PMID- 15148531
OWN - NLM
STAT- MEDLINE
DCOM- 20041018
LR  - 20191108
IS  - 1699-3993 (Print)
IS  - 1699-3993 (Linking)
VI  - 40
IP  - 3
DP  - 2004 Mar
TI  - Overview of treprostinil sodium for the treatment of pulmonary arterial 
      hypertension.
PG  - 225-34
AB  - Pulmonary arterial hypertension is a life-threatening disorder that refers to a 
      group of diseases characterized by an abnormal elevation of the blood pressure 
      within the pulmonary circulation due to a vasculopathy of the pulmonary 
      microcirculation (1). If left untreated, the overall prognosis of pulmonary 
      arterial hypertension is poor, with a 5-year survival rate of 34%. The most 
      common cause of death is progressive right-sided heart failure (2). There is no 
      pharmacologic cure for pulmonary arterial hypertension, and a team approach is 
      required for the proper care of these patients (3). Treatment is directed at 
      improving clinical symptoms, increasing exercise tolerance and extending 
      survival. Until just a few years ago, standard treatment options for the 
      treatment of pulmonary arterial hypertension were limited and included coumarin 
      derivatives, calcium channel blockers, diuretics, digoxin and oxygen 
      supplementation (4). In the last decade, the therapeutic options for pulmonary 
      arterial hypertension have made considerable advances. In at least three major 
      randomized controlled trials, the continuous intravenous infusion of 
      epoprostenol, a synthetic salt of prostacyclin with potent vasodilatory ability, 
      has been shown to improve exercise tolerance, hemodynamics, survival and quality 
      of life in patients with New York Heart Association (NYHA) functional classes III 
      and IV with either primary pulmonary hypertension or pulmonary arterial 
      hypertension associated with scleroderma (5-9). Epoprostenol has now become a 
      mainstay therapy in the long-term treatment of primary pulmonary hypertension or 
      pulmonary arterial hypertension associated with scleroderma. Nevertheless, 
      epoprostenol is far from an ideal form of therapy. Issues such as the short 
      half-life of the drug, need for continuous central intravenous access and 
      significant side effects have led to the development of more stable prostacyclin 
      analogues as alternative therapies for primary pulmonary hypertension. These 
      alternative therapies include iloprost (inhaled delivery) and treprostinil 
      (subcutaneous delivery). As a result, the Food and Drug Administration (FDA) 
      recently approved treprostinil for the treatment of pulmonary arterial 
      hypertension in patients with NYHA classes II-IV. This review will offer a 
      discussion of the basic pharmacology of treprostinil, its similarities to and 
      differences from epoprostenol, the animal studies as well as the initial 
      investigational studies leading to its FDA approval, and clinical uses of the 
      drug alone or in combination with newer therapies directed at pulmonary arterial 
      hypertension developed over the last decade.
CI  - c) 2004 Prous Science. All rights reserved
FAU - Budev, Marie M
AU  - Budev MM
AD  - Department of Pulmonary and Critical Care Medicine, The Cleveland Clinic 
      Foundation, Cleveland, Ohio 44195, USA. minaio@ccf.org
FAU - Minai, Omar A
AU  - Minai OA
FAU - Arroliga, Alejandro C
AU  - Arroliga AC
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Spain
TA  - Drugs Today (Barc)
JT  - Drugs of today (Barcelona, Spain : 1998)
JID - 101160518
RN  - 0 (Antihypertensive Agents)
RN  - DCR9Z582X0 (Epoprostenol)
RN  - RUM6K67ESG (treprostinil)
SB  - IM
MH  - Antihypertensive Agents/adverse effects/pharmacology/*therapeutic use
MH  - Endothelium, Vascular/drug effects/physiopathology
MH  - Epoprostenol/adverse effects/*analogs & derivatives/pharmacology/*therapeutic use
MH  - Humans
MH  - Hypertension, Pulmonary/*drug therapy
MH  - Lung/blood supply
MH  - Randomized Controlled Trials as Topic
RF  - 46
EDAT- 2004/05/19 05:00
MHDA- 2004/10/19 09:00
CRDT- 2004/05/19 05:00
PHST- 2004/05/19 05:00 [pubmed]
PHST- 2004/10/19 09:00 [medline]
PHST- 2004/05/19 05:00 [entrez]
AID - 820086 [pii]
AID - 10.1358/dot.2004.40.3.820086 [doi]
PST - ppublish
SO  - Drugs Today (Barc). 2004 Mar;40(3):225-34. doi: 10.1358/dot.2004.40.3.820086.