Efficacy of two lipid-lowering treatments on quantitative coronary angiographic endpoints

Citation
Wj. Mack et al., Efficacy of two lipid-lowering treatments on quantitative coronary angiographic endpoints, CARDIO DRUG, 14(4), 2000, pp. 411-418
Citations number
26
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CARDIOVASCULAR DRUGS AND THERAPY
ISSN journal
09203206 → ACNP
Volume
14
Issue
4
Year of publication
2000
Pages
411 - 418
Database
ISI
SICI code
0920-3206(200008)14:4<411:EOTLTO>2.0.ZU;2-S
Abstract
This study contrasts the sensitivity of four quantitative coronary angiogra phy (QCA) measures (percent diameter stenosis [%S], minimum lumen diameter, average segment diameter, and percent involvement) in detecting S-year tre atment effects of two lipid-lowering therapies and reports on the longitudi nal pattern after 4 years of treatment on the primary QCA trial endpoint (% S) for all, mild/moderate (<50%S), and severe lesions (greater than or equa l to 50%S). Patient cohorts were followed up from two randomized, placebo-c ontrolled clinical trials of lipid-lowering therapies-colestipol/niaein in the Cholesterol Lowering Atherosclerosis Study (CLAS) and lovastatin in the Monitored Atherosclerosis Regression Study (MARS). Identical QCA methodolo gy was used. In CLAS, the largest 2-year treatment effect size (=0.60) was noted for %S. In MARS, equivalent S-year effect sizes (=0.15) were noted fo r three QCA measures. The largest 2-year effect size in %S was found in CLA S for mild/moderate lesions (=0.55) and in MARS for severe lesions (=0.31). Treatment in CLAS led to regression of disease in the first 2 years; treat ment in MARS slowed progression of disease in the first 2 years and led to regression of disease after 4,years. Colestipol/niacin reduced progression of mild/moderate and severe lesions over the first 2 years of therapy; lova statin reduced the progression of severe lesions over the last 2 years of t herapy. We conclude that reducing the progression of atherosclerosis is not a simple proposition; maximal therapy for reducing and stabilizing atheros clerosis most likely will result from the selection of agents targeted at s pecific lesions.