作者
Na Li, David Y Chiang, Sufen Wang, Qiongling Wang, Liang Sun, Niels Voigt, Jonathan L Respress, Sameer Ather, Darlene G Skapura, Valerie K Jordan, Frank T Horrigan, Wilhelm Schmitz, Frank U Müller, Miguel Valderrabano, Stanley Nattel, Dobromir Dobrev, Xander HT Wehrens
发表日期
2014/3/25
期刊
Circulation
卷号
129
期号
12
页码范围
1276-1285
出版商
Lippincott Williams & Wilkins
简介
Background
The progression of atrial fibrillation (AF) from paroxysmal to persistent forms remains a major clinical challenge. Abnormal sarcoplasmic reticulum (SR) Ca2+ leak via the ryanodine receptor type 2 (RyR2) has been observed as a source of ectopic activity in various AF models. However, its potential role in progression to long-lasting spontaneous AF (sAF) has never been tested. This study was designed to test the hypothesis that enhanced RyR2-mediated Ca2+ release underlies the development of a substrate for sAF and to elucidate the underlying mechanisms.
Methods and Results
CREM-IbΔC-X transgenic (CREM) mice developed age-dependent progression from spontaneous atrial ectopy to paroxysmal and eventually long-lasting AF. The development of sAF in CREM mice was preceded by enhanced diastolic Ca2+ release, atrial enlargement, and marked conduction abnormalities. Genetic …
学术搜索中的文章
N Li, DY Chiang, S Wang, Q Wang, L Sun, N Voigt… - Circulation, 2014