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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. [ABSTRACT FROM PUBLISHER]

To investigate left and right ventricular involvement in acromegaly, 20 patients were studied by Doppler echocardiography. Nine of them had systemic hypertension. Right ventricular free wall thickness was significantly increased in acromegalic patients (8 ± 2 vs 4 ± 1 mm; P <0.001). Left ventricular mass index was augmented both in the whole group and in the subgroup of normotensive acromegalics, as compared with normals (134 ± 33 and 115 ± 20 vs 80 ± 18 g.m,. P <0.01). Ejection phase indices were normal in the patient group, while impaired left and right ventricular diastolic filling was found. In fact, isovolumic relaxation time was prolonged (118 ± 21 vs 78 ± 12 ms; P <0.001), ratio of early to late mitral (0. ± 0.3 vs 1.8±0.5 P<0.001) and tricuspid (1.0±0.2 vs 1.4±0.3 P<0.001 flow velocities were significantly decreased as compared with controls. Superior vena cava flowmetry was also abnormal showing a marked decrease of diastolic filling wave and, consequently, of the ratio between peak diastolic and peak systolic flow velocity. No significant differences observed between normotensive and hypertensive acromegalics, except for left ventricular mass index (115 ± 20 vs 156 ± 31 g.m; P <0.01). These findings indicate that abnormal diastolic filling patterns of transmitral, transtricuspid, and superior vena cava flowmetry suggesting ‘impaired relaxation’ associated with increased left and right ventricular mass, frequently occur in acromegaly. [ABSTRACT FROM PUBLISHER]

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