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Hyperinsulinaemia in ischaemic heart disease: the importance of myocardial infarction and left ventricular function
R A Wright1, A D Flapan, F Stenhouse
1Cardiovascular Research Unit, University of Edinburgh, UK.
Insights
Elevated insulin levels (hyperinsulinaemia) are common in heart conditions. This study found hyperinsulinaemia in patients with heart failure or after myocardial infarction, potentially explaining exercise-induced fatigue.
Area of Science:
- Cardiology
- Endocrinology
- Metabolic Syndrome
Background:
- Elevated circulating insulin levels are linked to ischemic heart disease.
- Previous research has not fully explored the impact of heart failure or myocardial infarction on insulin response, focusing instead on stable angina.
Purpose of the Study:
- To investigate insulin response to oral glucose challenge in men with normal glucose tolerance, stable angina, recent myocardial infarction, and chronic severe heart failure.
- To determine if heart failure or time since myocardial infarction influences hyperinsulinaemia.
Main Methods:
- Oral glucose tolerance test (75 g) was administered to five groups: normal controls, chronic stable angina, recent myocardial infarction (3 weeks and 3 months post), and chronic severe heart failure.
- Fasting and stimulated insulin levels were measured.
Main Results:
- Fasting hyperinsulinaemia was observed only in patients with chronic heart failure.
- Stimulated hyperinsulinaemia occurred in all patient groups, but was less pronounced and shorter in angina patients.
- At 120 minutes, hyperinsulinaemia persisted in heart failure and post-myocardial infarction groups.
- The degree of stimulated hyperinsulinaemia was not affected by heart failure or time post-infarction.
Conclusions:
- Hyperinsulinaemia is associated with impaired peripheral muscle glucose uptake and metabolism.
- This may contribute to exertional muscular fatigue in patients with myocardial infarction or heart failure.
Abstract:
Elevated circulating insulin levels have been reported in ischaemic heart disease, and may be of aetiological importance. Previous studies have not considered the potential influence of heart failure or of previous myocardial infarction, as opposed to stable angina. We therefore measured the insulin response to a 75 g oral glucose tolerance test in five groups with normal glucose tolerance, comparing normal male controls to men with chronic stable angina, men with recent myocardial infarction (two groups, 3 weeks and 3 months post infarction), and men with chronic severe heart failure. Only patients with chronic heart failure had fasting hyperinsulinaemia, probably reflecting associated neuroendocrine abnormalities. Stimulated hyperinsulinaemia was present in all patient groups, but was less pronounced and of shorter duration in patients with angina. At 120 min, only patients with heart failure or previous myocardial infarction were hyperinsulinaemic. The degree of stimulated hyperinsulinaemia was not influenced by the presence of heart failure or by the length of time from infarction. Hyperinsulinaemia is associated with impaired peripheral muscle glucose uptake and metabolism, and might contribute to muscular fatigue on exertion in patients with previous myocardial infarction or heart failure.