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Effect of sildenafil on ventilatory efficiency and exercise tolerance in pulmonary hypertension
Author(s) -
Oudiz Ronald J.,
Roveran Giorgio,
Hansen James E.,
Sun XingGuo,
Wasserman Karlman
Publication year - 2007
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2007.06.013
Subject(s) - sildenafil , medicine , diuretic , vascular resistance , cardiology , pulmonary hypertension , placebo , heart failure , cardiac output , hemodynamics , anesthesia , alternative medicine , pathology
Abstract 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 O 2 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 O 2 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 VO 2 , peak O 2 pulse, VE/CO 2 and PETCO 2 , 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 PETCO 2 , VE/VCO 2 , peak O 2 pulse and peak VO 2 during exercise compared to controls. A prospective, placebo‐controlled study is needed to validate these findings.