Abstract

Current literature suggests that the incidence of sudden cardiac arrest (SCA) attributable to mitral valve prolapse (MVP) is more common than historically presumed. Although its true incidence remains unknown, this novel realization suggests that the presence of MVP after resuscitated SCA should prompt exploratory identification of a causative association between MVP and SCA, even in the presence of other plausible explanatory findings. Case Description: A 60-year-old male with a history of hypertension presented with an out-of-hospital cardiac arrest due to ventricular fibrillation (VF). Coronary angiography revealed a 99% occluded 1st diagonal branch which was stented. TTE showed normal biventricular function and coincidentally found a myxomatous mitral valve with bileaflet prolapse. The patient was discharged without further work up under the rationale that the ischemic etiology of his arrest was reversed. 6 months later, he presented with another episode of VF arrest. EKG showed sinus bradycardia and a QTc of 534ms. Troponin was negative. Coronary angiography revealed a patent stent and coronary vessels. A cardiac MRI was obtained to investigate the arrhythmic significance of his MVP and showed late gadolinium enhancement in the basal inferolateral wall and tips of the mitral papillary muscles. A dual chamber implantable cardiac defibrillator was placed with a plan for future mitral valve repair. Discussion: Recent studies suggest that the estimated annual risk of SCA due to MVP is 0.2% to 1.9%, a figure higher than previously reported. Certain EKG, TTE and cardiac MRI findings have been associated with an increased risk of ventricular arrhythmias and SCA. In this patient, this included bileaflet MVP, mitral antral disjunction, and inferobasal wall and papillary muscle fibrosis. Currently, there are no society guidelines to assist in the identification of patients with MVP at high-risk for SCA. Nonetheless, in patients with MVP resuscitated from SCA, further workup to identify high risk features is reasonably justified to guide secondary SCA prophylaxis, even in the presence of other explanatory findings for SCA.

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