SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Severe aortic stenosis is known to be associated with a multitude of complications including heart failure, pulmonary hypertension, arrhythmias, acute coronary syndrome, and sudden cardiac death. We present a case of acute coronary syndrome in the setting of severe aortic stenosis. CASE PRESENTATION: 81-year-old man with PMH of moderate aortic stenosis(AVA 1.1cm2, gradient 29mmHg), atrial fibrillation, ascending aortic aneurysm, presented with sudden onset of chest pain. On arrival, he was hypoxic and was in bradycardic with HR in ’30s. After receiving atropine, his HR improved to ’50s. EKG showed junctional escape rhythm at 43 bpm, with significant ST Elevation of up to 4 mm in leads 2,3, aVF, V3-6, occasional PVCs with R on T phenomenon. Subsequently, he became pulseless and developed torsades requiring defibrillation X2 along with brief CPR to achieve spontaneous circulation. Troponin was elevated at 64.6 which later peaked to >200. Emergent LHC was done which showed normal coronary arteries with no significant blockages. Temporary femoral transvenous pacemaker placed for presumed bradycardia mediated torsades. CTA showed a stable aortic aneurysm and ECHO showed progression of aortic stenosis severity. Cardiac MRI was done to rule out myocarditis and other infiltrative etiologies. Cardiac MRI showed patchy focal fibrosis and edema of basal inferior septum most consistent with focal myocarditis. The magnitude of the troponin elevation way higher when compared with the area of focal myocarditis indicating there could be another mechanism of myocardial injury. The likely hypothesis is that patient developed Torsades secondary to bradycardia in the setting of Type II MI induced by severe aortic stenosis. Subsequently patient underwent TAVR and single chamber defibrillator as secondary prevention to prevent sudden cardiac death. DISCUSSION: AS when severe can cause various structural and autoregulatory changes leading to impairment of coronary flow reserve and myocardial ischemia in the absence of significant coronary artery disease. Compensatory LVH in AS increases the myocardial oxygen demand and also causes extravascular compression of the coronary microcirculation increasing the resistance in the microvasculature leading to impairment of myocardial perfusion. Severe AS is associated with a high risk of sudden cardiac death. A potential mechanism of SCD is activation of ventricular baroreceptors resulting in paradoxical bradycardia, decreased contractility, and hypotension (Bezold-Jarisch reflex). Timely valvular repair is known to decrease the complications of severe AS. Recent trials like RECOVERY are showing promising results of early surgery in asymptomatic severe AS Patients CONCLUSIONS: Severe aortic stenosis can result in sudden cardiac death secondary decreased coronary flow reserve in the absence of significant coronary artery disease. Reference #1: Circulation. 2003;107:3121–3123 Why Angina in Aortic Stenosis With Normal Coronary Arteriograms? K. Lance Gould and Blase A. Carabello Reference #2: Cardiol Res Pract. 2010;2010:423465. Published 2010 Jul 20. doi:10.4061/2010/423465 A case of critical aortic stenosis masquerading as acute coronary syndrome. Wayangankar SA, Dasari TW, Lozano PM, Beckman KJ. Reference #3: Nat Rev Cardiol 15, 420–431 (2018). https://doi.org/10.1038/s41569-018-0011-2 Pathophysiological coronary and microcirculatory flow alterations in aortic stenosis.Michail, M., Davies, J.E., Cameron, J.D. et al. DISCLOSURES: No relevant relationships by Tahreem Ahmad, source=Web Response No relevant relationships by Waqas Ali, source=Web Response No relevant relationships by Tariq Hassan, source=Web Response No relevant relationships by Pranali Santhoshini Pachika, source=Web Response
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