The Effects of Exercise on Right Ventricular Contractility and Right Ventricular–Arterial Coupling in Pulmonary Hypertension

• Published in: American journal of respiratory and critical care medicine Vol. 191; no. 9; pp. 1050 - 1057
• Main Authors: Spruijt, Onno A., de Man, Frances S., Groepenhoff, Herman, Oosterveer, Frank, Westerhof, Nico, Vonk-Noordegraaf, Anton, Bogaard, Harm-Jan
• Format: Journal Article
• Language: English
• Published: United States American Thoracic Society 01.05.2015
• Subjects: Adult; Exercise - physiology; Female; Humans; Hypertension, Pulmonary - physiopathology; Male; Middle Aged; Myocardial Contraction - physiology; Prospective Studies; Pulmonary Circulation - physiology; Ventricular Dysfunction, Right - physiopathology; Ventricular Function, Right - physiology; end-systolic elastance; contractile reserve; right ventricle; RV–arterial coupling
• DOI: 10.1164/rccm.201412-2271OC
• ISSN: 1073-449X; 1535-4970

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. 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). 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. 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. 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.