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Ann Thorac Surg 1995;60:833-838
© 1995 The Society of Thoracic Surgeons

Articles

Protection of evolving myocardial infarction and failed PTCA

MD Friedhelm Beyersdorf*

Department of Cardiovascular Surgery, Albert-Ludwigs-University Freiburg, Freiburg, Germany

* Address reprint requests to Dr Beyersdorf, Department of Cardiovascular Surgery, Albert-Ludwigs-University Freiburg, Hugstetterstr 55, D-79106 Freiburg, Germany.


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Acute myocardial infarction is caused by acute coronary occlusion and is the major cause of death in Europe and the United States. In-hospital mortality is due principally to cardiogenic shock because of extensive ischemic muscle damage. Previous surgical results of coronary artery bypass grafting for left ventricular power failure have been disappointing because intraoperative ischemic injury is superimposed on severe damage already sustained by the myocardium. Surgical revascularization has, in general, been restricted to patients with acute occlusion after elective percutaneous transluminal coronary angioplasty with or without thrombolytic therapy. During the last years new knowledge has been gained in the pathophysiology of acute coronary occlusion on ischemic and nonischemic (remote) myocardium that has evolved in a new surgical strategy for revascularization of patients with evolving myocardial infarctions and failed percutaneous transluminal coronary angioplasty. Studies of the natural history of acute regional ischemia have shown that acute occlusion of a coronary artery not only affects the ischemic myocardium but causes structural, functional, and metabolic alterations in the remote and adjacent myocardium. These changes in the remote myocardium are even more severe if the remote myocardium is supplied by a stenotic coronary artery. Furthermore, many experimental and clinical studies have shown that normal blood reperfusion of myocardium injured previously by ischemia leads to additional damage (reperfusion injury). This damage can be reduced or even avoided by therapeutic interventions during the initial reperfusion period. These observations on the pathophysiology of ischemic myocardium and myocardium remote from the ischemic zone led to the development of operative strategies intended both to restore early segmental contractility in the previously ischemic area and to restore or maintain hypercontractility in remote myocardium. These strategies involve use of mechanical cardiac decompression on total vented bypass, and use of warm, substrate-enriched blood cardioplegia to resuscitate both acute ischemic muscle and metabolically depleted remote muscle.


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Presented at the International Symposium on Myocardial Protection From Surgical Ischemic-Reperfusion Injury, Asheville, NC, Sep 25–28, 1994.


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