Pulmonary arterial hypertension (PAH) has a multifactorial aetiology that includes endothelial dysfunction as a key component. Phosphodiesterase-5 (PDE-5) inhibitors and endothelin-1 antagonists influence endothelial function and are used in the treatment of PAH. Statins improve endothelial nitric oxide synthase activity and vascular endothelial function in several vascular beds. However, the effects of statins on PAH are currently being investigated.
Different statins were shown to improve biomarkers, cardiovascular physiology and lung function in animal models of PAH. Human studies are limited, with one observational study showing benefits, but results from small, short-term randomized trials have been conflicting. A study with pravastatin showed general benefits on both biomarkers and lung physiology, whereas the Simvastatin as a Treatment for Pulmonary Hypertension Trial with simvastatin added to PDE-5 inhibitors and endothelin-1 antagonists showed transient improvement in biomarkers but not in physiological markers over 1 year. Similarly, rosuvastatin showed benefits on biomarkers but not on physiological function at 6 months.
Statins seem to improve biomarkers in human PAH, but as yet studies are too preliminary to indicate whether these effects are clinically relevant.
aDepartment of Clinical Biochemistry (Vascular Disease Prevention Clinics), Royal Free Hospital Campus, University College London Medical School, University College London, UK
bDepartment of Metabolic Medicine/Chemical Pathology, St Thomas' Hospital, London, UK
Correspondence to Dimitri P. Mikhailidis, BSc, MSc, MD, FRSPH, FCP, FFPM, FRCP, FRCPath, Academic Head, Department of Clinical Biochemistry (Vascular Disease Prevention Clinics), Royal Free Hospital Campus, University College London Medical School, University College London, Pond Street, London NW3 2QG, UK Tel: +44 20 7830 2258; fax: +44 20 7830 2235; e-mail: firstname.lastname@example.org