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Mechanisms Determining Course and Outcome of Diabetic Patients Who Have Had Acute Myocardial Infarction

Doron Aronson, MD; Elliot J. Rayfield, MD; and James H. Chesebro, MD
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From Joslin Diabetes Center, Boston, Massachusetts; and Mount Sinai Medical Center, New York, New York. Requests for Reprints: Doron Aronson, MD, Joslin Diabetes Center, Research Division, Metabolism Section, One Joslin Place, Boston, MA 02215. Current Author Addresses: Dr. Aronson: Joslin Diabetes Center, Research Division, Metabolism Section, One Joslin Place, Boston, MA 02215.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1997;126(4):296-306. doi:10.7326/0003-4819-126-4-199702150-00006
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Purpose: To review the pathogenic mechanisms that lead to the poor prognosis of diabetic patients after myocardial infarction and to determine the efficacy of current interventions for myocardial infarction in these patients.

Data Sources: Search of the MEDLINE database from 1985 to 1995, using the keywords diabetes, myocardial infarction, and cardiomyopathy, and a search of the reference citations of relevant articles.

Study Selection: Experimental and clinical studies on myocardial infarction in diabetic patients and basic research studies relevant to this topic.

Data Synthesis: The excess in-hospital mortality of diabetic patients results primarily from an increased incidence of congestive heart failure. Several combined mechanisms reduce the compensatory ability of the noninfarcted myocardium; such mechanisms include preexisting congestive heart failure caused by diabetic cardiomyopathy, severe coronary artery disease, decreased vasodilatory reserve of epicardial and resistance arteries, and possibly abnormal metabolism of myocardial substrate.

Late mortality results from increased reinfarction rates caused by the diffuse nature of the atherosclerotic disease and hypercoagulable state.Platelet hyperactivity, reduced fibrinolytic capacity, increased concentrations of hemostatic proteins, and endothelial dysfunction promote thrombosis at the site of plaque rupture. Autonomic neuropathy predisposes patients to ventricular arrhythmias. Thrombolytic agents, aspirin, β-blockers, and angiotensin-converting enzyme inhibitors are effective in patients with diabetes.

Conclusions: In the thrombolytic era, mortality rates of diabetic patients who have had acute myocardial infarction remain 1.5 to 2 times higher than those in nondiabetic patients. This increased mortality rate is caused by diverse mechanisms that affect myocardial function and blood supply and by the tendency toward thrombosis in diabetic patients. Current therapies for myocardial infarction are effective in these patients. Improved metabolic control may also decrease mortality rates.


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Figure 1.
Probable mechanisms promoting congestive heart failure and associated in-hospital mortality in diabetic patients who have had acute myocardial infarction.

Preexisting diabetic cardiomyopathy, impaired blood flow, and abnormal fuel use reduce the capacity of the noninfarcted myocardium to compensate.

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Grahic Jump Location
Figure 2.
Factors leading to poor long-term survival in diabetic patients after myocardial infarction.

Late mortality is primarily related to recurrent myocardial infarction and preexisting left ventricular dysfunction. Multivessel coronary artery disease and the hypercoaguable state promote recurrent infarctions. Autonomic imbalance may promote arrhythmic events.

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