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Circulation. 1997;96:1074-1077

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(Circulation. 1997;96:1074-1077.)
© 1997 American Heart Association, Inc.


Articles

Glucose-Insulin-Potassium in Acute Myocardial Infarction

The Time Has Come for a Large, Prospective Trial

Carl S. Apstein, MD; ; Heinrich Taegtmeyer, MD, DPhil

From the Boston University School of Medicine (C.S.A.), Boston, Mass, and The University of Texas–Houston Medical School (H.T.).

Correspondence to Carl S. Apstein, MD, Boston University School of Medicine, Cardiac Muscle Research Laboratory, Whitaker Cardiovascular Institute (Rm W-611), 80 E Concord St, Boston, MA 02118 () or Heinrich Taegtmeyer, MD, DPhil, University of Texas–Houston Medical School, Internal Medicine/Cardiology, 6431 Fannin St (Rm 1.246 MSB), Houston, TX 77030. e-mail capstein@bu.edu


Key Words: Editorials • myocardial infarction • glucose • insulin • potassium


*    Introduction
 
An important but nearly forgotten therapy for reducing mortality in acute MI has been reexamined and reported in this issue of Circulation.1 After performing a meta-analysis, Fath-Ordoubadi and Beatt came to the remarkable conclusion that glucose-insulin-potassium (GIK) had reduced in- hospital acute myocardial infarction (MI) mortality by 28% in nine prior clinical trials involving 1932 patients and by 48% in four studies in which GIK was administered at high concentrations to maximally suppress plasma free fatty acid (FFA) levels. This magnitude of mortality reduction is comparable to that achieved with thrombolytic therapy2 and supports the concept that metabolic protection of ischemic myocardium may be as important as reperfusion itself. However, the strength of this conclusion has the intrinsic weaknesses and limitations of the meta-analysis technique. In addition, all of the cited studies were done in the prethrombolytic era.

Before GIK can be considered as adjunctive therapy to revascularization in acute MI, confirmatory results are required from a modern, large-scale, prospectively randomized trial with adequate statistical power. Because urgent reperfusion, through thrombolytic therapy or primary angioplasty, is standard care for acute MI, the next target for therapeutic interventions is the myocardium. Restoration of blood flow and oxygen supply to the ischemic myocardium is critical but may not fully exploit the potential for salvage. Therefore, any trial of GIK should assess its value as an adjunctive agent to (1) delay cell death until reperfusion can occur and (2) optimize energy transfer in the postischemic heart.


*    Recent Related Studies
 
We believe that cautious optimism is . . . [Full Text of this Article]




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