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Circulation. 2008;117:2523-2533
doi: 10.1161/CIRCULATIONAHA.107.697979
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(Circulation. 2008;117:2523-2533.)
© 2008 American Heart Association, Inc.


Contemporary Reviews in Cardiovascular Medicine

Glucose-Insulin-Potassium for Acute Myocardial Infarction

Continuing Controversy Over Cardioprotection

Robert A. Kloner, MD, PhD; Richard W. Nesto, MD

From the Heart Institute (R.A.K.), Good Samaritan Hospital, and Division of Cardiovascular Medicine (R.A.K.), Keck School of Medicine, University of Southern California, Los Angeles, Calif; and the Department of Cardiovascular Medicine (R.W.N.), Lahey Clinic, Burlington, Mass.

Correspondence to Robert A. Kloner, MD, PhD, Heart Institute, Good Samaritan Hospital, 1225 Wilshire Blvd, Los Angeles, CA 90017. E-mail rkloner@goodsam.org


Key Words: diabetes mellitus • glucose • heart failure • myocardial infarction • pharmacology


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 
The "holy grail" in the field of cardioprotection is to develop pharmacological agents that can be administered as adjunctive treatment to reperfusion that will reduce myocardial infarct size and improve clinical outcomes. Numerous pharmacological agents and strategies have been studied over the years with variable results in both animal models and humans. Of drugs that have been studied, only a few have shown benefit in clinical trials. Aside from agents or devices than can restore and maintain reperfusion (thrombolytics, balloons, stents, aspirin, clopidogrel, IIb/IIIa inhibitors, low–molecular-weight heparin, and others), the only commonly used adjunctive agents shown to have cardioprotective effects when administered early after coronary occlusion and in addition to reperfusion are β-blockers. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are also used, but these can be given after infarction (as late as 1 week) and must be continued long-term to reduce left ventricular remodeling. Recently, adenosine and induced hypothermia have also shown promise as early adjunctive agents. For example, when intravenous adenosine was coupled with early reperfusion therapy, myocardial infarct size by single-photon emission computed tomography analysis and the composite end point of death and heart failure were reduced at 6 months.1 Hypothermia, induced by use of a heat-exchange cooling catheter, benefited a subgroup of patients who were successfully cooled to ≤35°C before reperfusion.2 Superoxide dismutase, magnesium, inhibitors of neutrophil adhesion, complement inhibitors, fluosol, RheothRx, the KATP channel/nitrate nicorandil, and others failed to show a benefit as adjuncts to reperfusion.3 Clinical research evaluating many of these agents in acute . . . [Full Text of this Article]




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