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Rapid Reduction of Left Ventricular Hypertrophy in Acromegaly after Suppression of Growth Hormone Hypersecretion

Michael J. Lim, BS; Ariel L. Barkan, MD; and Andrew J. Buda, MD
[+] Article and Author Information

Presented in part at the 62nd Scientific Session of the American Heart Association, 13-16 November 1989, New Orleans, Louisiana.

Grant Support: In part by the Veterans Affairs Medical Research Service and Geriatric Research, Education and Clinical Center; by National Institutes of Health grants R29-DK 38449 (Dr. Barkan) and 5MO-1-RR-42 (Clinical Research Center, University of Michigan Medical Center); and a student research fellowship from the American Heart Association of Michigan (Mr. Lim).

Requests for Reprints: Andrew J. Buda, MD, Chief, Section of Cardiology, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112.

Current Author Addresses: Mr. Lim: 1301 Orleans, Apartment 610, Detroit, MI 48207.

Dr. Buda: Chief, Section of Cardiology, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112.

Dr. Barkan: University of Michigan Medical School, Division of Endocrinology, Taubman Center 3920, Box 0354, Ann Arbor, MI 48109.


© 1992 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1992;117(9):719-726. doi:10.7326/0003-4819-117-9-719
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Objective: To examine the possible role of growth hormone as a pathogenetic factor in the development of myocardial hypertrophy in acromegaly.

Design: An uncontrolled clinical trial.

Setting: Tertiary-care medical center.

Patients: Sixteen patients with acromegaly were stratified into two groups: Group I (n = 10) had left ventricular hypertrophy (LVH), and group II (n = 6) did not have LVH.

Intervention: Therapy with octreotide acetate (SMS 201-995), a long-acting somatostatin analog (mean dose, 538 µg/d), was administered for 2 months.

Measurements: Plasma growth hormone and insulin-like growth factor I (IGF-I) concentrations, hand volume, and echocardiographic left ventricular dimensions and mass were measured at baseline and at 1 week and 2 months after the start of therapy.

Results: Before octreotide therapy, both groups had similar hand volumes and similar growth hormone and IGF-I hypersecretion. Both groups showed a reduction in growth hormone at 2 months (mean reduction, 13.7 µg/L in patients with LVH [P < 0.01] and 14.1 µg/L in patients without LVH [P < 0.05]). Plasma IGF-I was also decreased (mean reduction, 305 µg/L in patients with LVH [P < 0.01] and 304 µg/L in patients without LVH [P < 0.05]). Reduction of growth hormone and IGF-I hypersecretion in patients with LVH was associated with a rapid decrease in left ventricular mass (339 g to 299 g, P < 0.01) within 1 week, which was sustained at 2 months (274 g, P < 0.04). Patients without LVH showed no statistical change in left ventricular mass. In patients with LVH, the decrease in left ventricular mass correlated with the octreotide-induced decrease in growth hormone (r = 0.79, P < 0.05) but not with blood pressure. Blood pressure, left ventricular dimensions, and percent of fractional shortening were not altered by therapy in either group. Hand volume decreased in both groups.

Conclusions: Normalization of growth hormone secretion is associated with reduction of left ventricular mass in acromegalic patients with LVH within 1 week of initiating therapy with octreotide.

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