BACKGROUND: We hypothesized that unstable clinical presentation of coronary artery disease is associated with distinct characteristics of culprit lesions identifiable by multislice computed tomography (MSCT). METHODS: Patients with non-ST-elevation myocardial infarction (NSTEMI) (n = 57) or stable angina (SA) pectoris (n = 19) were studied. Coronary culprit lesions in patients with NSTEMI and symptomatic lesions in patients with SA were evaluated with 64-slice MSCT and a volumetric plaque imaging tool. Plaque volumes of lipid, fibrous tissue, or calcification according to signal intensity were determined. Plaque burden, mean signal intensity of the lesions, relative volumetric distribution of plaque components, and remodeling index were measured. RESULTS: Volumetric plaque burden of study lesions were similar in the 2 patient groups (P = .38). Mean signal intensity of study lesions were lower in patients with NSTEMI compared with patients with SA (74 [66-97] Hounsfield units vs 99 [77-154] Hounsfield units, P = .02). The volume of plaque occupied by calcified material was lower in patients with NSTEMI compared with patients with SA (15 mm(3) [3-58 mm(3)] vs 42 mm(3) [18-82 mm(3)], P = .045). In patients with NSTEMI, the lipid-rich plaque subtype was more frequent than in patients with SA, and the calcified plaque subtype was less frequent in patients with NSTEMI than in patients with SA (P = .032). Positive remodeling was observed in 19% of patients with NSTEMI, whereas this was absent in patients with SA (P = .04). CONCLUSION: Volumetric measurements with MSCT revealed that coronary culprit lesions in acute coronary syndrome frequently display low mean plaque signal intensity values, lipid-rich plaque subtype, and positive remodeling.
BACKGROUND: We hypothesized that unstable clinical presentation of coronary artery disease is associated with distinct characteristics of culprit lesions identifiable by multislice computed tomography (MSCT). METHODS:Patients with non-ST-elevation myocardial infarction (NSTEMI) (n = 57) or stable angina (SA) pectoris (n = 19) were studied. Coronary culprit lesions in patients with NSTEMI and symptomatic lesions in patients with SA were evaluated with 64-slice MSCT and a volumetric plaque imaging tool. Plaque volumes of lipid, fibrous tissue, or calcification according to signal intensity were determined. Plaque burden, mean signal intensity of the lesions, relative volumetric distribution of plaque components, and remodeling index were measured. RESULTS: Volumetric plaque burden of study lesions were similar in the 2 patient groups (P = .38). Mean signal intensity of study lesions were lower in patients with NSTEMI compared with patients with SA (74 [66-97] Hounsfield units vs 99 [77-154] Hounsfield units, P = .02). The volume of plaque occupied by calcified material was lower in patients with NSTEMI compared with patients with SA (15 mm(3) [3-58 mm(3)] vs 42 mm(3) [18-82 mm(3)], P = .045). In patients with NSTEMI, the lipid-rich plaque subtype was more frequent than in patients with SA, and the calcified plaque subtype was less frequent in patients with NSTEMI than in patients with SA (P = .032). Positive remodeling was observed in 19% of patients with NSTEMI, whereas this was absent in patients with SA (P = .04). CONCLUSION: Volumetric measurements with MSCT revealed that coronary culprit lesions in acute coronary syndrome frequently display low mean plaque signal intensity values, lipid-rich plaque subtype, and positive remodeling.
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