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Peripheral vascular structure and function in men with contrasting GH levels
R John Irving1, Maggie N Carson, David J Webb
1University of Edinburgh, Department of Medical Sciences, Western General Hospital, Edinburgh EH4 2XU, Scotland, UK.
Insights
Growth hormone (GH) deficiency and excess impact cardiovascular health. GH replacement therapy improved arterial stiffness and dermal capillary perfusion in GH-deficient men, suggesting modest direct vascular effects.
Area of Science:
- Endocrinology
- Cardiovascular Physiology
- Vascular Biology
Background:
- Growth hormone (GH) deficiency and excess are linked to cardiovascular disease, but direct vascular mechanisms remain unclear.
- Previous research suggests GH influences endothelium-dependent vasodilation and large artery structure.
Purpose of the Study:
- To comprehensively assess large artery and microvascular structure and function in individuals with varying GH levels.
- To investigate the direct vascular effects of GH deficiency and excess in men.
Main Methods:
- Studied healthy controls, men with acromegaly, and men with adult-onset GH deficiency.
- Measured arterial wall thickness, stiffness, microvascular flow, dermal capillary density, and endothelial function.
- Assessed cardiac output in GH-deficient patients and controls.
Main Results:
- GH-deficient patients showed trends toward increased arterial wall thickness and stiffness compared to controls.
- GH replacement therapy significantly reduced arterial stiffness and increased dermal capillary perfusion.
- No significant differences in forearm/dermal flow or endothelial function were observed between groups or with GH therapy.
Conclusions:
- Direct vascular effects of GH excess and deficiency in humans are modest.
- These direct vascular effects may not warrant the highest priority when assessing cardiovascular risks in pituitary disease patients.
Abstract:
Both GH deficiency and excess are associated with cardiovascular disease. The mechanisms are unclear, but direct effects of GH in the vessel wall may be important. Previous reports suggest that GH enhances endothelium-dependent vasodilatation and alters large artery structure. Here we report a detailed assessment of large artery and microvascular structure and function in patients with contrasting GH levels. We studied six age-matched healthy control men, five men with acromegaly, and seven men with adult-onset GH deficiency before and at the end of 16 wk of GH replacement therapy. We measured arterial wall thickness by ultrasound of the common carotid artery; arterial stiffness by pulse wave analysis at the radial artery; microvascular structure by measurement of flow during maximal dilatation in the forearm and dermal circulation and counting dermal capillaries using video microscopy; and endothelial function in the forearm during brachial artery infusion of vasodilators (acetylcholine and sodium nitroprusside). Cardiac output was measured by Doppler ultrasound in GH-deficient patients and controls. GH-deficient patients tended to have increased arterial wall thickness and arterial stiffness, compared with controls. GH replacement reduced arterial stiffness (radial augmentation index 0.28 +/- 0.07 to 0.20 +/- 0.12, P = 0.02) and increased the number of dermal capillaries perfused (28.6 +/- 5.0 to 30.9 +/- 6.5 cm(-2), P = 0.03), but a reduction in arterial wall thickness was not statistically significant. With respect to maximum flow in forearm and dermis and endothelial function, GH-deficient patients were not different from controls, and GH therapy had no effect. Moreover, acromegalic patients were not different from controls in any vascular parameters studied. We conclude that the direct vascular effects of GH excess and deficiency in man are of modest magnitude and should not therefore be given the highest priority in considering the risks of cardiovascular events in patients with pituitary disease.