© 2007 European Society of Cardiology
Effect of sildenafil on ventilatory efficiency and exercise tolerance in pulmonary hypertension
a Division of Cardiology USA
b Division of Respiratory and Critical Care Physiology and Medicine USA
c Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center Torrance, CA, USA
* Corresponding author. Liu Center for Pulmonary Hypertension 1124 W. Carson Street, #405 Torrance, CA 90502, USA. Tel.: +1 310 222 2515; fax: +1 310 787 0448. E-mail address: oudiz{at}humc.edu
| Abstract |
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Background: The pulmonary vasculopathy in pulmonary arterial hypertension (PAH) results in increased resistance to pulmonary blood flow, limiting the cardiac output required for the increased O2 demands of exercise.
Aims: We sought to determine the physiologic basis for clinical improvement in PAH patients receiving sildenafil, hypothesizing that the key mechanisms of improvement are improved blood flow and ventilatory efficiency, leading to improved exercise capacity and O2 pulse over time.
Methods: We studied 28P AH patients with (n=14) and without (n=14) sildenafil treatment. All received warfarin and diuretic therapy, and 13/14 sildenafil-treated patients were already receiving specific PAH drugs. Cardiopulmonary exercise testing was performed before and after sildenafil.
Results: Peak VO2, peak O2 pulse, VE/CO2 and PETCO2, were 0.84±0.1 L/min, 6.1±0.7 mL beat–1, 49±2 and 26±1.5 mm Hg, and improved after adding sildenafil to 0.91±0.1 L/min, 6.8±0.8 mL beat–1, 43±2, and 30±1.9, respectively, whereas control patients worsened (p=0.012, 0.008, 0.008 and 0.0002, treated vs. controls, respectively).
Conclusions: Sildenafil improves PETCO2, VE/VCO2, peak O2 pulse and peak VO2 during exercise compared to controls. A prospective, placebo-controlled study is needed to validate these findings.
Key Words: Pulmonary arterial hypertension Cardiopulmonary exercise testing Ventilatory efficiency Pulmonary heart disease
Received June 27, 2007; Accepted June 27, 2007
This research was supported by NIH grant # 1 K23 RR17596-01 and General Clinical Research Centers grant # MO1 RR 425.
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