BACKGROUND: Pulmonary hypertension (PH) is a rare but life-threatening disease characterized by significant increases in pulmonary arterial pressure (PAP) and right ventricular hypertrophy (RVH), therefore early diagnosis and proper treatment of PH is very important. Statins confer cardiovascular benefits beyond the reduction of serum cholesterol through antiproliferative and antiinflammatory mechanisms and induction of endothelial nitric oxide expression. In pneumonectomized rats injected with monocrotaline, simvastatin reversed established pulmonary hypertension and conferred a 100% survival advantage. OBJECTIVE: The aim of this study was to evaluate the potential effect of simvastatin treatment in patients with pulmonary hypertension (PH). PATIENTS AND METHODS: In this prospective before-after pilot trial, 19 patients with primary and secondary causes of PH referred to Khorrami Hospital in Qom, Iran were recruited. Patients were treated with simvastatin, beginning at 20 mg/daily for 2 months, then increasing to 40 mg/daily for another 4 months. Echocardiographic Doppler estimates of systolic pulmonary artery pressures (SPAP) were measured for each patient before prescribing simvastatin and at the end of treatment. Also demographic data, history of smoking and heart functional class (NYHA) before and after treatment were recorded. RESULTS: Out of 19 patients with PH, fifteen were males (78.95%) and four were females (21.1%) with the mean age of 66 (SD=15.28) yr, range between 18 to 83 years. The commonest cause of PH was chronic obstructive pulmonary disease (COPD) in 15 patients (78.9%). Simvastatin significantly ameliorated PH from 74.79 (SD=23.52) mmHg to 67.21 (SD=20.55) mmHg (P<0.001). Whereas, heart functional class changes were not statistically significant (P=0.157). CONCLUSION: In this study, we demonstrated that simvastatin treatment decreased SPAP in patients with PH. As the pathogenesis of PH involves inappropriate proliferation and constriction of vascular smooth-muscle cells, and deficiencies of endogenous vasodilators such as prostacyclin and endothelial-derived nitric oxide, the antiproliferative, antiinflammatory and antithrombogenic effect of simvastatin seems to be useful. This study has led physicians to believe that simvastatin may be beneficial for the treatment of PH.
BACKGROUND:Pulmonary hypertension (PH) is a rare but life-threatening disease characterized by significant increases in pulmonary arterial pressure (PAP) and right ventricular hypertrophy (RVH), therefore early diagnosis and proper treatment of PH is very important. Statins confer cardiovascular benefits beyond the reduction of serum cholesterol through antiproliferative and antiinflammatory mechanisms and induction of endothelial nitric oxide expression. In pneumonectomized rats injected with monocrotaline, simvastatin reversed established pulmonary hypertension and conferred a 100% survival advantage. OBJECTIVE: The aim of this study was to evaluate the potential effect of simvastatin treatment in patients with pulmonary hypertension (PH). PATIENTS AND METHODS: In this prospective before-after pilot trial, 19 patients with primary and secondary causes of PH referred to Khorrami Hospital in Qom, Iran were recruited. Patients were treated with simvastatin, beginning at 20 mg/daily for 2 months, then increasing to 40 mg/daily for another 4 months. Echocardiographic Doppler estimates of systolic pulmonary artery pressures (SPAP) were measured for each patient before prescribing simvastatin and at the end of treatment. Also demographic data, history of smoking and heart functional class (NYHA) before and after treatment were recorded. RESULTS: Out of 19 patients with PH, fifteen were males (78.95%) and four were females (21.1%) with the mean age of 66 (SD=15.28) yr, range between 18 to 83 years. The commonest cause of PH was chronic obstructive pulmonary disease (COPD) in 15 patients (78.9%). Simvastatin significantly ameliorated PH from 74.79 (SD=23.52) mmHg to 67.21 (SD=20.55) mmHg (P<0.001). Whereas, heart functional class changes were not statistically significant (P=0.157). CONCLUSION: In this study, we demonstrated that simvastatin treatment decreased SPAP in patients with PH. As the pathogenesis of PH involves inappropriate proliferation and constriction of vascular smooth-muscle cells, and deficiencies of endogenous vasodilators such as prostacyclin and endothelial-derived nitric oxide, the antiproliferative, antiinflammatory and antithrombogenic effect of simvastatin seems to be useful. This study has led physicians to believe that simvastatin may be beneficial for the treatment of PH.