Signal of Carotid Intraplaque Hemorrhage on MR T1-Weighted Imaging: Association with Acute Cerebral Infarct

BACKGROUND AND PURPOSE: Identifying the mere presence of carotid intraplaque hemorrhage would be insufficient to accurately discriminate the presence of acute cerebral infarct. We aimed to investigate the association between signal intensity ratios of carotid intraplaque hemorrhage on T1-weighted MR imaging and acute cerebral infarct in patients with hemorrhagic carotid plaques using MR vessel wall imaging.

MATERIALS AND METHODS: Symptomatic patients with carotid intraplaque hemorrhage were included. The signal intensity ratios of carotid intraplaque hemorrhage against muscle on T1-weighted, TOF, and MPRAGE images were measured. The acute cerebral infarct was determined on the hemisphere ipsilateral to the carotid intraplaque hemorrhage. The association between signal intensity ratios of carotid intraplaque hemorrhage and acute cerebral infarct was analyzed.

RESULTS: Of 109 included patients (mean, 66.8 ± 9.9 years of age; 96 men), 40 (36.7%) had acute cerebral infarct. Patients with acute cerebral infarct had significantly higher signal intensity ratios of carotid intraplaque hemorrhage on T1-weighted images than those without (Median, 1.44; 25–75 Percentiles, 1.14-1.82 versus Median, 1.27; 25–75 Percentiles, 1.06–1.55, P = .022). Logistic regression analysis revealed that the signal intensity ratio of carotid intraplaque hemorrhage on T1-weighted images was significantly associated with acute cerebral infarct before (OR, 4.08; 95% CI, 1.34–12.40; P = .013) and after (OR, 3.34; 95% CI, 1.08–10.31; P = .036) adjustment for clinical confounding factors. However, this association was not significant when further adjusted for occlusion of the carotid artery (P = .058) and volumes of intraplaque hemorrhage and lipid-rich necrotic core (P = .458).

CONCLUSIONS: The signal intensity ratio of carotid intraplaque hemorrhage on T1-weighted images is associated with acute cerebral infarct in symptomatic patients with carotid hemorrhagic plaques. This association is independent of traditional risk factors but not of the size of plaque composition. The possibility of applying T1 signals of carotid intraplaque hemorrhage to predict subsequent cerebrovascular ischemic events needs to be prospectively verified.