Effects of growth hormone therapy on cardiac and respiratory functions in growth hormone-deficient adults (original) (raw)
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Pituitary, 2009
The purpose of this study was to evaluate the effects of 5 years of GH substitution on cardiac structure and function, physical work capacity and blood pressure levels in adults with GH deficiency (GHD). Fourteen patients were clinically assessed every 3 months for 5 years. Transthoracic echocardiography and exercise test were performed at baseline, 24, 48 and 60 months. Blood pressure (BP) was measured by means of ambulatory monitoring of blood pressure at baseline, 6, 12, 24 and 60 months. Left ventricular mass and its index increased progressively during the 5 years of GH substitution (P = 0.008 and 0.007, respectively). There were no significant changes in all others cardiac parameters evaluated. It was observed a significant improve in functional capacity (P \ 0.001) and maximal oxygen uptake (P = 0.006) during the treatment. Diurnal systolic BP increased by 15 mmHg (P = 0.024) and diurnal diastolic BP by 4.5 mmHg (P = 0.037). There was no change in dirnal systolic pressure load but a considerable but non-statistically significant reduction in diurnal diastolic pressure load was observed during the study. During the night diastolic BP increased by 4 mmHg (P = 0.012) despite a substantial but non-statistically significant reduction in diastolic pressure load. We observed an increase in the proportion of persons with a non-physiological nocturnal fall (non-dippers) throughout the study (from 36.4% at baseline to 54.6% after 60 months of therapy). We concluded that 5 years of GH replacement promoted positive effects on exercise capacity and maximum oxygen uptake in spite of a modest increase in BP levels and left ventricular mass. Continuous monitoring is mandatory to arrive at further conclusions concerning the effects of GH substitution in adults on cardiovascular parameters with respect to possible unfavorable long term effects.
The Journal of Clinical Endocrinology & Metabolism, 2009
Background: GH-deficient (GHD) children have reduced left ventricular (LV) mass, but impairment of cardiac function has never been documented. Aim: The aim of the study was to evaluate effects of GHD and GH therapy on cardiac function using load-dependent and load-independent indices of myocardial contractility. Patients and Methods: Echocardiography was performed in 24 GHD children at baseline and 1 and 2 yr after GH therapy and in 24 controls. Results: Compared with controls, GHD children at baseline had lower LV mass (LV mass/BSA 50.6 Ϯ 1.8 vs. 60.5 Ϯ 2.4 g/m 2 ; P Ͻ 0.002, and LV mass/H 2.7 28.7 Ϯ 1.2 vs. 33.6 Ϯ 1.3 g/m 2.7 ; P Ͻ 0.009). Global systolic function was normal, with only a trend toward slight impairment of the fractional shortening (34.9 Ϯ 1.5 vs. 37.6 Ϯ 1.1%). However, subtle LV dysfunction was revealed by load-dependent and load-independent indices of myocardial contractility. In fact, GHD patients compared with controls showed lower rate-corrected mean velocity of circumferential fiber shortening (1.0 Ϯ 0.03 vs. 1.18 Ϯ 0.03 circ/sec; P ϭ 0.0001) and stress shortening index (0.10 Ϯ 0.02 vs. 0.18 Ϯ 0.02; P Ͻ 0.007) and higher end-systolic stress (49.2 Ϯ 1.4 vs. 45.7 Ϯ 1.0 g/cm 2 ; P Ͻ 0.05). One year of GH treatment was associated with a significant improvement of cardiac size (LV mass/BSA 67.8 Ϯ 2.9 g/m 2 ; LV mass/H 2.7 38.2 Ϯ 2.0 g/m 2.7 ; P Ͻ 0.0001 and P ϭ 0.0003, respectively) and myocardial contractility (mean velocity of circumferential fiber shortening 1.2 Ϯ 0.04 circ/sec; P Ͻ 0.0002; stress shortening index 0.19 Ϯ 0.02; P Ͻ 0.003) and reduced afterload (end-systolic stress 43.9 Ϯ 1.4 g/cm 2 ; P Ͻ 0.03). Conclusions: Our data indicate that GH deficiency is associated with abnormalities in morphology and function in not only adults but also children and further supports the beneficial effect of GH on the heart. (J Clin Endocrinol Metab 94: 3347-3355, 2009) E ven if the primary goal of GH replacement therapy is to promote linear growth in children, it has now been established that GH also has other important physiological functions influencing several key metabolic processes. Among the distinct features of GH deficiency (GHD), cardiovascular involvement has emerged as particularly important. Previous studies on GHD and GH therapy have documented that adults as well as adolescents with severe
Growth Hormone & IGF Research, 2005
Objective: There is accumulating evidence that growth hormone (GH) plays an important role in the maintenance of normal cardiac growth and function. Abnormalities in left ventricular diastolic function and impairment of systolic function have also been reported in patients with GHD. In this study, we investigated the effects of 12 months GH replacement therapy on cardiac functional indices measured by echocardiography, the ECG stress test and SPECT imaging.
Cardiac Effects of Growth Hormone in Adults With Growth Hormone Deficiency: A Meta-Analysis
Circulation, 2003
Background-Growth hormone (GH) treatment may improve morphological and functional cardiac parameters in adults with GH deficiency (GHD). However, clinical trials reported to date involved few patients and yielded variable effects. Methods and Results-We systematically reviewed blinded, placebo-controlled, randomized clinical trials of GH treatment in adults with GHD and open studies in patients with GHD before and after GH treatment, evaluating the effects of GH on cardiac parameters assessed by echocardiography. Sixteen trials (9 blinded and 7 open), involving a total of 468 patients, were identified in 3 bibliographic databases. GH dosage, duration of treatment, and study populations varied among the studies. We conducted a combined analysis of effects on left ventricular mass (LVM), interventricular septum thickness (IVS), left ventricular posterior wall (LVPW), left ventricular end-systolic (LVESD) and diastolic (LVEDD) diameters, stroke volume, E/A ratio, isovolumic relaxation time (IRT), and fractional shortening. Overall effect size was used to evaluate significance, and weighted mean difference between GH and control was given to appreciate size of the effect. GH treatment was associated with a significant increase in LVM: ϩ10.8 (SD: 9.3) g (Pϭ0.02); IVS: ϩ0.28 (0.38) mm (PϽ0.001), LVPW: 0.98 (0.22) mm (Pϭ0.05), LVEDD: ϩ1.34 (1.13) mm (PϽ0.001), and stroke volume: ϩ10.3 (8.7) mL (PϽ0.001). A trend toward a difference in fractional shortening was observed: ϩ1.1 (1.1)% (Pϭ0.06). Overall effect sizes were not significant for LVESD, E/A, and IRT.
Clinical Endocrinology, 1998
OBJECTIVE The impairment of heart structure and function in adults with childhood onset GH deficiency has been recently described. However, previous echocardiographic studies have reported no differences in cardiac mass and function between adulthood onset GH deficient patients and healthy subjects. DESIGN The aim of this study was to evaluate cardiac performance in adult patients with childhood and adulthood onset GH deficiency, using equilibrium radionuclide angiography, a method more accurate than echocardiography. PATIENTS Eleven patients with childhood onset GH deficiency, 9 patients with adulthood onset GH deficiency and 12 age-, gender-, height-and weightmatched healthy subjects entered the study. MEASUREMENTS All the study population underwent equilibrium radionuclide angiography at rest and during physical exercise. RESULTS Both childhood and adulthood onset GH deficient patients had an impaired left ventricular systolic performance both at rest (ejection fraction was 55 Ϯ 6%, 55 Ϯ 10% and 66 Ϯ 6% in childhood and adulthood onset GH deficient patients and control group, respectively; P < 0. 0001) and during physical exercise (ejection fraction was 54 Ϯ 9% in childhood onset GH deficient patients, 53 Ϯ 9% in adulthood onset GH deficient patients and 76 Ϯ 7% in normal subjects; P < 0. 0001). Peak ejection rate was 3. 2 Ϯ 0. 8 end-diastolic volume/second, 3. 0 Ϯ 0. 6 end-diastolic volume/second and 3. 9 Ϯ 0. 8 end-diastolic volume/ second in childhood and adulthood onset GH deficient patients and control group, respectively (P < 0. 01). Exercise-induced changes in end-systolic volume were increased in both groups of patients compared with 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 Ϯ 0. 7 end-diastolic volume/second, 2. 5 Ϯ 0. 7 end-diastolic volume/ second and 3. 1 Ϯ 0. 3 end-diastolic volume/second in the 2 groups of patients and healthy subjects, respectively (P < 0. 05). Reduced exercise tolerance in all patients, as shown by the significantly lower values of peak workload (P < 0. 0001), peak rate-pressure product (P < 0. 01) and exercise duration (P < 0. 0001) was observed. CONCLUSION Patients affected by GH deficiency have left ventricular systolic dysfunction at rest and during physical exercise, suggesting that GH plays a physiological role in maintaining normal cardiac performance in humans. Furthermore, no difference between childhood and adulthood onset GH deficient patients was found indicating that both group of patients have an impairment of cardiac function.
Growth Hormone Therapy and the Heart
The American Journal of Cardiology, 2006
The growth hormone (GH)-insulin-like growth factor-1 axis has great relevance for the regulation of cardiac growth, structure, and function. GH deficiency may result in impaired cardiac performance, manifest by a reduction in left ventricular mass and ejection fraction, but data are inconsistent. GH therapy is recommended treatment in adult patients with GH deficiency, but in acromegaly, in which there is excess GH, the main cause of mortality is cardiovascular disease. The purposes of this study were to perform (1) a case-controlled study comparing cardiac morphology and function in 53 GH-deficient patients (34 men, mean age 38.1 ؎ 15.2 years, 22 with childhoodonset GH deficiency) and 46 healthy controls (29 men, mean age 37.8 ؎ 12.4 years) and (2) a longitudinal study to assess the effect of introducing GH therapy in 37 subjects for a mean period of 26 ؎ 22 months. At study entry, all subjects underwent electrocardiography and 24-hour ambulatory electrocardiographic monitoring, systolic and diastolic blood pressure assessment, detailed echocardiography, and exercise tolerance tests. There were no significant differences in left ventricular mass, left ventricular dimensions, systolic or diastolic function indexes, or blood pressure at rest in patients compared with controls. Exercise duration was significantly shorter and peak heart rate during exercise (chronotropic response) lower in the GH-deficiency group than in controls (p <0.05). After GH treatment, there were no significant changes in echocardiographic parameters or blood pressure, but an improvement in exercise duration (p ؍ 0.019) was found, particularly in the subgroup with childhood-onset GH deficiency (n ؍ 16). In conclusion, patients with GH deficiency did not show cardiac structural or functional differences compared with healthy controls, with no significant changes after GH treatment. However, these patients exhibited improved exercise capacity, especially those with childhood-onset GH deficiency.
Cardiac structural and functional abnormalities in adult patients with growth hormone deficiency
The Journal of Clinical Endocrinology & Metabolism, 1993
Objectives: To identify in a prospective observational study the cardiac structural and functional abnormalities and mortality in patients with end stage renal disease (ESRD) with a raised cardiac troponin T (cTnT) concentration. Methods: 126 renal transplant candidates were studied over a two year period. Clinical, biochemical, echocardiographic, coronary angiographic, and dobutamine stress echocardiographic (DSE) data were examined in comparison with cTnT concentrations dichotomised at cut off concentrations of , 0.04 mg/l and , 0.10 mg/l. Results: Left ventricular (LV) size and filling pressure were significantly raised and LV systolic and diastolic function parameters significantly impaired in patients with raised cTnT, irrespective of the cut off concentration. The proportions of patients with diabetes and on dialysis were higher in both groups with raised cTnT. With a cut off cTnT concentration of 0.04 mg/l but not 0.10 mg/l, significantly more patients had severe coronary artery disease and a positive DSE result. The total ischaemic burden during DSE was similar in cTnT positive and negative patients, irrespective of the cut off concentration used. LV end systolic diameter index and E:Ea ratio were independent predictors of cTnT rises > 0.04 mg/l and > 0.10 mg/l, respectively. Diabetes was independently associated with cTnT at both cut off concentrations. Mortality was higher in all patients with raised cTnT. Conclusions: Patients with ESRD with raised cTnT concentrations have increased mortality. Raised concentrations are strongly associated with diabetes, LV dilatation, and impaired LV systolic and diastolic function, but not with severe coronary artery disease.