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Acromegalic cardiopathy: a left ventricular scintigraphic study
Insights
Acromegaly impairs heart diastolic function, specifically ventricular relaxation, due to excess growth hormone (GH). Systolic contractility remains unaffected in patients with acromegalic cardiomyopathy.
Area of Science:
- Cardiology
- Endocrinology
- Internal Medicine
Background:
- Acromegaly, caused by excess growth hormone (GH), can lead to cardiac complications.
- Acromegalic cardiomyopathy is a recognized concern in patients with this endocrine disorder.
Purpose of the Study:
- To investigate cardiac function in acromegalic patients.
- To differentiate between systolic and diastolic function impairments in acromegaly.
Main Methods:
- Gated radionuclide ventriculography was employed.
- Cardiac function was assessed in 18 acromegalic patients and 21 healthy controls.
Main Results:
- Ejection Fraction (EF), a measure of systolic function, showed no significant difference between groups.
- Peak Filling Rate (PFR) was significantly reduced in acromegalic patients.
- Time to Peak Filling Rate (TPFR) was significantly prolonged in acromegalic patients, indicating diastolic dysfunction.
Conclusions:
- Chronic GH hypersecretion in acromegaly primarily affects diastolic function, impairing ventricular relaxation.
- Systolic function (contractility) appears preserved in acromegaly.
- Early detection of diastolic dysfunction is crucial for managing acromegalic cardiomyopathy.
Abstract:
In order to study "acromegalic cardiomyopathy", cardiac function was examined, using gated radionuclide ventriculography, in 18 acromegalic patients and 21 control subjects with no clinical evidence of cardiac involvement. In these acromegalic subjects, while the Ejection Fraction (EF) did not appear to be significantly different, the Peak Filling Rate (PFR) was reduced while the Time to Peak Filling Rate (TPFR) resulted significantly greater than in control subjects. These findings indicate that chronic growth hormone (GH) hypersecretion, as observed in acromegaly, deteriorate the cardiac ventricular relaxation (diastolic phase) while it has no influence on contractility (systolic phase).