Reperfusion injury in acute myocardial infarction: from bench to cath lab. Part II: Clinical issues and therapeutic options.
Two forms of reperfusion injury can occur in patients with ST-segment elevation acute myocardial infarction who are undergoing primary angioplasty: no-reflow phenomenon and reperfusion syndrome. No-reflow, defined as low or no distal perfusion despite removal of epicardial occlusion, can be detected by angiographic flow, myocardial blush grade and contrast echocardiography. Reperfusion syndrome involves haemodynamic and rhythmic disturbances, but an overall paradoxical ST-segment increase. A variety of mechanisms give rise to no-reflow, including distal embolization, leucocyte plugging and vasoconstriction. Reperfusion syndrome reflects, at least in part, the cardiomyocyte component of reperfusion injury. Reperfusion injury can be predicted from the initial electrocardiogram, especially when QRS complex distortion is observed. Pharmacological prevention of reperfusion injury has been tested in a number of trials; the most useful drugs available currently are glycoprotein IIb/IIIa receptor blockers and adenosine. Thrombus aspiration leads to faster and greater ST-segment resolution. Postconditioning (also called staccato reperfusion) is a new strategy that has produced highly encouraging results, although it has been tested only in a small randomized study. New tools are required to enable thrombus aspiration and postconditioning to be carried out simultaneously. Pharmacological postconditioning can be anticipated in the near future, as many drugs appear to achieve the same positive effect as mechanical modified reperfusion.
Monassier
Jean-Pierre
JP
Cardiology Department, Emile Muller Hospital, 20, Laennec Street, 68000 Mulhouse, France. monassierj@ch-mulhouse.fr
D000241:Adenosine / Q000627:therapeutic use; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000818:Animals; D003326:Coronary Circulation; D004562:Electrocardiography; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D009203:Myocardial Infarction / Q000628:therapy*; D015425:Myocardial Reperfusion / Q000009:adverse effects*; D015428:Myocardial Reperfusion Injury / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D009206:Myocardium / Q000473:pathology*; D020108:Nicorandil / Q000627:therapeutic use; D054318:No-Reflow Phenomenon / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D017131:Thrombectomy / Q000295:instrumentation; D016896:Treatment Outcome; D014665:Vasodilator Agents / Q000627:therapeutic use
D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014665:Vasodilator Agents; D020108:Nicorandil; D000241:Adenosine