Atıf İçin Kopyala
Bourgonje V. J. A., Vos M. A., Ozdemir S., Doisne N., Acsai K., Varro A., ...Daha Fazla
CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY, cilt.6, sa.2, ss.371-379, 2013 (SCI-Expanded)
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Yayın Türü:
Makale / Tam Makale
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Cilt numarası:
6
Sayı:
2
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Basım Tarihi:
2013
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Doi Numarası:
10.1161/circep.113.000322
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Dergi Adı:
CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY
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Derginin Tarandığı İndeksler:
Science Citation Index Expanded (SCI-EXPANDED), Scopus
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Sayfa Sayıları:
ss.371-379
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Anahtar Kelimeler:
antiarrhythmic drug, calcium channel, heart failure, long QT syndrome, Na+/Ca2+ exchange, Torsade de Pointes, TORSADES-DE-POINTES, IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR, CHRONIC ATRIOVENTRICULAR-BLOCK, EARLY AFTERDEPOLARIZATIONS, DIASTOLIC DYSFUNCTION, NA+-CA2+ EXCHANGER, HEART-FAILURE, CA2+ RELEASE, IN-VIVO, INHIBITION
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Akdeniz Üniversitesi Adresli:
Evet
Özet
Background-L-type calcium channel (LTCC) and Na+/Ca2+ exchanger (NCX) have been implicated in repolarization-dependent arrhythmias, but also modulate calcium and contractility. Although LTCC inhibition is negative inotropic, NCX inhibition has the opposite effect. Combined block may, therefore, offer an advantage for hemodynamics and antiarrhythmic efficiency, particularly in diseased hearts. In a model of proarrhythmia, the dog with chronic atrioventricular block, we investigated whether combined inhibition of NCX and LTCC with SEA-0400 is effective against dofetilide-induced torsade de pointes arrhythmias (TdP), while maintaining calcium homeostasis and hemodynamics.