Document Detail


Insights into the role of thromboxane A2 and serotonin in the pathogenesis of unstable angina.
MedLine Citation:
PMID:  7873224     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
New research about platelet and endothelial functions is allowing us to better understand the pathogenesis of myocardial ischemic episodes in patients with unstable angina, creating new perspectives for the rational utilization of therapies. In patients with unstable angina, the episodes of symptomatic and silent ischemia are caused by repeated reductions of coronary blood flow. They are the result of the mechanical effect of the growing thrombus, which causes intermittent episodes of partial obstruction of the arterial lumen, in association with vasoconstriction at the stenotic site and dependent coronary arterial bed, produced by the cyclic release of platelet derived vasoactive products, namely thromboxane A2 and serotonin. Several studies, many of them in animal models of thrombosis, suggest that serotonin and thromboxane A2 are mediators of platelet aggregation, adynamic obstruction and coronary artery thrombosis. Because they cause coronary cyclic flow reductions, they are implicated in the pathogenesis of myocardial ischemic episodes during unstable angina. Drugs that interfere with the arachidonate pathway, and the 5-HT2-receptor antagonists, have been proven to decrease or abolish coronary cyclic flow variations in animal models and man. However, further studies should be done to test the hypothesis that the association of a 5-HT2-receptor antagonist with aspirin may contribute to decrease myocardial ischemia and prevent coronary occlusion in patients with unstable angina. Continuous Holter monitoring during the first week after admission in the hospital should be a good method to evaluate the eventual efficacy of this new class of drugs in abolishing or decreasing the frequency, intensity and duration of myocardial ischemic episodes in patients with unstable angina. The central role of serotonin in the pathogenesis of thrombotic events, and the presumed preventive effect of ketanserin, were the bases of a national multicenter pilot controlled study designed to evaluate the safety and efficacy of ketanserin plus aspirin in the secondary prevention of patients with unstable angina and non-Q wave myocardial infarction (KATUA Trial).
Authors:
A P Machado; J A Saavedra; C Ribeiro
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Revista portuguesa de cardiologia : orgão oficial da Sociedade Portuguesa de Cardiologia = Portuguese journal of cardiology : an official journal of the Portuguese Society of Cardiology     Volume:  13     ISSN:  0870-2551     ISO Abbreviation:  Rev Port Cardiol     Publication Date:  1994 Dec 
Date Detail:
Created Date:  1995-04-04     Completed Date:  1995-04-04     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8710716     Medline TA:  Rev Port Cardiol     Country:  PORTUGAL    
Other Details:
Languages:  eng     Pagination:  935-46, 893     Citation Subset:  IM    
Affiliation:
Serviço de Medicina I, Hospitalar de Medicina Interna do Hospital de Santa Maria.
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MeSH Terms
Descriptor/Qualifier:
Angina, Unstable / etiology*
Arachidonic Acid / physiology
Blood Platelets / physiology
Clinical Trials as Topic
Coronary Circulation
Endothelium, Vascular / physiology
Humans
Nitric Oxide / physiology
Platelet Aggregation / physiology
Platelet Aggregation Inhibitors
Receptors, Serotonin / physiology
Serotonin / physiology*
Serotonin Antagonists / pharmacology
Thromboxane A2 / physiology*
Chemical
Reg. No./Substance:
0/Platelet Aggregation Inhibitors; 0/Receptors, Serotonin; 0/Serotonin Antagonists; 10102-43-9/Nitric Oxide; 50-67-9/Serotonin; 506-32-1/Arachidonic Acid; 57576-52-0/Thromboxane A2

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


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