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Cardiac functional reserve is diminished in growth hormone-deficient adults
Robert Moisey1, Steve Orme, Diane Barker
1Department of Endocrinology, Leeds General Infirmary, Leeds, United Kingdom.
Insights
Patients with severe growth hormone deficiency (GHD) exhibit impaired cardiac functional reserve during peak exercise. This study reveals reduced cardiac power, chronotropic incompetence, and lower pressure-generating capacity in GHD patients compared to healthy individuals.
Area of Science:
- Cardiology
- Endocrinology
- Exercise Physiology
Background:
- Severe growth hormone deficiency (GHD) is linked to cardiac changes.
- Previous studies lack direct evidence of cardiac reserve during peak exercise in GHD.
Purpose of the Study:
- To test the hypothesis that severe GHD patients have reduced cardiac reserve function compared to healthy controls.
- To investigate peak cardiac power and cardiorespiratory fitness in severe GHD.
Main Methods:
- Noninvasive hemodynamic measurements during maximal cardiopulmonary exercise testing.
- Comparison of 18 severe GHD patients with 18 matched healthy controls.
- Assessment of peak cardiac power, VO2max, heart rate, and systolic blood pressure.
Main Results:
- GHD patients showed 15% lower peak cardiac power (4.4 W vs. 5.2 W, P=0.02).
- Similar aerobic exercise peaks (VO2max) and respiratory exchange ratios were observed.
- GHD patients had lower chronotropic reserve (peak HR 154 bpm vs. 174 bpm, P=0.001) and impaired pressure-generating capacity (peak SBP 160 mmHg vs. 200 mmHg, P<0.0001).
Conclusions:
- Severe GHD is associated with significantly impaired cardiac functional reserve.
- Chronotropic incompetence and reduced pressure-generating capacity contribute to this impairment.
- Noninvasive assessment confirms reduced cardiac pumping capacity in GHD during exercise.
Abstract:
Various studies have shown that patients with severe growth hormone deficiency (GHD) have diverse changes in left ventricular (LV) size or performance but so far there is no direct indication of cardiac reserve ability to maintain the circulation during peak exercise. We tested the hypothesis that patients with severe GHD have reduced cardiac reserve function compared with healthy controls. Eighteen patients with severe GHD were studied and compared with 18 age-, sex-, and body mass index (BMI)-matched healthy controls. Peak cardiac power and cardiorespiratory fitness were investigated using noninvasive hemodynamic measurements during maximal cardiopulmonary exercise testing. Compared with matched controls, the cardiac power of GHD patients during exercise to volitional exhaustion was significantly reduced by 15% (mean +/- SD: 4.4 +/- 1.0 watts (W) vs. 5.2 +/- 1.0 W, P= 0.02), despite attaining similar aerobic exercise peaks (VO(2max), GHD: 2390 +/- 822 mL/min vs. controls: 2461 +/- 872 mL/min, P= 0.80) and similar peak respiratory exchange ratios. The lower peak cardiac power could not be accounted for by peripheral alterations because both groups reached similar peak exercise systemic vascular resistances. Patients with GHD also had lower cardiac chronotropic reserve (peak heart rate: 154 +/- 21 bpm vs. 174 +/- 11 bpm, P= 0.001) and a lower cardiac pressure-generating capacity (systolic blood pressure [SBP] 160 +/- 25 mmHg vs. 200 +/- 15 mmHg, P < 0.0001). Using this robust noninvasive method of assessing functional cardiac pumping capacity we have for the first time shown that patients with severe GHD have a significantly impaired cardiac functional reserve associated with chronotropic incompetence and impaired pressure-generating capacity.
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