Vulnerable plaque: the devil is in the details.

Abstract

The notion of “vulnerable atherosclerotic plaque” introduced many years ago1,2 has been since used frequently and liberally, including by this investigator.3 We generally use this phrase to refer to intact lesions that look similar to those previously found to be disrupted and complicated by thrombosis on pathological examination. In doing so, we assume that given enough time or the right stimulus, these would become disrupted, thus triggering the formation of a thrombus. In an attempt to transform the potentiality into certainty, Virmani and colleagues4 have proposed that a descriptive terminology based on pathological characteristics of atherosclerotic lesions should be used instead. They proposed that the precursor lesion for disrupted plaques should be referred as “thin-cap fibroatheroma” (TCFA), a terminology that should encompass, along with ruptured plaques, the other types of plaques triggering thrombosis, ie, eroded plaques and calcified nodules. TCFA of patients dying from acute myocardial infarction are usually associated with <50% diameter stenosis, explaining the relatively recent realization of the danger these plaques may harbor. Other overall characteristics commonly associated with ruptured plaques include their propensity to have an eccentrically located lumen, as well as the significantly enhanced compensatory enlargement of the affected segment.4,5 See p 337 Morphologically, ruptured plaques are characterized by a thin fibrous cap covering a necrotic core containing macrophages and interstitial collagen, calling for improved imaging techniques that can reveal this level of structural detail in the plaques of patients.6 The precise measurements that can be performed on pathological specimens have yielded detailed dimensional parameters. For instance, the area of the necrotic core in at least 75% of cases of ruptured plaques examined was reported4 to be …