Left ventricular free wall rupture associated with a combination of acute myocardial infarction and stress-provoked cardiomyopathy: An autopsy case

Abstract

A 74-year-old female was admitted to our hospital due to prolonged chest pain that had lasted about 2 h. An electrocardiogram revealed ST-elevation in leads I, aVL, and V3-6, with an increase in myocardial necrosis markers. Emergency coronary angiography was performed, and left ventriculography showed the typical features of apical ballooning, and so a diagnosis of Takotsubo cardiomyopathy (TC) was made. On the 10th day after admission, the patient suddenly went into cardiopulmonary arrest because of a blow-out type left ventricular (LV) free wall rupture. Despite extensive cardiopulmonary resuscitation, the patient died. The autopsy revealed hemopericardium and a perforating wound located in the anterior wall of the LV. It was revealed that the diagonal branch of the coronary artery was occluded, and so a diagnosis of TC coexisting with acute myocardial infarction (AMI) was made. No previous case of TC accompanied by AMI has been reported. We present its clinical course during hospitalization and the result of a histopathologic examination.

Keywords: Acute myocardial infarction; Catecholamine cardiotoxicity; Left ventricular rupture; Takotsubo cardiomyopathy.

Figure 1

Cardiac catheterization. Coronary angiography revealed intact left anterior descending, circumflex (A), and right coronary arteries (B). Left ventriculography in the right anterior oblique view showed the typical features of apical ballooning (arrowhead), and basal hyperkinetics (asterisk), and an end-diastolic volume of 145 mL, an end-systolic volume of 106 mL, an ejection fraction of 27% (C and D). Left ventriculography in left anterior oblique view (E and F) showed concentric circles caused by apical ballooning (arrowhead), and basal hyperkinetics (asterisk) in systolic phase (F).

Figure 2

Autopsy findings. The perforating wound is indicated by an arrow (A–C). In the sectioned profile of the rupture site at the apex (B), transmural necrosis was seen in the anterior-lateral wall. A low power view of the same section with B is indicated by masson-trichrome stain (C). Microscopically, there was no contraction band necrosis in the border zone between infarct and non-infarct tissue on hematoxylin-eosin stain (D). The coronary tree shows an occlusion in the 2nd diagonal branch (arrow in E), the occlusive lesion has fibrous plaque, dissection, and thrombus on hematoxylin-eosin stain (F).