Original study
The relationship between growth of atherosclerotic plaques, variant angina and sudden death

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Abstract

Clinico-pathological findings are described in two patients with typical variant angina who died suddenly during an ischemic attack. In both cases, detailed pathologic examination of the coronary arteries disclosed severe focal atherosclerosis of the anterior descending coronary artery. The only distinctive histological finding was new intimal proliferation of smooth muscle cells enmeshed within mucoid substance, superimposed on the old fibrous cap of the plaque. These findings agree with experimental and clinical data which suggest that coronary vasospasm may be related to growth of atherosclerotic plaques. This study provides histological evidence that progression of an atherosclerotic plaque may underlie variant angina and sudden death.

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      The first experimental [37] and clinical demonstrations [38] of spastic changes date back to the nineties. We originally reported [39] two patients with variant angina who died suddenly with ECG-documented ischemia-induced ventricular fibrillation; at autopsy, a single-vessel CAD disease was observed in the left anterior descending coronary artery that consisted of a NAA plaque without thrombosis, with a well-preserved tunica media, and intimal SMCs hyperplasia, supporting the concept of functional instability with transient lumen occlusion (Supplemental Fig. 1). More recently, Shiomi and colleagues [40] provided the first in vivo experimental evidence that spasm can develop irrespectively of plaque composition.

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      Only in 30% of cases, VF is precipitated by acute occlusive coronary artery thrombosis, the latter usually occurring on a noncritical atherosclerotic plaque, triggered either by endothelial erosion or more rarely by fibrous cap rupture. In 70% of cases, the obstruction is most probably due to vasospasm, which has been proved to occur in SCD cases with transient ST-segment elevation at Holter monitoring, followed by onset of VF at reperfusion.13 Overt acute myocardial infarction, with classic histologic features of coagulative myocyte necrosis, was never observed in young SCD cases with atherosclerotic CAD.

    • Sudden cardiac death secondary to demonstrated reperfusion ventricular fibrillation in a woman with Takotsubo cardiomyopathy

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      In our case, the absence of significant arrhythmias during the hours preceding the cardiac arrest implies a strict connection of the onset of ventricular arrhythmias to the ischemic/reperfusion episode. The relationship between vasospasm and sudden death has been amply demonstrated in the literature since the early 1990s [4]. The massive reduction of the ST-segment elevation in less than 2 min indicates an abrupt reopening of the epicardial artery.

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    This study was supported by Veneto Region, Venice (Juvenile Sudden Death Research Project), Italy.

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