Use of Antiplatelet Agents Is Associated With Intraplaque Hemorrhage on Carotid Magnetic Resonance Imaging

Atherosclerosis in the carotid arteries is an important cause of ischemic stroke. Treatment decisions for carotid artery stenosis are currently based on the degree of luminal narrowing and the presence or absence of recent ipsilateral stroke or transient ischemic attack (TIA). However, there is increasing evidence that additional factors may be useful in stratifying a patient’s risk of stroke recurrence. A potent strategy may be the identification of so-called vulnerable plaque features, that is, intraplaque hemorrhage (IPH), a large lipid-rich necrotic core and a thin or ruptured fibrous cap. Plaques with these characteristics are associated with an increased risk of plaque rupture and subsequent embolization. A key feature of vulnerable plaques is IPH, which can be studied in vivo with highresolution carotid plaque magnetic resonance imaging (MRI). In cohort studies, IPH has shown to be a predictor of ipsilateral stroke and TIA in patients with symptomatic and to a lesser extend with asymptomatic carotid stenosis. Associations between clinical patient characteristics and vulnerable plaque characteristics have not been widely studied. It would be important to learn more about clinical determinants of IPH because it can give us information on the mechanism of vulnerable plaque development and Background and Purpose—Intraplaque hemorrhage (IPH), visualized by magnetic resonance imaging, has shown to be associated with the risk of stroke in patients with carotid artery stenosis. The mechanisms of IPH development are poorly understood. In this study, we investigated the association between clinical patient characteristics and carotid IPH on highresolution magnetic resonance imaging. Methods—Patients participate in the Plaque at Risk (PARISK) study. This prospective, multicenter cohort study included patients with recent amaurosis fugax, hemispheric transient ischemic attack, or nondisabling stroke in the internal carotid artery territory and an ipsilateral carotid stenosis of <70%, who were not scheduled for carotid revascularization procedure. One hundred patients, recruited between 2010 and 2012, underwent a 3-T high-resolution carotid magnetic resonance imaging. We documented clinical patient characteristics and performed multivariable logistic regression analysis to investigate their association with IPH. Results—IPH was observed in 45 patients (45%) in 1 or both carotid arteries. Male sex and the use of antiplatelet agents before the index event were associated with IPH in univariable analysis. In a multivariable analysis, only previous use of antiplatelet agents was significantly associated with IPH (odds ratio, 2.71; 95% confidence interval, 1.12–6.61). Risk factors of atherosclerotic arterial disease, including a history of symptomatic arterial diseases, were not associated with IPH. Conclusions—In this cohort of 100 patients with recently symptomatic carotid stenosis, the previous use of antiplatelet agents is associated with carotid IPH on magnetic resonance imaging. Antiplatelet therapy may increase the risk of IPH, but our findings need to be confirmed in larger patient cohorts. The implications for risk stratification remain to be determined. (Stroke. 2015;46:3411-3415. DOI: 10.1161/STROKEAHA.115.008906.)