title: Myocardial stunning and reperfusion injury in cardiac surgery.
abstract: This article reviews the evidence that myocardial stunning during surgical reperfusion after coronary revascularization or heart transplantation is not strictly due to myocardial injury sustained during ischemia, but results from pathophysiological events triggered by reperfusion (reperfusion injury). In sheep, left ventricular (LV) dP/dt and stroke work were reduced up to 50%, and 60% to 70% necrosis was observed in the area at risk during 3 hours reperfusion following coronary occlusion and cardioplegic arrest on bypass. Reperfusion with leukocyte depleted blood, or pharmacological blockade of either thromboxane or leukotriene receptors, provided significant improvements in LV function and myocardial blood flow, with a 40% to 50% reduction in necrosis. Similar results have been obtained using animal heart subjected to 2 to 3 hours arrest at either 4 degrees C or 15 degrees C, simulating cardiac preservation and reperfusion after transplantation. Diastolic pressure was significantly elevated, and increases in the time constant for relaxation of LV pressure and coronary vascular resistance were noted. These indices of myocardial stunning were reversed after blocking neutrophil-endothelial cell interaction with monoclonal antibodies against CD18 or ICAM-1 receptors, and significant improvements were also obtained after either thromboxane or leukotriene receptor blockade. We conclude that immediate postoperative myocardial stunning results largely from reperfusion injury that occurs due to an acute inflammatory response to ischemia and reperfusion, and that stunning can be largely reversed with appropriate pharmacological intervention.
authors: Department of Surgery, Harvard Medical School, Boston, Massachusetts.
authors: R F
authors: RF
authors: Appleyard
authors: L H
authors: LH
authors: Cohn
mesh_terms: D000818:Animals; D006348:Cardiac Surgical Procedures / Q000009:adverse effects*; D009202:Cardiomyopathies / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000276:immunology / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000276:immunology / Q000503:physiopathology; D009504:Neutrophils / Q000502:physiology; D011817:Rabbits; D012756:Sheep