TY - JOUR
T1 - Heart failure differentially modulates natural (Sinoatrial node) and ectopic (pulmonary veins) pacemakers
T2 - Mechanism and therapeutic implication for atrial fibrillation
AU - Chan, Chao Shun
AU - Lin, Yung Kuo
AU - Chen, Yao Chang
AU - Lu, Yen Yu
AU - Chen, Shih Ann
AU - Chen, Yi Jen
N1 - Funding Information:
Funding: This study was supported by the Ministry of Science and Technology of Taiwan (grant numbers MOST107-2314-B-281-009, and MOST107-2314-B-038-101-MY3), Taipei Medical University-Taipei Medical University Hospital (108TMU-TMUH-25) and Taipei Medical University-Wan Fang Hospital (107-wf-eva-01, 108-wf-eva-06, and 108-wf-swf-01).
Publisher Copyright:
© 2019 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2019/7/1
Y1 - 2019/7/1
N2 - Heart failure (HF) frequently coexists with atrial fibrillation (AF) and dysfunction of the sinoatrial node (SAN), the natural pacemaker. HF is associated with chronic adrenergic stimulation, neurohormonal activation, abnormal intracellular calcium handling, elevated cardiac filling pressure and atrial stretch, and fibrosis. Pulmonary veins (PVs), which are the points of onset of ectopic electrical activity, are the most crucial AF triggers. A crosstalk between the SAN and PVs determines PV arrhythmogenesis. HF has different effects on SAN and PV electrophysiological characteristics, which critically modulate the development of AF and sick sinus syndrome. This review provides updates to improve our current understanding of the effects of HF in the electrical activity of the SAN and PVs as well as therapeutic implications for AF.
AB - Heart failure (HF) frequently coexists with atrial fibrillation (AF) and dysfunction of the sinoatrial node (SAN), the natural pacemaker. HF is associated with chronic adrenergic stimulation, neurohormonal activation, abnormal intracellular calcium handling, elevated cardiac filling pressure and atrial stretch, and fibrosis. Pulmonary veins (PVs), which are the points of onset of ectopic electrical activity, are the most crucial AF triggers. A crosstalk between the SAN and PVs determines PV arrhythmogenesis. HF has different effects on SAN and PV electrophysiological characteristics, which critically modulate the development of AF and sick sinus syndrome. This review provides updates to improve our current understanding of the effects of HF in the electrical activity of the SAN and PVs as well as therapeutic implications for AF.
KW - Atrial fibrillation
KW - Heart failure
KW - Pulmonary veins
KW - Sinoatrial node
KW - Sinoatrial node dysfunction
KW - Heart Failure/drug therapy
KW - Animals
KW - Pulmonary Veins/drug effects
KW - Humans
KW - Sinoatrial Node/drug effects
KW - Atrial Fibrillation/drug therapy
KW - Anti-Arrhythmia Agents/pharmacology
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U2 - 10.3390/ijms20133224
DO - 10.3390/ijms20133224
M3 - Review article
C2 - 31262061
AN - SCOPUS:85069269935
SN - 1661-6596
VL - 20
JO - International Journal of Molecular Sciences
JF - International Journal of Molecular Sciences
IS - 13
M1 - 3224
ER -