Comparing culprit lesions in ST-segment elevation and non-ST-segment elevation acute coronary syndrome with 64-slice multidetector computed tomography

Background: Classifying acute coronary syndrome (ACS) as ST elevation ACS (STE-ACS) or non-ST elevation ACS (NSTE-ACS) is critical for clinical prognosis and therapeutic decision-making. Assessing the differences in composition and configuration of culprit lesions between STE-ACS and NSTE-ACS can clarify their pathophysiologic differences. Objective: This study focused on evaluating the ability of 64-slice multidetector computed tomography (MDCT) to investigate these differences in culprit lesions in patients with STE-ACS and NSTE-ACS. Methods: Of 161 ACS cases admitted, 120 who fit study criteria underwent MDCT and conventional coronary angiography. The following MDCT data were analyzed: calcium volume, Agatston calcium scores, plaque area, plaque burden, remodeling index, and plaque density. Results: The MDCT angiography had a good correlation with conventional coronary angiography regarding the stenotic severity of culprit lesions (r = 0.86, p < 0.001). The STE-ACS culprit lesions (n = 54) had significantly higher luminal area stenosis (78.6 ± 21.2% vs. 66.7 ± 23.9%, p = 0.006), larger plaque burden (0.91 ± 0.10 vs. 0.84 ± 0.12, p = 0.007) and remodeling index (1.28 ± 0.34 vs. 1.16 ± 0.22, p = 0.021) than those with NSTE-ACS (n = 66). The percentage of expanding remodeling index (remodeling index >1.05) was significantly higher in the STE-ACS group (81.5% vs. 63.6%, p = 0.031). The patients with STE-ACS had significantly lower MDCT density of culprit lesions than patients with NSTE-ACS (25.8 ± 13.9 HU vs. 43.5 ± 19.1 HU, p < 0.001). Conclusions: Sixty-four-slice MDCT can accurately evaluate the stenotic severity and composition of culprit lesions in selected patients with either STE-ACS or NSTE-ACS. Culprit lesions in NSTE-ACS patients had significantly lower luminal area stenosis, plaque burden, remodeling index and higher MDCT density, which possibly reflect differences in the composition of vulnerable culprit plaques and thrombi.