750-3 The Role of Triglyceride-Rich Lipoprotein Families in the Progression of Coronary Artery Atherosclerotic Lesions

The affect of triglyceride-rich lipoprotein particles on the progression of coronary artery atherosclerotic lesions is not known. In a subset of 270 subjects in the Monitored Atherosclerosis Regression Study, lovastatin significantly reduced apolipoprotein (Apo) B and cholesterol-rich lipoprotein (Lp) B levels without significantly affecting triglyceride-rich Lp (LpBc) particles, Lp-B:C, Lp-B:C:E, and Lp-AII:B:C:D:E. This differential affect of lovastatin on apoBcontaining lipoproteins offered the opportunity to determine the independent relationship of LpB and specific LpBc particles on the progression of coronary artery disease. Subjects were randomized to lovastatin 40mg b.i.d. or placebo for 2 years and progression determined by quantitative coronary angiography. There were 15 progressors (P) and 15 nonprogressors (NP) in the lovastatin group and 13 Pand 13 NP in the placebo group. In the placebo group, there was a significant difference between Pand NP (mean±SEM) in plasma triglyceride (259±33.6 vs 142.9±20.8, P=0.003), apoCIII (16.1±1.2 vs 11.9±0.7, P=0.02), and apoB (127.4±5.9 vs 112.4±4.7, P=0.04) levels. In the lovastatin group, there was a significant difference between P and NP in Lp-AII:B:C:D:E (8.4±1.3 vs 5.0±0.9, p=0.02) and apoAI (119.3±61 vs 134.0±3.6, p=0.02) levels. However, there was no significant difference in Lp-B:C or Lp-B:C:E levels between P and NP. These data confirm the atherogenic potential of LpB particles and show that after reduction of LpB particles to below 75mg/dL in the lovastatin group. LpBc particles in general, and Lp-AII:B:C:D:E specifically, play an important role in progression of coronary artery disease. The possible reason for the atherogenic potential of Lp-AII: B:C:D:E relative to other LpBc particles may be related to its lower reactivity toward lipoprotein lipase and therefore, longer residence time in the circulation