Coronary atherosclerosis stabilization: an achievable goal.
Coronary atherosclerotic plaques may restrict coronary blood flow producing angina or rupture causing unstable angina, myocardial infarction or sudden death. The rupture prone plaques are lipid rich, have thin fibrous caps and are often angiographically mild. Most treatment strategies are focused on relieving cardiac symptoms or salvaging myocardium in the wake of myocardial infarction rather than preventing plaque rupture. Animal studies revealed that atherosclerotic plaques can be modified and consequently trials were designed to test if lipid-altering strategies could favorably influence coronary artery disease in humans. Sixteen angiographic regression studies have been published to date and consistently show that favorably altering lipid levels results in retardation of coronary artery disease progression and markedly reduces cardiac events. The disparity between the extent of event reduction and angiographic disease change generated the concept that these favorable lipid alterations result in plaque stabilization. Therefore, the need to identify individuals at risk from these vulnerable plaques is more important than ever, knowing that such patients can now be effectively treated.
Maher
V M
VM
Department of Medicine, University of Washington Medical Center, Seattle 98195, USA.
D000818:Animals; D003324:Coronary Artery Disease / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D008055:Lipids / Q000097:blood; D008297:Male
D000960:Hypolipidemic Agents; D008055:Lipids