Effect of pravastatin on malondialdehyde-modified low-density lipoprotein levels and coronary plaque regression as determined by three-dimensional intravascular ultrasound.

We hypothesized that a reduction in atherogenic malondialdehyde-modified low-density lipoprotein (MDA-LDL) levels, which may antagonize the action of atheroprotective high-density lipoprotein cholesterol, leads to coronary plaque regression. This study investigated the effects of pravastatin on the serum levels of MDA-LDL and coronary atherosclerosis. In a 6-month prospective study, 75 patients with stable coronary artery disease were randomly assigned to a pravastatin-treatment group (n = 52) or a control group (n = 23). Volumetric analyses were performed in matched coronary artery segments by 3-dimensional intravascular ultrasound. Pravastatin therapy for 6 months resulted in a decrease in coronary plaque volume (14.4%, p <0.0001) and a corresponding reduction in serum MDA-LDL levels (12.7%, p = 0.0001). In the pravastatin treatment group, the percentage of change in plaque volume correlated with changes in the MDA-LDL and high-density lipoprotein cholesterol levels (r = 0.52 and -0.55, respectively, p <0.0001) but not with the changes in any other lipid levels. Multivariate regression analysis revealed that a reduced MDA-LDL level is an independent predictor of plaque regression, as was an increase in high-density lipoprotein cholesterol. In conclusion, these results suggest that the reduction in the MDA-LDL levels induced by pravastatin may serve as a novel marker of coronary atherosclerosis regression.

Effect of pravastatin on coronary plaque volume.

A volumetric analysis by 3-dimensional intravascular ultrasound revealed that lipid-lowering therapy with pravastatin significantly reduced coronary plaque volume. The changes in plaque volume were inversely correlated with the changes in plasma levels of high-density lipoprotein cholesterol but not with changes in levels of total cholesterol or low-density lipoprotein cholesterol.