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To the Editor: We have a number of concerns about the clinical features of the CREATE-ECLA trial.¹ First, heparin used in coronary reperfusion therapy, such as the CREATE-ECLA patients received, blocks the key GIK physiological effect of lowering free fatty acids.² Unfortunately, CREATE-ECLA did not report free fatty acid levels or look for this effect.

Second, not only should GIK have been given earlier, but also the sequence of GIK and reperfusion in CREATE-ECLA should have been reversed. In the GIK group, 68% received reperfusion therapy before GIK, largely eliminating the proposed benefit of GIK use in ST-segment elevation MI (STEMI) of extending the time window for benefit from reperfusion.^3-4 No reperfusion therapy was received by 17% of GIK patients, for whom no such effect was possible. For only 14% of these patients, GIK was started before reperfusion, although only briefly so. The investigators noted higher mortality in these . . . [Full Text of this Article]

Leonard A. Cobb, MD
Harborview Medical Center
Seattle, Wash

Thomas Killip, MD
Beth Israel Medical Center
New York, NY

Costas T. Lambrew, MD
Maine Medical Center
Portland, Me

Bruce A. MacLeod, MD
Mercy Hospital
Pittsburgh, Pa

Charles E. Rackley, MD
Georgetown University Hospital
Washington, DC

Harry P. Selker, MD, MSPH
hselker@tufts-nemc.org
Tufts–New England Medical Center
Boston, Mass

Robert J. Zalenski, MD
Wayne State University Health Center
Detroit, Mich

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