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 .
Cardiac function in growth hormone deficient patients before and after 1 year with replacement therapy: a magnetic resonance imaging study
Assessed by conventional echocardiography the influence of growth hormone deficiency ( GHD ) and effects of replacement therapy on left ventricle ( LV ) function and mass ( LVM ) have shown inconsistent results . We aim ed to evaluate cardiac function before and during replacement therapy employing the gold st and ard method cardiac magnetic resonance imaging ( CMRI ) and measurements of circulating levels of B-type natriuretic peptides .  Sixteen patients ( 8 males and 8 females , mean age 49 years ( range 18–75 ) ) with severe GHD and 16 matched control subjects were included . CMRI was performed at baseline and after 1 year of GH replacement therapy .  IGF-I , B-type natriuretic peptide ( BNP ) and N-terminal pro-BNP ( NT-proBNP ) were measured after 0 , 1 , 2 , 3 , 6 and 12 months of treatment . IGF-I Z-score increased from ( median ( IQR ) ) −2.3 ( −3.8 to −1.4 ) to 0.5 ( −0.3 to 1.7 ) . LVM index ( LVMI ) , ejection fraction ( range 63–80 % ) , cardiac output index and levels of BNP and NT-proBNP were similar at baseline in patients compared to controls ( P-values from 0.09 to 0.37 ) . The patients had significantly smaller LV end-diastolic volume index ( P = 0.032 ) and end-systolic volume index ( P = 0.038 ) . No significant change in LV systolic function or LVM occurred during 1 year of GH treatment . BNP levels were unchanged ( P = 0.88 ) , whereas NT-proBNP tended to decrease ( P = 0.052 ) . Assessed by the highly sensitive and precise CMRI method , untreated GHD was not associated with impaired systolic function or reduced LVMI and 1 year of GH replacement using physiological doses did not influence cardiac mass or function
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 .