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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 (

BACKGROUND AND PURPOSE: An important characteristic of vulnerable plaque, intraplaque hemorrhage, may predict plaque rupture. Plaque rupture can be visible on noninvasive imaging as a disruption of the plaque surface. We investigated the association between intraplaque hemorrhage and disruption of the plaque surface. MATERIALS AND METHODS: We selected the first 100 patients of the Plaque At RISK study, an ongoing prospective noninvasive plaque imaging study in patients with mild-to-moderate atherosclerotic lesions in the carotid artery. In carotid artery plaques, disruption of the plaque surface (defined as ulcerated plaques and/or fissured fibrous cap) and intraplaque hemorrhage were assessed by using MDCTA and 3T MR imaging, respectively. We used a chi2 test and multivariable logistic regression to assess the association between intraplaque hemorrhage and disrupted plaque surface. RESULTS: One hundred forty-nine carotid arteries in 78 patients could be used for the current analyses. Intraplaque hemorrhage and plaque ulcerations were more prevalent in symptomatic compared with contralateral vessels (hemorrhage, 38% versus 11%; P < .001; and ulcerations, 27% versus 7%; P = .001). Fissured fibrous cap was more prevalent in symptomatic compared with contralateral vessels (13% versus 4%; P = .06). After adjustment for age, sex, diabetes mellitus, and degree of stenosis, intraplaque hemorrhage was associated with disrupted plaque surface (OR, 3.13; 95% CI, 1.25-7.84) in all vessels. CONCLUSIONS: Intraplaque hemorrhage is associated with disruption of the plaque surface in patients with a carotid artery stenosis of

Objectives: Diastolic-systolic rise time characteristics of the distension waveform distribution, i.e., mean and inhomogeneity, might be modified by wave reflections from distal plaques. The aim of this study is to investigate the association between rise time characteristics for the common carotid artery (CCA) and composition of distal plaques. Methods: Longitudinal B-mode ultrasound (US) registrations of the CCA of 129 patients (age 69 ± 9) were performed with a Philips IU22 scanner. All patients had a plaque in the ipsilateral bifurcation and recently experienced a cerebrovascular accident. Distension waveforms were extracted by edge tracking and the diastolic-systolic rise time and its inhomogeneity, defined as standard deviation of systolic-diastolic rise time distribution for an artery segment, were derived. Plaque composition was extracted from 3T-MRI measurements (N = 125). Results: 118 subjects had both an adequate MRI and US registration. 58% of the plaques had a lipid-rich necrotic core (LRNC) of which 68% had a thin fibrous cap (FC). Lipids were demonstrated in the proximal part in 51 plaques (43%). Mean CCA diastolic-systolic rise time (162 ± 26 ms) did not vary with plaque composition (Student t-test, p-value > 0.2). The inhomogeneity, however, was significantly lower for vulnerable distal plaques (mean difference LRNC: 8ms, FC: 11ms, Student t-test, p-value < 0.02) and, more specifically, when lipids were present in the proximal part of the plaque (mean difference 12ms, Student t-test, p-value < 0.001). Conclusion: Diastolic-systolic rise time inhomogeneity of CCA distension is associated with the lipid presence of distal plaques. This research was supported by the Center for Translational Molecular Medicine and the Dutch Heart Foundation.