Effect of cholesterol lowering and cardiovascular risk factors on the progression of aortoiliac arteriosclerosis: a quantitative cineangiography study.
The post-Coronary Artery Bypass Graft (Post-CABG) trial has shown that aggressive compared to moderate lowering of low-density lipoprotein cholesterol (LDL-C) delayed the progression of obstructive disease in aortocoronary saphenous vein grafts and in the left main coronary artery. Patients had been allocated to high-and low-dose lovastatin therapy for a 4-5 year period. The present study evaluated the effect of LDL-C lowering and the role of cardiovascular risk factors on the progression of arteriosclerosis in the distal abdominal aorta and common iliac arteries. From one of the participating centers of the post-CABG trial, 145 patients who had adequate imaging of the aortoiliac arteries at baseline and follow-up were included. Angiographic outcomes, presumed to reflect progression of arteriosclerosis and obtained from lumen diameter (LD) measurements using quantitative cineangiography, were as follows: significant decrease of the minimum lumen diameter (LD) and increase of the maximum LD, percent lumen stenosis, and percent lumen dilatation. These outcomes were not significantly less frequent in patients randomly allocated to aggressive compared to moderate LDL-C lowering. Of 9 cardiovascular risk factors, only 2 were significantly related to progression of aortoiliac arteriosclerosis. Current smoking predicted both percent lumen stenosis increase and, to a lesser degree, percent lumen dilatation increase (p = 0.010 and p = 0.055, respectively). Abnormally high body mass index (BMI > or = 25 kg/m2) correlated with percent lumen dilatation increase (p = 0.006). Aggressive compared to moderate LDL-C lowering did not prevent or delay the progression of aortoiliac arteriosclerosis. Smoking predicted both lumen narrowing and dilatation presumably caused by arteriosclerosis. Abnormally high BMI, reflecting overweight or obesity, was strongly associated with vessel dilatation.
Campeau
Lucien
L
Montreal Heart Institute, Montreal, Quebec, Canada. lcampeau@cgocable.ca
Lespérance
Jacques
J
Bilodeau
Luc
L
Fortier
Annik
A
Guertin
Marie-Claude
MC
Knatterud
Genell L
GL
D000368:Aged; D000924:Anticholesteremic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001012:Aorta, Abdominal / Q000000981:diagnostic imaging; D001018:Aortic Diseases / Q000000981:diagnostic imaging / Q000188:drug therapy*; D001157:Arterial Occlusive Diseases / Q000000981:diagnostic imaging / Q000188:drug therapy; D008078:Cholesterol, LDL / Q000097:blood; D002792:Cholestyramine Resin / Q000008:administration & dosage / Q000009:adverse effects; D002932:Cineangiography; D018450:Disease Progression; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D006937:Hypercholesterolemia / Q000000981:diagnostic imaging / Q000188:drug therapy*; D007083:Iliac Artery / Q000000981:diagnostic imaging; D007383:Intermittent Claudication / Q000000981:diagnostic imaging / Q000188:drug therapy; D007511:Ischemia / Q000000981:diagnostic imaging / Q000188:drug therapy; D007866:Leg / Q000098:blood supply; D008148:Lovastatin / Q000008:administration & dosage* / Q000009:adverse effects; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D014664:Vasodilation / Q000187:drug effects; D014859:Warfarin / Q000008:administration & dosage / Q000009:adverse effects
D000924:Anticholesteremic Agents; D008078:Cholesterol, LDL; D002792:Cholestyramine Resin; D014859:Warfarin; D008148:Lovastatin