Cellular basis of triggered arrhythmias in heart failure.
Ventricular tachycardia in nonischemic heart failure (HF) initiates by a nonreentrant mechanism that appears to be due to triggered activity primarily from delayed afterdepolarizations that arise from altered cellular Ca handling and ionic currents. In HF, factors that conspire to enhance triggered arrhythmias include upregulated Na/Ca exchange, preserved beta-adrenergic responsiveness, and decreased I(K1). Overall, the further delineation of key factors that underlie triggered arrhythmias in HF will provide the basis for new therapeutic strategies directed toward novel targets that can reduce the high incidence of sudden death in patients with HF.
Pogwizd
Steven M
SM
Steven M. Pogwizd is at the Department of Medicine, University of Illinois at Chicago, Chicago, Illinois 60153, USA.
Bers
Donald M
DM
D000818:Animals; D001158:Arteries / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D016757:Death, Sudden, Cardiac / Q000517:prevention & control; D006333:Heart Failure / Q000150:complications / Q000503:physiopathology*; D006801:Humans; D007473:Ion Channels / Q000502:physiology; D023421:Models, Animal; D032342:Muscle Cells / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D017180:Tachycardia, Ventricular / Q000209:etiology / Q000503:physiopathology*
D007473:Ion Channels; D011943:Receptors, Adrenergic, beta; D019837:Ryanodine Receptor Calcium Release Channel; D012964:Sodium; D002118:Calcium