Article ID Journal Published Year Pages File Type
2929845 International Journal of Cardiology 2012 8 Pages PDF
Abstract

PurposeTo evaluate plaque image characteristics in coronary artery culprit-lesions in subjects with acute coronary syndromes (ACS), we retrospectively compared coronary arterial images by 64-slice CT before conventional-coronary-angiogram with those by intravascular ultrasound (IVUS).Materials-and-methodsRetrospective analysis of coronary arterial images from thirty-one subjects (26-males, mean age 59.3 ± 12.0 years) exhibiting acute symptoms with suspicion of ACS, where either (1) ECG was un-interpretable or (2) ECG was non diagnostic/cardiac biomarkers was equivocal; with significant stenosis on emergent 64 slice CT and subjects were finally diagnosed as having ACS confirmed by conventional-coronary-angiogram, followed by IVUS before coronary-intervention. After principal culprit-lesion components were classified into 1) thrombus, 2) soft plaques, and 3) fibrotic plaques by IVUS, corresponding culprit-lesion CT values were measured (two-observers).ResultsNineteen and 12 of 31 subjects were finally diagnosed as unstable angina pectoris and non-ST elevation acute myocardial infarction respectively. Main culprit-lesion components of ACS were identified on MSCT in all subjects. Culprit-lesion CT values diagnosed as soft plaques by IVUS (n = 6, 32.9 ± 8.7 HU) were not lower than those of thrombi (n = 18, 43.2 ± 10.7 HU, p = 0.268); both values were significantly lower than those of fibrotic plaques (n = 7, 82.5 ± 22.6 HU) (both p < 0.01). Calcification, spotty calcification, and positive arterial remodeling were observed in 67.7%, 61.3%, 58.1% (IVUS) and 58.1%, 51.6%, 74.2% (MSCT), respectively (all p = NS). CT value reproducibilities and culprit-lesion areas, were 0.87 and 0.86, respectively (two analyzers).Conclusions64-slice CT can non-invasively evaluate image characteristics in coronary artery culprit-lesions in ACS subjects accurately; this may help to differentiate soft plaques or thrombi generated by plaque rupture from fibrotic plaques.

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