Impact of malondialdehyde-modified low-density lipoprotein on coronary plaque vulnerability in patients not receiving lipid-lowering therapy: a whole coronary analysis with multislice-computed tomography.

Vulnerable plaque disruption was suggested as a primary cause of acute coronary syndrome. This study investigated the impact of malondialdehyde-modified low-density lipoprotein (MDA-LDL) on whole coronary plaque vulnerability, based on multislice-computed tomography (MSCT). We included 197 patients that were not receiving lipid-lowering therapy. We retrospectively analyzed MSCT and MDA-LDL measurements. We defined a CT-derived vulnerable plaque as a plaque with a remodeling index > 1.10 and a mean CT density value < 30 HU. Vulnerable plaques were detected in 60 patients (30%). Patients with vulnerable plaques had significantly higher MDA-LDL levels than patients without vulnerable plaques (151.3 ± 42.3 vs. 118.5 ± 41.7 U/L, p < 0.01). A univariate regression analysis showed that vulnerable plaques were significantly related to MDA-LDL levels [10 U/L groups, odds ratio (OR): 1.19; p < 0.01] and in a multivariate model (10 U/L groups, OR: 1.18; p < 0.01). Patients with multivessel vulnerable plaques had significantly higher MDA-LDL levels than those with single-vessel involvement or no vulnerable plaque (172.4 ± 28.5 vs. 142.8 ± 44.2 vs. 118.5 ± 41.7 U/L, respectively; p < 0.01). MDA-LDL difference was observed for all LDL tertiles (bottom; 128.9 ± 41.1 vs. 97.3 ± 25.0 U/L, p < 0.01, middle; 142.6 ± 42.7 vs. 122.5 ± 35.1 U/L, p = 0.05, top; 166.0 ± 38.1 vs. 143.5 ± 51.6 U/L, p = 0.05). Increased MDA-LDL levels were associated with the presence and extent of vulnerable plaques, regardless of LDL levels.