Cited 23 times since 2018 (3.9 per year) source: EuropePMC The American journal of cardiology, Volume 122, Issue 4, 4 1 2018, Pages 584-591 Relation of Echocardiographic Markers of Left Atrial Fibrosis to Atrial Fibrillation Burden. Leung M, Abou R, van Rosendael PJ, van der Bijl P, van Wijngaarden SE, Regeer MV, Podlesnikar T, Ajmone Marsan N, Leung DY, Delgado V, Bax JJ
In patients with atrial fibrillation (AF), left atrial (LA) fibrosis is a major determinant of the progression to, and burden of AF. LA reservoir strain and total atrial conduction time (PA-TDI) reflect LA fibrotic content. We aimed to investigate the relation between LA reservoir strain and PA-TDI in AF patients and control subjects. Six-hundred two patients (mean age 56 years, 53% men) with first episode of AF and 342 controls (mean age 64 years, 71% men) without structural heart disease underwent echocardiography. LA volumes, PA-TDI, LA reservoir strain, and left ventricular global longitudinal strain (GLS) were compared. Compared with controls, patients with paroxysmal AF and patients with persistent AF had longer PA-TDI (128 ± 25 millisecond, 140 ± 31 millisecond, and 154 ± 33 millisecond, respectively; p <0.001) and a progressive decline in LA reservoir strain (36.9 ± 11.6%, 29.8 ± 13.4%, 24.2 ± 12.3%, respectively; p <0.001). LA reservoir strain was negatively correlated with PA-TDI (r = -0.43, p <0.001). On multivariate analyses, LA reservoir strain, diabetes mellitus, and burden of AF were independent correlates of PA-TDI (R2 = 0.23, p <0.001); whereas only PA-TDI was an independent correlate of LA reservoir strain (R2 = 0.43, p <0.001); controlling for age, hypertension, coronary artery disease, body mass index, severity of mitral regurgitation, left ventricular global longitudinal strain, and LA volume. In conclusion, PA-TDI and LA reservoir strain are negatively correlated in all subjects, irrespective of the presence or burden of AF. Patients with persistent AF have longer PA-TDI and impaired LA reservoir strain compared with paroxysmal AF and controls, suggesting increasing burden of fibrosis and LA structural remodeling in the progression of AF.
