Cellular and molecular correlates of ectopic activity in patients with atrial fibrillation
Author(s) -
Niels Voigt,
Dobromir Dobrev
Publication year - 2012
Publication title -
ep europace
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.119
H-Index - 102
eISSN - 1532-2092
pISSN - 1099-5129
DOI - 10.1093/europace/eus282
Subject(s) - medicine , atrial fibrillation , pathophysiology , ectopic expression , cardiology , intracellular , mechanism (biology) , calcium in biology , clinical significance , bioinformatics , calcium , biochemistry , chemistry , philosophy , epistemology , biology , gene , microbiology and biotechnology
Atrial fibrillation (AF) is the most frequent arrhythmia and is associated with increased morbidity and mortality. Current drugs for AF treatment have limited efficacy and a substantial risk of proarrhythmic side effects, making novel drug development critical. Emerging evidence suggests that abnormal intracellular calcium (Ca(2+)) signalling is a key contributor to ectopic (triggered) electrical activity in human AF. Accordingly, atrial Ca(2+)-handling abnormalities underlying ectopic activity may constitute novel mechanism-based therapeutic approaches to treat AF. This article reviews the recent evidence for a role of cellular ectopic activity in human AF pathophysiology, discusses the molecular mechanisms underlying triggered activity in human atrial myocytes, and considers their relevance to the design of novel therapeutic options.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom