Emerging cardiovascular risk factors/markers such as proinflammatory cytokines , C-reactive protein , and adipokines are also increased in GHD patients .
Increased cardiovascular morbidity and mortality have also been reported in GHD .
GH treatment has been shown to improve both traditional and emerging cardiovascular risk factors and markers .
The GHD population may be considered at high cardiovascular risk , and GH substitution may be expected to bring an added value to patients with hypopituitarism in terms of cardiovascular protection .
CONTEXT GH deficiency ( GHD ) of the adult is a clinical condition characterized by the presence of several traditional and emerging cardiovascular risk factors that can significantly increase cardiovascular morbidity and mortality .
It is still an open issue whether GH replacement is able not only to improve cardiovascular risk factors but also to decrease cardiovascular morbidity and mortality .
EVIDENCE SYNTHESIS In untreated GHD , cardiovascular risk is increased due to abnormal lipid profile ( increased total and low-density lipoprotein cholesterol , increased triglycerides , and reduced high-density lipoprotein cholesterol ) and impaired glucose metabolism .
Cardiovascular effects of growth hormone treatment in growth-hormone-deficient adults: stimulation of the renin-aldosterone system.
1 . In adult humans with growth hormone deficiency , treatment with growth hormone has recently been shown to have major anabolic effects and to improve exercise performance . The cardiovascular effects of growth hormone in adults with growth hormone deficiency were examined in 24 patients treated with recombinant human growth hormone ( 0.07 units/kg at night ) in a double-blind , placebo-controlled trial lasting 6 months . 2 . Compared with placebo , resting M-mode echocardiography showed increases in left ventricular end-diastolic dimension and stroke volume in the group treated with recombinant human growth hormone . No differences were noted between the groups with respect to left ventricular end-systolic dimension , fractional shortening , wall thicknesses or mean arterial blood pressure . Left ventricular myocardial mass increased in the group given recombinant human growth hormone . 3 . The supine plasma renin activity was increased and remained elevated over the 6 months , whereas the plasma aldosterone concentration was unchanged , after treatment with recombinant human growth hormone . Clinical signs of sodium retention were evident during the first 3 months of treatment with recombinant human growth hormone . 4 . We conclude that treatment with recombinant human growth hormone in adults with growth hormone deficiency result ed in small increases in left ventricular pre-load , due to the sodium-retaining action of growth hormone . Activation of the renin-aldosterone system was involved in such changes . Myocardial hypertrophy was observed without changes in mean arterial pressure , reflecting the anabolic action of growth hormone
Emerging cardiovascular risk factors/markers such as proinflammatory cytokines , C-reactive protein , and adipokines are also increased in GHD patients .
Increased cardiovascular morbidity and mortality have also been reported in GHD .
GH treatment has been shown to improve both traditional and emerging cardiovascular risk factors and markers .
The GHD population may be considered at high cardiovascular risk , and GH substitution may be expected to bring an added value to patients with hypopituitarism in terms of cardiovascular protection .
CONTEXT GH deficiency ( GHD ) of the adult is a clinical condition characterized by the presence of several traditional and emerging cardiovascular risk factors that can significantly increase cardiovascular morbidity and mortality .
It is still an open issue whether GH replacement is able not only to improve cardiovascular risk factors but also to decrease cardiovascular morbidity and mortality .
EVIDENCE SYNTHESIS In untreated GHD , cardiovascular risk is increased due to abnormal lipid profile ( increased total and low-density lipoprotein cholesterol , increased triglycerides , and reduced high-density lipoprotein cholesterol ) and impaired glucose metabolism .