Patients with pulmonary hypertension were unable to increase right ventricular end-systolic elastance during submaximal exercise compared to controls (Pinteraction < 0.001), leading to a deterioration in right ventricular-arterial coupling.
Observational (n=24)
No
Does submaximal exercise reveal impaired right ventricular contractility and RV-arterial coupling in patients with precapillary pulmonary hypertension compared to controls?
Patients with pulmonary hypertension lack exertional right ventricular contractile reserve, leading to deteriorated RV-arterial coupling during exercise, which may explain their exercise intolerance.
p-value: p=<0.001
RATIONALE: Exercise tolerance is decreased in patients with pulmonary hypertension (PH). It is unknown whether exercise intolerance in PH coincides with an impaired rest-to-exercise response in right ventricular (RV) contractility. OBJECTIVES: To investigate in patients with PH the RV exertional contractile reserve, defined as the rest-to-exercise response in end-systolic elastance (ΔEes), and the effects of exercise on the matching of Ees and RV afterload (Ea) (i.e., RV-arterial coupling; Ees/Ea). In addition, we compared ΔEes with a recently proposed surrogate, the rest-to-exercise change in pulmonary artery pressure (ΔPAP). METHODS: We prospectively included 17 patients with precapillary PH and 7 control subjects without PH who performed a submaximal invasive cardiopulmonary exercise test between January 2013 and July 2014. Ees and Ees/Ea were assessed using single-beat pressure-volume loop analysis. MEASUREMENTS AND MAIN RESULTS: Exercise data in 16 patients with PH and 5 control subjects were of sufficient quality for analysis. Ees significantly increased from rest to exercise in control subjects but not in patients with PH. Ea significantly increased in both groups. As a result, exercise led to a decrease in Ees/Ea in patients with PH, whereas Ees/Ea was unaffected in control subjects (Pinteraction = 0.009). In patients with PH, ΔPAP was not related to ΔEes but significantly correlated to the rest-to-exercise change in heart rate. CONCLUSIONS: In contrast to control subjects, patients with PH were unable to increase Ees during submaximal exercise. Failure to compensate for the further increase in Ea during exercise led to deterioration in Ees/Ea. Furthermore, ΔPAP did not reflect ΔEes but rather the change in heart rate.
Spruijt et al. (Tue,) conducted a observational in Precapillary pulmonary hypertension (n=24). Precapillary pulmonary hypertension vs. Control subjects without pulmonary hypertension was evaluated on Rest-to-exercise response in right ventricular end-systolic elastance (ΔEes) (p=<0.001). Patients with pulmonary hypertension were unable to increase right ventricular end-systolic elastance during submaximal exercise compared to controls (Pinteraction < 0.001), leading to a deterioration in right ventricular-arterial coupling.