Inflammation, proinflammatory mediators and myocardial ischemia-reperfusion Injury.
Ischemic myocardium must be reperfused to terminate the ischemic event; otherwise the entire myocardium involved in the area at risk will not survive. However, there is a cost to reperfusion that may offset the intended clinical benefits of minimizing infarct size, postischemic endothelial and microvascular damage, blood flow defects, and contractile dysfunction. There are many contributors to this reperfusion injury. Targeting only one factor in the complex web of reperfusion injury is not effective because the untargeted mechanisms induce injury. An integrated strategy of reducing reperfusion injury in the catheterization laboratory involves controlling both the conditions and the composition of the reperfusate. Mechanical interventions such as gradually restoring blood flow or applying postconditioning may be used independently in or conjunction with various cardioprotective pharmaceuticals in an integrated strategy of reperfusion therapeutics to reduce postischemic injury.
Vinten-Johansen
Jakob
J
Department of Surgery (Cardiothoracic), Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center of Emory Crawford Long Hospital, Emory University, 550 Peachtree Street NE, Atlanta, GA 30308-2225, USA. jvinten@emory.edu
Jiang
Rong
R
Reeves
James G
JG
Mykytenko
James
J
Deneve
Jeremiah
J
Jobe
Lynetta J
LJ
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000276:immunology*; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000276:immunology*; D017202:Myocardial Ischemia / Q000188:drug therapy / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology
D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators