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Myocardial dysfunction and abnormal left ventricular exercise response in autonomic diabetic patients
R Scognamiglio1, G Fasoli, M Ferri
1Department of Cardiology, University of Padua, Medical School, Italy.
Clinical Cardiology
|May 1, 1995
Summary
Diabetic patients with autonomic dysfunction often show abnormal left ventricular (LV) responses to exercise. A defect in inotropic recruitment, not contractile reserve, contributes to exercise-induced LV dysfunction in these patients.
Area of Science:
- Cardiology
- Diabetology
- Exercise Physiology
Background:
- Exercise-induced left ventricular (LV) dysfunction in diabetic patients is poorly understood.
- Autonomic dysfunction is common in diabetes and may affect cardiac responses.
- Previous studies have not fully elucidated the mechanisms of abnormal LV function during exercise in this population.
Purpose of the Study:
- To investigate the role of myocardial contractility recruitment in abnormal LV response to exercise in diabetic patients with autonomic dysfunction.
- To differentiate between impaired contractile reserve and defective inotropic recruitment as causes of exercise-induced LV dysfunction.
Main Methods:
- Studied 14 diabetic patients with autonomic dysfunction, excluding ischemic heart disease.
- Assessed LV and myocardial function at rest and during isometric/isotonic exercise using 2D echocardiography.
- Evaluated inotropic reserve via post-extrasystolic potentiation at rest and peak handgrip.
Main Results:
- A high frequency of abnormal LV ejection fraction response to both isometric (9/14) and dynamic (8/14) exercise was observed.
- Patients exhibited normal baseline myocardial contractility and normal contractile reserve, evidenced by post-extrasystolic potentiation.
- Despite normal contractile reserve, impaired inotropic recruitment was suggested by altered LV ejection fraction-systolic wall stress relationships during exercise.
Conclusions:
- Diabetic patients with autonomic neuropathy frequently display abnormal LV function during exercise.
- A defective inotropic recruitment, rather than a lack of contractile reserve, is a key factor in exercise-induced LV dysfunction in this cohort.
- Post-extrasystolic potentiation can reverse exercise-induced LV dysfunction, highlighting the role of inotropic stimulation independent of adrenergic receptors.