The inflammatory response as a target to reduce myocardial ischaemia and reperfusion injury

• Published in: Thrombosis and haemostasis Vol. 102; no. 2; p. 240
• Main Authors: Steffens, Sabine, Montecucco, Fabrizio, Mach, François
• Format: Journal Article
• Language: English
• Published: Germany 01.08.2009
• Subjects: Adrenergic beta-Antagonists - therapeutic use; Adult; Angiotensin-Converting Enzyme Inhibitors - therapeutic use; Animals; Anti-Inflammatory Agents - therapeutic use; Anticoagulants - therapeutic use; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use; Immunosuppressive Agents - therapeutic use; Inflammation - physiopathology; Inflammation - prevention & control; Inflammation Mediators - physiology; Models, Cardiovascular; Myocardial Infarction - drug therapy; Myocardial Infarction - physiopathology; Myocardial Infarction - therapy; Myocardial Reperfusion Injury - physiopathology; Myocardial Reperfusion Injury - prevention & control; Platelet Aggregation Inhibitors - therapeutic use
• ISSN: 0340-6245
• DOI: 10.1160/TH08-12-0837

Acute myocardial infarction is the leading cause of morbidity and mortality in the adult population of developed and developing nations. Although the prompt restoration of antegrade blood flow in the infarct-related coronary artery is the mean therapy for improving survival, reperfusion itself may cause damage to ischaemic myocardial tissue. This event is well known as "reperfusion injury". Crucial mediators for cardiac damage in the reperfusion phases are oxidative stress, inflammation and leukocyte infiltration. Already approved and novel therapies might directly reduce these inflammatory processes. Treatments modulating chemokine secretion and activity should be considered as very promising approaches to reduce myocardial reperfusion injury.