Background: Sildenafil is a selective phosphodiesterase type 5 inhibitor which leads to nitric oxide-mediated vasodilatation decreases pulmonary vascular resistance. Sildenafil also significantly improves exercise tolerance and hemodynamic parameters in patients with idiopathic pulmonary hypertension (PAH), chronic congestive heart failure and consequent pulmonary hypertension. Objective: We hypothesized that sildenafil would improve pulmonary vasodilative potency and decrease pulmonary vascular resistance and sildenafil could augment exercise capacity by improving right ventricular (RV) function in patients with secondary pulmonary hypertension by chronic lung disease. Methods: Fifteen patients who had chronic lung disease and pulmonary hypertension (peak pulmonary artery pressure (PAP) > 40 mmHg & mean PAP > 25mmHg by echocardiography) without other left heart problem were included. Thirteen patients (mean age: 68.6 years, 9 men) tolerable to drug were given sildenafil 25mg tid everyday during 4weeks. BNP, hs-CRP, ABG, pulmonary function test and 6M walk test were also performed before and after treatment. Results: Pulmonary vascular resistance index was reduced by sildenafil (-21.3%, 5.02 to 3.32 Wood units, p=0.075). Peak PAP (-20.4%, 57.9 to 46.1 mmHg, p=0.043) and mean PAP (-8.7%, 39.3 to 35.9 mmHg, p=0.042) were all reduced after treatment. Exercise capacity measured by 6M walk test was also improved by sildenafil. (+10.5%, 190m to 210m, p=0.066). However RV fractional area change and RV diastolic, systolic function measured by tissue Doppler image (TDI) were not different. The hs-CRP level had tendency to be lower after treatment and concentration of O2, CO2 levels were not significantly changed during sildenafil administration. There were no adverse events. Conclusion: Sildenafil improves pulmonary vascular resistance, decreases pulmonary artery pressure and improves exercise tolerance in patients with chronic lung disease and secondary pulmonary hypertension.