Related Experiment Videos
Systolic and diastolic cardiac function in acromegaly. An echocardiographic study
G Galanti1, B Cappelli, G Diricatti
1Istituto di Clinica Medica Generale e Cardiologia, Università degli Studi di Firenze.
Insights
Acromegaly causes cardiac hypertrophy, but diastolic heart function is impaired, especially during exercise. This suggests a distinct acromegalic cardiomyopathy beyond typical cardiovascular issues.
Area of Science:
- Cardiology
- Endocrinology
- Internal Medicine
Background:
- Acromegaly, a condition of excess growth hormone (GH), is linked to cardiovascular complications.
- The existence of a primary acromegalic cardiomyopathy, distinct from other cardiovascular issues, requires further investigation.
Purpose of the Study:
- To determine if acromegaly causes a unique cardiomyopathy.
- To assess cardiac structure and function in acromegalic patients, with and without hypertension, compared to controls.
Main Methods:
- Echocardiographic studies were performed on 34 acromegalic patients (hypertensive and normotensive subgroups) and 34 matched controls.
- A handgrip test was used to evaluate cardiac function during isometric exercise in normotensive acromegalics, controls, and athletes.
Main Results:
- All acromegalic patients exhibited increased cardiac mass, with hypertensive patients showing a greater increase.
- Hypertensive acromegalics had altered systolic wall stress and impaired diastolic function compared to controls.
- Diastolic function, normal at rest, deteriorated during isometric exercise in acromegalics.
Conclusions:
- Growth hormone hypersecretion leads to cardiac hypertrophy that does not enhance cardiac function in acromegaly.
- Acromegalic cardiomyopathy is characterized by impaired diastolic function, particularly under the stress of isometric exercise.
Abstract:
The aim of this study was to establish the existence of primary acromegalic cardiomyopathy different from the cardiovascular complications often associated with acromegaly. Thirty-four acromegalic patients, referred to our non-invasive laboratory and divided into two groups on the basis of the presence of hypertension, underwent echocardiographic studies. A control group of 34 subjects individually matched with the patients for age, sex, and blood pressure values was also studied. To evaluate cardiac function during exercise, the normotensive acromegalics, the control group, and a group of 9 athletes with left ventricular mass comparable to that of the acromegalic subjects underwent a handgrip test. Cardiac mass was increased in all patients; hypertensive patients had a greater increase than normotensive patients (144.9 +/- 38 vs 120.9 +/- 20.8 g/m, p < 0.02). Systolic wall stress and percent fractional shortening, although similar to the values confirmed in controls, were modified in the hypertensive patients (wall stress 77.5 +/- 9.3 vs 60.8 +/- 9.4 dyne/cm2, p < 0.01). In all patients, diastolic function at rest was similar to that in controls, although the hypertensive patients had deteriorated diastolic function (E peak 56.9 +/- 12.4 vs 71 +/- 15 cm/s, p < 0.01; A peak 70.4 +/- 21.1 vs 52.3 +/- 16.4 cm/s, p < 0.03; E/A ratio 0.89 +/- 0.37 vs 1.38 +/- 0.35, p < 0.02). During handgrip testing, wall stress in both the normotensive acromegalics and the control subjects increased but remained unchanged in the athlete group; percent fractional shortening decreased in all patients and controls but increased slightly in the athlete group. In conclusion, cardiac hypertrophy caused by GH hyperincretion does not improve acromegalic heart activity: diastolic function, although normal at rest, appears deficient during isometric exercise.