(Circulation. 1997;96:1074-1077.)
© 1997 American Heart Association, Inc.
Articles |
From the Boston University School of Medicine (C.S.A.), Boston, Mass, and The University of TexasHouston 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 TexasHouston 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 |
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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.
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