LEFT-VENTRICULAR FUNCTION IN YOUNG-ADULTS WITH CHILDHOOD AND ADULTHOOD ONSET GROWTH-HORMONE DEFICIENCY

OBJECTIVE The impairment of heart structure and function in adults wit h childhood onset GH deficiency has been recently described. However, previous echocardiographic studies have reported no differences in car diac mass and function between adulthood onset GH deficient patients a nd healthy subjects. DESIGN The aim of this study was to evaluate card iac performance in adult patients with childhood and adulthood onset G H deficiency, using equilibrium radionuclide angiography, a method mor e accurate than echocardiography. PATIENTS Eleven patients with childh ood onset GH deficiency, 9 patients with adulthood onset GH deficiency and 12 age-, gender-, height-and weight-matched healthy subjects ente red the study. MEASUREMENTS All the study population underwent equilib rium radionuclide angiography at rest and during physical exercise. RE SULTS Both childhood and adulthood onset GH deficient patients had an impaired left ventricular systolic performance both at rest (ejection fraction was 55 +/- 6%, 55 +/- 10% and 66 +/- 6% in childhood and adul thood onset GH deficient patients and control group, respectively; P < 0.0001) and during physical exercise (ejection fraction was 54 +/- 9% in childhood onset GH deficient patients, 53 +/- 9% in adulthood onse t GH deficient patients and 76 +/- 7% in normal subjects; P < 0.0001). Peak ejection rate was 3.2 +/- 0.8 end-diastolic volume/second, 3.0 /- 0.6 end-diastolic volume/second and 3.9 +/- 0.8 end-diastolic volum e/second in childhood and adulthood onset GH deficient patients and,co ntrol group, respectively (P < 0.01). Exercise-induced changes in end- systolic volume were increased in both groups of patients compared wit h healthy subjects. In contrast, exercise-induced end-diastolic volume changes were not different between GH deficient patients and controls . Resting peak filling rate was 2.6 +/- 0.7 end-diastolic volume/secon d, 2.5 +/- 0.7 end-diastolic volume/second and 3.1 +/- 0.3 end-diastol ic volume/second in the 2 groups of patients and healthy subjects, res pectively (P < 0.05). Reduced exercise tolerance in all patients, as s hown by the significantly lower values of peak workload (P < 0.0001), peak rate-pressure product (P < 0.01) and exercise duration (P < 0.000 1) was observed. CONCLUSION Patients affected by GH deficiency have le ft ventricular systolic dysfunction at rest and during physical exerci se, suggesting that GH plays a physiological role in maintaining norma l cardiac performance in humans. Furthermore, no difference between ch ildhood and adulthood onset GH deficient patients was found indicating that both group of patients have an impairment of cardiac function.