Abstract 15591: Mechanical Dyssynchrony of the Left Atrium During Sinus Rhythm is Associated With Stroke in Patients With History of Atrial Fibrillation
Introduction: Depressed left atrial (LA) function during sinus rhythm is associated with stroke or transient ischemic attack (TIA) in patients with a history of atrial fibrillation (AF), independent of the CHA2DS2-VASc score.
Hypothesis: We hypothesized that mechanical dyssynchrony of the LA is associated with stroke or TIA independent of LA function in patients with a history of AF.
Methods: We conducted a retrospective case-control study of a total of 222 patients with a history of AF (60±10 years, 29% female, 24% nonparoxysmal AF) referred for catheter ablation to treat drug-refractory AF who underwent pre-ablation CMR in sinus rhythm. Using tissue tracking cardiac magnetic resonance (CMR) we measured the LA longitudinal strain and strain rate in each of 12 equi-length segments in two- and four-chamber views. Based on those time series we defined five indices of LA mechanical dyssynchrony, including the standard deviation of the time to the peak longitudinal strain (SD-TPS) (Figure 1A and 1B).
Results: Patients with a prior history of stroke or TIA (n=20) had a significantly higher SD-TPS (ms) than those without (n=202): 35.8 vs 23.6, p<0.001. Multivariable analysis showed that SD-TPS was associated with stroke/TIA (odds ratio (OR) 1.08; p<0.001) after adjusting for the CHA2DS2VASc score, LA minimum volume and the peak LA longitudinal strain. The receiver-operating characteristics curve showed that SD-TPS identified patients with stroke/TIA more sensitively and specifically than CHA2DS2 -VASC score alone (OR: 2.16 vs. 1.84, p =0.001; C-statistics: .83 vs .76, p<0.03) (Figure 1C).
Conclusions: Higher mechanical dyssynchrony of the left atrium during sinus rhythm is significantly associated with a history of stroke/TIA in patients with AF. Mechanical dyssynchrony of the left atrium may contribute to thrombogenesis by promoting reduction of regional blood flow within the left atrium due to a loss of coordinated contraction.
Author Disclosures: L. Ciuffo: None. Y. Inoue: None. S. Tao: None. E.G. Ipek: None. J.A. Lima: None. S. Nazarian: None. D.D. Spragg: None. J. Marine: None. R.D. Berger: None. H. Calkins: None. H. Ashikaga: None.
- © 2016 by American Heart Association, Inc.