First report on biventricular stress cardiomyopathy with concomitant atrio-ventricular high-grade conduction disorder

Abstract

Stress cardiomyopathy (takotsubo cardiomyopathy [TTC]) is an acute cardiac syndrome mimicking acute coronary syndrome (ACS) characterized by typical systolic dysfunction of left ventricle. Right ventricular involvement has been previously reported and represents an important predictor of adverse clinical outcomes. Biventricular involvement occurs in approximately one third of patients [1]. Atrio-ventricular (AV) block complicating TTC occurs in only 5% of patients [2]. Association of biventricular TTC, complete AV block and cardiogenic shock presenting as ACS is extremely rare and has never been reported to date.This study reports a case of an 82-year-old female known to have diabetes mellitus type II as well as CHILD B hepatic cirrhosis on beta-blocker treatment for oesophagal varices and was admitted to the Emergency Department for typical chest pain at rest and vasovagal syncope. Third degree AV block with high ventricular escape was noted on 12-lead electrocardiogram (Fig. 1A). Laboratory results showed an elevation of high-sensitivity cardiac troponin from 130 ng/L to 450 ng/L as well as N-terminal pro B-type natriuretic paptide (NTproBNP) elevation (3905 ng/L). During admission patient developed severe arterial hypotension, bradycardia, and cardiogenic shock. Urgent coronary angiography for very high-risk non-ST-segment elevation ACS was performed and demonstrated unobstructed coronary arteries. Severe biventricular systolic dysfunction with biventricular apical ballooning was noted on ventriculography ( Fig. 1D; Supplementary Movie 5 -see journal website). However, the patient presented persistent high-degree AV block requiring temporary endovenous pacing and finally implantation of a dual-chamber pacemaker at day 10. The patient was discharged on day 12 on enalapril, sitagliptin/ /metformin and simvastatin. At one one-year follow-up patient had remained free from cardiovascular symptoms and adverse cardiac events, though there was persistent high-degree AV block. Control echocardiogram demonstrated preserved left ventricular function (EF 60%) without wall motion abnormalities.Despite numerous known triggers [3][4][5], the underlying pathophysiological mechanism of timely stunned myocardium and AV conduction damage remains unclear. Whether AV blocks are the cause or consequence of TTC is still a matter of debate. The persistence of AV conduction disorders in the setting of transient left ventricle dysfunction inclines reconsideration clinical cardiology