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Mechanisms determining course and outcome of diabetic patients who have had acute myocardial infarction
D Aronson1, E J Rayfield, J H Chesebro
1Joslin Diabetes Center, Boston, Massachusetts, USA.
Insights
Diabetic patients face higher mortality after myocardial infarction due to heart failure and thrombosis. However, current therapies for myocardial infarction remain effective, with improved metabolic control potentially further reducing risks.
Area of Science:
- Cardiology
- Diabetology
- Pathophysiology
Background:
- Diabetic patients exhibit poor prognosis following myocardial infarction (MI).
- Understanding the mechanisms behind this increased mortality is crucial for developing targeted interventions.
- Diabetic cardiomyopathy and accelerated atherosclerosis contribute to adverse outcomes.
Purpose of the Study:
- To elucidate the pathogenic mechanisms driving poor prognosis in diabetic patients post-MI.
- To evaluate the effectiveness of contemporary MI interventions in this patient population.
Main Methods:
- Comprehensive literature search of MEDLINE (1985-1995) and relevant citations.
- Inclusion of experimental, clinical, and basic research studies on diabetes and MI.
- Keywords: diabetes, myocardial infarction, cardiomyopathy.
Main Results:
- Excess in-hospital mortality in diabetics is linked to congestive heart failure, exacerbated by diabetic cardiomyopathy, coronary artery disease, and impaired vasodilation.
- Late mortality is driven by reinfarction due to diffuse atherosclerosis, hypercoagulable state, and platelet hyperactivity.
- Autonomic neuropathy increases the risk of ventricular arrhythmias.
Conclusions:
- Diabetic patients have 1.5-2 times higher mortality post-MI compared to non-diabetics, attributed to complex pathophysiological mechanisms.
- Current MI therapies, including thrombolytics, aspirin, beta-blockers, and ACE inhibitors, are effective in diabetic patients.
- Enhanced glycemic control may further improve survival rates in diabetic individuals post-MI.
Purpose:
To review the pathogenic mechanism 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, beta-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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