Copyright © 1997 by the European Society of Cardiology.
© 1997 The European Society of Cardiology
Growth hormone and heart performance
A novel mechanism of cardiac wall stress regulation in humans
Departments of Internal Medicine and Endocrinology, University Federico II Naples, Italy
revised 10 May 1996; accepted 19 May 1996.
Correspondence: Luigi Saccà. MD. Medicina Interna, Via Pansini 5. 80131-Napoli. Italy
Abstract
OBJECTIVES: This study was designed to assess systolic wall stress and ventricular function in patients with deranged growth hormone secretion, in an attempt to elucidate the mechanisms of growth hormone interaction with heart performance.
DESIGN: A case-control study.
SUBJECTS: Thirty patients with active acromegaly, free of diabetes mellitus and coronary artery disease, and 25 subjects with congenital growth hormone deficiency were studied. Twelve growth hormone-deficient subjects were reevaluated after 12 months of recombinant human growth hormone therapy. Two groups of 30 normal subjects each were used as controls for the acromegalic and growth hormone-deficient patients, respectively.
RESULTS: In the acromegalics, end-systolic wall stress was reduced (20%; P<0·01) due to ventricular wall thickening (+26%; P<0·001), whereas cardiac output was significantly increased (+20%; P<0·01). The velocity of fibre shortening was unchanged. In growth hormone-deficient subjects, end-systolic wall stress was markedly increased (+38%; P<0·001) due to a significant reduction of ventricular wall thickness (28%; P<0·001), whereas cardiac output was significantly decreased (44%; P<0·001) Replacement therapy with recombinant human growth hormone produced a partial correction of wall thickness and stress. Consequently, systolic performance and cardiac output improved significantly.
CONCLUSION: This study demonstrates that growth hormone plays a role in the control of cardiac wall stress and performance through a mechanism mediated by the effect of growth hormone on myocardial tissue growth. The data may have therapeutic implications in cardiac diseases that lead to heart failure.
Key Words: Cardiac wall stress growth hormone excess growth hormone deficiency cardiac performance cardiac hypertrophy
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