European Heart Journal Advance Access originally published online on August 14, 2006
European Heart Journal 2006 27(17):2142-2143; doi:10.1093/eurheartj/ehl189
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Glucose, insulin, and acute myocardial infarction: reply
Department of Medicine
Division of Cardiology
Duke Clinical Research Institute and Duke University Medical Center
2400 Pratt Street
PO Box 3850
Durham, NC 27705
USA
E-mail address: a.goyal{at}duke.edu
Duke Clinical Research Institute and Duke University Medical Center
Durham, NC
USA
Duke Clinical Research Institute and Duke University Medical Center
Durham, NC
USA
Heart Institute
University of Sao Paulo Medical School
Sao Paulo
Brazil
Columbia University
New York, NY
USA
Henry Ford Hospital
Detroit, MI
USA
Instituto Dante Pazzanese de Cardiologia
Sao Paulo
Brazil
Proctor and Gamble Pharmaceuticals
Mason, OH
USA
Duke Clinical Research Institute and Duke University Medical Center
Durham, NC
USA
Dr Das comments that the association between the failure of glucose levels to drop during hospitalization and higher mortality following acute myocardial infarction (AMI) in the CARDINAL study1 is consistent with basic and translational work demonstrating the pro-inflammatory effects of glucose. In addition to its pro-inflammatory effects, glucose may also directly contribute to the pathogenesis of AMI by promoting thrombosis2 and impairing vasoreactivity.3 We and others4,5 concur that the maximal benefit of insulin therapy in AMI may be realized only when normalization of glucose levels have been achieved and maintained. This hypothesis is also supported by a meta-analysis of previous trials of insulin therapy in critically ill patients that demonstrated a benefit among trials in which insulin was dosed to achieve a glucose target, but not among trials in which a glucose target was not specified.6 Although it would be interesting to measure inflammatory markers during insulin infusion in AMI, it is currently impractical to dose insulin based on these markers, as they are markedly elevated in the setting of AMI, few assays are available at the point of care, and the dose of insulin would be necessarily limited by the occurrence of hypoglycaemia. It is our understanding that investigators are already planning a large, simple trial of intensive insulin therapy targeting normoglycaemia in AMI to determine whether this strategy improves clinical outcomes.
References
- Goyal A, Mahaffey KW, Garg J, Nicolau JC, Hochman JS, Weaver WD, Theroux P, Oliveira GBF, Todaro TG, Mojcik CF, Armstrong PW, Granger CB. (2006) Prognostic significance of the change in glucose level in the first 24 hours after acute myocardial infarction: results from the CARDINAL study. Eur Heart J 27:1289–1297.
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- Giugliano D, Marfella R, Coppola L, Verrazzo G, Acampora R, Giunta R, Nappo F, Lucarelli C, D'Onofrio F. (1997) Vascular effects of acute hyperglycemia in humans are reversed by L-arginine. Evidence for reduced availability of nitric oxide during hyperglycemia. Circulation 95:1783–1790.
[Abstract/Free Full Text] - Dandona P, Aljada A, Bandyopadhyay A. (2003) The potential therapeutic role of insulin in acute myocardial infarction in patients admitted to intensive care and in those with unspecified hyperglycemia. Diab Care 26:516–519.
[Free Full Text] - Mehta SR, Yusuf S, Diaz R, Paolasso E. (2005) Letters: glucose–insulin–potassium infusion and mortality in the CREATE-ECLA trial—reply. JAMA 293:2598.
[Free Full Text] - Pittas AG, Siegel RD, Lau J. (2004) Insulin therapy for critically ill hospitalized patients: a meta-analysis of randomized controlled trials. Arch Intern Med 164:2005–2011.
[Abstract/Free Full Text]
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