Int J Angiol 1996; 5(1): 55-58
DOI: 10.1007/BF02043466
Original Articles

© Georg Thieme Verlag KG Stuttgart · New York

Cardiac involvement in active uncomplicated acromegaly

Serafino Fazio1 , Domenico Sabatini1 , Antonello Cittadini1 , Manlio Cocozza1 , Alberto Cuocolo2 , Bartolomeo Merola3 , Annamaria Colao3 , Bernadette Biondi3 , Gaetano Lombardi3 , Luigi Saccà1
  • 1Department of Internal Medicine, Medical School of Federico II University, Naples, Italy
  • 3Department of Endocrinology, Medical School of Federico II University, Naples, Italy
  • 2Section of Nuclear Medicine, Medical School of Federico II University, Naples, Italy
Presented at the 36th Annual World Congress, International College of Angiology, New York, New York, July 1994
Further Information

Publication History

Publication Date:
23 April 2011 (online)

Abstract

Increased cardiovascular mortality is present in acromegaly. A late frequent complication of this disease is congestive heart failure. At present it is unclear whether the acromegalic heart disease is principally due to the growth hormone excess or to diabete mellitus, hypertension, and coronary artery disease often present in acromegalic patients. The aim of this study was an attempt to clarify this issue. Thus, we studied by echocardiography and radionuclide ventriculography at rest and during exercise 11 patients with active uncomplicated acromegaly in comparison with 12 normal subjects, comparable for age and sex distribution. The results have shown comparable heart rate and blood pressure in patients and control subjects. Moreover, increased left ventricular mass (117 ± 19 vs 79 ± 18 g/m2; p < 0.001) with normal internal dimensions; normal ejection fraction at rest, but impaired during exercise (59 ± 8 vs 74 ± 7 %, p < 0.001); impairment of diastolic function as documented by reduced peak filling rate (2.6 ± 0.6 vs 3.17 ± 0.3 EDV/s, p < 0.01) and prolonged time to peak filling rate (209 ± 78 vs 134 ± 53 ms, p < 0.01); and reduction of left ventricular end-systolic stress (49 ± 7 vs 62 ± 8 × 10 dynes/cm2, p < 0.001) were demonstrated in acromegalic patients. These results confirm those of the previous studies and better clarify the pathophysiological mechanisms at the base of acromegalic heart disease.

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