Pulmonary arterial hypertension and statins: an update

被引:25
作者
Katsiki, Niki [1 ]
Wierzbicki, Anthony S. [2 ]
Mikhailidis, Dimitri P. [1 ]
机构
[1] UCL, Sch Med, Vasc Dis Prevent Clin, Dept Clin Biochem, London NW3 2QG, England
[2] St Thomas Hosp, Dept Metab Med Chem Pathol, London, England
关键词
endothelium; nitric oxide; pulmonary hypertension; statin; treatment; SMOOTH-MUSCLE-CELLS; NITRIC-OXIDE SYNTHASE; REDUCTASE INHIBITORS; FUTURE-DIRECTIONS; PLASMA-LEVELS; SIMVASTATIN; ATORVASTATIN; RATS; APOPTOSIS; ROSUVASTATIN;
D O I
10.1097/HCO.0b013e32834659bf
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review 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. Recent findings 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. Summary Statins seem to improve biomarkers in human PAH, but as yet studies are too preliminary to indicate whether these effects are clinically relevant.
引用
收藏
页码:322 / 326
页数:5
相关论文
共 57 条
[1]  
Alnaeb ME, 2007, IN VIVO, V21, P1069
[2]   Pharmacotherapeutic Management of Pulmonary Arterial Hypertension [J].
Anderson, Joe R. ;
Nawarskas, James J. .
CARDIOLOGY IN REVIEW, 2010, 18 (03) :148-162
[3]  
Archer SL, 2006, CURR OPIN CARDIOL, V21, P385
[4]   Pleiotropic Effects of Statins - Clinical Evidence [J].
Athyros, Vasilios G. ;
Kakafika, Anna I. ;
Tziomalos, Konstantinos ;
Karagiannis, Asterios ;
Mikhailidis, Dimitri P. .
CURRENT PHARMACEUTICAL DESIGN, 2009, 15 (05) :479-489
[5]   Rosuvastatin and vascular dysfunction markers in pulmonary arterial hypertension: a placebo-controlled study [J].
Barreto, A. C. ;
Maeda, N. Y. ;
Soares, R. P. S. ;
Cicero, C. ;
Lopes, A. A. .
BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH, 2008, 41 (08) :657-663
[6]  
BATTISTINI B, 1993, LAB INVEST, V68, P600
[7]   Systematic review on the risk and benefit of different cholesterol-lowering interventions [J].
Bucher, HC ;
Griffith, LE ;
Guyatt, GH .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1999, 19 (02) :187-195
[8]   Fluvastatin inhibits hypoxic proliferation and p38 MAPK activity in pulmonary artery fibroblasts [J].
Carlin, Christopher M. ;
Peacock, Andrew J. ;
Welsh, David J. .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2007, 37 (04) :447-456
[9]   Acute actions and novel targets of matrix metalloproteinases in the heart and vasculature [J].
Chow, A. K. ;
Cena, J. ;
Schulz, R. .
BRITISH JOURNAL OF PHARMACOLOGY, 2007, 152 (02) :189-205
[10]   Statins decrease serotonin-induced contractions in coronary arteries of swine in vitro [J].
Crespo, MJ ;
Quidgley, JA .
PHARMACOLOGY, 2006, 76 (03) :141-147