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Multiple asymptomatic coronary plaque ruptures and fissures in acute myocardial infarction

To the Editor, Acute myocardial infarction (AMI) is a life‐threatening cardiovascular condition. Most AMI is caused by thrombus formation after disruption of atherosclerotic plaque. Several clinical studies of intravascular imaging showed that plaque ruptures were observed in the culprit lesions and other sites of coronary arteries, and multiple plaque ruptures were found in coronary arteries in 21.5% of patients with AMI. However, pathological features of asymptomatic plaque disruption in AMI have not been clearly described. Here, we describe an autopsy case of AMI with preceding multiple plaque disruptions in the three coronary arteries. The patient was a Japanese man in his early 70s. He was a habitual smoker (30 cigarettes per day) with no other significant medical history. He was admitted to the emergency room of our hospital because of sustained chest pain 2 days before death. Electrocardiography revealed ST‐segment elevation in leads II, III, aVF, V4‐V6, and V4R, and coronary angiography revealed total occlusion at the proximal part of the right coronary artery (RCA) (Segment 2), considered the culprit lesion, and also showed 90% stenosis in the proximal parts of the left anterior descending artery (Segment 6) and left circumflex artery (Segment 11). Primary percutaneous coronary intervention with thrombus aspiration and stent implantation was immediately performed for the culprit lesion of the RCA, which led to reperfusion of the RCA. Although the patient was cared for in the intensive care unit after the intervention, he died of ventricular fibrillation and cardiogenic shock. On post‐mortem macroscopic examination, the heart (weighing 420 g) showed dark mottling with central yellow‐tan and focal hemorrhage in the posterior wall and ventricular septa (Figure S1a). Histological examination revealed coagulative necrosis of the cardiomyocytes with neutrophil infiltration (Figure S1b,c). Additionally, some cholesterol emboli were found in the intramyocardial arterioles of the sepal and right ventricular walls. No foci of granulation tissue or scars were observed. The coronary arteries were cut into 3‐mm intervals with a knife or scissors, and the stents were removed under a stereomicroscope after the ethylenediaminetetraacetic acid decalcifying procedure. The stented proximal RCA (Segment 2) showed no luminal occlusion owing to thrombus aspiration. At the most proximal sites of the stent implantation, a plaque rupture was found with exposure of the lipid core with foamy macrophages (Figure S2a) and a small amount of fresh thrombus (Figure 1a) and intraplaque hemorrhage spread within distal plaques. The stented portion of the RCA was compatible with the culprit lesion of AMI and post‐thrombus aspiration state. In addition, five foci of plaque disruptions with various pathologic features were observed in Segment 3 of the RCA and Segments 5–7, and 11 of the left coronary artery. One feature of the plaque disruption was a small fibrous cap disruption with large atherosclerotic plaques (Segments 6, 7, and 11), accompanied by intraplaque hemorrhage, fibrin deposition, and their organizing reaction (Figure 1b–d). The plaque of Segment 6 showed a small healed rupture covered by a small organizing thrombus (Figures 1b, S3a,b). The plaques of Segments 7 and 11 showed plaque fissure and a tiny disruption of the fibrous cap without intramural thrombus formation (Figure 1c,d). Another feature of plaque disruption was ulceration of the atherosclerotic plaques, intraplaque hemorrhage, and mural organizing thrombus formation within the plaques (Segments 3 and 5) (Figures 1e,f, S3c–f). These disrupted plaques were not accompanied by occlusive thrombus formation and were considered non‐culprit lesions of AMI. Immunohistochemistry for CD68 highlighted intense accumulation of macrophages in all disrupted plaques, and infiltration of macrophages in the fibrous cap of the disrupted plaques, suggesting contribution of macrophage to plaque instability (Figure S2b–f). In addition, these thrombi and intraplaque hemorrhages in disrupted plaques showed various phases of time‐dependent organizing reactions with CD68‐immunopositive cell infiltration (Figure S2e,f), suggesting that asymptomatic coronary disruptions preceded fatal AMI events. The underlying mechanisms of the onset of cardiovascular events include plaque rupture, plaque erosion, or disruption of the calcified nodule. These