Atherosclerotic Plaque Rupture

Abstract

Abstract-It is generally established that the unstable plaque is the major cause of acute clinical sequelae of atherosclerosis.Unfortunately, terms indicating lesions prone to plaque instability, such as "vulnerable plaque," and the different phenotypes of unstable plaques, such as plaque rupture, plaque fissuring, intraplaque hemorrhage, and erosion, are often used interchangeably. Moreover, the different phenotypes of the unstable plaque are mostly referred to as plaque rupture.In the first part of this review, we will focus on the definition of true plaque rupture and the definitions of other phenotypes of plaque instability, especially on intraplaque hemorrhage, and discuss the phenotypes of available animal models of plaque instability. The second part of this review will address the pathogenesis of plaque rupture from a local and a systemic perspective. Plaque rupture is thought to occur because of changes in the plaque itself or systemic changes in the patient. Interestingly, contributing factors seem to overlap to a great extent and might even be interrelated. Finally, we will propose an integrative view on the pathogenesis of plaque rupture. Definition of Plaque RuptureIn 1995, the American Heart Association (AHA) Committee on Vascular Lesions developed a numerical classification of the composition and structure of human atherosclerotic lesions. In this classification, "complicated lesions" (type VI lesions), responsible for most of the morbidity and mortality from atherosclerosis, were defined as atheromata (type IV lesions) or fibroatheromata (type V lesions), containing 1 or more surface defects and/or hematoma-hemorrhage and/or thrombus. 1 In 2000, the classification was updated by Stary 2 and modified by Virmani et al. 3 They introduced a more detailed description of atherothrombotic plaques. In contrast to the AHA classification of 1995, the definition of "plaque rupture" is stricter, and the possibilities for atherothrombotic events are extended. Atherothrombotic events are clearly separated into plaque rupture, erosion, and eruptive calcified nodules. Moreover, intraplaque hemorrhages are described as phenomena in lesions that are not necessarily associated with plaque rupture (Figure 1).Because terms like "plaque instability," "plaque vulnerability," "plaque rupture," and "intraplaque hemorrhage" are often used interchangeably, one explanation for the apparent confusion in the literature is the use of a different definition of atherosclerotic plaque rupture. In this review, the stricter definitions of plaque rupture and intraplaque hemorrhage as proposed by Virmani et al 3 are used. Plaque rupture is defined as "an area of fibrous cap disruption whereby the overlying thrombus is in continuity with the lipid core". 3 Intraplaque hemorrhage is defined as the deposition of blood products inside the plaque and is not necessarily associated with atherosclerotic plaque rupture. 2 Because the pathogenesis of plaque erosion and calcified nodules is hardly known, these are excluded from this review. An...

Atherosclerotic Lesion Size and Vulnerability Are Determined by Patterns of Fluid Shear Stress

“…Intraplaque hemorrhages are considered prominent markers of plaque instability. 11,18,23,24 Without angiotensin II stimulation, the more extensive lesions that developed in the lowered shear stress regions showed small intraplaque hemorrhages close to the internal elastic lamina in 28% of the treated animals. Hemorrhages were never observed in the lesions in oscillatory shear stress regions.…”

“…Morphologically, the destabilizing components accumulate in pools underneath a thin, fibrous cap, with little infiltration of vascular smooth muscle cells. 17,18 Shear stress could determine the vulnerability of the lesion by altering the gene expression of endothelial cells (eg, upregulation of adhesion molecules, proinflammatory factors, and factors that mediate vascular wall permeability) and by increasing the interaction of proatherogenic components in the blood (lipoproteins and monocytes) with the activated endothelium. 19 -21 We found that lowered shear stress lesions contained more lipids, fewer vascular smooth muscle cells, and less collagen compared with lesions in the oscillatory shear stress region.…”

“…18 As a result, lesions induced by lowered shear stress contain relatively fewer vascular smooth muscle cells than do lesions induced by oscillatory shear stress. Thus, lowered shear stress appears to induce larger plaques with a stronger inflammatory response, giving rise to lesions with characteristics of a vulnerable plaque.…”

Original article Circulated CD4 + CD28 - lymphocytes rate and their cytotoxicity and morphological parameters of internal carotid artery atheromatous plaques in patients with atherosclerosis-related ischemic stroke

“…Research, including our previous studies, also shows that the symptomatic nature of carotid atherosclerotic plaques is rather an outcome of a combined effect of numerous, both intra-and extravascular factors [10,14]. CD4 + CD28 -Lc could have been only one of such factors by their involvement in the process of plaque destabilization.…”

Koroner Arter Hastalığı

“…Plak rüptürü, fissür plak, plak içi kanama ve erozyon unstable plakların farklı fenotipleri olup "hassas plak" gibi plak instabilitesine eğilimli lezyonları tanımlamakta ve maalesef terim olarak çoğunlukla birbirinin yerine kullanılmaktadır. Ayrıca, unstable plakların farklı fenotipleri ço-ğunlukla plak rüptürü olarak adlandırılır [15].…”