title: Concept of vulnerable/unstable plaque.
abstract: Today's concept of vulnerable plaque has evolved primarily from the early pioneering work uncovering the pivotal role of plaque rupture and coronary thrombosis as the major cause of acute myocardial infarction and sudden cardiac death. Since the first historical description of plaque rupture in 1844, several key studies by leading researchers and clinicians have lead to the current accepted views on lesion instability. Important to the complex paradigm of plaque destabilization and thrombosis are many discoveries beginning with the earliest descriptions of advanced plaques, reminiscent of abscesses encapsulated by fibrous tissue capable of rupture. It was not until the late 1980s that studies of remodeling provided keen insight into the growth of advanced plaques, beyond the simple accumulation of lipid. The emphasis in the next decade, however, was on a focused shift toward the mechanisms of lesion vulnerability based on the contribution of tissue proteolysis by matrix metalloproteinases as an essential factor responsible for thinning and rupture of the fibrous cap. In an attempt to unify the understanding of what constitutes a vulnerable plaque, morphological studies, mostly from autopsy, suggest the importance of necrotic core size, inflammation, and fibrous cap thickness. Definitive proof of the vulnerable plaque, however, remains elusive because animal or human data supporting a cause-and-effect relationship are lacking. Although emerging imagining technologies involving optical coherence tomography, high-resolution MRI, molecular biomarkers, and other techniques have far surpassed the limits of the early days of angiography, advancing the field will require establishing relevant translational animal models that produce vulnerable plaques at risk for rupture and further testing of these modalities in large prospective clinical trials.
authors.affiliation: Emory University School of Medicine, Atlanta, GA, USA.
authors.forename: Aloke V
authors.initials: AV
authors.lastname: Finn
authors.forename: Masataka
authors.initials: M
authors.lastname: Nakano
authors.forename: Jagat
authors.initials: J
authors.lastname: Narula
authors.forename: Frank D
authors.initials: FD
authors.lastname: Kolodgie
authors.forename: Renu
authors.initials: R
authors.lastname: Virmani
mesh_terms: D000818:Animals; D003324:Coronary Artery Disease / Q000150:complications / Q000266:history* / Q000473:pathology; D003952:Diagnostic Imaging / Q000379:methods; D018450:Disease Progression; D019317:Evidence-Based Medicine; D049672:History, 19th Century; D049673:History, 20th Century; D049674:History, 21st Century; D006801:Humans; D009203:Myocardial Infarction / Q000209:etiology / Q000266:history* / Q000473:pathology; D011237:Predictive Value of Tests; D018570:Risk Assessment; D012307:Risk Factors; D012421:Rupture; D013927:Thrombosis / Q000209:etiology / Q000266:history* / Q000473:pathology