Atorvastatin improves endothelial progenitor cell function and reduces pulmonary hypertension in patients with chronic pulmonary heart disease.

OBJECTIVE: To explore the effects of atorvastatin on the migration and adhesion of endothelial progenitor cells (EPCs) and on pulmonary artery pressure (PAP) in patients with chronic pulmonary heart disease.

METHODS: A total of 68 patients with chronic pulmonary heart disease were randomly assigned to either a control group (n=35) or a treatment group (n=33). In addition, 30 healthy volunteers (17 male, 13 female) were enrolled as healthy controls. Atorvastatin (20 mg per day) was administered to the treatment group. The migration and adhesion activities of EPCs in peripheral blood were assessed before and six months after the treatment. PAP was measured using echocardiography before and after the treatment.

RESULTS: EPC number, migration ability and adhesion activity in the peripheral blood of patients in the control and treatment groups were lower than in patients in the healthy control group at baseline (all P<0.05). After six months of atorvastatin therapy, the number of EPCs in the treatment group was greater than in the control group (P<0.05). Migration and adhesion functions of EPCs in the treatment group were greater than in the control group (all P<0.05). The reduction in PAP in the treatment group was greater than in the untreated control group following six months of therapy (P<0.05).

CONCLUSION: Atorvastatin therapy increased the migration and adhesion activities of EPCs in patients with chronic pulmonary heart disease. Atorvastatin treatment was also associated with a reduction in PAP in these patients.