Proximal Region of Carotid Atherosclerotic Plaque Shows More Intraplaque Hemorrhage: The Plaque at Risk Study

Abstract

BACKGROUND AND PURPOSE: Intraplaque hemorrhage contributes to lipid core enlargement and plaque progression, leading to plaque destabilization and stroke. The mechanisms that contribute to the development of intraplaque hemorrhage are not completely understood. A higher incidence of intraplaque hemorrhage and thin/ruptured fibrous cap (upstream of the maximum stenosis in patients with severe [$70%] carotid stenosis) has been reported. We aimed to noninvasively study the distribution of intraplaque hemorrhage and a thin/ruptured fibrous cap in patients with mild-to-moderate carotid stenosis.MATERIALS AND METHODS: Eighty-eight symptomatic patients with stroke (,70% carotid stenosis included in the Plaque at Risk study) demonstrated intraplaque hemorrhage on MR imaging in the carotid artery plaque ipsilateral to the side of TIA/stroke. The intraplaque hemorrhage area percentage was calculated. A thin/ruptured fibrous cap was scored by comparing pre-and postcontrast black-blood TSE images. Differences in mean intraplaque hemorrhage percentages between the proximal and distal regions were compared using a paired-samples t test. The McNemar test was used to reveal differences in proportions of a thin/ruptured fibrous cap. RESULTS:We found significantly larger areas of intraplaque hemorrhage in the proximal part of the plaque at 2, 4, and 6 mm from the maximal luminal narrowing, respectively: 14.4% versus 9.6% (P ¼ .04), 14.7% versus 5.4% (P , .001), and 11.1% versus 2.2% (P ¼ .001). Additionally, we found an increased proximal prevalence of a thin/ruptured fibrous cap on MR imaging at 2, 4, 6, and 8 mm from the MR imaging section with the maximal luminal narrowing, respectively: 33.7% versus 18.1%, P ¼ .007; 36.1% versus 7.2%, P , .001; 33.7% versus 2.4%, P ¼ .001; and 30.1% versus 3.6%, P ¼ .022. CONCLUSIONS:We demonstrated that intraplaque hemorrhage and a thin/ruptured fibrous cap are more prevalent on the proximal side of the plaque compared with the distal side in patients with mild-to-moderate carotid stenosis. ABBREVIATIONS: FC ¼ fibrous cap; IPH ¼ intraplaque hemorrhage; QIR TSE ¼ quadruple inversion recovery turbo spin-echo; TRFC ¼ thin/ruptured fibrous cap R upture of a vulnerable atherosclerotic plaque is an important underlying cause of myocardial infarction and stroke. 1 Noninvasive visualization of plaque vulnerability has demonstrated that intraplaque hemorrhage (IPH) contributes to enlargement of the lipid core and plaque progression, leading to plaque destabilization. 2,3 Indeed, we and others have demonstrated that IPH on MR imaging is a strong predictor of future cerebrovascular events. [4][5][6] This finding has led to the recognition of IPH as a key marker and pathologic factor contributing to plaque vulnerability.

A Spontaneous Extracranial Internal Carotid Artery Dissection with Autosomal Dominant Polycystic Kidney Disease: A Case Report and Literature Review

“…Intra-plaque hemorrhage can also be observed in atherosclerotic carotid plaques. In such situations, however, similar findings are detected in only a part of the plaque [ 19 , 20 ]. Therefore, if the condition is homogenous throughout the lesion, as in this case, it is likely that the lesion would be an intramural hematoma due to arterial dissection.…”

Carotid geometry is independently associated with complicated carotid artery plaques

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Lipid Content Distribution and its Clinical Implication in Patients with Acute Myocardial Infarction-Plaque Erosion: Results from the Prospective OCTAMI Study

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