Inflammation and infection in acute coronary syndrome.
Basic science research has revealed that monocytes and macrophages are important factors in atherogenesis. Immune system activation occurs at all stages of plaque formation, from the fatty streak to an advanced, complicated lesion. The inflammatory response not only stimulates changes in coronary artery endothelial cells causing endothelial injury and dysfunction, but also plays a role in plaque instability and rupture. New perspectives of atherosclerosis and acute coronary syndromes will be discussed in relation to inflammation. In addition, discussion will focus on bacterial and viral infectious microorganisms as a potential factor that may induce and promote inflammation and lead to acute coronary events. Clinical studies in humans have provided insight relating inflammation and infectious agents to atherosclerosis and plaque vulnerability. Other studies focus on specific interventions that may aid in diagnosis and treatment.
Albert
N M
NM
Kaufman Center for Heart Failure, The Cleveland Clinic Foundation, Ohio 44195, USA. albertn@ccf.org
D000818:Animals; D001161:Arteriosclerosis / Q000188:drug therapy / Q000209:etiology / Q000276:immunology; D002690:Chlamydia Infections / Q000150:complications / Q000188:drug therapy; D016993:Chlamydophila pneumoniae; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000209:etiology / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D014777:Virus Diseases / Q000150:complications