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J Thorac Cardiovasc Surg 2002;123:842-844
© 2002 The American Association for Thoracic Surgery
Editorials |
From the Department of Cardiothoracic Surgery, Boston Medical Center, Boston, Mass.
Received for publication Sept 7, 2001. Accepted for publication Sept 28, 2001. Address for reprints: Harold L. Lazar, MD, Department of Cardiothoracic Surgery, Boston Medical Center, 88 E Newton St, Suite B-404, Boston, MA 02118.
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Introduction |
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In 1965 Sodi-Pollares and colleagues
1 first used glucose-insulin-potassium (GIK) solutions to treat patients with acute myocardial infarctions and found that this limited infarct size, reduced ventricular ectopy, and improved survival. Early studies in isolated heart preparations with regional ischemia showed that GIK decreased infarct size, increased high-energy phosphate levels, and improved ventricular function. 2 Clinical studies in patients with acute myocardial infarction demonstrated that GIK enhanced myocardial performance. 3 However, enthusiasm for GIK was dampened by a British Medical Research Council clinical trial of patients with acute myocardial infarction that failed to show any survival benefit with GIK therapy. 4 In that study, GIK protocols were inconsistent, such that different doses and volumes of GIK were administered at various times from the onset of the infarct, making it difficult to determine the effectiveness of GIK therapy. The role of glucose and insulin in cardiac surgery was further diminished by the introduction of cold chemical cardioplegia and hypothermic cardiopulmonary bypass because of the inhibitory effects of hypothermia on glucose and insulin metabolism. However, the increased numbers of patients requiring urgent coronary artery bypass grafting (CABG) for acute coronary syndromes, many with reduced ventricular function, and the introduction of warm cardioplegia and cardiopulmonary bypass techniques have prompted a renewed interest in substrate enhancement with glucose and insulin in an attempt to augment myocardial protection and improve clinical outcomes for these high-risk patients.
There are several mechanisms by which glucose and insulin protect the ischemic myocardium. Although the primary energy source for the nonischemic myocardium is free fatty acids, glucose is the preferred substrate during periods of ischemia. Adenosine triphosphate
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J. Thorac. Cardiovasc. Surg. 2002 123: 928-935.
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