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    "title": "Clinical Cases",
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    "text": "These are a list of all the conferences and talks that I have given during clinical training, ranging from residency, fellowship, and in practice. Most of these are focused on clinical cases, which have all been de-identified."
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    "title": "Clinical Cases",
    "section": "Cardiology Fellowship",
    "text": "Cardiology Fellowship\n\nJanuary 24, 2023 Brief cardiac catheterization case conference on complex/staged PCI.\nDecember 07-08, 2022 A lecture series on AVNRT, including an introduction, an overview of typical AVNRT, These include surface ECG, EGM, and pacing maneuvers.\nMay 24, 2022 Brief cardiac catheterization case conference discussion of a triple-vessel disease patient with UGIB that was surgically turned down for bypass, pending surgery for infection.\nFebruary 16, 2022 Pulmonary Embolism Response Team introduction and overview at the Jesse Brown VA system for the internal medicine residency.\nFebruary 08, 2022 Pulmonary Embolism Response Team introduction and overview at the Jesse Brown VA system for both medicine residents and cardiology fellows.\nDecember 07, 2021 Short cardiac catheterization case conference on a NSTEMI that may benefit from CABG, a ICM that may benefit from protected PCI, and a complex, heavily calcific peripheral case.\nNovember 30, 2021 Illinois Medical District Cath Conference presentation on Wellen’s Syndrome in a LAD STEMI patient.\nNovember 23, 2021 Short cardiac catheterization case conference on a late-presenting STEMI at the time of a massive CVA, and a standard peripheral intervention to the left iliac arteries.\nNovember 16, 2021 Short cardiac catheterization case conference with a two-vessel CAD pre-transplant that was revascularized, and two STEMI cases.\nNovember 16, 2021 An introduction to antiplatelet agents in atherosclerotic disease.\nNovember 09, 2021 Short cardiac catheterization case conference with an anterior STEMI and no-reflow to LAD.\nOctober 18, 2021 A mortality and morbidity conference on rheumatic heart disease and mitral stenosis, deferring percutaneous balloon mitral valvuloplasty for surgical mechanical mitral valve replacement.\nOctober 12, 2021 Short cardiac catheterization case conference, with RCA Shockwave, interesting coronary anatomy, and a case of false-positive stress testing with anginal symptoms.\nOctober 05, 2021 Short cardiac catheterization case conference, with LM bifurcation disease using DK crush, a LAD orbital atherectomy case, and a high right radial with severe spasm.\nSeptember 28, 2021 Short cardiac catheterization case conference, with a focus on severe disease\nSeptember 28, 2021 An introduction to femoral access for new cardiology fellows.\nSeptember 09, 2021 Short cardiac catheterization case conference, with a focus on CABG revascularization\nJune 01, 2021 Cardiac catheterization lab conference, with a few STEMIs from call.\nMarch 16, 2021 Cardiac catheterization lab conference, with a focus of three PCI cases.\nFebruary 01, 2021 A journal club on GALACTIC-HF\nDecember 23, 2020 A brief overview of cardiac tamponade for the POCUS curriculum for internal medicine residents.\nDecember 14, 2020 An interesting case of restrictive cardiomyopathy, including workup and consideration of alternative etiologies."
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    "title": "Clinical Cases",
    "section": "Internal Medicine Residency",
    "text": "Internal Medicine Residency\n\nFebruary 18, 2019 As a medical resident, we complete a senior grand rounds, a summative talk of an area of our choosing. I researched psychological triggers for sudden cardiac death, and gave a “chalk talk” style presentation. There was an associated handout and notes with references. The concept of psychological triggers as affecting the ventricular substrate is fascinating, particularly as we learn more of the role of the autonomic nervous system in cardiovascular disease.\nSeptember 26, 2018 Another bite-sized teaching mode talk on transfusions in sickle cell. Gave this talk again on October 4, 2018 at the Southern Hospital Medicine conference as an example of alternative teaching methods.\nMarch 21, 2018 With literature from early-terminated trials during 2018, I gave a journal club lecture on the updated guidelines on thrombectomy for ischemic strokes. My notes for it serve as a reference and series of citations, with a handout to improve viewer interaction. The largest issue I find was in the interpretation of their Table 1 showing non-adjusted odds ratios for an ordinal scale, listed next to a P-value.\nMarch 15, 2018 As a resident, there is a shift into becoming a teacher to both medical students and near-peers while being a learner as well. A significant amount of residents actually develop critical failures in the learning process. Here is an approach I presented, with supporting literature and an outline to be shared.\nFebruary 28, 2018 I gave a bite-sized teaching mode talk on treating rashes. The purpose of this style of talk is to explain and actually teach a topic in less than 8 minutes. Giving the talk itself emphasized learning how to teach."
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    "text": "As part of clinical training (internal medicine residency, cardiovascular disease fellowship, clinical cardiac electrophysiology fellowship), clinical and procedural volume are important in the development of skills/competence. The following is a summary of volume received during training thus far:\n\n\n\n\n\n\n\n\nProcedure Log\n\n\n\nTotal\nNotes\n\n\n\n\nMagnetic Resonance Imaging\n\n\nCardiac MRI (performed)\n18\n—\n\n\nCardiac MRI (interpreted)\n38\n—\n\n\nNuclear Imaging\n\n\nStress myocardial perfusion imaging\n361\nThallium, technetium, ammonium (SPECT/PET)\n\n\nElectrophysiology\n\n\nCardioversion or defibrillation\n63\n—\n\n\nTransvenous pacemaker insertion\n12\n—\n\n\nDevice interrogation\n126\n—\n\n\nImplantable loop recorders\n52\n—\n\n\nPermanent pacemaker insertion\n55\n—\n\n\nCardiac Catheterization\n\n\nDiagnostic left heart catheterization\n362\nCoronary angiography, aortic valve studies\n\n\nRight heart catheterization\n68\n—\n\n\nAdvanced catheterization procedures\n81\nPCI, MCS, pericardiocentesis, IVUS, OCT\n\n\nEchocardiography\n\n\nTransthoracic echocardiography (performed)\n200\n—\n\n\nTransthoracic echocardiography (interpreted)\n900\n—\n\n\nTransesophageal echocardiography\n160\n—\n\n\nStress echocardiography\n135\nDobutamine and treadmill"
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    "title": "AVNRT: Part 1",
    "section": "Epidemiology",
    "text": "Epidemiology\nApproximately 50% of SVT cases in adults are from an AVNRT mechanism (Issa, Miller, and Zipes 2018)"
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    "title": "AVNRT Mechanisms",
    "section": "Objectives",
    "text": "Objectives"
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    "title": "AVNRT: Part 1",
    "section": "Objectives",
    "text": "Objectives"
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    "title": "AVNRT: Part 1",
    "section": "Definition",
    "text": "Definition"
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    "title": "AVNRT: Part 1",
    "section": "Nodal Pathways",
    "text": "Nodal Pathways"
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    "title": "AVNRT: Part 1",
    "section": "Cellular Level",
    "text": "Cellular Level"
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    "title": "AVNRT: Part 1",
    "section": "Initiation",
    "text": "Initiation"
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    "title": "AVNRT: Part 1",
    "section": "Maintenance",
    "text": "Maintenance"
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    "title": "Typical AVNRT",
    "section": "Objectives",
    "text": "Objectives\n\nUnderstand the relevant anatomy and physiology that allow for AVNRT\nKnow how to diagnose typical AVNRT from …\n\nClinical history\nSurface ECG\nIntracardiac electrograms\n\nUnderstand the underlying mechanisms behind treatment strategies"
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    "title": "Typical AVNRT",
    "section": "Definition",
    "text": "Definition\n\nSVT implies involvement of ≥ 1 structure above bifurcation of the His bundle (HB).\nAVNRT is usually a narrow-complex tachycardia that uses the AV node, and functional/anatomical pathways (slow/fast)\n\n\nRemains unclear if there are anatomical correlates with the regions of slow versus fast conduction."
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    "title": "Typical AVNRT",
    "section": "Incidence",
    "text": "Incidence\nApproximately 50% of SVT cases in adults are from an AVNRT mechanism (Issa, Miller, and Zipes 2018)"
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    "title": "Typical AVNRT",
    "section": "Definitions",
    "text": "Definitions\nAbbreviation | Definition |\nHB | His bundle |\nSAN | sinoatrial node |\nAV | atrioventricular |\nAVN | AV node |\nCS | coronary sinus |\nST | sinus tachycardia |\nSVT | supraventricular tachycardia |\nAVNRT | AVN reentrant tachycardia |\nAVRT | AV reentrant tachycardia |\nAT | atrial tachycardia |"
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    "title": "Typical AVNRT",
    "section": "Overview",
    "text": "Overview\n\nAVNRT is typically a narrow-complex tachycardia\n\n\n\n\nSVT implies involvement of ≥ 1 structure above the bifurcation of the His bundle (HB)."
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    "title": "Typical AVNRT",
    "section": "Abbreviations",
    "text": "Abbreviations\n\n\n\nAbbr.\nAbbreviation\n\n\n\n\nHB\nHis bundle\n\n\nSAN\nsinoatrial node\n\n\nAV\natrioventricular\n\n\nCS\ncoronary sinus\n\n\nSVT\nsupraventricular tachycardia\n\n\nST\nsinus tachycardia\n\n\nAVNRT\nAV nodal reentrant tachycardia\n\n\nAVRT\nAV reentrant tachycardia\n\n\nAT\natrial tachycardia"
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    "title": "Typical AVNRT",
    "section": "What’s the rhythm? {background-image=“svt-example.png”]}",
    "text": "What’s the rhythm? {background-image=“svt-example.png”]}"
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    "section": "{background-image=“svt-example.png”]}",
    "text": "{background-image=“svt-example.png”]}\nWhat’s the rhythm?"
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    "title": "Typical AVNRT",
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    "text": "{background-image=“./svt-example.png”]}\nWhat’s the rhythm?"
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    "title": "Typical AVNRT",
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    "text": "Abbr.\nAbbreviation\n\n\n\n\nAAD\nantiarrhythmia drugs\n\n\nAH\natrial-His\n\n\nAP\naccessory pathway\n\n\nAVNRT\nAV nodal reentrant tachycardia\n\n\nd/pCS\ndistal/proximal coronary sinus\n\n\nDAD\ndelayed after-depolarization\n\n\nEAD\nearly after-depolarization\n\n\nHPS\nHis-Purkinje system\n\n\nHB\nHis bundle\n\n\nHA\nHis-atrial interval\n\n\nHV\nHis-ventricular interval\n\n\nST\nsinus tachycardia\n\n\nSVT\nsupraventricular tachycardia\n\n\nTCL\ntachycardia cycle length"
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    "section": "{background-image=“svt-example.png”, background-size=“contain”}",
    "text": "{background-image=“svt-example.png”, background-size=“contain”}\n\nWhat’s the rhythm?"
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    "title": "Typical AVNRT",
    "section": "Does the history and physical matter?",
    "text": "Does the history and physical matter?\n\nDizziness and hypotension occur more commonly in short RP tachycardias\nPolyuria/diuresis during tachycardia or at termination due to increased ANP secretion [Abe1997b]\nNeck pounding manifests with continuous pulsing cannon A waves, as the RA contracts against a closed tricuspid valve, described as the frog sign (5)\n\nDoes not occur in orthodromic AVRT, as longer VA interval separates the chamber contractions\n7-fold increase in AVNRT over other SVT with this symptom"
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    "title": "Typical AVNRT",
    "section": "A differential for a regular SVT?",
    "text": "A differential for a regular SVT?\n\n\nNarrow QRS\n\nAVNRT\nAT\nOrthodromic AVRT due to an accessory pathway\nAFL with fixed AV conduction\nSANRT\nHigh septal VT\nST\n\n\nWide QRS\n\nAVNRT or AT with aberrancy\nAVNRT with a bystander accessory pathway\nAntidromic AVRT due to an accessory pathway\nSVT with wider QRS due to electrolyte/AAD therapies"
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    "title": "Typical AVNRT",
    "section": "Does the physical matter?",
    "text": "Does the physical matter?\n\nDizziness and hypotension occur more commonly in short RP tachycardias\nNeck pounding manifests with continuous pulsing cannon A waves, as the RA contracts against a closed tricuspid valve, described as the frog sign (5)\n\nDoes not occur in orthodromic AVRT, as longer VA interval separates the chamber contractions\n7-fold increase in AVNRT over other SVT with this symptom"
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    "title": "Typical AVNRT",
    "section": "Does the history matter?",
    "text": "Does the history matter?\n\nSudden onset and termination (often positional) more often re-entrant\nAbortive measures such as drinking iced water\nDizziness and hypotension occur more commonly in short RP tachycardias\nPolyuria/diuresis during tachycardia or at termination due to increased ANP secretion (5)"
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    "title": "Typical AVNRT",
    "section": "Does the exam matter?",
    "text": "Does the exam matter?\n\nNeck pounding manifests with continuous pulsing cannon A waves, as the RA contracts against a closed tricuspid valve, described as the frog sign (6)\n\nDoes not occur in orthodromic AVRT, as longer VA interval separates the chamber contractions\n7-fold increase in AVNRT over other SVT with this symptom"
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    "title": "Typical AVNRT",
    "section": "Outline",
    "text": "Outline\n\nIntroduction to AVNRT\nNon-invasive diagnosis\nNon-invasive treatment approach\nRelevant anatomy and physiology\nElectrograms"
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    "title": "Typical AVNRT",
    "section": "Guidelines",
    "text": "Guidelines\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n2019 ESC SVT Guidelines (7)"
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    "section": "Vagal Maneuvers",
    "text": "Vagal Maneuvers"
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    "title": "Typical AVNRT",
    "section": "Adenosine",
    "text": "Adenosine\n90% success rate:\n\n6 mg bolus\n12 mg bolus\n18 mg bolus\n\nAdenosine works on Y2a receptor by increasing XXX\n\n\nCan repeat doses after 1 minute, as end-organ effects are complete within 30 seconds."
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    "text": "What’s the rhythm?"
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    "text": "1. Kwaku KF, Josephson ME. Typical AVNRT - An update on mechanisms and therapy. 2002;6:414–421. Available at: https://link.springer.com/article/10.1023/A:1021140509804.\n\n\n2. Issa ZF, Miller JM, Zipes DP. Clinical arrhythmology and electrophysiology: A companion to braunwald’s heart disease. Elsevier; 2018:1–752. Available at: https://linkinghub.elsevier.com/retrieve/pii/C20140032935.\n\n\n3. Goyal R, Zivin A, Souza J, et al. Comparison of the ages of tachycardia onset in patients with atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia. American Heart Journal 1996;132:765–767. Available at: https://pubmed.ncbi.nlm.nih.gov/8831363/.\n\n\n4. Porter MJ, Morton JB, Denman R, et al. Influence of age and gender on the mechanism of supraventricular tachycardia. Heart Rhythm 2004;1:393–396.\n\n\n5. Abe H, Nagatomo T, Kobayashi H, Miura Y, Masaru Araki AK, Nakashima Y. Neurohumoral and hemodynamic mechanisms of diuresis during atrioventricular nodal reentrant tachycardia. PACE - Pacing and Clinical Electrophysiology 1997;20:2783–2788. Available at: https://pubmed.ncbi.nlm.nih.gov/9392809/.\n\n\n6. Sakhuja R, Smith LM, Tseng ZH, et al. Test characteristics of neck fullness and witnessed neck pulsations in the diagnosis of typical AV nodal reentrant tachycardia. Clinical Cardiology 2009;32:E13. Available at: /pmc/articles/mid/NIHMS319317/ /pmc/articles/mid/NIHMS319317/?report=abstract https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3200305/.\n\n\n7. Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for themanagement of patients with supraventricular tachycardia. European Heart Journal 2020;41:655–720. Available at: www.escardio.org/guidelines."
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    "text": "1. Kwaku KF, Josephson ME. Typical AVNRT - An update on mechanisms and therapy. 2002;6:414–421. Available at: https://link.springer.com/article/10.1023/A:1021140509804.\n\n\n2. Issa ZF, Miller JM, Zipes DP. Clinical arrhythmology and electrophysiology: A companion to braunwald’s heart disease. Elsevier; 2018:1–752. Available at: https://linkinghub.elsevier.com/retrieve/pii/C20140032935.\n\n\n3. Goyal R, Zivin A, Souza J, et al. Comparison of the ages of tachycardia onset in patients with atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia. American Heart Journal 1996;132:765–767. Available at: https://pubmed.ncbi.nlm.nih.gov/8831363/.\n\n\n4. Porter MJ, Morton JB, Denman R, et al. Influence of age and gender on the mechanism of supraventricular tachycardia. Heart Rhythm 2004;1:393–396.\n\n\n5. Abe H, Nagatomo T, Kobayashi H, Miura Y, Masaru Araki AK, Nakashima Y. Neurohumoral and hemodynamic mechanisms of diuresis during atrioventricular nodal reentrant tachycardia. PACE - Pacing and Clinical Electrophysiology 1997;20:2783–2788. Available at: https://pubmed.ncbi.nlm.nih.gov/9392809/.\n\n\n6. Sakhuja R, Smith LM, Tseng ZH, et al. Test characteristics of neck fullness and witnessed neck pulsations in the diagnosis of typical AV nodal reentrant tachycardia. Clinical Cardiology 2009;32:E13. Available at: /pmc/articles/mid/NIHMS319317/ /pmc/articles/mid/NIHMS319317/?report=abstract https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3200305/.\n\n\n7. Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for themanagement of patients with supraventricular tachycardia. European Heart Journal 2020;41:655–720. Available at: www.escardio.org/guidelines."
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    "text": "1. Kwaku KF, Josephson ME. Typical AVNRT - An update on mechanisms and therapy. 2002;6:414–421. Available at: https://link.springer.com/article/10.1023/A:1021140509804.\n\n\n2. Issa ZF, Miller JM, Zipes DP. Clinical arrhythmology and electrophysiology: A companion to braunwald’s heart disease. Elsevier; 2018:1–752. Available at: https://linkinghub.elsevier.com/retrieve/pii/C20140032935.\n\n\n3. Goyal R, Zivin A, Souza J, et al. Comparison of the ages of tachycardia onset in patients with atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia. American Heart Journal 1996;132:765–767. Available at: https://pubmed.ncbi.nlm.nih.gov/8831363/.\n\n\n4. Porter MJ, Morton JB, Denman R, et al. Influence of age and gender on the mechanism of supraventricular tachycardia. Heart Rhythm 2004;1:393–396.\n\n\n5. Abe H, Nagatomo T, Kobayashi H, Miura Y, Masaru Araki AK, Nakashima Y. Neurohumoral and hemodynamic mechanisms of diuresis during atrioventricular nodal reentrant tachycardia. PACE - Pacing and Clinical Electrophysiology 1997;20:2783–2788. Available at: https://pubmed.ncbi.nlm.nih.gov/9392809/.\n\n\n6. Sakhuja R, Smith LM, Tseng ZH, et al. Test characteristics of neck fullness and witnessed neck pulsations in the diagnosis of typical AV nodal reentrant tachycardia. Clinical Cardiology 2009;32:E13. Available at: /pmc/articles/mid/NIHMS319317/ /pmc/articles/mid/NIHMS319317/?report=abstract https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3200305/.\n\n\n7. Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for themanagement of patients with supraventricular tachycardia. European Heart Journal 2020;41:655–720. Available at: www.escardio.org/guidelines."
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    "text": "Differential\n\nAtypical AVNRT\nNon-reentrant junctional tachycardia (junctional ectopic tachycardia)\nNon-paroyxsmal junctional tachycardia (d/t digitalis-induced DADs)\nDual AV nodal tachycardia (repetitive retrograde concealment or “linking” phenomenon)"
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    "text": "Objectives\n\nUnderstand the relevant anatomy and physiology that allow for AVNRT\nKnow how to diagnose typical AVNRT from …\n\nClinical history\nSurface ECG\nIntracardiac electrograms\n\nUnderstand the underlying mechanisms behind treatment strategies"
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    "text": "Abbr.\nAbbreviation\n\n\n\n\nAAD\nantiarrhythmia drugs\n\n\nAH\natrial-His\n\n\nAP\naccessory pathway\n\n\nAVNRT\nAV nodal reentrant tachycardia\n\n\nCS\ncoronary sinus\n\n\nHPS\nHis-Purkinje system\n\n\nHB\nHis bundle\n\n\nHA\nHis-atrial interval\n\n\nHV\nHis-ventricular interval\n\n\nST\nsinus tachycardia\n\n\nSVT\nsupraventricular tachycardia\n\n\nTCL\ntachycardia cycle length"
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    "text": "Definition\n\nSVT implies involvement of ≥ 1 structure above bifurcation of the His bundle (HB).\nAVNRT is usually a narrow-complex tachycardia that uses the AV node, and functional/anatomical pathways (slow/fast)\n\n\nRemains unclear if there are anatomical correlates with the regions of slow versus fast conduction."
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    "text": "What’s the rhythm?"
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    "section": "A differential for a regular SVT?",
    "text": "A differential for a regular SVT?\n\n\nNarrow QRS\n\nAVNRT\nAT\nOrthodromic AVRT due to an accessory pathway\nAFL with fixed AV conduction\nSANRT\nHigh septal VT\nST\n\n\nWide QRS\n\nAVNRT or AT with aberrancy\nAVNRT with a bystander accessory pathway\nAntidromic AVRT due to an accessory pathway\nSVT with wider QRS due to electrolyte/AAD therapies"
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    "section": "Does the history matter?",
    "text": "Does the history matter?\n\nSudden onset and termination (often positional) more often re-entrant\nAbortive measures such as drinking iced water\nDizziness and hypotension occur more commonly in short RP tachycardias\nPolyuria/diuresis during tachycardia or at termination due to increased ANP secretion (5)\n\n\nWhat next?\n\n\nPhysical exam?\n\n\n\n24-48 hour Holter?\n2-4 weeks of cardiac event monitoring?\nExercise testing?\nEchocardiogram?\nEP testing?\n\n\n\nVideo\n\n\nhttps://youtu.be/csVn_kvdeBM"
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    "section": "Does the exam matter?",
    "text": "Does the exam matter?\n\nNeck pounding manifests with continuous pulsing cannon A waves, as the RA contracts against a closed tricuspid valve, described as the frog sign (6)\n\nDoes not occur in orthodromic AVRT, as longer VA interval separates the chamber contractions\n7-fold increase in AVNRT over other SVT with this symptom"
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    "section": "Guidelines",
    "text": "Guidelines\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n2019 ESC SVT Guidelines (7)"
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    "section": "Vagal Maneuvers",
    "text": "Vagal Maneuvers\n\n\nValsalva maneuver\n\nAlso called Flack’s test, where intrapleural pressure is raised to 40 mm Hg (expiration against closed airway)\nBradycardia effect seen within first 10-15 seconds\n\n\n\n\n\n\n\n\n\n\n\nCarotid sinus massage\n\nHolding constant pressure (not a “massage”) for 5-10 seconds\nIncreases pressure in carotid body, firing baroreceptors\nSNS afferent response leads to PNS efferents via vagus (right = SA, left = AV)\nResponses…\n\ncardioinhibitory with ≥ 3s pause\nvasodepressor is drop of ≥ 50 mm Hg in pressure\nmixed\n\n\n\n\n\nAdenosine\n\n\n\nan endogenous purine nuceloside, binding to cardiac adenosine A1 receptors\ndose-related prolongation of AV conduction at AH interval\n\n\n90% success rate:\n\n6 mg bolus\n12 mg bolus\n18 mg bolus\n\nRepeat dosing after 1 minute (30 seconds for complete effect). Better efficacy with “single syringe strategy” (8)"
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    "text": "1. Kwaku KF, Josephson ME. Typical AVNRT - An update on mechanisms and therapy. 2002;6:414–421. Available at: https://link.springer.com/article/10.1023/A:1021140509804.\n\n\n2. Issa ZF, Miller JM, Zipes DP. Clinical arrhythmology and electrophysiology: A companion to braunwald’s heart disease. Elsevier; 2018:1–752. Available at: https://linkinghub.elsevier.com/retrieve/pii/C20140032935.\n\n\n3. Goyal R, Zivin A, Souza J, et al. Comparison of the ages of tachycardia onset in patients with atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia. American Heart Journal 1996;132:765–767. Available at: https://pubmed.ncbi.nlm.nih.gov/8831363/.\n\n\n4. Porter MJ, Morton JB, Denman R, et al. Influence of age and gender on the mechanism of supraventricular tachycardia. Heart Rhythm 2004;1:393–396.\n\n\n5. Abe H, Nagatomo T, Kobayashi H, Miura Y, Masaru Araki AK, Nakashima Y. Neurohumoral and hemodynamic mechanisms of diuresis during atrioventricular nodal reentrant tachycardia. PACE - Pacing and Clinical Electrophysiology 1997;20:2783–2788. Available at: https://pubmed.ncbi.nlm.nih.gov/9392809/.\n\n\n6. Sakhuja R, Smith LM, Tseng ZH, et al. Test characteristics of neck fullness and witnessed neck pulsations in the diagnosis of typical AV nodal reentrant tachycardia. Clinical Cardiology 2009;32:E13. Available at: /pmc/articles/mid/NIHMS319317/ /pmc/articles/mid/NIHMS319317/?report=abstract https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3200305/.\n\n\n7. Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for themanagement of patients with supraventricular tachycardia. European Heart Journal 2020;41:655–720. Available at: www.escardio.org/guidelines."
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    "text": "Differential\n\nAtypical AVNRT\nNon-reentrant junctional tachycardia (junctional ectopic tachycardia)\nNon-paroyxsmal junctional tachycardia (d/t digitalis-induced DADs)\nDual AV nodal tachycardia (repetitive retrograde concealment or “linking” phenomenon)"
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    "text": "Evaluation\n\nMode of initiation of tachycardia\nAtrial activation sequence during tachycardia\nInfluence of bundle branch block on conduction and cycle length during tachycardia\nRequirement of atria/ventricle for initiation and maintenance of tachcyardia\nEffect of atrial/ventricular stiulation during tachycardia\nEffect of drugs or physiological maneuvers on tachycardia"
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    "text": "Requirements\nTo initiate and maintain a re-entrant rhythm:\n\n≥ 2 functionally/anatomically distinct pathways that join proximally and distally to form a closed circuit of conduction\nunidirectional block in one of those potential pathways\nslow conduction down the unblocked pathway, allowing the previous pathway to recover\n\nSina qua non of reentrant arrhythmia is the ability to reproducibly intiate the tachycardia by timed extrastimuli"
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    "text": "tach_start <- read_lspro(file.path(loc, \"tmf_data/lsp-tach-initiation.txt\"))\n\nggm(data = tach_start,\n        channels = c(\"I\", \"CS\", \"RV\", \"HIS d\", \"HIS m\")) |>\n    add_intervals(channel = \"I\")\n\n\n\n\nTachycardia initiation\n\n\n\n\n\n\nggm(data = tach_start,\n        channels = c(\"I\", \"CS\", \"RV\", \"HIS d\", \"HIS m\"),\n        time_frame = c(2.6, 2.9))\n\n\n\n\nA beat from the tachycardia\n\n\n\n\n\n\nggm(data = tach_start,\n        channels = c(\"I\", \"CS\", \"RV\", \"HIS d\", \"HIS m\"),\n        time_frame = c(0.6, 1.0))\n\n\n\n\nA beat from the sinus\n\n\n\n\n\n\nggm(data = tach_start,\n        channels = c(\"I\", \"CS\", \"RV\", \"HIS d\", \"HIS m\"),\n        time_frame = c(1.5, 3.0))\n\n\n\n\nAPD leads to tachycardia\n\n\n\n\n\n\navnrt <-\n    ra_grey +\n    geom_sf(data = pathways, fill = \"white\", color = NA_character_) +\n    geom_sf(\n        data = filter(pathways,\n                                    structure == \"slow\" & component == \"middle\"),\n        fill = orange[3]\n    ) +\n    geom_sf(\n        data = filter(\n            pathways,\n            (structure == \"slow\" & component == \"distal\") |\n                (structure == \"bridge\" & component == \"distal\")\n            ),\n        fill = orange[3]\n    ) +\n    geom_sf(\n        data = filter(pathways, structure == \"lower_common\"), \n        fill = orange[3]\n    ) +\n    geom_sf(\n        data = filter(pathways,\n                                    structure == \"fast\" & component == \"distal\"),\n        fill = red[2]\n    ) +\n    geom_sf(\n        data = filter(pathways,\n                                    structure == \"fast\" & component == \"middle\"),\n        fill = red[2]\n    ) +\n    geom_sf(\n        data = filter(\n            pathways,\n            (structure == \"fast\" & component == \"proximal\") |\n                (structure == \"bridge\" & component == \"proximal\")\n            ),\n        fill = red[2]\n    ) +\n    geom_sf(\n        data = filter(\n            pathways,\n            (structure == \"upper_common\" & component == \"distal\") |\n                (structure == \"upper_common\" & component == \"upper_fast\")\n            ),\n        fill = red[2]\n    ) +\n    geom_sf(\n        data = filter(pathways,\n                                    structure == \"upper_common\" & component == \"upper_slow\"),\n        fill = orange[2]\n    ) +\n    geom_sf(\n        data = filter(\n            pathways, \n            (structure == \"atrial_extension\") |\n                (structure == \"slow\" & component == \"proximal\")\n        ),\n        fill = c(red[2], orange[3], rep(red[2], 4))\n    ) \n\navnrt +\n    transition_layers(\n        keep_layers = c(Inf, Inf, rep(1, 9)),\n        layer_length = 1,\n        from_blank = FALSE\n    ) +\n    enter_fade() +\n    exit_fade(alpha = 0)\n\n\n\n\n\n\ndecremental_800 <-\n    read_lspro(file.path(loc, \"tmf_data/lsp-cs-pacing-800.txt\")) \n\nggm(decremental_800, channels = c(\"I\", \"CS\", \"HIS\")) |>\n    add_intervals(channel = \"CS 9-10\")\n\n\n\n\nDecremental pacing at 800 ms\n\n\n\n\n\n\ndecremental_400 <-\n    read_lspro(file.path(loc, \"tmf_data/lsp-cs-pace-decremental-400ms-jump.txt\"))\n\nggm(decremental_400, channels = c(\"I\", \"CS\", \"HIS\")) |>\n    add_intervals(channel = \"CS 9-10\")\n\n\n\n\nDecremental pacing at 400 ms"
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    "text": "Objectives\n\nUnderstand the concepts of dual node physiology\nKnow the requirements for typical AVNRT\nEvaluate the response of standard EP maneuvers in typical AVNRT"
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    "text": "Abbr.\nAbbreviation\n\n\n\n\nDAD\ndelayed after-depolarization\n\n\nEAD\nearly after-depolarization\n\n\nAPD\natrial premature depolarization\n\n\nVPD\nventricular premature depolarization\n\n\nRAAS\nretrograde atrial activation sequence"
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    "text": "Criteria\n\nInitiation and termination by APD/VPD during AV nodal Wenckebach cycles\nDual AV nodal physiology (differential refractory curves during APD)\nInitiation dependent on critical AH interval during slow pathway conduction\nRetrograde atrial activation with variable VA activation in Triangle of Koch\nInitiated, terminated, or reset without atrial activation\n\n\n\nSlow-fast AVNRT has atrial activation close to QRS complex, such that AH/HA > 1"
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    "text": "Differential…\n\nTypical AVNRT\nOrthodromic AVRT\nAtypical AVNRT\nAtrial tachycardia always a possibility\nNon-reentrant junctional tachycardia (junctional ectopic tachycardia)\nNon-paroyxsmal junctional tachycardia (d/t digitalis-induced DADs)\nDual AV nodal tachycardia (repetitive retrograde concealment or “linking” phenomenon)"
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    "text": "SVT features prior to diagnostic pacing maneuvers\nFor typical AVNRT, there are some findings to help eliminate options.\n\nVA Relationship: any pattern, but most commonly V=A and V<A\nVA Interval: VA ≤ 70\nAtrial Activation Sequence: concentric\nSpontaneous Termination: end either in A or V response\nVA Increase with BBB: no"
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    "text": "1. Kwaku KF, Josephson ME. Typical AVNRT - An update on mechanisms and therapy. 2002;6:414–421. Available at: https://link.springer.com/article/10.1023/A:1021140509804.\n\n\n2. Issa ZF, Miller JM, Zipes DP. Clinical arrhythmology and electrophysiology: A companion to braunwald’s heart disease. Elsevier; 2018:1–752. Available at: https://linkinghub.elsevier.com/retrieve/pii/C20140032935.\n\n\n3. Goyal R, Zivin A, Souza J, et al. Comparison of the ages of tachycardia onset in patients with atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia. American Heart Journal 1996;132:765–767. Available at: https://pubmed.ncbi.nlm.nih.gov/8831363/.\n\n\n4. Porter MJ, Morton JB, Denman R, et al. Influence of age and gender on the mechanism of supraventricular tachycardia. Heart Rhythm 2004;1:393–396.\n\n\n5. Abe H, Nagatomo T, Kobayashi H, Miura Y, Masaru Araki AK, Nakashima Y. Neurohumoral and hemodynamic mechanisms of diuresis during atrioventricular nodal reentrant tachycardia. PACE - Pacing and Clinical Electrophysiology 1997;20:2783–2788. Available at: https://pubmed.ncbi.nlm.nih.gov/9392809/.\n\n\n6. Sakhuja R, Smith LM, Tseng ZH, et al. Test characteristics of neck fullness and witnessed neck pulsations in the diagnosis of typical AV nodal reentrant tachycardia. Clinical Cardiology 2009;32:E13. Available at: /pmc/articles/mid/NIHMS319317/ /pmc/articles/mid/NIHMS319317/?report=abstract https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3200305/.\n\n\n7. Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for themanagement of patients with supraventricular tachycardia. European Heart Journal 2020;41:655–720. Available at: www.escardio.org/guidelines.\n\n\n8. Kotruchin P, Chaiyakhan I on, Kamonsri P, et al. Comparison between the double-syringe and the single-syringe techniques of adenosine administration for terminating supraventricular tachycardia: A pilot, randomized controlled trial. Clinical Cardiology 2022;45:583–589."
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    "text": "Criteria for typical AVNRT\n\nInitiation and termination by APD/VPD during AV nodal Wenckebach cycles\nDual AV nodal physiology (differential refractory curves during APD)\nInitiation dependent on critical AH interval during slow pathway conduction\nRetrograde atrial activation with variable VA activation in Triangle of Koch\nInitiated, terminated, or reset without atrial activation\n\n\n\nSlow-fast AVNRT has atrial activation close to QRS complex, such that AH/HA > 1"
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    "text": "Case setup\n\n\nAccess: RCFV x 3\nCatheters:\n\nCS: decapolar catheter\nHis: quadrapolar catheter\nRV: quadrapolar catheter\nAblation: STSF 4 mm\n\nClosure: collagen-plug x 3\n\nStudy plan:\n\nBaseline EP study\nRA and RV pacing maneuvers (including decremental pacing)\nHis-refractory PVC\nInduction of tachycardia\nEntrainment\n3D anatomical mapping (CART) with His cloud\nAblation\nPost-ablation testing"
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    "text": "Sinus Rhythm\n\nNormal P and R axis\nRR = 900\nPP = 900\nQRS = 80\nP = 120\nPR = 160\nQT = 440\n\n\nSVT\n\nSuspected retro-grade P\nRR = 350\nQRS = 70\nPR = 300\n\n\n\nRP = 40"
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    "text": "ra_colors <-\n    ra_grey +\n    geom_sf(data = chambers, fill = red[5], alpha = 0.1) +\n    geom_sf(data = septum, fill = red[5], alpha = 0.1) +\n    geom_sf(data = vessels, fill = blue[5], alpha = 0.1) +\n    geom_sf(data = projections, fill = red[2], alpha = 0.1) +\n    geom_sf(data = valves, fill = grey[9], alpha = 0.1) +\n    geom_sf(data = conduction, fill = orange[1], alpha = 0.3) \n\nra_colors\n\n\n\n\n\n\nra_colors + \n    geom_sf(data = pathways, fill = \"white\", color = NA, alpha = 0.8) +\n    geom_sf_label(data = filter(pathways, type == \"pathway\"), aes(label = label), nudge_y = 1)\n\nWarning: Removed 12 rows containing missing values (`geom_label()`).\n\n\n\n\n\n\n\nnsr <-\n    ra_grey +\n    geom_sf(data = pathways, fill = \"white\", color = NA_character_) +\n    geom_sf(data = filter(pathways, structure == \"atrial_extension\"),\n                    fill = orange[3]) +\n    geom_sf(data = filter(pathways, structure == \"upper_common\"),\n                    fill = orange[3]) +\n    geom_sf(\n        data = filter(\n            pathways,\n            (structure == \"fast\" & component == \"proximal\") |\n                (structure == \"bridge\" & component == \"proximal\")\n            ),\n        fill = orange[3]\n    ) +\n    geom_sf(\n        data = filter(\n            pathways,\n            (structure == \"fast\" & component == \"middle\") |\n                (structure == \"slow\" & component == \"proximal\")\n            ),\n        fill = orange[3]\n    ) +\n    geom_sf(\n        data = filter(\n            pathways,\n            (structure == \"fast\" & component == \"distal\") |\n                (structure == \"bridge\" & component == \"distal\")\n            ),\n        fill = orange[3]\n    ) +\n    geom_sf(\n        data = filter(pathways, structure == \"lower_common\"),\n        fill = orange[3]\n    ) + \n    geom_sf(\n        data = filter(\n            pathways,\n            (structure == \"slow\" & component == \"distal\") |\n                (structure == \"slow\" & component == \"middle\")\n            ),\n        fill = c(red[2], orange[3])\n    ) \n\nnsr +\n    transition_layers(\n        keep_layers = c(Inf, Inf, rep(2, 7)),\n        layer_length = 1,\n        from_blank = FALSE\n    ) +\n    enter_fade() +\n    exit_fade(alpha = 0)\n\n\n\n\n\n\nnsr_egm <- read_lspro(file.path(loc, \"tmf_data/lsp-single-pvc.txt\"))\n\nggm(data = nsr_egm,\n        channels = c(\"I\", \"CS\", \"RV\", \"HIS D\", \"HIS M\", \"HIS P\"),\n        time_frame = c(0.25, 0.7)) \n\n\n\n\nNormal sinus beat on multiple electrodes"
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    "text": "I am developing a clinical volume dashboard for the work that I have done. This will include work from residency through fellowship(s)."
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    "text": "Overview\n\nThought to be more rare, but now diagnosed more commonly\nIncidence of 1:200 to 1:500\nRange of phenotypic presentations, 15 mm to ≥ 30 mm LV wall thickness\nClinical presentation along the spectrum of disease:\n\nstable/benign\nsudden death\nobstructive physiology + heart failure\natrial fibrillation + stroke\n\n\n\n\nMaron et al. JACC 2022"
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    "text": "Clinical evaluation\n\nDiscuss: disease and its treatment strategies - genetic conditions necessitate both clinical and psychosocial considerations\nHPI: focuses on syncope, prolonged palpitations, chest pain, family history of HCM or sudden death\nEstablish: LV morphology, stratify sudden death risk, classify if obstructive or not, family screening needs, and follow-up\nEvaluate: TTE, ECG (12-lead + ambulatory), CMR, ESE, genetic testing\nFollow-up: repeat imaging every 1-2 years (based on clinical setting)"
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    "text": "Diagnostic requirements\n\nLV wall thickness > 15 mm (13 to 14 mm with other risk features)\nUnassociated with other cardiometabolic or systemic disease\nSarcomere mutation or other genetic variant\n\n\n\nGersh, BJ, et al. JACC 2011"
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    "text": "Non-mandatory findings\n\nAsymmetrical septal hypertrophy\nSystolic anterior motion\nDynamic LVOT obstruction"
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    "section": "Where is the LVH?",
    "text": "Where is the LVH?\n\n\n\n\n\nFigure 2: Frequency of LVH location\n\n\n\n\n\n\nKlues HG, JACC 1995;"
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    "title": "Hypertrophic Cardiomyopathy",
    "section": "LVH variant morphology",
    "text": "LVH variant morphology\n\n\n\nFigure 3: Variant sub-type correlated with frequency of genetic mutations: sigmoid, reversse, neutral, apical (respectively)\n\n\n\n\nBinder J, et al. Mayo Clin Proc 2006"
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    "href": "chalk_talks/02-22-23_hcm-overview/hcm-overview.html#overview",
    "title": "Hypertrophic Cardiomyopathy",
    "section": "Overview",
    "text": "Overview\n\nThought to be more rare, but now diagnosed more commonly\nIncidence of 1:200 to 1:500\nRange of phenotypic presentations, 15 mm to ≥ 30 mm LV wall thickness\nClinical presentation along the spectrum of disease:\n\nstable/benign\nsudden death\nobstructive physiology + heart failure\natrial fibrillation + stroke\n\n\n\n\nMaron et al. 2022, JACC"
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    "href": "chalk_talks/02-22-23_hcm-overview/hcm-overview.html#clinical-evaluation",
    "title": "Hypertrophic Cardiomyopathy",
    "section": "Clinical evaluation",
    "text": "Clinical evaluation\n\nDiscuss: disease and its treatment strategies - genetic conditions necessitate both clinical and psychosocial considerations\nHPI: focuses on syncope, prolonged palpitations, chest pain, family history of HCM or sudden death\nEstablish: LV morphology, stratify sudden death risk, classify if obstructive or not, family screening needs, and follow-up\nEvaluate: TTE, ECG (12-lead + ambulatory), CMR, ESE, genetic testing\nFollow-up: repeat imaging every 1-2 years (based on clinical setting)"
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    "href": "chalk_talks/02-22-23_hcm-overview/hcm-overview.html#diagnostic-requirements",
    "title": "Hypertrophic Cardiomyopathy",
    "section": "Diagnostic requirements",
    "text": "Diagnostic requirements\n\nLV wall thickness > 15 mm (13 to 14 mm with other risk features)\nUnassociated with other cardiometabolic or systemic disease\nSarcomere mutation or other genetic variant\n\n\n\nGersh, BJ, et al. 2011, JACC"
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    "href": "chalk_talks/02-22-23_hcm-overview/hcm-overview.html#non-mandatory-findings",
    "title": "Hypertrophic Cardiomyopathy",
    "section": "Non-mandatory findings",
    "text": "Non-mandatory findings\n\nAsymmetrical septal hypertrophy\nSystolic anterior motion\nDynamic LVOT obstruction"
  },
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    "objectID": "chalk_talks/02-22-23_hcm-overview/hcm-overview.html#where-is-the-lvh",
    "href": "chalk_talks/02-22-23_hcm-overview/hcm-overview.html#where-is-the-lvh",
    "title": "Hypertrophic Cardiomyopathy",
    "section": "Where is the LVH?",
    "text": "Where is the LVH?\n\n\n\n\n\nFigure 3: Frequency of LVH location\n\n\n\n\n\n\nKlues HG, 1995, JACC"
  },
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    "href": "chalk_talks/02-22-23_hcm-overview/hcm-overview.html#lvh-variant-morphology",
    "title": "Hypertrophic Cardiomyopathy",
    "section": "LVH variant morphology",
    "text": "LVH variant morphology\n\n\n\nFigure 3: Variant sub-type correlated with frequency of genetic mutations: sigmoid, reversse, neutral, apical (respectively)\n\n\n\n\nBinder et al. Mayo Clin Proc 2006"
  },
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    "href": "chalk_talks/02-22-23_hcm-overview/hcm-overview.html#classify-lvh-morphology",
    "title": "Hypertrophic Cardiomyopathy",
    "section": "Classify LVH morphology",
    "text": "Classify LVH morphology\n\n\n\n\n\n\n\n(a) Sigmoid\n\n\n\n\n\n\n\n(b) Reverse\n\n\n\n\n\n\n\n(c) Apical\n\n\n\n\nFigure 4: Location of hypertrophy defines the morphology. No matter where, any region > 30 mm increases risk of SCD, as well as apical pouch.\n\n\n\n\nOmmen et al. 2016, JASE"
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    "href": "chalk_talks/02-22-23_hcm-overview/hcm-overview.html#sam",
    "title": "Hypertrophic Cardiomyopathy",
    "section": "SAM",
    "text": "SAM\n\n\n\nFigure 5: The Venturi effect. LV ejection → obstruction → MR.\n\n\n\n\nSilbinger 2016, JASE"
  },
  {
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    "href": "chalk_talks/02-22-23_hcm-overview/hcm-overview.html#lvh-associated-with-genetic-variants",
    "title": "Hypertrophic Cardiomyopathy",
    "section": "LVH associated with genetic variants",
    "text": "LVH associated with genetic variants\n\n\n\nFigure 2: Variant sub-type correlated with frequency of genetic mutations: sigmoid, reversse, neutral, apical (respectively)\n\n\n\n\nBinder et al. 2006, Mayo Clin Proc"
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    "title": "Hypertrophic Cardiomyopathy",
    "section": "Gradients",
    "text": "Gradients\nWe can compare LV systolic pressure with systemic systolic pressure to estimate obstructive gradients:\n\\[ LV\\ Systolic\\ Pressure = 4 \\times (MR\\ velocity)^{2} + LA\\ Pressure\\]\n\nPeak LVOT gradient of ≥ 50 mmHg at rest or with provocation or exercise indicates obstruction\nDifferentiate SAM-mediated LVOT obstruction from mid-ventricular obstruction (MVO; “dagger” shaped)\n\nMR signal is both higher and longer, thus may contaminate LVOT signal"
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    "title": "Hypertrophic Cardiomyopathy",
    "section": "Pre-operative strategies",
    "text": "Pre-operative strategies\nSurgical septal myectomy and alcohol septal ablation should have TEE support. Measure:\n\nIVS maximum thickness\nanterior leaflet length\napical extent of the septal “bulge”\ndistance between aortic annulus to mitral-septal continuity\n\nFollow-up TTE in 3-6 months."
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    "title": "Mortality and Morbidity",
    "section": "Outline",
    "text": "Outline\n\nOverview of M&M Conference\nObjectives\nCase Introduction\nPre-interventional Planning\nOperative Course\nPacemaker\nLeft Atrial Appendage\nAortic Valve\nDiscussion, Conclusion"
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    "title": "Mortality and Morbidity",
    "section": "Objectives",
    "text": "Objectives\n\nIdentify system-based issues in a complex case\nDescribe interdisciplinary challenges in cardiovascular care\nPropose potential system-based implementations to improve outcomes\nConsider changes in clinical knowledge and evidence that may impact medical decision-making\n“Be kind” ~ Professor Avital"
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    "title": "Mortality and Morbidity",
    "section": "Questions",
    "text": "Questions\n\nDid the surgeon know the patient was in AF?\nWas it paroxysmal or persistent?\nWas the patient ever in junctional escape? Or was this AF with SVR?\nWhy did the LAA not get closed?\nIs a TEE needed prior to MVR?\nWhat is the need for a pacemaker?"
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    "title": "Mortality and Morbidity",
    "section": "Problems",
    "text": "Problems\n\nPatient taking half dose of DOAC d/t bleeding concerns\nPatient prosthetic mismatch\nNo LAA ligation\nDescribed as paroxysmal AF\nIndication for pacemaker"
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    "title": "Mortality and Morbidity",
    "section": "Summary",
    "text": "Summary\n\nDay 0: SMVR/SAVR, ?CHB\nDay 1: Intermittent pacing needed\nDay 3: LA mass seen on TTE, concern for HIT/thrombycytopenia, and AoV PPM\nDay 4: TEE shows large, mobile LAA thrombus\nDay 5: SC-PPM placed\nDay 10: MV with thickening/vegetation + large pericardial effusion\nDay 17: Pericardial window made\nDay 21: Discharged home"
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    "title": "Mortality and Morbidity",
    "section": "Aortic valve evaluation 1",
    "text": "Aortic valve evaluation 1\n\nBi-ventricular pressure overload\nLow cardiac index at baseline\nLow-flow low gradient severe aortic valve stenosis with improvement following dobutamine infusion suggestive of moderate to severe aortic valve stenosis.\nNo angiographic evidence of obstructive coronary artery disease\n\nTimeline = 2 years, 4 months prior"
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#initial-structural-consultation",
    "title": "Mortality and Morbidity",
    "section": "Initial structural consultation",
    "text": "Initial structural consultation\nFindings:\n\nNYHA II\nAF on apixiban\nCVA\nESRD with transplant, baseline creatinine of 1.8\nModerate to severe AS\nCardiac cath with low-flow, low-gradient AS (mean of 23, AVA 0.86)\n\nRecommendations: 1\n\nGiven his thorough evaluation his aortic stenosis remains the most likely cause of his symptoms and I would favor proceeding with aortic valve replacement. Given his young age, surgical aortic valve replacement is probably favored. His STS PROM is 1.7%. If TAVR is chosen he will need a TAVR protocol CTA of chest, abdomen and pelvis. I will refer him to be evaluated by cardiac surgery and then we will have a heart team meeting and decide the best route to go. I discussed this with the patient and his wife and they expressed understanding.\n\nTimeline = 2 years, 4 months prior"
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    "title": "Mortality and Morbidity",
    "section": "Initial CTS consult",
    "text": "Initial CTS consult\nFindings: 1\n\nMr. Powell is a 56-year-old man who has history of hypertension, chronic renal failure status post kidney transplant in 2015 with reasonable function with a recent creatinine of 1.8. The patient has also history of atrial fibrillation on apixaban and since May he has been experiencing symptoms of shortness of breath on exertion.\n\n\nAtrial fibrillation on apxiban\nTTE: mild AS, moderate MR, valve area of 1.4 cm\nLHC: with valve area estimate at 0.8 cm\nTEE: unable to be found\n\nRecommendations:\n\nTEE to eval type of aortic valve anatomy, and etiology of mitral regurgitation\n\nTimeline = 2 years, 2 months prior"
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    "title": "Mortality and Morbidity",
    "section": "Follow-up with CTS",
    "text": "Follow-up with CTS\nGiven TTE/TEE, at this time pt does not meet hemodynamic criteria for surgical valve replacement either for aortic or mitral valve. Given pt only with mild symptoms of dyspnea on exertion; recommend follow conservatively at this point and repeat TTE in 6 months.\nTimeline = 2 years, 0 months prior"
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    "title": "Mortality and Morbidity",
    "section": "CT chest",
    "text": "CT chest\nHEART AND GREAT VESSELS: Cardiomegaly. There is trace pericardial effusion. There is conventional three-vessel anatomy of the aortic great vessels. Mild atherosclerotic calcification of the ascending aorta, aortic arch, descending thoracic aorta. Coronary atherosclerotic disease. There is dense circumferential atherosclerotic calcification of the aortic valve and leaflets as well as dense atherosclerotic calcification of the mitral valve (also appreciable on scout images). There is dense linear high attenuation material within the left brachiocephalic vein, likely representing chronic calcified thrombus. 4.2 cm ectasia of the ascending thoracic aorta."
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    "section": "Optimal outcome",
    "text": "Optimal outcome"
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    "title": "Mortality and Morbidity",
    "section": "Root cause analyses",
    "text": "Root cause analyses"
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#future-recommendations",
    "title": "Mortality and Morbidity",
    "section": "Future recommendations",
    "text": "Future recommendations\n\n\n\n\n\n\n1. George SA, Faye NR, Murillo-Berlioz A, Lee KB, Trachiotis GD, Efimov IR. At the atrioventricular crossroads: Dual pathway electrophysiology in the atrioventricular node and its underlying heterogeneities. Arrhythmia and Electrophysiology Review 2017;6:179–185. Available at: http://onlinelibrary.wiley.com/doi/10.1002/ar.20631/full."
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    "title": "Mortality and Morbidity",
    "section": "Aortic valve evaluation (2y, 4mo prior)",
    "text": "Aortic valve evaluation (2y, 4mo prior)"
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    "title": "Mortality and Morbidity",
    "section": "Initial structural consultation (2y, 4mo prior)",
    "text": "Initial structural consultation (2y, 4mo prior)\n\nGiven his thorough evaluation his aortic stenosis remains the most likely cause of his symptoms and I would favor proceeding with aortic valve replacement. Given his young age, surgical aortic valve replacement is probably favored. His STS PROM is 1.7%. If TAVR is chosen he will need a TAVR protocol CTA of chest, abdomen and pelvis. I will refer him to be evaluated by cardiac surgery and then we will have a heart team meeting and decide the best route to go. I discussed this with the patient and his wife and they expressed understanding."
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    "title": "Mortality and Morbidity",
    "section": "Initial CTS consult (2y, 2mo prior)",
    "text": "Initial CTS consult (2y, 2mo prior)\n\nNAME REDACTED 56-year-old man who has history of hypertension, chronic renal failure status post kidney transplant in 2015 with reasonable function with a recent creatinine of 1.8. The patient has also history of atrial fibrillation on apixaban and since May he has been experiencing symptoms of shortness of breath on exertion."
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    "title": "Mortality and Morbidity",
    "section": "CT chest (2y, 1 mo prior)",
    "text": "CT chest (2y, 1 mo prior)\n\nHEART AND GREAT VESSELS: Cardiomegaly. There is trace pericardial effusion. There is conventional three-vessel anatomy of the aortic great vessels. Mild atherosclerotic calcification of the ascending aorta, aortic arch, descending thoracic aorta. Coronary atherosclerotic disease. There is dense circumferential atherosclerotic calcification of the aortic valve and leaflets as well as dense atherosclerotic calcification of the mitral valve (also appreciable on scout images)."
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    "title": "Mortality and Morbidity",
    "section": "Follow-up with CTS (2y prior)",
    "text": "Follow-up with CTS (2y prior)\n\nGiven TTE/TEE, at this time pt does not meet hemodynamic criteria for surgical valve replacement either for aortic or mitral valve. Given pt only with mild symptoms of dyspnea on exertion; recommend follow conservatively at this point and repeat TTE in 6 months.\n\n\nPatient was “lost to follow-up” for almost 2 years"
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    "title": "Mortality and Morbidity",
    "section": "Follow-up with CTS (4mo prior)",
    "text": "Follow-up with CTS (4mo prior)\n\nIn light of the persistent and increasing symptoms of shortness of breath as well as symptoms of rapid heart rate with severe biatrial enlargement on echocardiography in the past as well as the significant murmur that I hear today on physical examination, I suspect that the amount of mitral regurgitation that this patient has is more than what is reported in the echocardiogram that was done 2 years ago. In light of the above, I would like to recommend that the patient would obtain a transesophageal echocardiogram and see his cardiologist, ~~ NAME REDACTED~~, so that we can assess his severity of his mitral regurgitation and aortic stenosis and regurgitation more thoroughly. If the patient had evidence of severe mitral regurgitation, then I would strongly recommend considering him for open-heart surgery and mitral valve repair or replacement, at the time of which we will address the aortic pathology as well."
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    "title": "Mortality and Morbidity",
    "section": "Follow-up with structural (3mo prior)",
    "text": "Follow-up with structural (3mo prior)\n\nTwo valve disease. Will obtain TEE to assess degree of mitral regurgitation. IF at least moderate would plan for surgical AVR and MVR. Will follow-up with Surgeon after TEE"
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    "title": "Mortality and Morbidity",
    "section": "01/31/23 TEE",
    "text": "01/31/23 TEE\n\nLeft atrial appendage has a thrombus. Large mobile thrombus on the interior of the left atrial appendage."
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    "title": "Mortality and Morbidity",
    "section": "01/04/23 RHC/LHC",
    "text": "01/04/23 RHC/LHC\nLeft Ventricle | LV systolic pressure is normal. LV end diastolic pressure is normal. |\nMitral Valve | The annulus is calcified. Severe mitral annular calcification |\nAortic Valve | There is mild aortic valve stenosis. The aortic valve is calcified. Mean gradient 4.7 mm2 |\n\n\n\n\n\n\n\n\n\n\n\nAortic Valve\nTime\nDate\nMean Gradient (mmHg)\nValve Area (cm2)\nValve Area Index (cm2/m2)\n\n\n\n\nAortic Valve Fick\n9:41 AM\n1/4/23\n22.43\n1.07\n0.53\n\n\nAortic Valve Thermo\n9:41 AM\n1/4/23\n22.43\n0.93\n0.46\n\n\n\nConclusion\n\nAngiographically normal coronary arteries\nNormal LVEDP and moderately elevated PCWP\nModerate-severe pulmonary hypertension\nNormal resting cardiac output\nSevere mitral annular calcification"
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    "title": "Mortality and Morbidity",
    "section": "Pre-operative visit with CTS (1mo prior)",
    "text": "Pre-operative visit with CTS (1mo prior)\nFindings:\n\nIn AFIB on xarelto, states he is not able to take his full rx dose since has episodes of bleeding when takes prescribed dose.\n\nRecommendations:\n\nDiscussed valve types including risks/benefits of both bioprosthetic and mechanical. Patient would like to move forward with bioprosthetic valve if possible. Discussed possibility of necessity of mechanical valve depending on intraoperative findings."
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    "title": "Mortality and Morbidity",
    "section": "Operation",
    "text": "Operation\n\n\nPREOPERATIVE DIAGNOSES:\n\nChronic renal failure, status post kidney transplant with some allograft dysfunction.\nSymptomatic severe aortic stenosis and severe mitral regurgitation in the setting of calcific rheumatic valvular disease.\nHypertension.\n\n\nOPERATIONS:\n\nMedian sternotomy.\nTotal cardiopulmonary bypass.\nAortic valve replacement with a 23 mm Carpentier-Edwards pericardial bovine tissue valve.\nMitral valve replacement with a 25 mm Carpentier-Edwards pericardial bovine tissue valve.\nInsertion of 2 temporary ventricular bipolar pacing wires.\nInsertion of 2 mediastinal and 1 right pleural chest tubes."
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    "title": "Mortality and Morbidity",
    "section": "Post-op Note (1d after)",
    "text": "Post-op Note (1d after)\n\nOn dobutamine 8mcg, attempted to wean overnight but cardiac index dropped to 1.6. Epinephrine used initially post op but was weaned overnight and turned off. V paced at 80 overnight, turned down this AM patient does have underlying rhythm at 60. ABT completed, ABG without hypoxia or hypercarbia, OK parameters and patient was extubated to NC at 640AM."
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    "title": "Mortality and Morbidity",
    "section": "CTS Attending Note (3d after)",
    "text": "CTS Attending Note (3d after)\n\nPt seen and examined while I chair. BP stable. Rhythm paced at 62/min. His intrinsic rate was 44 bpm. No afib.\n\n\nPt will need a permanent pacemaker prior to discharge. EP on board. Appreciate input. We hope to have the pacemaker placed Monday or Tuesday so he can be discharged mid week."
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    "title": "Mortality and Morbidity",
    "section": "Post-op Note (4d after)",
    "text": "Post-op Note (4d after)\n\nNPO overnight for possible PPM with EP. V paced at 60, has intrinsic rhythm of mid 50s. Feels SOB for the past 6 hours or so. No BM, making good urine. Received 1u plt overnight count is 83 from 51 yesterday."
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    "title": "Mortality and Morbidity",
    "section": "01/30/23 TTE",
    "text": "01/30/23 TTE\n\nThere is a well seated, bioprosthetic valve in the mitral position (25mm Carpentier Edwards, Surgeon). Leaflet tips are not well visualized. Mean transmitral diastolic gradient is 4 mm Hg at a HR of 60 bpm. There is at least some degree of regurgitation, but difficult to visualize due to shadowing. There is a well seated, bioprosthetic valve in the aortic position (23mm Carpentier Edwards; Surgeon). Leaflet tips are not well visualized. Mean gradient 26 mmHg and peak velocity of 3.5 m/s. There is trace periprosthetic regurgitation. There is also some degree of intraprosthetic regurgitation, but difficult to quantify on current study. There is a large left atrial echodensity that is concerning for thrombus."
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#tee-1",
    "title": "Mortality and Morbidity",
    "section": "01/31/23 TEE",
    "text": "01/31/23 TEE\n\nLeft atrial appendage has a thrombus. Large mobile thrombus on the interior of the left atrial appendage."
  },
  {
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#eps",
    "title": "Mortality and Morbidity",
    "section": "02/01/23 EPS",
    "text": "02/01/23 EPS\n\nA Boston Scientific Model Number 7841, Serial Number 1240738 ventricular pacing electrode was advanced into the RA (is is to note that the RA is markedly dilated) and we recorded the electrical activity at multiple locations. The Atria in in AF with significant portion of the atria is either in very fine AF or silent, likely scarred tissues. An organized Afib was noted in the PL at the AV junction. Furthermore, we have given consideration to placed CS LV pacing lead but the recent MVR makes this effort difficult. Given this presentation a decision was made to place a SC PM.\n\nProcedure Performed: Placement of a single chamber permanent pacemaker via the right subclavian vein under fluoroscopy.\nDevice parameters: Mode: VVIR Base/max track: 60/120 BPM RV lead: Paced V waves 609 ohms/0.4 mV@0.4 ms; programmed 2.5 mV, 3.5V (0.4ms?)"
  },
  {
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#tte-1",
    "title": "Mortality and Morbidity",
    "section": "02/04/23 TTE",
    "text": "02/04/23 TTE\n\nThere is a well-seated bioprosthetic valve in the aortic position (bioAVR, 23mm Carpentier Edwards). Bioprosthetic leaflets not well seen, though appear to be normally thin and mobile consistent with normal leaflet function. Mean gradient 26 mmHg and peak velocity of 3.5 m/s and acceleration time around 95msec and DI 0.45 suggestive of patient prosthesis mismatch. There appears to be very eccentric, mild-moderate bioAVR regurgitation that is likely periprosthetic, seen along the mitral-aortic continuity. There is a well-seated bioprosthetic valve in the mitral position (bioMVR, 25mm Carpentier Edwards). Bioprosthetic leaflets not well seen, though there appears to be some leaflet thickening and reduced excursion of one of the leaflets. Elevated mean transmitral diastolic gradient 6 mm Hg at a HR of 60 bpm. There is a small highly-mobile echodensity seen along the ventricular surface of the bioMVR measuring approximately 7mm in length and 3mm in width (i.e. image 34); similar echodensity not well seen on prior TTE 1/30/2023 or TEE 1/31/2023. Differential includes residual chordal structure (not seen on prior echos) or possibly a new vegetation. Consider further evaluation with TEE if clinically indicated."
  },
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#pacemaker-placement-6d-after",
    "title": "Mortality and Morbidity",
    "section": "Pacemaker placement (6d after)",
    "text": "Pacemaker placement (6d after)\n\nA Boston Scientific Model Number 7841, Serial Number 1240738 ventricular pacing electrode was advanced into the RA (is is to note that the RA is markedly dilated) and we recorded the electrical activity at multiple locations. The Atria in in AF with significant portion of the atria is either in very fine AF or silent, likely scarred tissues. An organized Afib was noted in the PL at the AV junction. Furthermore, we have given consideration to placed CS LV pacing lead but the recent MVR makes this effort difficult. Given this presentation a decision was made to place a SC PM.\n\nDevice parameters:\nMode: VVIR\nBase/max track: 60/120 BPM\nRV lead: Paced V waves 609 ohms/0.4 mV@0.4 ms; programmed 2.5 mV, 3.5V (0.4ms?)"
  },
  {
    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#transesophageal-echocardiogram-3mo-prior",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#transesophageal-echocardiogram-3mo-prior",
    "title": "Mortality and Morbidity",
    "section": "Transesophageal echocardiogram (3mo prior)",
    "text": "Transesophageal echocardiogram (3mo prior)\n\nSevere biatrial enlargement.\n\n\nAortic valve tricuspid. There is moderate to severe calcification of all three leaflets, resulting in moderate aortic stenosis and moderate aortic regurgitation.\n\n\nMitral valve is rheumatic. There is significant calcification of the anterior and posterior leaflets, with resulting moderate mitral regurgitation. There is no evidence of significant mitral stenosis. There is significant mitral annular calcificaiton."
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#structural-consult-2y-4mo-prior",
    "title": "Mortality and Morbidity",
    "section": "Structural consult (2y, 4mo prior)",
    "text": "Structural consult (2y, 4mo prior)\n\nGiven his thorough evaluation his aortic stenosis remains the most likely cause of his symptoms and I would favor proceeding with aortic valve replacement. Given his young age, surgical aortic valve replacement is probably favored. His STS PROM is 1.7%. If TAVR is chosen he will need a TAVR protocol CTA of chest, abdomen and pelvis. I will refer him to be evaluated by cardiac surgery and then we will have a heart team meeting and decide the best route to go. I discussed this with the patient and his wife and they expressed understanding."
  },
  {
    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#cts-consult-2y-2mo-prior",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#cts-consult-2y-2mo-prior",
    "title": "Mortality and Morbidity",
    "section": "CTS consult (2y, 2mo prior)",
    "text": "CTS consult (2y, 2mo prior)\n\nPatient 56-year-old man who has history of hypertension, chronic renal failure status post kidney transplant in 2015 with reasonable function with a recent creatinine of 1.8. The patient has also history of atrial fibrillation on apixaban and since May he has been experiencing symptoms of shortness of breath on exertion."
  },
  {
    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#cts-follow-up-2y-prior",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#cts-follow-up-2y-prior",
    "title": "Mortality and Morbidity",
    "section": "CTS follow-up (2y prior)",
    "text": "CTS follow-up (2y prior)\n\nGiven TTE/TEE, at this time pt does not meet hemodynamic criteria for surgical valve replacement either for aortic or mitral valve. Given pt only with mild symptoms of dyspnea on exertion; recommend follow conservatively at this point and repeat TTE in 6 months.\n\n\nPatient was “lost to follow-up” for almost 2 years subseuqnetly"
  },
  {
    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#cts-follow-up-4mo-prior",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#cts-follow-up-4mo-prior",
    "title": "Mortality and Morbidity",
    "section": "CTS follow-up (4mo prior)",
    "text": "CTS follow-up (4mo prior)\n\nIn light of the persistent and increasing symptoms of shortness of breath as well as symptoms of rapid heart rate with severe biatrial enlargement on echocardiography in the past as well as the significant murmur that I hear today on physical examination, I suspect that the amount of mitral regurgitation that this patient has is more than what is reported in the echocardiogram that was done 2 years ago. In light of the above, I would like to recommend that the patient would obtain a transesophageal echocardiogram and see his cardiologist, Physician, so that we can assess his severity of his mitral regurgitation and aortic stenosis and regurgitation more thoroughly. If the patient had evidence of severe mitral regurgitation, then I would strongly recommend considering him for open-heart surgery and mitral valve repair or replacement, at the time of which we will address the aortic pathology as well."
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#tee-3mo-prior",
    "title": "Mortality and Morbidity",
    "section": "TEE (3mo prior)",
    "text": "TEE (3mo prior)\n\nSevere biatrial enlargement.\n\n\nAortic valve tricuspid. There is moderate to severe calcification of all three leaflets, resulting in moderate aortic stenosis and moderate aortic regurgitation.\n\n\nMitral valve is rheumatic. There is significant calcification of the anterior and posterior leaflets, with resulting moderate mitral regurgitation. There is no evidence of significant mitral stenosis. There is significant mitral annular calcificaiton."
  },
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#cardiac-cath-1mo-prior",
    "title": "Mortality and Morbidity",
    "section": "Cardiac cath (1mo prior)",
    "text": "Cardiac cath (1mo prior)\n\n\n\n\n\n\n\nLeft coronary artery\n\n\n\n\n\n\n\nRight coronary artery\n\n\n\n\nFigure 4: Cardiac catheterization with aortic valve study"
  },
  {
    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#cts-pre-op-1mo-prior",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#cts-pre-op-1mo-prior",
    "title": "Mortality and Morbidity",
    "section": "CTS pre-op (1mo prior)",
    "text": "CTS pre-op (1mo prior)\nFindings:\n\nIn AFIB on xarelto, states he is not able to take his full rx dose since has episodes of bleeding when takes prescribed dose.\n\nRecommendations:\n\nDiscussed valve types including risks/benefits of both bioprosthetic and mechanical. Patient would like to move forward with bioprosthetic valve if possible. Discussed possibility of necessity of mechanical valve depending on intraoperative findings."
  },
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    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#ecg-changes",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#ecg-changes",
    "title": "Mortality and Morbidity",
    "section": "ECG changes",
    "text": "ECG changes"
  },
  {
    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#ep-consult-3d-after",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#ep-consult-3d-after",
    "title": "Mortality and Morbidity",
    "section": "EP consult (3d after)",
    "text": "EP consult (3d after)\n\nPrior to surgery, patient has one prior ECG in our system from 10/2022 that shows afib rate 80’s. No known ECG’s in sinus rhythm. Since the surgery, telemetry examined shows a lack of p waves and patient 100% v-paced, has epicardial pacer since surgery. Setting: VVI rate: 60"
  },
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#ep-follow-up-4d-after",
    "title": "Mortality and Morbidity",
    "section": "EP Follow-up (4d after)",
    "text": "EP Follow-up (4d after)\n\nJunctional escape pattern after SMVR/SAVR, concern for high grade AV block, in setting of AF:\n\n\n1. Agree with the CTS consideration of DC-PPM.\n2. Normal LVEF suggests resynchronization not needed at this time.\n3. Would prefer to have PLT closer to 100k prior to procedure\n4. Recommend IV diuresis today to help c- edema (to facilitate positioning for procedure)\n5. Will plan for placement tomorrow AM (NPO @ MN) unless other imaging or interventions are needed for TTE finding.\n6. Will call CTS in AM to confirm plan."
  },
  {
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#aortic-valve-evaluation--2y-4m",
    "title": "Mortality and Morbidity",
    "section": "Aortic valve evaluation (-2y, 4m)",
    "text": "Aortic valve evaluation (-2y, 4m)"
  },
  {
    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#structural-consult--2y-4m",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#structural-consult--2y-4m",
    "title": "Mortality and Morbidity",
    "section": "Structural consult (-2y, 4m)",
    "text": "Structural consult (-2y, 4m)\n\nGiven his thorough evaluation his aortic stenosis remains the most likely cause of his symptoms and I would favor proceeding with aortic valve replacement. Given his young age, surgical aortic valve replacement is probably favored. His STS PROM is 1.7%. If TAVR is chosen he will need a TAVR protocol CTA of chest, abdomen and pelvis. I will refer him to be evaluated by cardiac surgery and then we will have a heart team meeting and decide the best route to go. I discussed this with the patient and his wife and they expressed understanding."
  },
  {
    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#cts-consult--2y-2m",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#cts-consult--2y-2m",
    "title": "Mortality and Morbidity",
    "section": "CTS consult (-2y, 2m)",
    "text": "CTS consult (-2y, 2m)\n\nPatient 56-year-old man who has history of hypertension, chronic renal failure status post kidney transplant in 2015 with reasonable function with a recent creatinine of 1.8. The patient has also history of atrial fibrillation on apixaban and since May he has been experiencing symptoms of shortness of breath on exertion."
  },
  {
    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#ct-chest--2y-1m",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#ct-chest--2y-1m",
    "title": "Mortality and Morbidity",
    "section": "CT chest (-2y, 1m)",
    "text": "CT chest (-2y, 1m)\n\nHEART AND GREAT VESSELS: Cardiomegaly. There is trace pericardial effusion. There is conventional three-vessel anatomy of the aortic great vessels. Mild atherosclerotic calcification of the ascending aorta, aortic arch, descending thoracic aorta. Coronary atherosclerotic disease. There is dense circumferential atherosclerotic calcification of the aortic valve and leaflets as well as dense atherosclerotic calcification of the mitral valve (also appreciable on scout images)."
  },
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    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#cts-follow-up--2y",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#cts-follow-up--2y",
    "title": "Mortality and Morbidity",
    "section": "CTS follow-up (-2y)",
    "text": "CTS follow-up (-2y)\n\nGiven TTE/TEE, at this time pt does not meet hemodynamic criteria for surgical valve replacement either for aortic or mitral valve. Given pt only with mild symptoms of dyspnea on exertion; recommend follow conservatively at this point and repeat TTE in 6 months.\n\n\nPatient was “lost to follow-up” for almost 2 years subsequently, although seen in general/internal medicine clinics per EPIC"
  },
  {
    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#cts-follow-up--4m",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#cts-follow-up--4m",
    "title": "Mortality and Morbidity",
    "section": "CTS follow-up (-4m)",
    "text": "CTS follow-up (-4m)\n\nIn light of the persistent and increasing symptoms of shortness of breath as well as symptoms of rapid heart rate with severe biatrial enlargement on echocardiography in the past as well as the significant murmur that I hear today on physical examination, I suspect that the amount of mitral regurgitation that this patient has is more than what is reported in the echocardiogram that was done 2 years ago. In light of the above, I would like to recommend that the patient would obtain a transesophageal echocardiogram and see his cardiologist, Physician, so that we can assess his severity of his mitral regurgitation and aortic stenosis and regurgitation more thoroughly. If the patient had evidence of severe mitral regurgitation, then I would strongly recommend considering him for open-heart surgery and mitral valve repair or replacement, at the time of which we will address the aortic pathology as well."
  },
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#follow-up-with-structural--3m",
    "title": "Mortality and Morbidity",
    "section": "Follow-up with structural (-3m)",
    "text": "Follow-up with structural (-3m)\n\nTwo valve disease. Will obtain TEE to assess degree of mitral regurgitation. IF at least moderate would plan for surgical AVR and MVR. Will follow-up with Surgeon after TEE"
  },
  {
    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#tee--3m",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#tee--3m",
    "title": "Mortality and Morbidity",
    "section": "TEE (-3m)",
    "text": "TEE (-3m)\n\n\n\n\n\n\n\nAI\n\n\n\n\n\n\n\nAS\n\n\n\n\n\n\n\n\n\nLAA\n\n\n\n\n\n\n\nMR\n\n\n\n\nFigure 5: TEE for valvular heart disease re-evaluation"
  },
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#cardiac-cath--1m",
    "title": "Mortality and Morbidity",
    "section": "Cardiac cath (-1m)",
    "text": "Cardiac cath (-1m)\n\n\n\n\n\n\n\nLeft coronary artery\n\n\n\n\n\n\n\nRight coronary artery\n\n\n\n\nFigure 6: Pre-operative cardiac catheterization with repeat aortic valve study"
  },
  {
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#cts-pre-op--1mo",
    "title": "Mortality and Morbidity",
    "section": "CTS pre-op (-1mo)",
    "text": "CTS pre-op (-1mo)\nFindings:\n\nIn AFIB on xarelto, states he is not able to take his full rx dose since has episodes of bleeding when takes prescribed dose.\n\nRecommendations:\n\nDiscussed valve types including risks/benefits of both bioprosthetic and mechanical. Patient would like to move forward with bioprosthetic valve if possible. Discussed possibility of necessity of mechanical valve depending on intraoperative findings."
  },
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#operation-note-0d",
    "title": "Mortality and Morbidity",
    "section": "Operation Note (=0d)",
    "text": "Operation Note (=0d)\n\n\nPREOPERATIVE DIAGNOSES:\n\nChronic renal failure, status post kidney transplant with some allograft dysfunction.\nSymptomatic severe aortic stenosis and severe mitral regurgitation in the setting of calcific rheumatic valvular disease.\nHypertension.\n\n\nOPERATIONS:\n\nMedian sternotomy.\nTotal cardiopulmonary bypass.\nAortic valve replacement with a 23 mm Carpentier-Edwards pericardial bovine tissue valve.\nMitral valve replacement with a 25 mm Carpentier-Edwards pericardial bovine tissue valve.\nInsertion of 2 temporary ventricular bipolar pacing wires.\nInsertion of 2 mediastinal and 1 right pleural chest tubes."
  },
  {
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#post-op-note-1d",
    "title": "Mortality and Morbidity",
    "section": "Post-op Note (+1d)",
    "text": "Post-op Note (+1d)\n\nOn dobutamine 8mcg, attempted to wean overnight but cardiac index dropped to 1.6. Epinephrine used initially post op but was weaned overnight and turned off. V paced at 80 overnight, turned down this AM patient does have underlying rhythm at 60. ABT completed, ABG without hypoxia or hypercarbia, OK parameters and patient was extubated to NC at 640AM."
  },
  {
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#cts-attending-note-3d",
    "title": "Mortality and Morbidity",
    "section": "CTS Attending Note (+3d)",
    "text": "CTS Attending Note (+3d)\n\nPt seen and examined while I chair. BP stable. Rhythm paced at 62/min. His intrinsic rate was 44 bpm. No afib.\n\n\nPt will need a permanent pacemaker prior to discharge. EP on board. Appreciate input. We hope to have the pacemaker placed Monday or Tuesday so he can be discharged mid week."
  },
  {
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#post-op-note-4d",
    "title": "Mortality and Morbidity",
    "section": "Post-op Note (+4d)",
    "text": "Post-op Note (+4d)\n\nNPO overnight for possible PPM with EP. V paced at 60, has intrinsic rhythm of mid 50s. Feels SOB for the past 6 hours or so. No BM, making good urine. Received 1u plt overnight count is 83 from 51 yesterday."
  },
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#summary-1",
    "title": "Mortality and Morbidity",
    "section": "Summary",
    "text": "Summary"
  },
  {
    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#ep-consult-3d",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#ep-consult-3d",
    "title": "Mortality and Morbidity",
    "section": "EP consult (+3d)",
    "text": "EP consult (+3d)\n\nPrior to surgery, patient has one prior ECG in our system from 10/2022 that shows afib rate 80’s. No known ECG’s in sinus rhythm. Since the surgery, telemetry examined shows a lack of p waves and patient 100% v-paced, has epicardial pacer since surgery. Setting: VVI rate: 60"
  },
  {
    "objectID": "cases/03-27-23-mm-conference/mm-conference.html#ep-follow-up-4d",
    "href": "cases/03-27-23-mm-conference/mm-conference.html#ep-follow-up-4d",
    "title": "Mortality and Morbidity",
    "section": "EP Follow-up (+4d)",
    "text": "EP Follow-up (+4d)\n\nJunctional escape pattern after SMVR/SAVR, concern for high grade AV block, in setting of AF:\n1. Agree with the CTS consideration of DC-PPM. \n2. Normal LVEF suggests resynchronization not needed at this time.\n3. Would prefer to have PLT closer to 100k prior to procedure\n4. Recommend IV diuresis today to help c- edema (to facilitate positioning for procedure)\n5. Will plan for placement tomorrow AM (NPO @ MN) unless other imaging or interventions are needed for TTE finding.\n6. Will call CTS in AM to confirm plan."
  },
  {
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#ep-follow-up-5d",
    "title": "Mortality and Morbidity",
    "section": "EP follow-up (+5d)",
    "text": "EP follow-up (+5d)\n\nHigh grade AV block in setting of persistent AF after SMVR/SAVR, with new dx of LA thrombus d/t ?HIT:\n1. As pt may have changes in AC options d/t this, we will defer DC-PPM placement until resolution or a plan is solidified. We can do this procedure under oral AC but would wait until this LA thrombus issue has resolved before proceeding.\n\nOf note, he is less rate dependent on the pacemaker, as has been able to generate rates as high as mid-60s. We set his back-up rate at 50 for now.\nWill continue to follow along, and have initiated the conversation with IC/general cards about interventions. TEE pending."
  },
  {
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#pacemaker-placement-6d",
    "title": "Mortality and Morbidity",
    "section": "Pacemaker placement (+6d)",
    "text": "Pacemaker placement (+6d)\n\nA Boston Scientific Model Number 7841, Serial Number 1240738 ventricular pacing electrode was advanced into the RA (is is to note that the RA is markedly dilated) and we recorded the electrical activity at multiple locations. The Atria in in AF with significant portion of the atria is either in very fine AF or silent, likely scarred tissues. An organized Afib was noted in the PL at the AV junction. Furthermore, we have given consideration to placed CS LV pacing lead but the recent MVR makes this effort difficult. Given this presentation a decision was made to place a SC PM.\n\nDevice parameters:\nMode: VVIR\nBase/max track: 60/120 BPM\nRV lead: Paced V waves 609 ohms/0.4 mV@0.4 ms; programmed 2.5 mV, 3.5V@0.4ms\n\nWhen would you have placed a pacemaker?"
  },
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    "href": "cases/03-27-23-mm-conference/mm-conference.html#tte-post-op-3d",
    "title": "Mortality and Morbidity",
    "section": "TTE post-op (+3d)",
    "text": "TTE post-op (+3d)\n\nThere is a large left atrial echodensity that is concerning for thrombus."
  },
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    "title": "Mortality and Morbidity",
    "section": "TEE post-op (+4d)",
    "text": "TEE post-op (+4d)\n\n\n\n\n\n\n\nNo intra-cardiac mass seen\n\n\n\n\n\n\n\nLarge thrombus seen in LAA\n\n\n\n\nFigure 8: Post-op TEE for left atrial evaluation"
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    "title": "Mortality and Morbidity",
    "section": "TTE post-op (+3d)",
    "text": "TTE post-op (+3d)\n\nThere is a well seated, bioprosthetic valve in the mitral position (25mm Carpentier Edwards, Surgeon). Leaflet tips are not well visualized. Mean transmitral diastolic gradient is 4 mm Hg at a HR of 60 bpm. There is at least some degree of regurgitation, but difficult to visualize due to shadowing. There is a well seated, bioprosthetic valve in the aortic position (23mm Carpentier Edwards; Surgeon). Leaflet tips are not well visualized. Mean gradient 26 mmHg and peak velocity of 3.5 m/s. There is trace periprosthetic regurgitation. There is also some degree of intraprosthetic regurgitation, but difficult to quantify on current study."
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    "title": "Mortality and Morbidity",
    "section": "TTE prior to discharge (+10d)",
    "text": "TTE prior to discharge (+10d)\n\nThere is a well-seated bioprosthetic valve in the aortic position (bioAVR, 23mm Carpentier Edwards). Bioprosthetic leaflets not well seen, though appear to be normally thin and mobile consistent with normal leaflet function. Mean gradient 26 mmHg and peak velocity of 3.5 m/s and acceleration time around 95msec and DI 0.45 suggestive of patient prosthesis mismatch. There appears to be very eccentric, mild-moderate bioAVR regurgitation that is likely periprosthetic, seen along the mitral-aortic continuity. There is a well-seated bioprosthetic valve in the mitral position (bioMVR, 25mm Carpentier Edwards). Bioprosthetic leaflets not well seen, though there appears to be some leaflet thickening and reduced excursion of one of the leaflets. Elevated mean transmitral diastolic gradient 6 mm Hg at a HR of 60 bpm. There is a small highly-mobile echodensity seen along the ventricular surface of the bioMVR measuring approximately 7mm in length and 3mm in width (i.e. image 34); similar echodensity not well seen on prior TTE 1/30/2023 or TEE 1/31/2023. Differential includes residual chordal structure (not seen on prior echos) or possibly a new vegetation. Consider further evaluation with TEE if clinically indicated."
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    "title": "Mortality and Morbidity",
    "section": "CTS pre-op (-1m)",
    "text": "CTS pre-op (-1m)\nFindings:\n\nIn AFIB on xarelto, states he is not able to take his full rx dose since has episodes of bleeding when takes prescribed dose.\n\nRecommendations:\n\nDiscussed valve types including risks/benefits of both bioprosthetic and mechanical. Patient would like to move forward with bioprosthetic valve if possible. Discussed possibility of necessity of mechanical valve depending on intraoperative findings."
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    "title": "Mortality and Morbidity",
    "section": "Discharge (+21d)",
    "text": "Discharge (+21d)\n\nMr. Powell is a 58 year old male who underwent a mitral and aortic valve replacement for symptomatic moderate mitral regurgitation and moderate aortic stenosis and regurgitation. He received 1 platelet intraop. He was transferred to the ICU in stable condition. He was noted to be baseline bradycardic after surgery and EP was consulted for PPM which was placed on 2/1."
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    "text": "Summary"
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    "title": "Mortality and Morbidity",
    "section": "Overview of M&M Conference",
    "text": "Overview of M&M Conference\n\nM&M have evolved to focus on system-level problems (e.g. root cause analyses), a paradignm shift after the publication “To Err is Human” (~ Institute of Medicine, 1999)\nM&M conferences originally developed for surgical/procedure fields, but now have spread to medical discplines\nCertain medical disciplines have developed M&M subspecialty guidelines\nRecently, a proposed framework has been identified for Cardiology M&Ms, emphasizing roles of fellows and early-career physicians"
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    "title": "Mortality and Morbidity",
    "section": "Plan",
    "text": "Plan\n58 year-old gentleman with VHD, chronic/persistent AF, and CKD III after transplant who has had worsening moderate-to-severe AS, moderate MR and suspected symptomatic MS.\n\nBioprosthetic SMVR\nBioprosthetic SAVR\n\n\nWould anyone amend or addend this plan?"
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    "title": "Mortality and Morbidity",
    "section": "Concerns I",
    "text": "Concerns I\n\nWhat is the underlying disorder causing this rapidly degenerating VHD?\nDid a Heart Team meeting occur to discuss pre-operative strategies?\nWas further imaging indicated prior to making operative decision?\nDoes inadequate AC suggest need for repeat pre-operative evaluation of LAA?\nShould LAA occlusion/exclusion be considered for this patient?"
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    "title": "Mortality and Morbidity",
    "section": "Patient Summary",
    "text": "Patient Summary\nPatient:\n\n58 year old gentleman\nPrior kidney transplant in 2015, on immunosuppression\nLong-standing persistent AF on DOAC\nPH on sildenafil, multifactorial\nmoderate to severe AS, low-flow low gradient\nModerate MR with moderate MS\n\nPresentation:\n\nIncreasing exertional dyspnea/fatigue\nIn the setting of chronic smoking, valvular disease, and AF\nEvaluation for potential valve replacement"
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    "title": "Mortality and Morbidity",
    "section": "Questions I",
    "text": "Questions I\n\nWhy was the TEE not able to be seen by the surgeon, or why was it referenced by physician if not done?\nDid a Heart Team meeting occur to discuss pre-operative strategies?\nWhy is there not an ECG in the system?"
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    "title": "Mortality and Morbidity",
    "section": "Questions I",
    "text": "Questions I\n\nWhat is the underlying disorder causing this rapidly degenerating VHD?\nDid a Heart Team meeting occur to discuss pre-operative strategies?\nWas further imaging indicated prior to making operative decision?\nDoes inadequate AC suggest need for repeat pre-operative evaluation of LAA?\nShould LAA occlusion/exclusion be considered for this patient?"
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    "title": "Mortality and Morbidity",
    "section": "Questions I",
    "text": "Questions I\n\nWhat is the underlying disorder causing this rapidly degenerating VHD?\nDid a Heart Team meeting occur to discuss pre-operative strategies?\nWas further imaging indicated prior to making operative decision?\nDoes inadequate AC suggest need for repeat pre-operative evaluation of LAA?\nShould LAA occlusion/exclusion be considered for this patient?"
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    "title": "Mortality and Morbidity",
    "section": "Questions I",
    "text": "Questions I\n\nWhat is the underlying disorder causing this rapidly degenerating VHD?\nDid a Heart Team meeting occur to discuss pre-operative strategies?\nWas further imaging indicated prior to making operative decision?\nDoes inadequate AC suggest need for repeat pre-operative evaluation of LAA?\nShould LAA occlusion/exclusion be considered for this patient?"
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    "section": "Questions II",
    "text": "Questions II\n\nWhy was the TEE not able to be seen by the surgeon, or why was it referenced by physician if not done? CERNER and EPIC changeover did happen at about this time\nDid a Heart Team meeting occur to discuss pre-operative strategies? Unclear\nAlthough ordered, why were no ECGs made? Rhythm strip found buried in media\nWhat follow-up system do we have in place for patients after consultation/referral?"
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    "title": "Mortality and Morbidity",
    "section": "Questions III",
    "text": "Questions III\n\nWhy was the TEE not able to be seen by the surgeon, or why was it referenced by physician if not done? CERNER and EPIC changeover did happen at about this time\nDid a Heart Team meeting occur to discuss pre-operative strategies? Unclear\nAlthough ordered, why were no ECGs made? Rhythm strip found buried in media\nWhat follow-up system do we have in place for patients after consultation/referral? No orders for follow-up were placed\nWhat is the underlying disorder causing this rapidly degenerating VHD?\nWas further imaging indicated prior to making operative decision?\nDoes inadequate AC suggest need for repeat pre-operative evaluation of LAA?\nShould LAA occlusion/exclusion be considered for this patient?"
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    "title": "Mortality and Morbidity",
    "section": "Clinical Questions",
    "text": "Clinical Questions\n\nWhat is the underlying disorder causing this rapidly degenerating VHD?\nWas further imaging indicated prior to making operative decision?\nDoes inadequate AC suggest need for repeat pre-operative evaluation of LAA?\nShould LAA occlusion/exclusion be considered for this patient?"
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    "title": "Mortality and Morbidity",
    "section": "System Issues",
    "text": "System Issues\n\nWhy was the TEE not able to be seen by the surgeon, or why was it referenced by physician if not done? CERNER and EPIC changeover did happen at about this time\nDid a Heart Team meeting occur to discuss pre-operative strategies? Unclear\nAlthough ordered, why were no ECGs made? Rhythm strip found buried in media\nWhat follow-up system do we have in place for patients after consultation/referral? Order for RTC not seen in system"
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    "title": "Mortality and Morbidity",
    "section": "System Issues",
    "text": "System Issues\n\nWhy was the need for pacemaker escalated/rushed?Are there timelines required for discharge?\nDoes the underlying indication matter for the intervention? Difference between junctional escape and AF with slow response"
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    "title": "Mortality and Morbidity",
    "section": "Clinical Questions",
    "text": "Clinical Questions\n\nWhat was the underlying rhythm? AF with slow ventricular response and surgical IVCD?\nDid the patient need a pacemaker now, or could this have waited?"
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    "title": "Mortality and Morbidity",
    "section": "System Issues",
    "text": "System Issues\n\nWould knowing the underlying diagnosis change management? Discrepancy between ECG read and rhythm assessment multiple times throughout chart"
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    "section": "Clincial Questions",
    "text": "Clincial Questions\n\nWhy was the LAA not closed or ligated during surgery?"
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    "title": "Mortality and Morbidity",
    "section": "Potential issues",
    "text": "Potential issues\n\nWhy was the TEE not able to be seen by the surgeon, or why was it referenced by physician if not done? CERNER and EPIC changeover did happen at about this time\nDid a Heart Team meeting occur to discuss pre-operative strategies? Unclear\nWas further imaging indicated prior to making operative decision?\nShould LAA occlusion/exclusion be considered for this patient?\nAlthough ordered, why were no ECGs made? Rhythm strip found buried in media\nWhat follow-up system do we have in place for patients after consultation/referral? Order for RTC not seen in system\nDoes inadequate AC suggest need for repeat pre-operative evaluation of LAA?\nWhat is the underlying disorder causing this rapidly degenerating VHD?"
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    "title": "Mortality and Morbidity",
    "section": "Potential issues",
    "text": "Potential issues\n\nWhy was the LAA not closed or ligated during surgery?\nHow do we decide appropriate secondary interventions at time of surgery? Ex: addressing aortic valve at the same time as mitral valve\nShould cases routinely be discussed in an interdisciplinary/multidisciplinary manner? Heart Team meetings\nWould having the LAA closed or ligated during surgery improve stroke risk?\nDoes the patient have an increased risk of stroke now?"
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    "title": "Mortality and Morbidity",
    "section": "Potential issues",
    "text": "Potential issues\n\nHow are surgical valves sized?\nShould adjunctive imaging be performed prior to surgery? Undersizing is a risk that may not be seen intra-operatively\nIs the patient symptomatic from these increased gradients (compared to before valve replacement)?"
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    "title": "Mortality and Morbidity",
    "section": "Valvular status",
    "text": "Valvular status\n\n\nAortic valve\n\nSeverely calcified leaflets\nmean gradient 24 mmHg\npeak velocity of 3.2 m/s\nAVA 1.4 cm2\n\n\n\nNormal bioprosthetic leaflets\nMean gradient 26 mm Hg\nPeak velocity of 3.5 m/s\nAT of 95 ms, DI of 0.45\n\n\nMitral valve\n\nRheumatic mitral valve\nMild anterior/posterior leaflet thickening\nMean gradient 5 mmHg @ 70 bpm\nModerate mitral regurg\nSevere MAC\n\n\n\nBioprosthetic mitral valve\nLeaflet thickening and reduced excursion\nMobile echodensity seen (new), 7 mm x 3 mm\nMean gradient 6 mm Hg @ 60 bpm"
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    "title": "Mortality and Morbidity",
    "section": "Potential issues",
    "text": "Potential issues\n\nWhat was the underlying rhythm? AF with slow ventricular response and surgical IVCD?\nWould knowing the underlying diagnosis change management? Discrepancy between ECG read and rhythm assessment multiple times throughout chart\nWhy was the need for pacemaker escalated/rushed?Are there timelines required for discharge?\nDoes the underlying indication matter for the intervention? Difference between junctional escape and AF with slow response\nDid the patient need a pacemaker now, or could this have waited?\nWill the patient develop cardiomyopathy from RV pacing? Particularly in setting of LFLG AS\nWas his native, post-op conduction disease better or worse than RV pacing?\nHow do we assess post-operative conduction disease? What is the expected risk?"
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    "title": "Mortality and Morbidity",
    "section": "Surgical closure…",
    "text": "Surgical closure…\n\nJTCVS 2018:(Ando2018?) Meta-analysis of for LAA closure during surgery, 7 articles (n = 4k) showed reduction in mortality (HR = 0.4) and CVA (HR = 0.6)\nJAMA 2018:(Yao2018?) Retrospective cohort study (n = 75k) of surgical LAAO versus not showed lower risk of stroke (HR = 0.7) and mortality (HR = 0.7)\nNEJM 2021:(Whitlock2021?) RCT (n = 4.7k) of CHA2DS2VASC ≥ 2 showed LAAO had reduced CVA/embolism risk (HR = 0.7) … LAAOS III trial stopped early due to efficacy (Verma2021?)"
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    "title": "Mortality and Morbidity",
    "section": "Valve sizing…",
    "text": "Valve sizing…\n\nFor SAVR, sizing occurs intra-operatively, incorporating valve external diameter, stent structure, internal diameter, etc.\nSmall study of individuals undergoing SAVR (n = 80) had CT imaging to predict TAVR size, and over 40% the SAVR was undersized compared to predicted TAVR (1)\nHemodynamic differences by valve type occur due to idiosyncratic patient factors that interact with valve profile\nValve hemodynamics can be predicted per-patient using CT imaging,(Deeb2020?) suggesting potential benefit for more liberal pre-SAVR testing (Houtom2020?)\nImaging can also help with predicting those at risk for PPM (Pibarot2019?)"
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    "title": "Mortality and Morbidity",
    "section": "Conduction system damage…",
    "text": "Conduction system damage…\n\n\nRisk of PPM placement is rare (<2%) after SAVR alone (n = 663) (Hwang2017?)\nHigh grade AVB after mitral valve surgery is also rare (<4%), however on autopsy, 25% of AV nodal arteries run by the annulus of the MV (Berdajs2008?)\nRate of conduction disease after MV repair/replacement (n = 69) had 2% rate of pacemaker placement, associated with 1) bypass time (OR = 3.2) and 2) pre-existing RBBB (OR = 2.0) (VilesGonzales2021?)\nSAVR using suture-less valve (n = 184) had 1/5 develop new LBBB post-op, with… of these, 1/3 had recover (Lam2021?)\nCTSN investigators (DeRose2019?) showed that AF ablation, multivalve surgery (with MV replacement), and NYHA ≥ III had increased risk of PPM"
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    "title": "Mortality and Morbidity",
    "section": "RV pacing alone…",
    "text": "RV pacing alone…\n\n\nCurrently, CHB is managed with RV pacing, however may be benefit to CRT (BLOCK HF, (Curtis2013?)):\n\nGuidelines recommend LVEF ≤ 35 (IIa), although some benefit in intermediate LVEF\nLess evidence for ≥ 50%\n\n\n\n\n\nFigure 14: Indications for CRT in AVB"
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    "title": "Mortality and Morbidity",
    "section": "TTE of AV prior to discharge (+10d)",
    "text": "TTE of AV prior to discharge (+10d)\n\nThere is a well-seated bioprosthetic valve in the aortic position (bioAVR, 23mm Carpentier Edwards). Bioprosthetic leaflets not well seen, though appear to be normally thin and mobile consistent with normal leaflet function. Mean gradient 26 mmHg and peak velocity of 3.5 m/s and acceleration time around 95msec and DI 0.45 suggestive of patient prosthesis mismatch.\n\n\n\nThere appears to be very eccentric, mild-moderate bioAVR regurgitation that is likely periprosthetic, seen along the mitral-aortic continuity."
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    "title": "Mortality and Morbidity",
    "section": "TTE of MV prior to discharge (+10d)",
    "text": "TTE of MV prior to discharge (+10d)\n\nThere is a well-seated bioprosthetic valve in the mitral position (bioMVR, 25mm Carpentier Edwards). Bioprosthetic leaflets not well seen, though there appears to be some leaflet thickening and reduced excursion of one of the leaflets. Elevated mean transmitral diastolic gradient 6 mm Hg at a HR of 60 bpm.\n\n\n\nThere is a small highly-mobile echodensity seen along the ventricular surface of the bioMVR measuring approximately 7mm in length and 3mm in width (i.e. image 34); similar echodensity not well seen on prior TTE 1/30/2023 or TEE 1/31/2023. Differential includes residual chordal structure (not seen on prior echos) or possibly a new vegetation. Consider further evaluation with TEE if clinically indicated."
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    "title": "Clinical Case Conference",
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    "text": "Understand the cognitive processes involved in the case-based diagnostic reasoning\nIdentify diagnostic assumptions that may lead towards case-specific biases\nPractice contextualizing clinical data in the framework of cardiovascular physiology"
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    "section": "Presentation",
    "text": "Presentation\n\n30 year old gentleman with a history of acid reflux on PPI therapy, generalized anxiety disorder without long-term therapy, exercise-induced asthma on SABA inhaler therapy.\n\n\nHe had recurrent episodes of wheezing and cough over past 4-6 months, and was sent to the emergency room after being found to have a arterial saturation of 87% on room air.\n\n\nReports that he most prominently noted his dyspnea during sexual intercourse with his wife.\n\n\nHe improved with nebulizer therapy. An ECG was made during his ER visit however."
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    "section": "History",
    "text": "History\n\n\nPatient describes a 10+ year history of anabolic steroid usage, initiated by his coach as he trained as a body-builder. He continued as he was unsure on how to taper. He had been on multiple testosterone and anabolic steroid supplements, and had most recently (past 3-6 months) trialed growth hormone. Growth hormone was DC due to lower extremity and hand swelling.\nMaternal grandfather died of sudden death at age 40, and mother has a potential “mitral valve prolapse”. Father was a body-builder and had taken steroids previously. No foreign travel, raised in Canada and lives in Chicago currently. Has a 1-year old son with his wife, who are both healthy.\n\nMedications:\n\nChlorodehydromethyltestosterone (CDMT, a.k.a. turinabol)\nOxandrolone (active)\nTestosterone supplementation (active)\nGrowth hormone injections (for 3-6 months prior to presentation)"
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    "section": "Additional histories",
    "text": "Additional histories\n. . .\nMaternal grandfather died of sudden death at age 40, and mother has a potential “mitral valve prolapse”. Father was a body-builder and had taken steroids previously. No foreign travel, raised in Canada and lives in Chicago currently.\n. . .\nNo pets. Has a 1-year old son with his wife, who are both healthy."
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    "section": "Medications",
    "text": "Medications\n\nChlorodehydromethyltestosterone (CDMT, a.k.a. turinabol)\nOxandrolone (active)\nTestosterone supplementation (active)\nGrowth hormone injections (for 3-6 months prior to presentation)\nAlbuterol inhaler PRN\nOmeprazole 40 mg PO daily"
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    "section": "Labs",
    "text": "Labs\n\n\n\nSodium 138\nPotassium 4.0\nChloride 102\nCO2 24\nBUN 29\n\nCreatinine 1.96\n\nAST 35\n\nALT 52\n\n\n\n\nHg 17.5\nWBC 8 (normal differential)\nPLT 208\nHbA1c 5.2%\n\nLDL 165, HDL 34\nTroponin I 105 (ng/L)\nBNP 289\n\nUDS negative"
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    "section": "Additional Labs",
    "text": "Additional Labs\n\n\nTSH/T4 normal\n\nACTH 20.4\nFree cortisol 1.0\nAM cortisol 13\nFSH &lt; 0.2\nLH &lt; 0.2\nTestosterone 1445 ng/dL\n\nLp(a) 21, ApoB100 126 (mg/dL)\nCystatin 0.9 (eGFR 81)\n\nFerritin 194\nIron 70\nNormal cerruloplasmin\nTB negative\nHIV negative\nRVP negative\nHepatitis panel negative\nTrypanasoma cruzi IgG negative\nANA/Anti-SM negative\nSPEP/UPEP negative"
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    "section": "Differential",
    "text": "Differential\n\n\n\nGenetic\n\n\nTTN\nLMNA\nMYH7\nFLNC (filamin C)\nRBM20 (RNA-binding motif-20)\nTNNT2\nTTNC1\nPLN (phospholamban)\nDSP (desmoplakin)\nACTC1\nSCN5A\nTPM1 (tropomyosin)\n\n\n\nInfectious\n\n\nCOVID/viral myocarditis\nChagas disease\nEndomyocardial fibrosis\n\n\nImmune-mediated\n\n\nGiant-cell myocarditis\nEosinophilic myocarditis\nSarcoidosis\n\n\nIschemic\n\n\nPlaque rupture syndrome\nCoronary artery spasm\nSpontaneous coronary artery dissection\n\n\n\nOthers\n\n\nThiamine deficiency (beri-beri)\nSelenium deficiency\nHypocalcemia\nHyper/hypo-thyroidism\nTachycardia-induced\nAlcohol-induced\nAmphetamine-induced\nCatecholamine-induced (stress-induced, e.g. Takotsubo)\nAnabolic steroid-induced\nHemochromatosis\nWilson’s disease"
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    "section": "Reasoning",
    "text": "Reasoning\n\n\n\nSinus tachycardia\n\n\n\nRight axis deviation with inferior qR and lateral rS pattern\n\n\n\n\nComplete interpolation of ventricular ectopy with superior axis and inverted transition at V2-V3\n\n\n\n\nEnlarged left-sided heart border with narrow vascular pedicle\n\n\n\n\nEarlier completely interpolated atrial depolarization, as compared with PVC, at similar cycle length.\n\n\n\n\n\nLeft posterior fascicular block\n\n\n\n\nInferior/posterior-septal PVC\n\n\n\n\nCardiomegaly\n\n\n\n\nPoor or abnormal VA conduction?"
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    "title": "Clinical Case Conference",
    "section": "Gadolinium contrast!",
    "text": "Gadolinium contrast!\n. . .\nGadolinium (Gd) is a paramagnetic substance (becomes temporarily magnetized), out of four elements (Fe, Ni, Co). Gd induces T1 relaxation.\n. . .\nT1 is the time it takes for net magnetization to return to initial maximum value (shortened by Gd).\n. . .\nInitially, T1 scouting identifies the inversion time at which viable myocardium is “dark”.\n\n\n\nhttps://mriquestions.com/ps-phase-sensitive-ir.html"
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    "section": "Reasoning",
    "text": "Reasoning\n\n\n\n\nSeverely reduced LV systolic function with EF &lt; 20%\n\n\n\n\nLV cavity during diastole of ~7.5 cm\n\n\n\n\nLVOT VTI of 9 cm and RVOT VTI of 6 cm\n\n\n\n\nRegional wall motion abnormalities with inferior hypokinesis/akinesis\n\n\n\n\nModerate to severe mitral regurgitation\n\n\n\n\nEchodensity in apex\n\n\n\n\nGrade III diastolic dysfunction\n\n\n\nLeft posterior fascicular block\nInferior/posterior septal PVC\n\nCardiomegaly\n\n\n\nSevere systolic dysfunction\n\n\n\n\nDilated cardiomyopathy\n\n\n\n\nMitral regurgitation IIIb\n\n\n\n\nLow cardiac output state\n\n\n\n\nApical thrombus"
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    "section": "Differential",
    "text": "Differential\n\n\n\nGenetic\n\n\nTTN\nLMNA\nMYH7\nFLNC (filamin C)\nRBM20 (RNA-binding motif-20)\nTNNT2\nTTNC1\nPLN (phospholamban)\nDSP (desmoplakin)\nACTC1\nSCN5A\nTPM1 (tropomyosin)\n\n\n\nInfectious\n\n\n\nCOVID/viral myocarditis\nChagas disease\nEndomyocardial fibrosis\n\n\n\nImmune-mediated\n\n\n\nGiant-cell myocarditis\nEosinophilic myocarditis\nSarcoidosis\n\n\n\nIschemic\n\n\nPlaque rupture syndrome\nCoronary artery spasm\nSpontaneous coronary artery dissection\n\n\n\nOthers\n\n\n\nThiamine deficiency (beri-beri)\nSelenium deficiency\nHypocalcemia\nHyper/hypo-thyroidism\n\nTachycardia-induced\n\nAlcohol-induced\nAmphetamine-induced\nCatecholamine-induced (stress-induced, e.g. Takotsubo)\n\nAnabolic steroid-induced\n\nHemochromatosis\nWilson’s disease\n\n\n\n\n\n\n\nSteroid-induced cardiomyopathy\n\nGenetic/dilated cardiomyopathy\n\nTachycardia-mediated cardiomyopathy\n\nIschemic cardiomyopathy"
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    "section": "Examination",
    "text": "Examination\n. . .\nInitial vitals of 173/92 and heart rate of 122 bpm that decreased to 137/75 and 109 bpm after rest. SaO2 of 94-96% on room air. BMI 28, 93 kg.\n. . .\nAnxious appearing young gentleman, mildly pressured speech. Skin is warm and dry, Fitzpatrick class I. Mild androgenic alopecia. Not overly-muscular.\n. . .\nJVP at level of clavicle at 30˚. Normal carotid upstroke. PMI is laterally displaced. No obvious thrills or heaves. S1 with physiologically split S2. III/VI systolic murmur apparent at axilla. No peripheral edema, with +2 radial and posterior tibialis pulses."
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    "text": "More"
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    "text": "Sliwa et al. (2023)"
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    "section": "Differential",
    "text": "Differential\n\n\n\n\nGenetic\n\n\n\nTTN\nLMNA\nMYH7\nFLNC (filamin C)\nRBM20 (RNA-binding motif-20)\nTNNT2\nTTNC1\nPLN (phospholamban)\nDSP (desmoplakin)\nACTC1\nSCN5A\nTPM1 (tropomyosin)\n\n\n\nInfectious\n\n\n\nCOVID/viral myocarditis\nChagas disease\nEndomyocardial fibrosis\n\n\n\nImmune-mediated\n\n\n\nGiant-cell myocarditis\nEosinophilic myocarditis\nSarcoidosis\n\n\n\nIschemic\n\n\n\nPlaque rupture syndrome\nCoronary artery spasm\n\n\nSpontaneous coronary artery dissection\n\n\n\n\nOthers\n\n\n\nThiamine deficiency (beri-beri)\nSelenium deficiency\nHypocalcemia\nHyper/hypo-thyroidism\n\n\nTachycardia-induced\n\n\nAlcohol-induced\nAmphetamine-induced\nCatecholamine-induced (stress-induced, e.g. Takotsubo)\n\n\nAnabolic steroid-induced\n\n\nHemochromatosis\nWilson’s disease"
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    "text": "Tachycardia-mediated cardiomyopathy\nIschemic cardiomyopathy"
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    "text": "Genetic/dilated cardiomyopathy\nTachycardia-mediated cardiomyopathy\nIschemic cardiomyopathy"
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    "text": "Steroid-induced cardiomyopathy\nGenetic/dilated cardiomyopathy\nTachycardia-mediated cardiomyopathy\nIschemic cardiomyopathy"
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    "section": "Problems",
    "text": "Problems\n\n\n\nSinus tachycardia\n\n\n\nRight axis deviation with inferior qR and lateral rS pattern\n\n\n\n\nComplete interpolation of ventricular ectopy with superior axis and inverted transition at V2-V3\n\n\n\n\nEnlarged left-sided heart border with narrow vascular pedicle\n\n\n\n\nEarlier completely interpolated atrial depolarizations, as compared with PVC, at similar cycle length.\n\n\n\n\n\nLeft posterior fascicular block\n\n\n\n\nInferior/posterior-septal PVC\n\n\n\n\nCardiomegaly\n\n\n\n\nPoor or abnormal VA conduction?\n\n\n\n\n\nPatient describes a 10+ year history of anabolic steroid usage, initiated by his coach while he trained as a body-builder.\n. . .\nHe continued as he was unsure on how to taper.\n. . .\nHe had been on multiple testosterone and anabolic steroid supplements, and had most recently (past 3-6 months) trialed growth hormone.\n. . .\nGrowth hormone was stopped due to lower extremity and hand swelling."
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    "section": "Problems",
    "text": "Problems\n\n\n\n\nSeverely reduced LV systolic function with EF &lt; 20%\n\n\n\n\nLV cavity during diastole of ~7.5 cm\n\n\n\n\nLVOT VTI of 9 cm and RVOT VTI of 6 cm\n\n\n\n\nRegional wall motion abnormalities with inferior hypokinesis/akinesis\n\n\n\n\nModerate to severe mitral regurgitation\n\n\n\n\nEchodensity in apex\n\n\n\n\nGrade III diastolic dysfunction\n\n\n\nLeft posterior fascicular block\nInferior/posterior septal PVC\n\nCardiomegaly\n\n\n\nSevere systolic dysfunction\n\n\n\n\nDilated cardiomyopathy\n\n\n\n\nMitral regurgitation IIIb\n\n\n\n\nLow cardiac output state\n\n\n\n\nApical thrombus"
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    "section": "Coronary pressures during exercise",
    "text": "Coronary pressures during exercise\nTODO"
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    "title": "Clinical Case Conference",
    "section": "Steroid-induced cardiomyopathy",
    "text": "Steroid-induced cardiomyopathy\n. . .\nAnabolic-androgenic steroid (AAS) misuse, above that of replacement hormone levels, is common - up to 2% of men in the US (Pope et al., 2014)\n. . .\nAAS abuse tends to involve dosing 5-30 times greater than recommended by the Endocrine Society (Garner et al., 2018).\n. . .\nIn a small study (n = 140), AAS users had an LVEF 10% lower than age-matched non-users (Baggish et al., 2017).\n\n\n\nBaggish et al. (2017)"
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    "section": "Problems",
    "text": "Problems\n\n\n\n\nHypovolemic “shock” requiring nor epinephrine with light sedation\n\n\n\n\nLarge diameter coronary vessels (4-5 mm) without obstructive disease\n\n\n\n\nDiffuse ectasia of RCA with diminutive branch vessels\n\n\n\nLeft posterior fascicular block\nInferior/posterior septal PVC\nSevere systolic dysfunction\nDilated cardiomyopathy\nMitral regurgitation IIIb\n\nLow cardiac output state\n\nApical thrombus\n\n\nSpontaneous coronary artery dissection?"
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    "section": "TEMPORARY SLIDE",
    "text": "TEMPORARY SLIDE\nEMPTY"
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    "title": "Clinical Case Conference",
    "section": "Arterial Pressure During Resistance Training",
    "text": "Arterial Pressure During Resistance Training\n\nTesting the acute hypertensing response to resistance training, with invasive brachial artery pressure transduction.\nMacDougall et al. (1985)"
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    "section": "Arterial pressure and resistance training",
    "text": "Arterial pressure and resistance training\n. . .\nMacDougall et al. (1985) tested the acute hypertensing response to resistance training, with invasive brachial artery pressure transduction.\n\nSingle-arm curls of 255/190\nDouble-leg press of 320/250 (peak 480/350)"
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    "text": "Sliwa et al. (2023)"
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    "section": "AAS agents?",
    "text": "AAS agents?\n\nTestosterone is predominately bound to sex hormone-binding globulin, with only 1-2% being free\nOnce bound to androgen receptors, initiates gene transcription\nAAS agents mimic testosterone, but maximize anabolic effect and minimize androgenic effects\nAvailable orally or as injectable agents\nUsed in “cycles” however can become dependent, develop tolerance and have withdrawal with cessation (Garner et al., 2018)\nAdditional effect leads to dyslipidemia with high LDL and lower HDL, including increased coronary plaque volume (Fadah et al., 2023)\n\n\n\n\nFadah et al. (2023)"
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    "title": "Clinical Case Conference",
    "section": "But the growth hormone?",
    "text": "But the growth hormone?\n\nGrowth hormone deficiency is common in heart failure\nSalzano et al. (2018) reviewed studies on the effect on treatment with growth hormone on cardiac function, however mixed results:\n\nImproved functional class and exercise duration/capacity\nImproved VO2\nDecreased LV size, reverse remodeling, and improved LVEF\nDecrease HF-associated inflammatory cytokines\n\nDid on-and-off growth hormone mask some of the effects of AAS?\n\n\n\n\nSalzano et al. (2018)"
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    "section": "Problems",
    "text": "Problems\n\n\n\n\nDilated LV with severely reduced LV function\n\n\n\n\nInferior wall akinesis\n\n\n\n\nInferior wall showed transmural, from base to apex late gadolinium enhancement\n\n\n\n\nThrombus seen in the apex\n\n\n\nLeft posterior fascicular block\nInferior/posterior septal PVC\n\nSevere systolic dysfunction\nDilated cardiomyopathy\n\nMitral regurgitation IIIb\nLow cardiac output state\n\nApical thrombus\n\n\nSpontaneous coronary artery dissection?"
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    "section": "",
    "text": "MacDougall et al. (1985)"
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    "text": "Hospitalization:\n\nPatient was admitted to the cardiology service\nNephrology and endocrine consultation\nUnderwent coronary angiography and right heart catheterization\nUnderwent cardiac magnetic resonance imaging\nDischarged with LifeVest\n\n\nTreatment:\n\natorvastatin 20\napixaban 5 bid\nsacubitril-valsartan 24/26\nempagliflozin 10"
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    "section": "",
    "text": "Rare cases of SCAD seen with resistance training (Aghasadeghi & Aslani, 2008)\n. . .\nFahmy et al. (2016) described a population of men and women with SCAD. Men (v. women) had a higher rate of…\n\nBeing younger\nIsometric exercise\nHeavy-weight resistance training\nRecreational drugs\n\n\n\n\nAghasadeghi & Aslani (2008)"
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    "text": "Hospitalization:\n\nPatient was admitted to the cardiology service\nNephrology and endocrine consultation\nUnderwent coronary angiography and right heart catheterization\nUnderwent cardiac magnetic resonance imaging\nDischarged with LifeVest\n\n\nTreatment:\n\ncessation of AAS\natorvastatin 20\napixaban 5 bid\nsacubitril-valsartan 24/26\nempagliflozin 10"
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    "section": "Cine imaging",
    "text": "Cine imaging\n. . .\nGenerally, steady-state free precession (SSFP) is used in the generation of cine imaging.\n. . .\nRF pulses produce free induction decay curves or signals, and corresponding echos. When in rapid sequence, the signal will began to merge and never reach zero, achieving a continuous signal of varying amplitude \\(\\rightarrow\\) SSFP.\n. . .\nFor CMR, these sequences are repeated throughout a cardiac cycle."
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    "title": "Mendelian Randomization in Practice",
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    "text": "About\nBjörnson, Elias, Martin Adiels, Marja-Riitta Taskinen, Stephen Burgess, M. John Chapman, Chris J. Packard, and Jan Borén. “Lipoprotein(a) Is Markedly More Atherogenic Than LDL: An Apolipoprotein B-Based Genetic Analysis.” Journal of the American College of Cardiology 83, no. 3 (January 23, 2024): 385–95. https://doi.org/10.1016/j.jacc.2023.10.039.\n\nBjörnson et al. (2024)"
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    "text": "::: #refs\n\n\n\n\n\n\n\n\nBjörnson, E., Adiels, M., Taskinen, M.-R., Burgess, S., Chapman, M. J., Packard, C. J., & Borén, J. (2024). Lipoprotein(a) Is Markedly More Atherogenic Than LDL: An Apolipoprotein B-Based Genetic Analysis. Journal of the American College of Cardiology, 83(3), 385–395. https://doi.org/10.1016/j.jacc.2023.10.039"
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    "title": "Mendelian Randomization in Practice",
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    "text": "Article\n\n\n\n\n\n\n\nPaper\n\n\nBjörnson, Elias, Martin Adiels, Marja-Riitta Taskinen, Stephen Burgess, M. John Chapman, Chris J. Packard, and Jan Borén. Lipoprotein(a) Is Markedly More Atherogenic Than LDL: An Apolipoprotein B-Based Genetic Analysis Journal of the American College of Cardiology 83, no. 3 (January 23, 2024): 385–95. https://doi.org/10.1016/j.jacc.2023.10.039.\n\n\n\n\n\nBjörnson et al. (2024)"
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    "title": "Mendelian Randomization in Practice",
    "section": "References",
    "text": "References\n\n\nBjörnson, E., Adiels, M., Taskinen, M.-R., Burgess, S., Chapman, M. J., Packard, C. J., & Borén, J. (2024). Lipoprotein(a) Is Markedly More Atherogenic Than LDL: An Apolipoprotein B-Based Genetic Analysis. Journal of the American College of Cardiology, 83(3), 385–395. https://doi.org/10.1016/j.jacc.2023.10.039"
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    "text": "Objectives\n\nReview the role of lipids in atherosclerosis\nUnderstand the effect of genetic variants on lipid particles\nDescribe the principles of mendelian randomization\nConsider the intersection of epidemiology/causality using this methodology"
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    "text": "Outline\n\n\n\nIntroduction\n\nPurpose\nBackground on lipids\nOverview of Lp(a)\n\nMethods\n\nStatistical approach\nGenetics of ApoB100\n(Re)-introduction to mendelian randomization\n\nResults\n\nMajor findings\nSupplemental findings\n\nConclusions\n\nInnovation of approach\nValidity"
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    "section": "Basics of lipids",
    "text": "Basics of lipids\n\n\n\n\n\nCholesterol\n\n\n\n\n\nTriglycerides\n\n\n\n\nHigh-density lipoprotein (HDL)\nLow-density lipoprotein (LDL)\nVery low-density lipoprotein (VLDL)\n\n\n\n\nCholesterols (and triglycerides) are insoluble in water, and must be transported via protein structures called lipoproteins.\n\n\n\n\n\n\n\n\nFigure 2: Diagram of structure of a lipoprotein particle\n\n\n\n\n\n\n\nhttps://my.clevelandclinic.org/health/articles/23229-lipoprotein"
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    "text": "Types of MR\n\nOne-sample v. two-sample\n\n\nSanderson et al. (2022)"
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    "text": "References\n\n\nBjörnson, E., Adiels, M., Taskinen, M.-R., Burgess, S., Chapman, M. J., Packard, C. J., & Borén, J. (2024). Lipoprotein(a) Is Markedly More Atherogenic Than LDL: An Apolipoprotein B-Based Genetic Analysis. Journal of the American College of Cardiology, 83(3), 385–395. https://doi.org/10.1016/j.jacc.2023.10.039\n\n\nHolmes, D. N., Piccini, J. P., Allen, L. A., Fonarow, G. C., Gersh, B. J., Kowey, P. R., O’Brien, E. C., Reiffel, J. A., Naccarelli, G. V., Ezekowitz, M. D., Chan, P. S., Singer, D. E., Spertus, J. A., Peterson, E. D., Thomas, L., & null, null. (2019). Defining Clinically Important Difference in the Atrial Fibrillation Effect on Quality-of-Life Score. Circulation: Cardiovascular Quality and Outcomes, 12(5), e005358. https://doi.org/10.1161/CIRCOUTCOMES.118.005358\n\n\nSanderson, E., Glymour, M. M., Holmes, M. V., Kang, H., Morrison, J., Munafò, M. R., Palmer, T., Schooling, C. M., Wallace, C., Zhao, Q., & Davey Smith, G. (2022). Mendelian randomization. Nature Reviews Methods Primers, 2(1, 1), 1–21. https://doi.org/10.1038/s43586-021-00092-5"
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    "section": "Lipoprotein classification",
    "text": "Lipoprotein classification\n\nCore of cholesterol & triglycerides wrapped in phospholipid layer containing apolipoproteins\n\nHDL (12 nm) contains ApoA1\nLDL (18-25 nm) contains ApoB100\nIDL (&lt; 50 nm) and VLDL (&gt; 50 nm) are similar to LDL, but do not enter arterial intima\n\nLDL (IDL & VLDL) contain only one ApoB100 protein\n\n\n\n\n\n\n\n\nFigure 3: Classification of cholesterol types\n\n\n\n\nHolmes et al. (2019)"
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    "section": "What is lipoprotein(a)?",
    "text": "What is lipoprotein(a)?\n\nLp(a) is a type of LDL particle\nContains an additional protein called apolipoprotein (a), which binds directly to ApoB100 via a disulfide bond\nThis means that Apo(a) and ApoB100 exist in a 1:1 molar ratio\nClinical relevance\n\nIncreased atherogenicity\nDriver of CVD mortality\nMay represent clinical benefits of PCSK9i (and future siRNA therapies, e.g. pelacarsen)"
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    "section": "Why do we care about Lp(a)?",
    "text": "Why do we care about Lp(a)?\n\nIncreased atherogenecity\nDriver of CVD mortality\nMay represent clinical benefits of PCSK9i"
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    "section": "Study populations",
    "text": "Study populations\n\n\nUK Biobank\n\n502,000 UK residents (primarily European ancestry)\n487,202 with genetic data\n402,387 not on lipid lowering agents\nGenotyping performed using UK BiLEVE Axiom or UK Biobank Axiom array, which evaluated 805,426 SNPs\n\n\nCARDIoGRAMplusC4D\n\nCoronary ARtery DIsease Genome wide Replication and Meta-analysis plust The Coronary Artery Disease Genetics dataset\nUsed as a replication cohort to test generalizability"
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    "text": "Approach\n\nIdentify SNPs associated with LDL and Lp(a) by GWAS\n\nLDL cluster of SNPs\nLp(a) cluster of SNPs\n\nEnsure appropriate SNP estimates/weights on LDL/Lp(a)\n\nCheck that LDL-cluster of SNPs not associated with Lp(a) mass\nCheck that Lp(a) cluster of SNPs associated in linear manner with apoB and Lp(a) mass\n\nOutcomes (CHD events) analysis using exposure of LDL-apoB or Lp(a)-apoB"
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    "section": "Lipid measurements",
    "text": "Lipid measurements\n\n\nLDL\n\nLDL-c was directly measured\nTriglyceride-rich lipoprotein cholesterol remnants (TRL) = total cholesterol - (HDL + LDL)\nTRL were removed from analysis, including associated SNPs\n\n\nLp(a)\n\nLp(a) mass concentration measured in 377,572 participants\nLp(a) is meausured as a concentration, which is an approximation as Lp(a) has a range of molecular weights\nNot used for MR analysis directly, but for validation of SNP effects\n\n\nApoB\n\nApoB measured in g/L\nConverted to plasma concentrations in nmol/L by assuming molecular weight of 550 kDa"
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    "section": "Polygenic scores",
    "text": "Polygenic scores\n\nGWAS x2 performed, wadjusting for age, sex, and genomic principal components (PC1 - PC5)\nSNPs meeting threshold of \\(p &lt; 5 \\times 10^{-8}\\) were included\nSNPs pruned for linkage disequilibrium (\\(r^{2} &lt; 0.1\\)) and minor allele frequency (\\(MAF &gt; 0.01\\))\n\nLinkage disequilibrium (LD) is the non-random association of alleles at linked loci\n\\(r^{2}\\) is the correlation coefficient between pairs of loci\n\nPolygenic scores calculated for the Lp(a) SNP cluster and the LDL SNP cluster\nEach SNP was weighted by effect size on apoB\nEach subject received a score as the weighted sum of all the effect sizes present"
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    "section": "Statistical approach",
    "text": "Statistical approach\n\nMendelian randomization (MR) using the R package {MendelianRandomization}\nCox proportional hazard for incident CHD outcomes\nCHD outcomes defined as…\n\nNon-fatal myocardial infarction\nFatal MI\nCoronary revascularization\n\nPGS terms scaled according to relationshp between PGS and apoB\nHazard ratio calculated per 50 nmol/L increase in apoB"
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    "text": "Outline and objectives\n\n\nOutline\n\n\nIntroduction\n\nPurpose\nBackground on lipids\nOverview of Lp(a)\n\nMethods\n\nStatistical approach\nGenetics of ApoB100\n(Re)-introduction to mendelian randomization\n\nResults\n\nMajor findings\nSupplemental findings\n\nConclusions\n\nInnovation of approach\nValidity\n\n\n\n\nObjectives\n\n\nIntroduction\n\nPurpose\nBackground on lipids\nOverview of Lp(a)\n\nMethods\n\nStatistical approach\nGenetics of ApoB100\n(Re)-introduction to mendelian randomization\n\nResults\n\nMajor findings\nSupplemental findings\n\nConclusions\n\nInnovation of approach\nValidity"
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    "section": "Overview",
    "text": "Overview\n\n\nOutline\n\n\nIntroduction\n\nPurpose\nBackground on lipids\nOverview of Lp(a)\n\nMethods\n\nStatistical approach\nGenetics of ApoB100\n(Re)-introduction to mendelian randomization\n\nResults\n\nMajor findings\nSupplemental findings\n\nConclusions\n\nInnovation of approach\nValidity\n\n\n\n\nObjectives\n\n\nReview the role of lipids in atherosclerosis\nUnderstand the effect of genetic variants on lipid particles\nDescribe the principles of mendelian randomization\nConsider the intersection of epidemiology/causality using this methodology"
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    "section": "Polygenic scores (PGS)",
    "text": "Polygenic scores (PGS)\n\nGWAS x2 performed, adjusting for age, sex, and genomic principal components (PC1 - PC5)\nSNPs meeting threshold of \\(p &lt; 5 \\times 10^{-8}\\) were included\nSNPs pruned for linkage disequilibrium (\\(r^{2} &lt; 0.1\\)) and minor allele frequency (\\(MAF &gt; 0.01\\))\n\nLinkage disequilibrium (LD) is the non-random association of alleles at linked loci\n\\(r^{2}\\) is the correlation coefficient between pairs of loci\n\nPolygenic scores calculated for the Lp(a) SNP cluster and the LDL SNP cluster\nEach SNP was weighted by effect size on apoB\nEach subject received a score as the weighted sum of all the effect sizes present"
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    "section": "Statistical analysis",
    "text": "Statistical analysis\n\nMendelian randomization (MR) using the R package {MendelianRandomization}\nCox proportional hazard for incident CHD outcomes\nCHD outcomes defined as…\n\nNon-fatal myocardial infarction\nFatal MI\nCoronary revascularization\n\nPGS terms scaled according to relationshp between PGS and apoB\nHazard ratio calculated per 50 nmol/L increase in apoB"
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    "section": "Mendelian randomization",
    "text": "Mendelian randomization\n\nInstrumental variable (IV) analysis\n\nIV related to exposure but not to outcome (except through exposure)\nAvoids bias from unobserved confounding of outcome ~ exposure\n\nIV require three assumptions\n\nRelevance: IV is associated with exposure\nIndependence: IV is independent of confounders\nExclusion: IV affects outcome only through exposure\n\nWhen using multiple IV (e.g. many SNPs), must account for weak instrument bias, that can be partially mitigated by two-sample approach and/or jackknife resampling"
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    "section": "Key findings",
    "text": "Key findings\n\nGenetic variants in SNPs were be separated into LDL and Lp(a) clusters\nChanges in apoB can be attributed to differences by SNP clusters, which were then associated with CHD risk\nComparative CHD risk suggests per particle, Lp(a) is 4-12 times more atherogenic than LDL\nProvides causal evidence based on study design"
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    "section": "Study strengths and limitations",
    "text": "Study strengths and limitations\n\n\nStrengths\n\nLp(a)-apoB translates to apo(a) levels in 1:1 fashion\nApoB served as a common denominator to directly compare Lp(a) and LDL risk\nApoB is a standardized test, compared to the variability in Lp(a) testing\n\n\nLimitations\n\nVariable nature of Lp(a) particles (e.g. number of kringle 4 copy numbers) could not be assessed\nSNPs used for Lp(a) were located in a small region of chromosome 6 at the \\(LPA\\) locus"
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    "section": "Study design considerations",
    "text": "Study design considerations\n\n\nStrengths\n\nLp(a)-apoB translates to apo(a) levels in 1:1 fashion\nApoB served as a common denominator to directly compare Lp(a) and LDL risk\nApoB is a standardized test, compared to the variability in Lp(a) testing\nEnrollment cohort included those with and without CHD at baseline\n\n\nLimitations\n\nVariable nature of Lp(a) particles (e.g. number of kringle 4 copy numbers) could not be assessed\nSNPs used for Lp(a) were located in a small region of chromosome 6 at the LPA locus (although attempted stringent linkage disequilibrium for SNP pruning)\nPrimarily European ancestry"
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    "section": "Questions?",
    "text": "Questions?"
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    "section": "Application to this study",
    "text": "Application to this study\n\nUse of genetic variant prediction of Lp(a)-apoB and LDL-apoB as IV\n\nDoes not require actual apo(a) measurement, which is a difficult assay\nCalibrated on measures of apoB\n\nUse summary-level data and causal-estimation using {MendelianRandomization} package in R, with variation in weights\nUse both one-sample and two-sample approach (previously published GWAS)"
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    "section": "Example in R",
    "text": "Example in R\n\n\n\n\nlibrary(MendelianRandomization)\n\nMRInputObject &lt;-\n  mr_input(\n    bx = ldlc,\n    bxse = ldlcse,\n    by = chdlodds,\n    byse = chdloddsse\n  )\n\nMRAllObject_all &lt;-\n  mr_allmethods(MRInputObject,\n                method = \"all\")\n\nmr_plot(MVMRInputObject)\nmr_plot(MRAllObject_all)"
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    "title": "Mortality and Morbidity",
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    "text": "Hospital course\nMaria D Valdez is a 69 y.o. female with PMH of ESRD s/p DDKT 2018 due to HTN and SLE c/b lupus nephritis, afib on apixaban, IDDM, hypothyroidism, T6-T7 meningioma s/p meningioma resection and laminectomy, and CAD s/p PCI to LAD 1/28/23 who presents from OSH for further management of gross hematuria and recurrent UTI. Pt presented to OSH for chest pain and was found to have STEMI and had PCI placed in LAD and was started on DAPT in addition to home medication of apixaban. Developed gross hematuria and also had some minimal bleeding from access site at groin which had resolved.\nWorkup revealed UA concerning for UTI, per documentation culture was growing E. Coli and was started on CTX then switched to nitrofurantoin 100mg BID once susceptibilities came back at NW OSH (1 day worth of it). Escalated to impenem here due to concern for ESBL without susceptibilities in hand. Transplant ultrasound without signs of pyelo but there is mild hydronephrosis  Per documentation urology was consulted and signed off since hematuria was resolving and likely from DAPT. Goal was to have patient start losartan but appears blood pressure was low end of normal so this was held and carvedilol was also decreased to 3.25 mg BID. Eliquis has been held since gross hematuria began, but DAPT continued because of high risk given very recent stent placement. Immunosuppressives were continued.   Overall pt feels well and that she is recovering. Reports having worked with physical therapy while at the OSH. States that all day today her urine was not bloody. Denies dysuria. Has had purewick in place. Of note pt tested positive for COVID while at OSH but has remained asymptomatic, she is fully vaccinated.    MEDICINE TEAM E COURSE: Escalated to impenem here due to concern for ESBL without susceptibilities in hand. Per ID, de-escalated to nitrofurantoin for appropriate coverage (last day 2/9). Diuretics were held per transplant nephro given possible transplant rejection noted at OSH. Apixaban was continued to be held on admission in setting of gross hematuria, with apixaban restarted on 2/5.   On 2/6, patient was noted to have desaturated to 84-86% on RA. Saturating appropriately on 2L O2 NC. CXR obtained showing pulmonary edema, IVF were stopped with plan to diurese if no signs of improvement.   When seen in the AM, patient was noted to be hypoxic, desaturating to the mid-80s on 2L O2 NC, improved to low 90s on 6L. Patient endorsed chest pain with exertion that had started overnight. EKG w/ possible ST depressions, troponin elevated to 1900, though difficult to interpret in setting of recent STEMI (last troponin &gt;25000 at OSH on 1/29). It was identified that DAPT had not been re-ordered upon admission. Cardiology was consulted, who recommended urgent cardiac cath and transfer to CCU.   CCU COURSE (2/7-2/11): Transferred to CCU, had cardiac cath w/o evidence of stent thrombosis. Briefly hypotensive after cath requiring levophed, now weaned off. Intubated given hypoxemic respiratory failure 2/2 to volume overload, extubated 2/9 now on room air.   TTE on 2/8 showed EF of 29% with RWA, LV mural thrombus. Patient was initially on triple therapy but descalated to Plavix and Eliquis as DAPT. Pt’s AKI initially improved after diuresis but worsened in setting of GI losses from diarrhea on 2/10. Felt to be iatrogenic 2/2 medication side effect for constipation. S/p 500 cc bolus NS. Currently holding ACE/ARB given AKI.   Medicine Team A Course (2/11-2/13): Patient had some hematemesis/hemoptysis with suctioning and went for EGD on 2/12 without an identifiable bleeding lesion. Bleeding thought to be in setting of intubation trauma and has now resolved. On 2/13 AM patient with mild acidosis, worsening LFT and AKI c/f continued congestion and IV depletion. Acute liver workup and transplant nephrology consulted. Patient with decreasing urine output and downtrending Na to 118, necessitating ICU care per Dr. Tang, attending transplant nephrologist. Prior to transfer patient was made NPO since we would like to fluid restrict her (food is ok) and we started a sodium bicarb drip to correct her acidosis.   MICU 2 Course (2/13- 2/14): Patient transferred to MICU for management of moderate hyponatremia to 120 and AKI (kidney transplant 11/9/18) likely cardiorenal etiology with EF 30% given sacral edema and pulmonary congestion on CXR. POCUS on arrival to MICU demonstrated moderate circumferential pericardial effusion which is larger than noted posterior pericardial effusion on TTE from (2/8). She was diuresed and Cardiology was contacted regarding the effusion where pericardiocentesis was done with 600 cc of bloody fluid with hemodynamic changes suggestive of pericardial tamponade. Of notes, ventricular tachycardia with successful synchronized cardioversion, biventricular overload with normal C.O., and Severe LV dysfx c/w free wall rupture. Patent LAD stent. Transfuse PRBC in lab with plan for cardiac surgery with repair of free wall rupture. R IJ accessed and swan catheter placed. Transferred to OR under cardiothoracic surgery now s/p pericardial window, intubated and on norepinephrine/epinephrine. Accepted and Transferred to CCU service.   CCU course (2/14-2/17) Per transplant nephrology, pt continued on sodium bicarbonate drip for acidosis and AKI for 1 day. Given concern for volume overload, pt then started on CVVH, D5W added on to prevent sodium from overcorrecting. Pt had worsening lactic acid, started on imipenem and infectious workup sent. Repeat TTE obtained which was similar to prior with EF &lt;20%. Hepatology consulted for worsening LFTs concerning for ischemic hepatitis, recommended supportive care. Pt had worsening INR, started on IV Vitamin K and given FFP. Also noted to have thrombocytopenia, 2 units platelets given and HIT workup sent. Started on dobutamine drip 2/15 given worsening urine output. UOP did not improve, but patient was weaned off norepi, and lactate began to normalize, with LFTs peaking in the thousands presumable secondary to resolving shock liver. Patient overall appeared stable, and eventual transfer for durable LVAD was discussed with advance cardiology providers at NMH.   On the morning of 2/17, patient self-extubated and was comfortable on room air, awake/responsive. Pulmonary pressures and lactate had also been improving on dobutamine 2.5, with CVVH pulling 50mL/hr for cardiogenic shock with oliguric patient. Around 11:30am, patient entered Vtach rhythm and pulse was lost. She received CPR and 1mg epi was given prior to ROSC. Sinus rhythm devolved into recurrent Vtach and patient was shocked. Subsequent rhythm was also irregular and devolved into asystole. During this interval, patient was reintubated. During second code, she received another 1mg epi and further CPR was provided. ROSC was obtained again with sinus rhythm, stable. Despite full oxygenation via ventilator, she was saturating in mid 70s, and dobutamine was restarted after previously being held over concern it might have contributed to the initial arrhythmia. Saturation recovered, and norepi was initiated at 40, with appropriate BP obtained. POCUS demonstrated severely reduced LVEF ~10%, similar to prior. Given initial Atach, she began amio loading. Patient’s son was at bedside and requested full code until his sister arrived.   Upon the daughter’s arrival, she and her brother were given the option of pursuing transfer to NMH for possible LVAD, but after discussing, they elected palliative extubation and comfort care. They reported that the patient had previously expressed her wish not to be reintubated, and felt the decision best reflected the patients goals for care when last decisional. Patient was extubated around 5pm with family present and prompty passed away. Family declined autopsy."
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    "text": "Cardio last saw cardiology 10/12/22 (+) Aortic stenosis (moderate AS and moderate AR on TEE 10/2022) (+) Benign essential hypertension (on metoprolol, reports at home BPs 130s/80s, BP in office 106/74 today) (+) Congestive heart failure (CMS/HCC) (EF 55 to 60% on TEE 10/2022, on Lasix, denies pedal edema or SOB (but wife reports patient “sounds like he has difficulty breathing at times”), +1-3 pillow orthopnea as well as sleeps with head of bed elevated (chronic, stable/unchanged), does not follow low salt diet) (+) Longstanding persistent atrial fibrillation (CMS/HCC) (on Eliquis) (+) Pulmonary hypertension (CMS/HCC) (moderate-severe on RHC 1/4/23, on sildenafil) (-) Chest pain (-) MI (myocardial infarction) (CMS/HCC) (-) Stented coronary artery\nPulmonary wife reports apneic episodes for patient but no previous sleep study\n\n\n\n\n\nMr. Powell is a 58 year old male who underwent a mitral and aortic valve replacement for symptomatic moderate mitral regurgitation and moderate aortic stenosis and regurgitation. He received 1 platelet intraop. He was transferred to the ICU in stable condition. Large pericardial effusion noted on CT chest 2/3/23.\nCardiovascular: -S/p AVR and MVR on 1/27 -POD1 single chamber pacemaker, V paced at 60 -Boston Scientific Model Number L310, Serial Number 834450 -no evidence of pocket hematoma -hemodynamically stable -Increased lasix to 40mg BID -Preop medications: Toprol XL 25mg daily, Lasix 40 daily. - restarted home lasix, not started BB as patient is baseline bradycardic and requiring pacing -LAA thrombus seen on TEE -discussed indications for coumadin in the case with a history of valvular afib and left atrial thrombus. Patient prefers to be on Eliquis. -Continue ASA 81mg and pre op statin -Preop LCEF 55% - repeat TTE stat - NPO 2/2 hemoptysis\n\n\n\n\n\n\n58 yr old M with MR, AS and AR s/p surgical MVR and AVR with carpenter-edwards bioprosthetic valves (23mm aortic, 25mm mitral) on 1-27-2023, kidney transplant in 2015, pAF, pHTN who was admitted for the valve replacement surgery. Postoperatively he had persistent junctional escape needing transvenous pacing, being planned for PPM. Yesterday he had a TTE that showed a large left atrial echodensity concerning for thrombus, so he presents today for TEE for better evaluation.\n\n\n\n58M h/o ESRD s/p transpant in 2015 (on IS), persistent AF, and calcific VHD now s/p SMVR/SAVR on 01/27 c- Edwards-Carpentier bovine bioprosthetic valves. He had ?junctional escape in 40s, and epicardial pacer was left on 60 to help c- this block.\nPt feels much better now, overall, and is on top of his pain medications. There was some suspicion of HIT in setting of his thrombocytopenia and need for platelets, along with this new found suspected thrombus in LA. He hasn’t noticed any stroke like sx, and feels his pain is better controlled. Doesn’t note any dizzy/LH/syncopal sx when his PM rate is decreased.\nCurrently c- HR in 60s c- irregular wide complex pattern and underlying AF. S1/S2 observed, distant. Less crackles noted on lateral lung fields. TTE with potential LA thrombus.\nHigh grade AV block in setting of persistent AF after SMVR/SAVR, with new dx of LA thrombus d/t ?HIT:\n\nAs pt may have changes in AC options d/t this, we will defer DC-PPM placement until resolution or a plan is solidified. We can do this procedure under oral AC but would wait until this LA thrombus issue has resolved before proceding.\nOf note, he is less rate dependent on the pacemaker, as has been able to generate rates as high as mid-60s. We set his back-up rate at 50 for now.\nWill continue to follow along, and have initiated the conversation with IC/general cards about interventions. TEE pending.\n\n\n\n\nEcho 1/30/23: Mild LVH, normal LV function EF 55-60%, severely dilated LA and RA, moderate to severely elevated pulmonary artery pressure, well seated mitral and aortic valve. Large left atrial echodensity concerning for thrombus.\nAssessment/Plan: Calvin D Powell is an 58 y.o. male with MR, AR, AS, kidney transplant in 2015, on immunosuppression, afib, pHTN on sildenafil who was admitted on 1/26/2023 for aortic and mitral valve replacement on 1/27. Cardiology consulted for recommendations regarding LA thrombus seen on TTE.\nProblem List: Left atrial thrombus Bradycardia with pacemaker at 60bpm Mitral and Aortic Regurgitation s/p bioprosthetic valve replacements on 1/27 hx of kidney transplant on immunosuppression AKI thrombocytopenia, concern for HIT\nRecommendations: - Obtain TEE to further characterize LA thrombus - Anticoagulation per CT surgery, but no objection to keep the patient on AC for now from a cardiology standpoint\n\n\n\nMr. Powell is a 58 year old AA M w/ hx of kidney transplant in 2015, on immunosuppression, afib, pHTN on sildenafil, mod-severe calcified AS/moderate AI/mod-severe MR s/p 23mm Bioprosthetic AVR and 25mm bioprosthetic MVR on 1/27/23 c/b Patient-prostheis mismatch and mild-mod periprosthetic regurgitation, CHB s/p Boston Scientific SC-ppm 2/1/23, Long standing persistent Atrial Fibrillation, large posterior pericardial effusion who remains in ICU with volume overload and suboptimal urine output (currently Cr 2.26, hovering close to ~2 since surgery). This AM paged that patient has not been feeling well, poor urine output and he is V-paced at 60 bpm.\nTTE 2/4/23: 1. Ventricular wall thickness is mildly increased. There is normal global left ventricular function. Overall left ventricular ejection fraction by visual estimate is 60%. 2. There is a well-seated bioprosthetic valve in the aortic position (bioAVR, 23mm Carpentier Edwards; placed 1/26/23). Bioprosthetic leaflets not well seen, though appear to be normally thin and mobile consistent with normal leaflet function. Mean gradient 26 mmHg and peak velocity of 3.5 m/s and acceleration time around 95msec and DI 0.45 suggestive of patient prosthesis mismatch. 3. There appears to be very eccentric, mild-moderate bioAVR regurgitation that is likely periprosthetic, seen along the mitral-aortic continuity. 4. There is a well-seated bioprosthetic valve in the mitral position (bioMVR, 25mm Carpentier Edwards, placed 1/26/23). Bioprosthetic leaflets not well seen, though there appears to be some leaflet thickening and reduced excursion of one of the leaflets. Elevated mean transmitral diastolic gradient 6 mm Hg at a HR of 60 bpm. 5. There is a small highly-mobile echodensity seen along the ventricular surface of the bioMVR measuring approximately 7mm in length and 3mm in width (i.e. image 34); similar echodensity not well seen on prior TTE 1/30/2023 or TEE 1/31/2023. Differential includes residual chordal structure (not seen on prior echos) or possibly a new vegetation. Consider further evaluation with TEE if clinically indicated. 6. Mild tricuspid valve regurgitation. The estimated right ventricular systolic pressure is elevated at 55 mmHg. 7. IVC size is dilated with &lt;50% collapse consistent with an RA pressure of 15 - 20 mmHg. 8. There is a large, mostly posteriorly-located pericardial effusion measuring only about 0.5cm in diameter anteriorly at end-ventricular diastole and and approximately 2.6 cm in diameter posteriorly at end-ventricular diastole in the parasternal long axis view. Limited study to evaluate for respiratory changes, though no clear significant intracardiac hemodynamic compromise (no clear chamber collapse) from this predominantly posteriorly-located pericardial effusion.\nMr. Powell is a 58 year old AA M admitted to ICU with the following:\nVolume overload Stage C chronic systolic HF with preserved EF, NYHA class III-IV symptoms AKI in setting of prior kidney transplant in 2015 on immunosuppression, pHTN\nmod-severe calcified AS with moderate AI s/p 23mm Carpentier Edwards Bioprosthetic AV on 1/27/23 mod-severe MR s/p 25mm Carpentier Edwards bioprosthetic MV on 1/27/23 Patient-prostheis mismatch mild-mod periprosthetic regurgitation CHB s/p Boston Scientific SC-ppm 2/1/23 Long standing persistent Atrial Fibrillation large posterior pericardial effusion\nImpression: discussed with Dr. Avitall with EP and increased patient’s back-up ventricular rate to 80 bpm with hopes to augment CO. From EP perspective, we are limited in further optimizing device as it is single lead ppm. Patient also seen and assessed with Dr. Ibrahim. Low concern that there is tamponade physiology from the posterior effusion and that the bioprostethetic valves are responsible for the current issues. He is clinically volume overloaded and out diuretic strategy thus far appears to be suboptimal. No stigmata of cardiogenic shock at this time.\nRecommendations: 1. Please increase our lasix dosing and frequency to lasix 80mg BID for goal urine output of 1-2 L in 24 hours. If patient is not achieving this goal, we will need to increase to a lasix drip +/- thiaxide diuretic such as metolazone. Suspect that we may see transient Cr rise with diuresis but suspect that is cardiorenal and will improve once we diuresis and relieve the venous congestion.\n\n\n\n\nVolume overload/large posterior pericardial effusion\nS/p 23 mm Carpentier Edwards bioprosthetic AVR 1/26/23. Elevated Vmax 3.5 m/s mm MG 26 mm Hg c/w PPM (normal AT, DI). Mild-moderate periprosthetic aortic regurgitation not well characterized on TTE or TEE 1/31/23, which will need f/u\nS/p 25 mm Carpentier Edwards bioprosthetic MVR 1/26/23. MG elevated 6 mm Hg (HR 60 BPM). Valve appears normal on TEE 1/31/23\nLAA thrombus\nHigh grade AV block post operative, now s/p single lead Boston Scientific PM implanted 2/1/23\nParoxysmal atrial fibrillation\nRenal transplant 2015 on immunosuppression\nPulmonary hypertension on sildenafil\n\n58 y.o. M, cardiology following for volume overload, LA thrombus management.\nAgree with continued IV diuresis, can increase to lasix 80 mg IV TID, goal -2-3L/day as he remains quite overloaded. BUN/Cr are stable, no contraction alkalosis. He reports improvement, but dyspnea not completely resolved. No clinical evidence of tamponade from the predominantly posterior pericardial effusion. No c/o chest pain beyond incisional discomfort to suggest marked pericarditis; patient is already on prednisone for renal tx. Otherwise, continue apixaban AC for LA thrombus.\n\n\n\n\nPatient: Calvin D Powell Admission Date: 1/26/2023 Discharge Date: 2/16/2023 Discharge Disposition: Home with family\nDischarge Service: Cardiothoracic Surgery Discharge Attending: Malek Massad, MD Primary Diagnosis: S/P aortic valve and mitral valve replacement for mitral valve insufficiency and aortic valve stenosis.\nSecondary Diagnosis Bradycardia symptomatic requiring PPM Hx of atrial fibrilation Left atrial thrombus on DOAC Hemorrhoids Bloody stools Right lower lobe consolidation Constipation BPH Deconditioning Surgical blood loss anemia Large pericardial effusion ATN AKI non oliguric Pulmonary hypertension Restrictive Lung disease Orthopnea Surgeries Performed\n1/26/2023 OPERATIONS: 1. Median sternotomy. 2. Total cardiopulmonary bypass. 3. Aortic valve replacement with a 23 mm Carpentier-Edwards pericardial bovine tissue valve. 4. Mitral valve replacement with a 25 mm Carpentier-Edwards pericardial bovine tissue valve. 5. Insertion of 2 temporary ventricular bipolar pacing wires. 6. Insertion of 2 mediastinal and 1 right pleural chest tubes.\n2/1/2023 Procedure Performed: Placement of a single chamber permanent pacemaker via the right subclavian vein under fluoroscopy.\n2/14/2023 OPERATIONS:\n7. Subxiphoid pericardiostomy with drainage of 650 cc of nonclotting serosanguineous fluid. 8. Insertion of a Jackson-Pratt catheter in the pericardial sac.\nHospital Course Mr. Powell is a 58 year old male who underwent a mitral and aortic valve replacement for symptomatic moderate mitral regurgitation and moderate aortic stenosis and regurgitation. He received 1 platelet intraop. He was transferred to the ICU in stable condition. He was noted to be baseline bradycardic after surgery and EP was consulted for PPM which was placed on 2/1. Transplant nephrology was consulted given patient had a kidney transplant in 2016. Post operative echo showed large left atrial appendage thrombus and patient preferred to be anticoagulated with eliquis. GI was consulted for intermittent bloody stools and thought likely to be internal hemorrhoids and deferred colonoscopy to 3 months post discharge. Aspirin held and eliquis continued given risks of stroke remain high given size and location of thrombus, hemoglobin and hemodynamics remained stable and concern for large bleed were low. Pacemaker set to 80 BPM to help with cardiac output. Ongoing diuresis with IV lasix given patient had enlarged IVC on echo. On 2/14 patient underwent pericardial window with drainage of 650cc of serosanguineous fluid and immediate improvement in hemodynamics. Renal function continued to improve. Sleep medicine consult was placed as RN noticed patient would snore and desaturate at night- patient preferred to do sleep study after discharge. Patient was deemed stable for discharge. Extensive time was taken to explain discharge instructions to both patient and wife. Numbers were given in the event patient would need to contact the team prior to follow up visit 2/21/2023."
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    "text": "Cardio last saw cardiology 10/12/22 (+) Aortic stenosis (moderate AS and moderate AR on TEE 10/2022) (+) Benign essential hypertension (on metoprolol, reports at home BPs 130s/80s, BP in office 106/74 today) (+) Congestive heart failure (CMS/HCC) (EF 55 to 60% on TEE 10/2022, on Lasix, denies pedal edema or SOB (but wife reports patient “sounds like he has difficulty breathing at times”), +1-3 pillow orthopnea as well as sleeps with head of bed elevated (chronic, stable/unchanged), does not follow low salt diet) (+) Longstanding persistent atrial fibrillation (CMS/HCC) (on Eliquis) (+) Pulmonary hypertension (CMS/HCC) (moderate-severe on RHC 1/4/23, on sildenafil) (-) Chest pain (-) MI (myocardial infarction) (CMS/HCC) (-) Stented coronary artery\nPulmonary wife reports apneic episodes for patient but no previous sleep study"
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    "text": "Mr. Powell is a 58 year old male who underwent a mitral and aortic valve replacement for symptomatic moderate mitral regurgitation and moderate aortic stenosis and regurgitation. He received 1 platelet intraop. He was transferred to the ICU in stable condition. Large pericardial effusion noted on CT chest 2/3/23.\nCardiovascular: -S/p AVR and MVR on 1/27 -POD1 single chamber pacemaker, V paced at 60 -Boston Scientific Model Number L310, Serial Number 834450 -no evidence of pocket hematoma -hemodynamically stable -Increased lasix to 40mg BID -Preop medications: Toprol XL 25mg daily, Lasix 40 daily. - restarted home lasix, not started BB as patient is baseline bradycardic and requiring pacing -LAA thrombus seen on TEE -discussed indications for coumadin in the case with a history of valvular afib and left atrial thrombus. Patient prefers to be on Eliquis. -Continue ASA 81mg and pre op statin -Preop LCEF 55% - repeat TTE stat - NPO 2/2 hemoptysis"
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    "text": "58 yr old M with MR, AS and AR s/p surgical MVR and AVR with carpenter-edwards bioprosthetic valves (23mm aortic, 25mm mitral) on 1-27-2023, kidney transplant in 2015, pAF, pHTN who was admitted for the valve replacement surgery. Postoperatively he had persistent junctional escape needing transvenous pacing, being planned for PPM. Yesterday he had a TTE that showed a large left atrial echodensity concerning for thrombus, so he presents today for TEE for better evaluation.\n\n\n\n58M h/o ESRD s/p transpant in 2015 (on IS), persistent AF, and calcific VHD now s/p SMVR/SAVR on 01/27 c- Edwards-Carpentier bovine bioprosthetic valves. He had ?junctional escape in 40s, and epicardial pacer was left on 60 to help c- this block.\nPt feels much better now, overall, and is on top of his pain medications. There was some suspicion of HIT in setting of his thrombocytopenia and need for platelets, along with this new found suspected thrombus in LA. He hasn’t noticed any stroke like sx, and feels his pain is better controlled. Doesn’t note any dizzy/LH/syncopal sx when his PM rate is decreased.\nCurrently c- HR in 60s c- irregular wide complex pattern and underlying AF. S1/S2 observed, distant. Less crackles noted on lateral lung fields. TTE with potential LA thrombus.\nHigh grade AV block in setting of persistent AF after SMVR/SAVR, with new dx of LA thrombus d/t ?HIT:\n\nAs pt may have changes in AC options d/t this, we will defer DC-PPM placement until resolution or a plan is solidified. We can do this procedure under oral AC but would wait until this LA thrombus issue has resolved before proceding.\nOf note, he is less rate dependent on the pacemaker, as has been able to generate rates as high as mid-60s. We set his back-up rate at 50 for now.\nWill continue to follow along, and have initiated the conversation with IC/general cards about interventions. TEE pending.\n\n\n\n\nEcho 1/30/23: Mild LVH, normal LV function EF 55-60%, severely dilated LA and RA, moderate to severely elevated pulmonary artery pressure, well seated mitral and aortic valve. Large left atrial echodensity concerning for thrombus.\nAssessment/Plan: Calvin D Powell is an 58 y.o. male with MR, AR, AS, kidney transplant in 2015, on immunosuppression, afib, pHTN on sildenafil who was admitted on 1/26/2023 for aortic and mitral valve replacement on 1/27. Cardiology consulted for recommendations regarding LA thrombus seen on TTE.\nProblem List: Left atrial thrombus Bradycardia with pacemaker at 60bpm Mitral and Aortic Regurgitation s/p bioprosthetic valve replacements on 1/27 hx of kidney transplant on immunosuppression AKI thrombocytopenia, concern for HIT\nRecommendations: - Obtain TEE to further characterize LA thrombus - Anticoagulation per CT surgery, but no objection to keep the patient on AC for now from a cardiology standpoint\n\n\n\nMr. Powell is a 58 year old AA M w/ hx of kidney transplant in 2015, on immunosuppression, afib, pHTN on sildenafil, mod-severe calcified AS/moderate AI/mod-severe MR s/p 23mm Bioprosthetic AVR and 25mm bioprosthetic MVR on 1/27/23 c/b Patient-prostheis mismatch and mild-mod periprosthetic regurgitation, CHB s/p Boston Scientific SC-ppm 2/1/23, Long standing persistent Atrial Fibrillation, large posterior pericardial effusion who remains in ICU with volume overload and suboptimal urine output (currently Cr 2.26, hovering close to ~2 since surgery). This AM paged that patient has not been feeling well, poor urine output and he is V-paced at 60 bpm.\nTTE 2/4/23: 1. Ventricular wall thickness is mildly increased. There is normal global left ventricular function. Overall left ventricular ejection fraction by visual estimate is 60%. 2. There is a well-seated bioprosthetic valve in the aortic position (bioAVR, 23mm Carpentier Edwards; placed 1/26/23). Bioprosthetic leaflets not well seen, though appear to be normally thin and mobile consistent with normal leaflet function. Mean gradient 26 mmHg and peak velocity of 3.5 m/s and acceleration time around 95msec and DI 0.45 suggestive of patient prosthesis mismatch. 3. There appears to be very eccentric, mild-moderate bioAVR regurgitation that is likely periprosthetic, seen along the mitral-aortic continuity. 4. There is a well-seated bioprosthetic valve in the mitral position (bioMVR, 25mm Carpentier Edwards, placed 1/26/23). Bioprosthetic leaflets not well seen, though there appears to be some leaflet thickening and reduced excursion of one of the leaflets. Elevated mean transmitral diastolic gradient 6 mm Hg at a HR of 60 bpm. 5. There is a small highly-mobile echodensity seen along the ventricular surface of the bioMVR measuring approximately 7mm in length and 3mm in width (i.e. image 34); similar echodensity not well seen on prior TTE 1/30/2023 or TEE 1/31/2023. Differential includes residual chordal structure (not seen on prior echos) or possibly a new vegetation. Consider further evaluation with TEE if clinically indicated. 6. Mild tricuspid valve regurgitation. The estimated right ventricular systolic pressure is elevated at 55 mmHg. 7. IVC size is dilated with &lt;50% collapse consistent with an RA pressure of 15 - 20 mmHg. 8. There is a large, mostly posteriorly-located pericardial effusion measuring only about 0.5cm in diameter anteriorly at end-ventricular diastole and and approximately 2.6 cm in diameter posteriorly at end-ventricular diastole in the parasternal long axis view. Limited study to evaluate for respiratory changes, though no clear significant intracardiac hemodynamic compromise (no clear chamber collapse) from this predominantly posteriorly-located pericardial effusion.\nMr. Powell is a 58 year old AA M admitted to ICU with the following:\nVolume overload Stage C chronic systolic HF with preserved EF, NYHA class III-IV symptoms AKI in setting of prior kidney transplant in 2015 on immunosuppression, pHTN\nmod-severe calcified AS with moderate AI s/p 23mm Carpentier Edwards Bioprosthetic AV on 1/27/23 mod-severe MR s/p 25mm Carpentier Edwards bioprosthetic MV on 1/27/23 Patient-prostheis mismatch mild-mod periprosthetic regurgitation CHB s/p Boston Scientific SC-ppm 2/1/23 Long standing persistent Atrial Fibrillation large posterior pericardial effusion\nImpression: discussed with Dr. Avitall with EP and increased patient’s back-up ventricular rate to 80 bpm with hopes to augment CO. From EP perspective, we are limited in further optimizing device as it is single lead ppm. Patient also seen and assessed with Dr. Ibrahim. Low concern that there is tamponade physiology from the posterior effusion and that the bioprostethetic valves are responsible for the current issues. He is clinically volume overloaded and out diuretic strategy thus far appears to be suboptimal. No stigmata of cardiogenic shock at this time.\nRecommendations: 1. Please increase our lasix dosing and frequency to lasix 80mg BID for goal urine output of 1-2 L in 24 hours. If patient is not achieving this goal, we will need to increase to a lasix drip +/- thiaxide diuretic such as metolazone. Suspect that we may see transient Cr rise with diuresis but suspect that is cardiorenal and will improve once we diuresis and relieve the venous congestion.\n\n\n\n\nVolume overload/large posterior pericardial effusion\nS/p 23 mm Carpentier Edwards bioprosthetic AVR 1/26/23. Elevated Vmax 3.5 m/s mm MG 26 mm Hg c/w PPM (normal AT, DI). Mild-moderate periprosthetic aortic regurgitation not well characterized on TTE or TEE 1/31/23, which will need f/u\nS/p 25 mm Carpentier Edwards bioprosthetic MVR 1/26/23. MG elevated 6 mm Hg (HR 60 BPM). Valve appears normal on TEE 1/31/23\nLAA thrombus\nHigh grade AV block post operative, now s/p single lead Boston Scientific PM implanted 2/1/23\nParoxysmal atrial fibrillation\nRenal transplant 2015 on immunosuppression\nPulmonary hypertension on sildenafil\n\n58 y.o. M, cardiology following for volume overload, LA thrombus management.\nAgree with continued IV diuresis, can increase to lasix 80 mg IV TID, goal -2-3L/day as he remains quite overloaded. BUN/Cr are stable, no contraction alkalosis. He reports improvement, but dyspnea not completely resolved. No clinical evidence of tamponade from the predominantly posterior pericardial effusion. No c/o chest pain beyond incisional discomfort to suggest marked pericarditis; patient is already on prednisone for renal tx. Otherwise, continue apixaban AC for LA thrombus."
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    "text": "Patient: Calvin D Powell Admission Date: 1/26/2023 Discharge Date: 2/16/2023 Discharge Disposition: Home with family\nDischarge Service: Cardiothoracic Surgery Discharge Attending: Malek Massad, MD Primary Diagnosis: S/P aortic valve and mitral valve replacement for mitral valve insufficiency and aortic valve stenosis.\nSecondary Diagnosis Bradycardia symptomatic requiring PPM Hx of atrial fibrilation Left atrial thrombus on DOAC Hemorrhoids Bloody stools Right lower lobe consolidation Constipation BPH Deconditioning Surgical blood loss anemia Large pericardial effusion ATN AKI non oliguric Pulmonary hypertension Restrictive Lung disease Orthopnea Surgeries Performed\n1/26/2023 OPERATIONS: 1. Median sternotomy. 2. Total cardiopulmonary bypass. 3. Aortic valve replacement with a 23 mm Carpentier-Edwards pericardial bovine tissue valve. 4. Mitral valve replacement with a 25 mm Carpentier-Edwards pericardial bovine tissue valve. 5. Insertion of 2 temporary ventricular bipolar pacing wires. 6. Insertion of 2 mediastinal and 1 right pleural chest tubes.\n2/1/2023 Procedure Performed: Placement of a single chamber permanent pacemaker via the right subclavian vein under fluoroscopy.\n2/14/2023 OPERATIONS:\n7. Subxiphoid pericardiostomy with drainage of 650 cc of nonclotting serosanguineous fluid. 8. Insertion of a Jackson-Pratt catheter in the pericardial sac.\nHospital Course Mr. Powell is a 58 year old male who underwent a mitral and aortic valve replacement for symptomatic moderate mitral regurgitation and moderate aortic stenosis and regurgitation. He received 1 platelet intraop. He was transferred to the ICU in stable condition. He was noted to be baseline bradycardic after surgery and EP was consulted for PPM which was placed on 2/1. Transplant nephrology was consulted given patient had a kidney transplant in 2016. Post operative echo showed large left atrial appendage thrombus and patient preferred to be anticoagulated with eliquis. GI was consulted for intermittent bloody stools and thought likely to be internal hemorrhoids and deferred colonoscopy to 3 months post discharge. Aspirin held and eliquis continued given risks of stroke remain high given size and location of thrombus, hemoglobin and hemodynamics remained stable and concern for large bleed were low. Pacemaker set to 80 BPM to help with cardiac output. Ongoing diuresis with IV lasix given patient had enlarged IVC on echo. On 2/14 patient underwent pericardial window with drainage of 650cc of serosanguineous fluid and immediate improvement in hemodynamics. Renal function continued to improve. Sleep medicine consult was placed as RN noticed patient would snore and desaturate at night- patient preferred to do sleep study after discharge. Patient was deemed stable for discharge. Extensive time was taken to explain discharge instructions to both patient and wife. Numbers were given in the event patient would need to contact the team prior to follow up visit 2/21/2023."
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    "text": "Understand the cognitive processes involved in the case-based diagnostic reasoning\nIdentify diagnostic assumptions that may lead towards case-specific biases\nPractice contextualizing clinical data in the framework of cardiovascular physiology"
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    "text": "Phase-corrected inversion recovery sequences are less reliant on a set inversion time\n. . .\nNext sequence is done with free-breathing."
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    "text": "History\n81M with RV lead migration\n\nSingle-chamber pacemaker implanted September 2023 for high grade AV block\nParoxysmal AF on apixaban and digoxin\nCOPD on home O2, HTN, DM, distant MI (1987)"
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    "text": "Presentation\n\n3-4 days of left-sided chest pain & increased dyspnea\nPresents to St. Luke’s (Idaho), and CT scan showing…\n\n\n“…pacer lead that transverses the apex of the right ventricle with a small pericardial hematoma and a few small foci of air within the pericardial region.”\n\n\nTransferred to St. Alphonsus (Idaho), with urgent chest tube placement (7/14)\nTVP placed for worsening lead measurements and intermittent heart block (7/17)\nTransferred to University for “higher level of care” (7/18)"
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    "text": "Current status\n\nLast anticoagulant dose 7/13 AM (Hb 14, PLT 100)\nSmall hemopericardium seen on echo and CT\nResolving left pneumothorax with chest tube\nHas intrinsic rhythm with current adequate permanent pacemaker parameters (VVI 60)\nTVP in place with (backup VVI 40)"
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    "text": "Considerations\nLead explantation/extraction with cardiothoracic surgery support:\n\nLikely mobile and not adherent to pericardium\nRisk of worsening pericardial bleeding (may benefit from prophylactic pericardial drain)\nHigh risk of inpatient mortality if requiring emergent surgery/sternotomy\nWill need long-term AC for CVA protection, difficult with migrating RV lead\nIf delayed (weeks to months), may lead to more difficult extraction due to fibrosis/adherence to pericardium/RV apex"
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