ABC | Volume 110, Nº4, April 2018

Anatomopathological Correlation Nunes et al. A 73 year-old man with ischemic heart disease and cachexia Arq Bras Cardiol. 2018; 110(4):388-392 Figure 2 – A and B: Cross sections of the ventricles in the middle-basal and apical regions, respectively. Healed transmural infarction in the left ventricular anterior and lateral walls and in the anterior two-thirds of the ventricular septum, with aneurysmal formation. Myocardial hypertrophy of the left ventricular walls not affected by the infarction is evident. Organizing thrombus in the endocardium of the left ventricular anterior and septal walls (arrow) in the middle-basal region, extending to the apical region (tr). Organizing thrombus in the right ventricular endocardium of the apex (arrow). C and D: Histological sections of the left ventricular aneurysm showing an isolated group of cardiomyocytes (m) and focal calcification (ca) amid mural fibrosis (f). Hematoxylin-eosin, 25x. Postmortem examination The external examination revealed significant weight loss and moderate edema in the subcutaneous tissue, more marked in the lower limbs. On opening of the abdomen, 280 mL of yellow translucent ascitic fluid escaped. The heart weighed 644g (normal: 300-350g), and both ventricles were enlarged. Cross sections of the ventricles evidenced healed transmural myocardial infarction in the left ventricular anterior and anterolateral walls, involving at least 45% of the left ventricular myocardial mass and the anterior two-thirds of the ventricular septum, from the heart base to its tip (Figure 2). Significant left ventricular aneurysmatic dilatationwas observed, with important fibrosis and thinning of the anterior wall, whose thickness ranged from 0.2 cm to 1.4 cm. In the middle and apical thirds of the left ventricle, an organizing laminated thrombus was identified, adhered to the endocardial surface of the anterior wall and ventricular septum (Figure 2). The myocardium not affected by the infarction in the left ventricle was hypertrophied. The right ventricle showed moderate mural hypertrophy and dilatation, with an organizing thrombus in the apical region. Themicroscopic study of the epicardial coronary arteries showed atherosclerotic impairment with fibrosis and calcification in atheromatous plaques and important obstruction of the vascular lumen of the major branches (Figure 3). The branches of the left coronary artery showed: maximal luminal obstruction of 75% in the first centimeter of the circumflex artery (CX), and 90% in the fourth centimeter of the anterior interventricular artery (AD). In addition, to aggravate the obstruction of the latter, in the fourth centimeter, there was an old recanalized thrombus in a calcified atherosclerotic plaque. The right coronary artery (RC) showed a maximal obstruction of 60% in its first centimeter, and 70% in the first centimeter of its posterior interventricular branch (PD). Neither recent myocardial infarction nor coronary thrombosis nor intracoronary stent s were seen. The lungs, liver and spleen showed morphological changes of chronic passive congestion secondary to CHF (Figure 4). The aorta and cerebral arteries of the Willis polygon evidenced moderate atherosclerosis with calcification. The brain showed neither recent nor old ischemic infarction. There were benign nephrosclerosis, represented by hyalinization of the wall of the glomerular afferent arterioles, and myocardial sclerosis, with multifocal perivascular fibrosis in the left ventricular myocardium, due to systemic arterial hypertension. The lungs showed bilateral suppurative aspiration pneumonia, with particulate food matter and Gram-positive filamentous bacterial aggregates, morphologically compatible with Actinomyces sp , which are saprophyte microorganisms of the mouth (Figure 5). There was benign nodular prostatic hyperplasia, accompanied by a distended and thickened urinary bladder, with no morphological evidence of infection. There were acute tubular necrosis in the kidneys, hepatic centrilobular necrosis in the liver, and recent multifocal subendocardial infarctions in both ventricles, resulting from low cardiac output. Although the patient had reported coronary angioplasty with stent implantation 8 years before, no stent was identified in the coronary arteries. Neither malignant neoplasms nor morphological evidence of infection in other organs were found. (Léa Maria Macruz Ferreira Demarchi, MD) Anatomopathological diagnoses: 1) systemic atherosclerosis; 2) coronary atherosclerosis; 3) ischemic heart disease, with healed infarction in the left ventricular anterior and anterolateral walls and in the anterior two-thirds of the ventricular septum; 4) left ventricular aneurysmatic dilatation 390