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Cardiac involvement in acromegaly: specific myocardiopathy or consequence of systemic hypertension?
R López-Velasco1, H F Escobar-Morreale, B Vega
1Department of Endocrinology, Hospital Ramón y Cajal, Madrid, Spain.
Insights
This study reveals that both growth hormone (GH) hypersecretion and hypertension independently contribute to cardiac abnormalities in acromegaly. Treating active acromegaly can reverse some cardiac changes, suggesting a specific acromegalic myocardiopathy.
Area of Science:
- Cardiology
- Endocrinology
- Internal Medicine
Background:
- Acromegaly, caused by excess growth hormone (GH), is associated with cardiac abnormalities.
- The independent contributions of GH hypersecretion and hypertension to these cardiac changes are not fully understood.
Purpose of the Study:
- To evaluate the distinct roles of past/present GH hypersecretion and hypertension in acromegaly-related cardiac abnormalities.
- To assess cardiac morphology and function in patients with acromegaly compared to controls.
Main Methods:
- Echocardiography-Doppler was used to measure cardiac indexes in 39 acromegaly patients and control groups.
- Serum GH, IGF-I, and blood pressure were measured.
- Patients included those with active or cured acromegaly.
Main Results:
- Hypertension was common in active (42.8%) and cured (28.0%) acromegaly.
- Hypertension independently worsened cardiac morphology and function.
- Acromegaly itself increased left ventricular mass and altered systolic/diastolic function, independent of hypertension.
- Successful acromegaly treatment reduced left ventricular mass and posterior wall thickness.
Conclusions:
- Cardiac abnormalities in acromegaly result from independent effects of GH excess and hypertension.
- A specific acromegalic myocardiopathy exists, potentially aggravated by coexisting hypertension.
- Treatment of acromegaly can lead to cardiac improvements.
Abstract:
To evaluate the relative contributions of past or present GH hypersecretion and of hypertension to the cardiac abnormalities present in acromegaly, we have studied the serum GH and insulin-like growth factor I concentrations, systolic and diastolic blood pressures, and morphological and functional cardiac indexes as measured by echocardiography-Doppler, in 39 patients with active or cured acromegaly, 16 hypertensive controls, and 17 normotensive controls. Hypertension was present in 42.8% of patients with active acromegaly and in 28.0% of patients in which acromegaly was cured. Hypertension was independently related to an increase in indexes of cardiac morphology (left ventricular mass, left ventricular posterior wall thickness, interventricular septum thickness, relative wall thickness with respect to the diastolic diameter of the left ventricle, and left atrial end-systolic diameter), systolic function (stroke volume, fractional shortening, and end-systolic stress), and diastolic function (isovolumic relaxation time and maximal late diastolic flow velocity) and to a reduction in the early to late maximal diastolic flow velocity ratio. Acromegaly was related to an increase in left ventricular mass, stroke volume, cardiac output, and isovolumic relaxation time, which were independent from the presence of hypertension. End-systolic stress was reduced by acromegaly. In the five patients in which active acromegaly was successfully treated, left ventricular mass and left ventricular posterior wall thickness were reduced 1 yr later. In conclusion, the asymptomatic morphological and functional cardiac abnormalities present in acromegalic patients are independently related to acromegaly and hypertension, pointing to the existence to a specific acromegalic myocardiopathy that might be aggravated by the coexistence of hypertension.