Diagnosis of myocardial infarction at autopsy: AECVP reappraisal in the light of the current clinical classification

Abstract

Ischemic heart disease is one of the leading causes of morbidity and death worldwide. Consequently, myocardial infarctions are often encountered in clinical and forensic autopsies, and diagnosis can be challenging, especially in the absence of an acute coronary occlusion. Precise histopathological identification and timing of myocardial infarction in humans often remains uncertain while it can be of crucial importance, especially in a forensic setting when third person involvement or medical responsibilities are in question. A proper post-mortem diagnosis requires not only up-to-date knowledge of the ischemic coronary and myocardial pathology, but also a correct interpretation of such findings in relation to the clinical scenario of the deceased. For these reasons, it is important for pathologists to be familiar with the different clinically defined types of myocardial infarction and to discriminate myocardial infarction from other forms of myocardial injury. This article reviews present knowledge and post-mortem diagnostic methods, including post-mortem imaging, to reveal the different types of myocardial injury and the clinical-pathological correlations with currently defined types of myocardial infarction.

Keywords: Acute coronary syndromes; Autopsy; Immunohistochemistry; Myocardial infarction; Myocardial injury; Post-mortem imaging.

Fig. 1

Coronary artery segments with different degrees of atherosclerotic stenosis. The diagrams demonstrate a 50% area stenosis, 75% stenosis and 90% stenosis; diameter x will usually be less than 2 mm in the left main stem and less than 1 mm in other major coronary arteries

Fig. 2

Patterns of topographic distribution of MI in the heart: regional transmural infarction; regional subendocardial infarction; circumferential subendocardial infarction; diffuse multifocal infarction

Fig. 3

Visualization of coronary collaterals in post-mortem angiograms. Contrast filling of right coronary artery (RCA) shows retrograde filling through collaterals of a large marginal branch of occluded left coronary artery (a). Contrast filling of RCA of another heart shows extensive ‘bridging collaterals’ surrounding a chronic total occlusion of the artery (b)

Fig. 4

Histological features of MI at different stages, without reperfusion; myofiber waviness (a); interstitial oedema (b); hypereosinophilia and coagulative necrosis of cardiomyocytes (c); heavy granulocyte infiltration with karyorrhexis (d); macrophages and lymphocyte infiltration with early removal of necrotic debris (e); granulation tissue with formation of microvessels (f); fibroblast proliferation and early collagen deposition (g); dense fibrous scar replacing myocyte loss (h). All sections are stained with haematoxylin and eosin

Fig. 5

Nitro blue tetrazolium (NBT)-stained myocardium; myocardial slice (middle) with circumferential subendocardial infarction indicated by loss of staining (pale area); purple-stained tissue represents vital myocardium, heart and apical slice are not NBT treated

Fig. 6

Immunostaining of early myocardial infarction. Positive staining for fibronectin (a) and C5b-9 (b) in irreversibly injured cardiomyocytes. Scale bars = 50 μm. Courtesy from Aljakna et al., Int J Legal Med, 2018; acute myocardial infarction in papillary muscle immunostained with C4d antibody (brown). Low power view, bar = 0.25 mm, highlights exact delineation of necrotic areas (geographic zones, and multifocal cells) (c); Higher magnification, bar = 50 μm, shows abrupt border between vital tissue and necrotic area (d)

Fig. 7

Histological features of MI with reperfusion; Detail of myocardium with contraction band necrosis (a); microvascular damage and extravasation of erythrocytes (b); macroscopic image of the heart with left ventricular widespread circumferential subendocardial haemorrhage(c); embolus of guide wire coating (blue material) surrounded by giant cells and some lymphocytic infiltration in myocardial microvessel of a previously PCI treated (stented) coronary artery (d); Histologic sections stained with haematoxylin and eosin