An autopsy case of tako-tsubo cardiomyopathy presenting ventricular tachycardia after pacemaker implantation

Abstract

We herein report a rare autopsy case of tako-tsubo cardiomyopathy (TTC) presenting ventricular tachycardia after pacemaker implantation. A 69-year-old male received a dual-chamber pacemaker implantation for complete atrioventricular block. He had no chest symptoms after the operation. Three days later, he developed severe chest pain, followed by syncope. Electrocardiogram showed sustained monomorphic ventricular tachycardia. Despite the use of amiodarone and frequent electrical defibrillation, ventricular tachycardia and ventricular fibrillation were repeated incessantly. He died 24 h after the syncope. The autopsy revealed no hemopericardial effusion, or perforation of leads. There were also no obstructive lesions in the coronary arteries. Myocardial necrosis was observed in the entire circumference and the all layers of the left ventricle. Microscopically, myocardial necrosis was plurifocal and contraction band necrosis. We speculate that catecholamine cardiotoxicity caused ventricular tachycardia in this case. Further studies are needed to clarify the heterogeneity of this disease. <Learning objective: Tako-tsubo cardiomyopathy should be considered a potential complication of pacemaker implantation. Physicians should recognize that this disorder can occur unexpectedly during medical examination or treatment.>.

Keywords: Contraction band necrosis; Pacemaker implantation; Tako-tsubo cardiomyopathy; Ventricular tachycardia.

Fig. 1

(A) Twelve-lead electrocardiogram at hospital admission; (B) twelve-lead electrocardiogram after pacemaker implantation; and (C) chest X-ray after pacemaker implantation.

Fig. 2

(A) Sustained monomorphic ventricular tachycardia with left bundle branch block and right axis with a frequency of 160 beats per minute; (B) an urgent echocardiography at the bedside (parasternal long axis view); (C) chest X-ray at the time of sudden change and (D) twelve-lead electrocardiogram after cardioversion.

Fig. 3

(A) Cross-section of the heart; (B) distribution of the myocardial necrosis sites; (C) the specimen from the left ventricle (hematoxylin–eosin staining; scale bar, 200 μm). The enclosed areas show the pleurifocal myocardial necrosis. (D) Area of contraction band necrosis in a left ventricle myocardium section, cellular degeneration typical of Tako-tsubo cardiomyopathy (hematoxylin-eosin staining; scale bar, 50 μm).