Recent angiographic trials with intensive lipid-lowering therapy have documented regression or slowing of progression in coronary lesions with less than 50% stenosis. Clinical trials in coronary artery disease with HMG-CoA reductase inhibitors have reported decrease in clinical events which are out of proportion with changes in coronary angiogram. A decline in lipid values was seen within 6 months whereas angiographic changes required 1 to 3 years. We hypothesized that HMG-CoA reductase inhibitors might modify the oxidized LDL in patients with hypercholesterolemia. Lipid profile and autoantibody titers to oxidized LDL in 9 patients were obtained at baseline, 2 to 6 months, and 7 to 12 months after treatment. Baseline < 6m. < 12m. Autoantibody titers (OD) 0.170 ± 0.170 0.242 ± 0.182 * 0.225 ± 0.211 Total cholesterol (mg/dl) 235±53 219±40 217±43 LDL (mg/dl) 165±46 141±37 145±39 * p-value < 0.0.5 vs. baseline by paired t-test OD: optical density Conclusion: In patients with hypercholesterolemia: 1) HMG-CoA reductase inhibitors cause a rise in ox-LDL autoantibodies during the first 6 months of therapy. 2) Increase in autobodies to ox-LDL is probably due to mobilization of ox-LDL. 3) Mobilization of ox-LDL and formation of autoantibody/ox-LDL complex may lead to acceleration of clearance and help explain the decrease in ischemic events in clinical trials.
|Original language||English (US)|
|Journal||Journal of Investigative Medicine|
|State||Published - Jan 1 1996|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)