|
 |
|
|||||||
|
|||||||||
Copyright ©ERS Journals Ltd 2006
A study of aspirin and clopidogrel in idiopathic pulmonary arterial hypertension
1 Dept of Medicine, Vanderbilt University Medical Center, Nashville, TN, Depts of 2 Medicine, 4 Paediatrics, College of Physicians and Surgeons, and 3 Epidemiology, Joseph L. Mailman School of Public Health, Columbia University, New York, NY, 5 Dept of Medicine, 8 Center for Clinical Epidemiology and Biostatistics, and 6 Center for Experimental Therapeutics, University of Pennsylvania School of Medicine, Philadelphia, PA, and 7 Dept of Medicine, Brigham and Women's Hospital, Boston, MA, USA, 9 Authors contributed equally to this paper.
CORRESPONDENCE: S. M. Kawut, Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons, PH 8E, Rm 101, 622 W, 168th Street, New York, NY 10032, USA. Fax: 1 2123425382. E-mail: sk2097{at}columbia.edu
Keywords: Aspirin, clinical trial, hypertension, platelets, pulmonary
Received: August 17, 2005
Accepted November 9, 2005
Idiopathic pulmonary arterial hypertension (IPAH) is characterised by in situ thrombosis and increased thromboxane (Tx) A2 synthesis; however, there are no studies of antiplatelet therapy in IPAH. The aim of the current study was to determine the biochemical effects of aspirin (ASA) and clopidogrel on platelet function and eicosanoid metabolism in patients with IPAH.
A randomised, double-blind, placebo-controlled crossover study of ASA 81 mg once daily and clopidogrel 75 mg once daily was performed. Plasma P-selectin levels and aggregometry were measured after exposure to adenosine diphosphate, arachidonic acid and collagen. Serum levels of TxB2 and urinary metabolites of TxA2 and prostaglandin I2 (Tx-M and PGI-M, respectively) were assessed.
A total of 19 IPAH patients were enrolled, of whom nine were being treated with continuous intravenous epoprostenol. ASA and clopidogrel significantly reduced platelet aggregation to arachidonic acid and adenosine diphosphate, respectively. ASA significantly decreased serum TxB2, urinary Tx-M levels and the Tx-M/PGI-M ratio, whereas clopidogrel had no effect on eicosanoid levels. Neither drug significantly lowered plasma P-selectin levels. Epoprostenol use did not affect the results.
In conclusion, aspirin and clopidogrel inhibited platelet aggregation, and aspirin reduced thromboxane metabolite production without affecting prostaglandin I2 metabolite synthesis. Further clinical trials of aspirin in patients with idiopathic pulmonary arterial hypertension should be performed.
This article has been cited by other articles:
|
|
 |
|
  K. M. Chin, R. N. Channick, J. A. de Lemos, N. H. Kim, F. Torres, and L. J. Rubin Hemodynamics and Epoprostenol Use Are Associated With Thrombocytopenia in Pulmonary Arterial Hypertension Chest, January 1, 2009; 135(1): 130 - 136. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Gomberg-Maitland Traditional and Alternative Designs for Pulmonary Arterial Hypertension Trials Proceedings of the ATS, July 15, 2008; 5(5): 610 - 616. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Rousseau, M. Tartas, B. Fromy, A. Godon, M.-A. Custaud, J. L. Saumet, and P. Abraham Platelet inhibition by low-dose aspirin but not by clopidogrel reduces the axon-reflex current-induced vasodilation in humans Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2008; 294(5): R1420 - R1426. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |