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dc.contributor.authorRiegger, GAJ
dc.contributor.authorErdmann, J
dc.contributor.authorHolmer, S
dc.contributor.authorWollnik, B
dc.contributor.authorSchunkert, H
dc.contributor.authorJeron, A
dc.contributor.authorHengstenberg, C
dc.date.accessioned2021-03-06T21:12:53Z
dc.date.available2021-03-06T21:12:53Z
dc.date.issued2004
dc.identifier.citationJeron A., Hengstenberg C., Holmer S., Wollnik B., Riegger G., Schunkert H., Erdmann J., "KCNJ11 polymorphisms and sudden cardiac death in patients with acute myocardial infarction", JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, cilt.36, ss.287-293, 2004
dc.identifier.issn0022-2828
dc.identifier.othervv_1032021
dc.identifier.otherav_fdad6b19-e07f-407a-a265-bd58106fe493
dc.identifier.urihttp://hdl.handle.net/20.500.12627/165938
dc.identifier.urihttps://doi.org/10.1016/j.yjmcc.2003.11.009
dc.description.abstractPurpose. Patients with an acute myocardial infarction (AMI) are of high risk to develop ischemia-induced ventricular arrhythmias, leading to sudden cardiac death (SCD) in about one third of all AMI patients. The individual susceptibility to ischemia-induced arrhythmias may be modified by polymorphisms in genes encoding ion channels. The cardiac ATP-dependent potassium channel (K-ATP) current is generated by ion channels encoded by the KCNJ11 gene and the SUR2a gene. Opening of the K-ATP channel during ischemia results in action potential shortening in various studies and may therefore influence the outcome of AMI patients.
dc.language.isoeng
dc.subjectTemel Tıp Bilimleri
dc.subjectHistoloji-Embriyoloji
dc.subjectDahili Tıp Bilimleri
dc.subjectKardiyoloji
dc.subjectYaşam Bilimleri
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectTemel Bilimler
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectTıp
dc.subjectSağlık Bilimleri
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectHÜCRE BİYOLOJİSİ
dc.subjectKlinik Tıp (MED)
dc.subjectKlinik Tıp
dc.subjectCARDIAC ve CARDIOVASCULAR SİSTEMLER
dc.titleKCNJ11 polymorphisms and sudden cardiac death in patients with acute myocardial infarction
dc.typeMakale
dc.relation.journalJOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
dc.contributor.department, ,
dc.identifier.volume36
dc.identifier.issue2
dc.identifier.startpage287
dc.identifier.endpage293
dc.contributor.firstauthorID170872


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