title: Effects of statins on inflammation in patients with acute and chronic coronary syndromes.
abstract: Inflammation plays a crucial role in the cell biology of atherosclerosis. Coronary risk factors, and particularly low-density lipoprotein (LDL) cholesterol, injure the endothelium and decrease the bioavailability of nitric oxide to promote the expression of proinflammatory genes, cellular adhesion molecules, cytokines, chemokines, and growth factors. For example, the expression of CD40/CD40 ligand increases cell-mediated immune responses to activate a number of inflammatory cells and destabilize atherosclerosis. As part of this response, soluble markers of inflammation that are released into the blood offer insights into the cell biology of inflammation in atherosclerosis. In groups of patients, these markers have provided a means to study inflammatory mechanisms and have supported the value of many of our interventions that prevent cardiovascular disease. Statins have potent effects to reduce LDL cholesterol in the plasma and the artery wall and also appear to have a number of nonlipid effects that decrease inflammatory stimuli. Because statins also reduce some soluble markers of inflammation, it is likely that at least part of their benefit reflects a reduction in vascular inflammation in stable and unstable coronary syndromes. Although these inflammatory markers are valuable tools for studying the mechanisms of atherosclerosis, their use in clinical practice to stratify cardiovascular risk or assess treatment in individual patients requires further evaluation.
authors.affiliation: Cardiovascular Division and the Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. skinlay@rics.bwh.harvard.edu
authors.forename: Scott
authors.initials: S
authors.lastname: Kinlay
authors.forename: Andrew P
authors.initials: AP
authors.lastname: Selwyn
mesh_terms: D000208:Acute Disease; D000924:Anticholesteremic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D002097:C-Reactive Protein / Q000187:drug effects; D008078:Cholesterol, LDL / Q000097:blood / Q000187:drug effects / Q000378:metabolism; D002908:Chronic Disease; D003327:Coronary Disease / Q000188:drug therapy* / Q000503:physiopathology*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D007249:Inflammation / Q000188:drug therapy / Q000503:physiopathology; D016032:Randomized Controlled Trials as Topic; D013577:Syndrome
chemical_list: D000924:Anticholesteremic Agents; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D002097:C-Reactive Protein