Data on plaque components of nonculprit subclinical atherosclerosis in patients with acute coronary syndrome at baseline and 1-year follow-up

Regression of nonculprit subclinical atherosclerosis at 1-year follow-up was mainly caused by regression of the lipid component in plaque in patients with acute coronary syndrome who underwent lipid-lowering therapy with conventional doses of statins. In the lesion regression (LR) group which was defined by a decrease in percent atheroma volume (PAV), changes in normalized total atheroma volume (ΔTAVn) from baseline to 1 year measured by optical flow ratio (OFR) software was significantly positively correlated only with lipid ΔTAVn (r=0.482, p<0.001), no significant correlation was found between ΔTAVn and fibrous ΔTAVn (r=0.454, p=0.058) or calcium ΔTAVn (r=0.053, p=0.624).

A similar positive correlation was found between changes in PAV (ΔPAV) and lipid ΔPAV (r=0.315, p=0.003), while ΔPAV was not correlated with either fibrous ΔPAV or calcium ΔPAV. 2. The degree of low-density lipoprotein cholesterol (LDL-C) reduction based on statin therapy was positively correlated with the regression of nonculprit subclinical atherosclerosis. Multivariate logistic regression analysis showed that nondiabetic status, use of beta-blockers, baseline lipid PAV, and ΔLDL-C% were correlated with LR. 3.