Key result
Untreated growth hormone deficiency is linked to ~8% lower LVEF and reduced exercise capacity.
Why the study?
Growth hormone deficiency is known to cause higher rates of cardiovascular mortality, but the structural, functional, and autonomic cardiovascular changes in these patients require further analysis.
Does growth hormone deficiency cause structural, functional, and autonomic changes in the cardiovascular system compared to healthy controls?
Case-Control (n=26)
Does growth hormone deficiency cause structural, functional, and autonomic changes in the cardiovascular system compared to healthy controls?
Absolute Event Rate: 57.4% vs 65.5%
p-value: p=<0.001
Growth hormone deficiency is associated with decreased left ventricular mass, lower ejection fraction, and reduced sympathetic components of heart rate variability, which may contribute to increased cardiovascular risk.
BACKGROUND: Growth hormone deficiency (GHD) is known to cause higher rates of cardiovascular mortality. The purpose of the study was to analyze the structural and functional changes in the heart and investigate their relation to autonomic function as assessed with heart rate variability (HRV). METHODS: Eleven untreated GHD patients (mean age 50.4 +/- 10.7 years, M/F: 3/8) and 15 age- and sex-matched healthy persons (mean age 45.3 +/- 10.4 years, M/F: 5/10) were compared. Both groups were examined with echocardiography, HRV, and exercise testing and findings were analyzed. RESULTS: The groups were similar in height, weight, body mass index, body surface area, systolic and diastolic blood pressure, heart rate. The GHD patients had lower exercise duration and metabolic equivalent (MET) compared to controls (7.94 +/- 1.26 vs. 9.8 +/- 1.9 min, P < 0.001, for MET 8.85 +/- 0.86 vs. 10.7 +/- 2.23, P = 0.03). On echocardiography, GHD patients had lower interventricular septum diastolic diameter (9 +/- 0.89 vs. 10.7 +/- 0.88 mm, P < 0.001) and posterior wall thickness (8.4 +/- 0.93 vs. 9.8 +/- 0.91 mm, P = 0.002), and lower left ventricle mass index (90.9 +/- 20 vs. 112 +/- 8 g/m2, P = 0.01). Left ventricular ejection fraction was lower in the GHD patients (57.4 +/- 5.12% vs. 65.5 +/- 4.1%, P < 0.001). Time and frequency domain heart rate variability parameters, SDNN, SDANN, VLF, LF ve LF/HF were lower in GHD patients compared to controls. There was a significant correlation between left ventricle diastolic diameter and LF (r = 0.62, P = 0.02). CONCLUSION: GHD seemed to cause decreased left ventricle mass and decreases in the sympathetic components of HRV that may have a bearing on the increased cardiovascular risk seen in these patients.
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Erdoğan et al. (2004) conducted a case-control in Growth hormone deficiency (n=26). Growth hormone deficiency vs. Age- and sex-matched healthy controls was evaluated on Left ventricular ejection fraction (p=<0.001). Untreated growth hormone deficiency was associated with lower left ventricular ejection fraction (57.4% vs 65.5%, P<0.001) and reduced exercise capacity compared to healthy controls.
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