Document Detail

Endothelin receptor antagonists for pulmonary arterial hypertension: an overview.
MedLine Citation:
PMID:  20406243     Owner:  NLM     Status:  In-Process    
The last decade has seen major advances in the pharmacotherapy of pulmonary arterial hypertension (PAH). One of these advances has been the discovery of endothelin receptor antagonists (ERAs). ERAs are a class of potent vasodilators and antimitotic substances, which could specifically dilate and remodel pulmonary arterial system, and have been proposed as an alternative to traditional therapies for PAH. Current available evidence suggests that ERAs improve exercise capacity, functional status, pulmonary hemodynamics, and delay the time to clinical worsening for patients with PAH. This review attempts to provide an overview of the pharmacology, therapeutic benefits, and safety profile of ERAs in patients with PAH.
Shahzad G Raja
Related Documents :
20152223 - Systematic review of trials using vasodilators in pulmonary arterial hypertension: why ...
9264443 - Usefulness of atrial septostomy as a treatment for primary pulmonary hypertension and g...
7638713 - Retroperitoneal aortoiliac reconstruction.
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Cardiovascular therapeutics     Volume:  28     ISSN:  1755-5922     ISO Abbreviation:  Cardiovasc Ther     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-11-05     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101319630     Medline TA:  Cardiovasc Ther     Country:  England    
Other Details:
Languages:  eng     Pagination:  e65-71     Citation Subset:  IM    
Copyright Information:
© 2010 Blackwell Publishing Ltd.
Department of Cardiothoracic Surgery, Great Ormond Street Hospital, London, UK.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Anacetrapib: Hope for CETP Inhibitors?
Next Document:  Drug-induced hERG Block and Long QT Syndrome.