title: Drug therapies to prevent coronary plaque rupture and erosion: present and future.
abstract: Patients at high risk for coronary heart disease usually have a number of atherosclerotic plaques in their coronary arteries. Some plaques grow inward and, once they have caused a critical degree of luminal stenosis, lead to chronic anginal symptoms. Other plaques grow outward and remain silent unless they disrupt and trigger an acute coronary event. Either type of plaque may become vulnerable to rupture or erosion once they have reached an advanced stage. Typically, a highly stenotic fibrotic plaque is prone to erosion, whereas an advanced lipid-rich thin-cap fibroatheroma is prone to rupture. Because of the multitude and complex nature of the coronary lesions and our inability to detect silent rupture-prone plaques, the best practical approach to prevent acute coronary events is to treat the vulnerable patient, i.e., to eliminate the risk factors of coronary disease. Despite such preventive measures, a sizable number of patients still experience acute coronary events due to plaque erosion or rupture. Thus, there is room for new avenues to pharmacologically stabilize vulnerable plaques. The development of new noninvasive tools to detect the progression and regression of individual non-stenotic rupture-prone plaques will allow testing of such novel pharmacotherapies. Because no specific plaque-targeted therapies are available at present, we give an overview of the current pharmacotherapy to treat the vulnerable patient and also discuss potential novel therapies to prevent acute coronary events.
authors.affiliation: Wihuri Research Institute, Helsinki, Finland. petri.kovanen@wri.fi
authors.forename: P T
authors.initials: PT
authors.lastname: Kovanen
authors.forename: M
authors.initials: M
authors.lastname: Mäyranpää
authors.forename: K A
authors.initials: KA
authors.lastname: Lindstedt
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D003324:Coronary Artery Disease / Q000188:drug therapy*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D008407:Mast Cells / Q000187:drug effects; D047495:PPAR gamma / Q000819:agonists; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011480:Protease Inhibitors / Q000627:therapeutic use; D012422:Rupture, Spontaneous; D014611:Vaccination
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000900:Anti-Bacterial Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D047495:PPAR gamma; D010975:Platelet Aggregation Inhibitors; D011480:Protease Inhibitors