Source: Annual Congress 2011 - Physiology of human pulmonary hypertension
Disease area: Pulmonary vascular diseases

Abstract

Schistosomiasis is the most common cause of pulmonary arterial hypertension (PAH) worldwide. It has been reported that schistosomiasis-associated PAH (Sch-PAH) has better hemodynamic profile at diagnosis and a more benign clinical course as compared with idiophatic PAH (IPAH) [Fernandes, C.J.C.S. et al. JACC 2010; 59:715-20]. We hypothesized that Sch-PAH subjects have better physiological responses to incremental cardiopulmonary exercise test (CPET) than IPAH patients, even at similar resting pulmonary hemodynamic impairment. We performed CPET and hemodynamic study in 8 Sch-PAH and 9 IPAH patients. None of them had received any PAH therapy. There were no significant between-group differences on cardiac index (2.1 ± 0.3 vs 2.4 ± 0.7 L/min, p=0.21), pulmonary vascular resistance (p=0.32) and mean pulmonary artery pressure (p=0.48). However, the peak oxygen uptake (V´O₂) was greater in Sch-PAH (75 ± 21 vs 54 ± 16%pred, p=0.016), as well as the ratio of increases of V´O₂ to work rate (8.2 ± 1.1 vs 6.8 ± 1.8 mL/min/W^_, p=0.024). Also, the slope of the ventilatory response as a function of CO₂ output was lower in Sch-PAH (41 ± 4 vs 59 ± 18 L²/min², p= 0.04), with a shallower heart rate response for a given change in V´O₂ (80 ± 21 vs 123 ± 39 beats.ml/min², p=0.02), and a greater peak oxygen pulse (p<0.05). In conclusion, Sch-PAH patients had better physiological responses to exercise than IPAH subjects at similar resting hemodynamic profile. Our data suggest a more preserved hemodynamic response to exercise in Sch-PAH, that might explain its better clinical course as compared with IPAH.

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Citations should be made in the following way:
F. Valois, R. Ramos, E. Ferreira, J. Arakaki, J. A. Neder, L. E. Nery (São Paulo, Brazil). Contrasting cardiopulmonary responses to incremental exercise in patients with schistosomiasis-associated and idiopathic pulmonary arterial hypertension with similar resting hemodynamic impairment. Eur Respir J 2011; 38: Suppl. 55, 2307

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