Plaque hemorrhage in carotid artery disease: Pathogenesis, clinical and biomechanical considerations

Abstract

Stroke remains the most prevalent disabling illness today, with internal carotid artery luminal stenosis due to atheroma formation responsible for the majority of ischemic cerebrovascular events. Severity of luminal stenosis continues to dictate both patient risk stratification and the likelihood of surgical intervention. But there is growing evidence to suggest that plaque morphology may help improve pre-existing risk stratification criteria. Plaque components such a fibrous tissue, lipid rich necrotic core and calcium have been well investigated but plaque hemorrhage (PH) has been somewhat overlooked. In this review we discuss the pathogenesis of PH, its role in dictating plaque vulnerability, PH imaging techniques, marterial properties of atherosclerotic tissues, in particular, those obtained based on in vivo measurements and effect of PH in modulating local biomechanics.

Intraplaque Hemorrhage and the Plaque Surface in Carotid Atherosclerosis: The Plaque At RISK Study (PARISK)

“…As stated previously, the common viewpoint is that these small leaky neovessels are responsible for the occurrence of intraplaque hemorrhage and subsequently the development of an unstable rupture-prone plaque. 5,[9][10][11][12]32 Our results-if confirmed in serial studies-can support the pathophysiologic relation between intraplaque hemorrhage and disrupted plaque surface. An alternative viewpoint to explain this relationship is that repeated fissuring of the plaque and associated formation of nonocclusive luminal thrombus incorporated in the plaque could be the cause of intraplaque hemorrhage.…”

“…In addition, our overall prevalence of intraplaque hemorrhage of 26% is in accordance with that in the literature. 4,5,15 Correction for MR imaging protocol used in the multivariate model did not change our results. A second limitation is the lack of histology.…”

“…4 Prevalence of intraplaque hemorrhage has been shown to be higher in symptomatic than in asymptomatic lesions. 5 Moreover, the presence of intraplaque hemorrhage in carotid artery disease is associated with an increased risk of cerebral ischemic events. [6][7][8] The pathophysiologic mechanism leading to intraplaque hemorrhage is a topic of debate.…”

“…However, a common viewpoint is that small leaky neovessels in the atherosclerotic plaques are a likely source of intraplaque hemorrhage. 5,9,10 The presence of intraplaque hemorrhage is thought to initiate several biologic processes like phagocytosis and local inflammation, leading to the release of proteolytic enzymes, deposition of free cholesterol and subsequently plaque growth, plaque destabilization, and possible plaque rupture. 5,[9][10][11][12] Plaque rupture can be visible on imaging as a disruption of the atherosclerotic plaque surface (plaque ulceration and/or a fissured fibrous cap).…”

“…5,9,10 The presence of intraplaque hemorrhage is thought to initiate several biologic processes like phagocytosis and local inflammation, leading to the release of proteolytic enzymes, deposition of free cholesterol and subsequently plaque growth, plaque destabilization, and possible plaque rupture. 5,[9][10][11][12] Plaque rupture can be visible on imaging as a disruption of the atherosclerotic plaque surface (plaque ulceration and/or a fissured fibrous cap). 13,14 A previous study reported that plaque ulceration on CTA was useful for the prediction of intraplaque hemorrhage on MR imaging in a broad group of symptomatic patients referred for carotid artery imaging.…”