期刊
CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY
卷 9, 期 3, 页码 -出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCEP.115.002897
关键词
arrhythmias; cardiac; atrial fibrillation; fibrosis; magnetic resonance imaging; regression analysis
资金
- Biosense-Webster grant
- National Institutes of Health (NIH) [K23HL089333, R01HL116280]
- Dr Francis P. Chiaramonte Foundation
- Norbert and Louise Grunwald Cardiac Arrhythmia Fund
- Marv Weiner Cardiac Arrhythmia Fund
- Marilyn and Christian Poindexter Research Fund
Background Prior studies have demonstrated regional left atrial late gadolinium enhancement (LGE) heterogeneity on magnetic resonance imaging. Heterogeneity in regional conduction velocities is a critical substrate for functional reentry. We sought to examine the association between left atrial conduction velocity and LGE in patients with atrial fibrillation. Methods and Results LGE imaging and left atrial activation mapping were performed during sinus rhythm in 22 patients before pulmonary vein isolation. The locations of 1468 electroanatomic map points were registered to the corresponding anatomic sites on 469 axial LGE image planes. The local conduction velocity at each point was calculated using previously established methods. The myocardial wall thickness and image intensity ratio defined as left atrial myocardial LGE signal intensity divided by the mean left atrial blood pool intensity was calculated for each mapping site. The local conduction velocity and image intensity ratio in the left atrium (meanSD) were 0.98 +/- 0.46 and 0.95 +/- 0.26 m/s, respectively. In multivariable regression analysis, clustered by patient, and adjusting for left atrial wall thickness, conduction velocity was associated with the local image intensity ratio (0.20 m/s decrease in conduction velocity per increase in unit image intensity ratio, P<0.001). Conclusions In this clinical in vivo study, we demonstrate that left atrial myocardium with increased gadolinium uptake has lower local conduction velocity. Identification of such regions may facilitate the targeting of the substrate for reentrant arrhythmias.
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