Key result
Obesity in patients with unexplained exercise intolerance was associated with significant exercise right ventriculo-arterial uncoupling (peak Ees/Ea 0.67 and 0.56 vs 1.45 in controls, p<0.001).
Why the study?
Does obesity impair right ventricular-arterial coupling and contractile reserve during exercise in patients with unexplained exercise intolerance?
Observational (n=55)
No
Does obesity impair right ventricular-arterial coupling and contractile reserve during exercise in patients with unexplained exercise intolerance?
p-value: p=<0.001
Obesity-related exercise intolerance is characterized by exercise-induced right ventriculo-arterial uncoupling and reduced RV contractile reserve, which can occur independently of elevated left ventricular filling pressures.
Small invasive study of RV coupling in obesity is hypothesis-generating; leaves open clinical relevance of ePVH.
BACKGROUND: Right ventricular (RV) dysfunction and heart failure with preserved ejection fraction may contribute to exercise intolerance in obesity. To further define RV exercise responses, we investigated RV-arterial coupling in obesity with and without development of exercise pulmonary venous hypertension (ePVH). METHODS: RV-arterial coupling defined as RV end-systolic elastance/pulmonary artery elastance (Ees/Ea) was calculated from invasive cardiopulmonary exercise test data in 6 controls, 8 obese patients without ePVH (Obese-ePVH) and 8 obese patients with ePVH (Obese+ePVH) within a larger series. ePVH was defined as a resting pulmonary arterial wedge pressure < 15 mmHg but ≥ 20 mmHg on exercise. Exercise haemodynamics were further evaluated in 18 controls, 20 Obese-ePVH and 17 Obese+ePVH patients. RESULTS: Both Obese-ePVH and Obese+ePVH groups developed exercise RV-arterial uncoupling (peak Ees/Ea = 1.45 ± 0.26 vs 0.67 ± 0.18 vs 0.56 ± 0.11, p < 0.001, controls vs Obese-ePVH vs Obese+ePVH respectively) with higher peak afterload (peak Ea = 0.31 ± 0.07 vs 0.75 ± 0.32 vs 0.88 ± 0.62 mL/mmHg, p = 0.043) and similar peak contractility (peak Ees = 0.50 ± 0.16 vs 0.45 ± 0.22 vs 0.48 ± 0.17 mL/mmHg, p = 0.89). RV contractile reserve was highest in controls (ΔEes = 224 ± 80 vs 154 ± 39 vs 141 ± 34% of baseline respectively, p < 0.001). Peak Ees/Ea correlated with peak pulmonary vascular compliance (PVC, r = 0.53, p = 0.02) but not peak pulmonary vascular resistance (PVR, r = - 0.20, p = 0.46). In the larger cohort, Obese+ePVH patients on exercise demonstrated higher right atrial pressure, lower cardiac output and steeper pressure-flow responses. BMI correlated with peak PVC (r = - 0.35, p = 0.04) but not with peak PVR (r = 0.24, p = 0.25). CONCLUSIONS: Exercise RV-arterial uncoupling and reduced RV contractile reserve further characterise obesity-related exercise intolerance. RV dysfunction in obesity may develop independent of exercise LV filling pressures.
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McCabe et al. (2018) conducted an observational in Unexplained exercise intolerance in obesity (n=55). Obesity vs. Non-obese controls was evaluated on Peak exercise right ventriculo-arterial coupling (peak Ees/Ea) (p=<0.001). Obesity in patients with unexplained exercise intolerance was associated with significant exercise right ventriculo-arterial uncoupling (peak Ees/Ea 0.67 and 0.56 vs 1.45 in controls, p<0.001).
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