Document Detail


Pharmacologic preconditioning of estrogen by activation of the myocardial adenosine triphosphate-sensitive potassium channel in patients undergoing coronary angioplasty.
MedLine Citation:
PMID:  11869855     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: The purpose of this study was to determine whether administration of estrogen produces cardioprotective effects in patients undergoing coronary angioplasty. BACKGROUND: We have previously demonstrated that estrogen can provide cardioprotection by activating the mitochondrial adenosine triphosphate-sensitive potassium (K(ATP)) channel, a major contributor to ischemic cardioprotection. METHODS: Fifty patients undergoing angioplasty of a major epicardial coronary artery were randomly allocated to either ischemic preconditioning or intracoronary estrogen administration in the presence or absence of glibenclamide (glyburide). RESULTS: The coronary collateral circulation, as quantitatively assessed by an intracoronary Doppler flow wire, was similar during balloon inflation among the groups. Patients in the preconditioned and estrogen-treated groups significantly lowered their ischemic burden, as assessed by an ST-segment shift, chest pain score and myocardial lactate extraction ratio, as compared with control subjects. The reduction in the ST-segment shift afforded by estrogen during the first inflation (-63% vs. first inflation in the preconditioned group) was similar to that afforded by preconditioning during the second inflation (-68% vs. first inflation). In contrast, the patients given glibenclamide developed significantly higher ischemic burden during the first and second inflations, as compared with those in the estrogen-treated group alone. CONCLUSIONS: It is concluded that intracoronary administration of estrogen before balloon angioplasty rendered the myocardium relatively resistant to subsequent ischemia, and the degree of cardioprotective effect was comparable to that afforded by ischemic preconditioning. The effect of estrogen was abolished by glibenclamide, suggesting that the cardioprotective effect of estrogen may result from activation of myocardial K(ATP) channels.
Authors:
Tsung Ming Lee; Sheng Fang Su; Tsai Fwu Chou; Chang Her Tsai
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Publication Detail:
Type:  Clinical Trial; Journal Article; Randomized Controlled Trial    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  39     ISSN:  0735-1097     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  2002 Mar 
Date Detail:
Created Date:  2002-02-28     Completed Date:  2002-03-20     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  871-7     Citation Subset:  AIM; IM    
Affiliation:
Departments of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / physiology*
Angioplasty, Transluminal, Percutaneous Coronary*
Cardiotonic Agents / pharmacology*
Collateral Circulation / drug effects,  physiology
Coronary Artery Disease / physiopathology*,  therapy*
Coronary Circulation / drug effects,  physiology
Electrocardiography
Estrogens, Conjugated (USP) / pharmacology*
Female
Humans
Ischemic Preconditioning, Myocardial*
Male
Middle Aged
Potassium Channels / drug effects*,  physiology*
Prospective Studies
Chemical
Reg. No./Substance:
0/Cardiotonic Agents; 0/Estrogens, Conjugated (USP); 0/Potassium Channels; 56-65-5/Adenosine Triphosphate

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


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