THE CARDIOVASCULAR EFFECTS OF OCTREOTIDE TREATMENT IN ACROMEGALY: AN ECHOCARDIOGRAPHIC STUDY

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Abstract
SUMMARY: Nine acromegalic patients were treated by the somatostatin analogue SMS 201–995 octreotide (Sandostatin (octreotide), Sandoz, Basle, Switzerland)) 250 μg/ day in 4 divided s.c. injections (50 + 50 + 50 +100 μg) for 1 month, 250 μg/24 h as continuous s.c. infusions for another month and thereafter 200 μg three times daily as s.c. injections. Echocardiography was performed before the treatment, following 1 month of octreotide s.c. infusion/injection and after 6 and after 12 months of octreotide treatment. No differences in serum growth hormone, heart rate, blood pressure, cardiac contractility or left ventricular wall mass or wall thickness were found between the infusion and the injection periods. As compared to the pretreatment levels serum growth hormone decreased by 62 and 66%, respectively following 6 and 12 months octreotide treatment. The heart rate per minute (± SD) decreased from the pretreatment level of 75 ± 12 to 63·13 (P> 0.007) at month 12. The systolic and the diastolic blood pressure decreased from the pretreatment level of 121 ± 8 and 79 ± 5 mmHg respectively to 108 ± 7 (P> 0.0007) and 71 ± 7 mmHg (P> 0.0001) respectively at month 12. The left ventricular wall thickness was reduced from 26 ± 3 mm before treatment to 24 ± 3 mm (P> 0.05) at month 6 and to 24 ± 4 mm (P> 0.04) at month 12. The left ventricular wall mass was 168 ± 48 g/m2 before octreotide treatment, 156 ± 46 g/m2 (NS) after 6 months and 157 ± 52 g/m2 after 12 months (P> 0.08) of octreotide treatment. In age and sex‐matched normal control subjects the left ventricular wall thickness was 20 ± 2 mm, and the left ventricular wall mass was 122 ± 26 g/m2. The wall thickness and the wall mass were increased in the acromegalic patients as compared to the controls before and following the octreotide treatment periods. We suggest that reduction of serum growth hormone levels by octreotide in acromegalic patients is associated with a decrease of the left ventricular wall thickness, but the wall thickness is not reduced to levels of normal control subjects.