| Insights into the role of thromboxane A2 and serotonin in the pathogenesis of unstable angina. | |
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MedLine Citation:
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PMID: 7873224 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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). |
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Authors:
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A P Machado; J A Saavedra; C Ribeiro |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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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:
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Created Date: 1995-04-04 Completed Date: 1995-04-04 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8710716 Medline TA: Rev Port Cardiol Country: PORTUGAL |
Other Details:
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Languages: eng Pagination: 935-46, 893 Citation Subset: IM |
Affiliation:
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Serviço de Medicina I, Hospitalar de Medicina Interna do Hospital de Santa Maria. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Angina, Unstable
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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:
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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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