title: Growth hormone and heart performance. A novel mechanism of cardiac wall stress regulation in humans.
abstract: OBJECTIVE
  This study was designed to assess systolic wall stress and ventricular function in patients with deranged growth hormone secretion, in an attempt to elucidate the mechanisms of growth hormone interaction with heart performance.
  
  
  METHODS
  A case-control study.
  
  
  METHODS
  Thirty patients with active acromegaly, free of diabetes mellitus and coronary artery disease, and 25 subjects with congenital growth hormone deficiency were studied. Twelve growth hormone-deficient subjects were reevaluated after 12 months of recombinant human growth hormone therapy. Two groups of 30 normal subjects each were used as controls for the acromegalic and growth hormone-deficient patients, respectively.
  
  
  RESULTS
  In the acromegalics, end-systolic wall stress was reduced (-20%; P < 0.01) due to ventricular wall thickening (+ 26%; P < 0.001), whereas cardiac output was significantly increased (+ 20%; P < 0.01). The velocity of fibre shortening was unchanged. In growth hormone-deficient subjects, end-systolic wall stress was markedly increased (+ 38%; P < 0.001) due to a significant reduction of ventricular wall thickness (- 28%; P < 0.001), whereas cardiac output was significantly decreased (-44%; P < 0.001). Replacement therapy with recombinant human growth hormone produced a partial correction of wall thickness and stress. Consequently, systolic performance and cardiac output improved significantly.
  
  
  CONCLUSIONS
  This study demonstrates that growth hormone plays a role in the control of cardiac wall stress and performance through a mechanism mediated by the effect of growth hormone on myocardial tissue growth. The data may have therapeutic implications in cardiac diseases that lead to heart failure.
authors.affiliation: Department of Internal Medicine, University Federico II, Naples, Italy.
authors.forename: S
authors.initials: S
authors.lastname: Fazio
authors.forename: A
authors.initials: A
authors.lastname: Cittadini
authors.forename: D
authors.initials: D
authors.lastname: Sabatini
authors.forename: B
authors.initials: B
authors.lastname: Merola
authors.forename: A
authors.initials: A
authors.lastname: Colao
authors.forename: B
authors.initials: B
authors.lastname: Biondi
authors.forename: S
authors.initials: S
authors.lastname: Longobardi
authors.forename: G
authors.initials: G
authors.lastname: Lombardi
authors.forename: L
authors.initials: L
authors.lastname: Saccà
mesh_terms: D000172:Acromegaly / Q000378:metabolism / Q000503:physiopathology; D000328:Adult; D001794:Blood Pressure; D002302:Cardiac Output; D016022:Case-Control Studies; D004452:Echocardiography; D015444:Exercise; D005260:Female; D013006:Growth Hormone / Q000502:physiology* / Q000627:therapeutic use; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D015588:Observer Variation; D014655:Vascular Resistance
chemical_list: D013006:Growth Hormone