Pharmacologic preconditioning of estrogen by activation of the myocardial adenosine triphosphate-sensitive potassium channel in patients undergoing coronary angioplasty

The purpose of this study was to determine whether administration of estrogen produces cardioprotective effects in patients undergoing coronary angioplasty. We have previously demonstrated that estrogen can provide cardioprotection by activating the mitochondrial adenosine triphosphate-sensitive pot...

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Published inJournal of the American College of Cardiology Vol. 39; no. 5; pp. 871 - 877
Main Authors Lee, Tsung-Ming, Su, Sheng-Fang, Chou, Tsai-Fwu, Tsai, Chang-Her
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 06.03.2002
Elsevier Science
Elsevier Limited
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Online AccessGet full text
ISSN0735-1097
1558-3597
DOI10.1016/S0735-1097(01)01816-2

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Abstract The purpose of this study was to determine whether administration of estrogen produces cardioprotective effects in patients undergoing coronary angioplasty. We have previously demonstrated that estrogen can provide cardioprotection by activating the mitochondrial adenosine triphosphate-sensitive potassium (KATP) channel, a major contributor to ischemic cardioprotection. 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). 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. 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 KATPchannels.
AbstractList 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 (KATP) 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 KATPchannels.
The purpose of this study was to determine whether administration of estrogen produces cardioprotective effects in patients undergoing coronary angioplasty. We have previously demonstrated that estrogen can provide cardioprotection by activating the mitochondrial adenosine triphosphate-sensitive potassium (KATP) channel, a major contributor to ischemic cardioprotection. 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). 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. 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 KATPchannels.
The purpose of this study was to determine whether administration of estrogen produces cardioprotective effects in patients undergoing coronary angioplasty.OBJECTIVESThe purpose of this study was to determine whether administration of estrogen produces cardioprotective effects in patients undergoing coronary angioplasty.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.BACKGROUNDWe 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.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).METHODSFifty 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).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.RESULTSThe 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.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.CONCLUSIONSIt 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.
The purpose of this study was to determine whether administration of estrogen produces cardioprotective effects in patients undergoing coronary angioplasty. 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. 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). 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. 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.
Author Su, Sheng-Fang
Lee, Tsung-Ming
Tsai, Chang-Her
Chou, Tsai-Fwu
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  organization: Surgery, Cardiology Section, National Taiwan University Hospital, Taipei, Taiwan
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Issue 5
Keywords ECG
MLER
KATP
ANOVA
PTCA
HERS
Human
Prognosis
Potassium ion
Coronary artery
Estrogen
Instrumentation therapy
Cardiovascular disease
Ionic channel
Instrumental dilatation
Coronary heart disease
Biological activity
Treatment
Sex steroid hormone
ATP
Preconditioning
Language English
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SSID ssj0006819
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Snippet The purpose of this study was to determine whether administration of estrogen produces cardioprotective effects in patients undergoing coronary angioplasty. We...
Objectives The purpose of this study was to determine whether administration of estrogen produces cardioprotective effects in patients undergoing coronary...
The purpose of this study was to determine whether administration of estrogen produces cardioprotective effects in patients undergoing coronary...
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StartPage 871
SubjectTerms Adenosine Triphosphate - physiology
Angina pectoris
Angioplasty
Angioplasty, Balloon, Coronary
Biological and medical sciences
Cardiology
Cardiology. Vascular system
Cardiotonic Agents - pharmacology
Collateral Circulation - drug effects
Collateral Circulation - physiology
Coronary Artery Disease - physiopathology
Coronary Artery Disease - therapy
Coronary Circulation - drug effects
Coronary Circulation - physiology
Coronary heart disease
Electrocardiography
Estrogens, Conjugated (USP) - pharmacology
Female
Heart
Heart attacks
Humans
Ischemic Preconditioning, Myocardial
Male
Medical sciences
Middle Aged
Potassium Channels - drug effects
Potassium Channels - physiology
Prospective Studies
Rodents
Title Pharmacologic preconditioning of estrogen by activation of the myocardial adenosine triphosphate-sensitive potassium channel in patients undergoing coronary angioplasty
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0735109701018162
https://dx.doi.org/10.1016/S0735-1097(01)01816-2
https://www.ncbi.nlm.nih.gov/pubmed/11869855
https://www.proquest.com/docview/1506096385
https://www.proquest.com/docview/71489357
Volume 39
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