Epidemiological data suggest that adults with hypopituitarism have reduced life expectancy compared with healthy controls, with a greater than twofold increase in mortality from cardiovascular disease (35,36). GH-deficiency has been proposed as the variable accounting for this increased mortality, and the hypothesis that long standing GH-deficiency predisposes to the development of premature atherosclerosis. The mecha nisms responsible for the increased cardiovascular mortality remain largely unknown, but increased intima-medial thickening, intimal plaque formation (37), and reduced arterial compliance (38) in the carotid artery have been demonstrated in hypopituitary adults on conventional replacement therapy.
A study comparing echocardiography findings in GH-deficient adults with healthy controls demonstrated reduced left ventricular mass and impaired cardiac systolic function in the patients (15). Similar findings were reported from a study using radionuclide scanning (39). In both of these studies treatment with GH for six months normalized these indices, and six months following cessation of therapy, cardiac function had returned to baseline. Six months GH replacement has been shown to increase left ventricular mass (18%), and cardiac output (43%) in GH-deficient adults (40), and studies suggest that these benefits are sustained to three years following commencement and continuation of GH therapy (23,41).
A recent study investigating total blood volume measuring red cell mass and plasma volume has shown that erythropoiesis is impaired in adult GH-deficiency. GH therapy stimulates erythropoiesis (oxygen capacity) and increases plasma volume and total blood volume and may, therefore, contribute to observed increased in exercise performance associated with GH therapy (18).
In summary, adults with GH-deficiency have an increased cardiovascular mortality compared to matched controls. Cardiac function is impaired in GH-deficiency and GH replacement reverses these deficits in studies lasting up to three years.
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