Changes in exercise hemodynamics during treatment in pulmonary arterial hypertension

¹ Centre des maladies vasculaires pulmonaires (UPRES EA 2705), Service de pneumologie et reanimation respiratoire, AP-HP-Université Paris Sud XI, Hôpital Antoine Béclère, 157 rue de la Porte de Trivaux, 92140 Clamart, France; and Centre de recherche de l'Hôpital Laval, Institut universitaire de cardiologie et de pneumologie de l'Université Laval, Québec, Canada
² Centre chirurgical Marie-Lannelongue, 92350 Le Plessis-Robinson, France
³ Centre des maladies vasculaires pulmonaires (UPRES EA 2705), Service de pneumologie et reanimation respiratoire, AP-HP-Université Paris Sud XI, Hôpital Antoine Béclère, 157 rue de la Porte de Trivaux, 92140 Clamart, France
⁴ Service de physiologie, EA4046, CHU de Bicêtre, 94275 Le Kremlin-Bicêtre, France

^* To whom correspondence should be addressed. E-mail: steve.provencher{at}crhl.ulaval.ca.

	Abstract

Improvement in exercise capacity may not be associated with significant changes in resting pulmonary hemodynamics. Our prospective study documented the relations between improvement in six-minute walking distance (6MWD) and changes in resting and exercise pulmonary hemodynamics after treatment in idiopathic pulmonary arterial hypertension (IPAH).

42 IPAH patients underwent supine submaximal exercise hemodynamics at baseline and after 5(2) months on therapy. The 6MWD, the corresponding chronotropic response (peak-resting heart rate) and resting and exercise hemodynamic variables were analyzed. The isoflow was defined as the lowest of the pre- and post-treatment peak cardiac index. The extrapolated isoflow mPAP was used to characterize changes in mPAP-cardiac index regression lines following treatment.

Patients were given bosentan (n=28), epoprostenol (n=12) or both. The 6MWD increased from 399(88) to 442(86) meters (P<0.001). In univariate analysis changes in 6MWD correlated with changes in isoflow mPAP (R2=0.54, P<0.01), chronotropic response, resting hemodynamics (cardiac index, pulmonary vascular resistance and mixed venous oxygen saturation) and exercise hemodynamics (peak cardiac index). In multivariate analysis, only changes in isoflow mPAP and chronotropic response were independently associated with changes in 6MWD.

Improvement in exercise tolerance with chronic therapy is independently related to improvement in pulmonary hemodynamics measured in exercise but not in resting conditions.