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Ann Thorac Surg 2001;71:2086
© 2001 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery and Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA
e-mail: galmassi{at}mcw.edu
To the Editor
Endogenous release or exogenous administration of adenosine or agents that enhance levels of adenosine in ischemic myocardium are cardioprotective. The antiischemic action of adenosine has been shown to be due to stimulation of A1 receptors in myocytes linked by G-proteins to K+ ATP channels. Furthermore, K+ ATP channels open in the presence of reduced intracellular ATP during ischemia. K+ ATP channels in the heart and coronary circulation may be important in the regulation of blood flow during ischemia and hypoxia and may offer an endogenous myocardial protective mechanism during ischemia [1]. K+ ATP channel opening during ischemia has been suggested to produce a rapid reduction in myocardial oxygen consumption, preserve intracellular ATP and counteract ischemia-induced calcium overload, and beneficially affect the oxidative state of the myocyte. Examples of K+ ATP channel openers include pinacidil, cromakalim, and aprikalim. Selective blockers of K+ ATP channels include the sulfonylurea hypoglycemic agents glibenclamide (glyburide) and tolbutamide and the structurally unrelated compound 5-hydroxydecanoate.
A number of studies have shown that various K+ ATP channel openers produce cardioprotective effects. Intracoronary administration of cromakalim or pinacidil in doses that produce no systemic hemodynamic effects significantly reduced myocardial infarct size [2]. In a similar investigation, intravenous administration of aprikalim caused reduction of myocardial infarct size, which was antagonized by pretreatment with glibenclamide. A 30-minute coronary artery occlusion followed by 3 hours of reperfusion in pentobarbital-anesthetized rabbits has been shown to produce infarction, which was significantly increased by glibenclamide [3]. The University Group Diabetes Program [4] has previously documented the deleterious actions of the K+ ATP channel antagonists. The study showed that patients receiving tolbutamide had an increased incidence of cardiovascular death compared with those treated with insulin or placebo. It is, however, not known if this deleterious effect of oral hypoglycemic agents contributes to an increase in adverse outcomes in patients who undergo coronary artery bypass grafting. Identification of these agents as deleterious may have important significance for this patient population.
To examine a possible difference in myocardial infarction rate, other adverse cardiac events and mortality between patients on oral hypoglycemic agents versus patients receiving insulin or control patients without diabetes, the STS National Database for the entire patient population undergoing coronary artery bypass grafting between 1994 and 1997 was analyzed. Of a total number of 636,826 patients, 451,928 were nondiabetics. Diabetic patients were divided into insulin treated (65,301 patients), oral hypoglycemic treated (82,201 patients), and diet/no treatment controls (37,396 patients). Mortality was 2.90% for nondiabetics, 5.01% for insulin treated, 3.54% for oral hypoglycemic treated, and 3.96% for diet/no treatment groups. Although the mortality rate for insulin-treated diabetics is higher compared to nondiabetics, there was no significant difference among the different groups. Similarly, the rate of perioperative myocardial infarction was similar for all groups (1.42% nondiabetics, 1.31% insulin treated, 1.25% oral hypoglycemic treated, and 1.30% diet/no control group). There was no significant difference in operative mortality and perioperative myocardial infarction between men and women.
In summary despite the theoretical adverse effects of oral hypoglycemic agents, the analysis of STS data for patients undergoing coronary artery bypass grafting does not show an increased risk of adverse outcome for diabetic patients taking oral hypoglycemic agents.
References
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