Background Four-dimensional (4D) flow cardiovascular magnetic resonance (CMR) allows sophisticated quantification of left atrial (LA) blood flow, and could yield novel biomarkers of propensity for intra-cardiac thrombus formation and embolic stroke. As reproducibility is critically important to diagnostic performance, we systematically investigated technical and temporal variation of LA 4D flow in atrial fibrillation (AF) and sinus rhythm (SR). Methods Eighty-six subjects (SR, n = 64; AF, n = 22) with wide-ranging stroke risk (CHA2DS2VASc 0–6) underwent LA 4D flow assessment of peak and mean velocity, vorticity, vortex volume, and stasis. Eighty-five (99%) underwent a second acquisition within the same session, and 74 (86%) also returned at 30 (27–35) days for an interval scan. We assessed variability attributable to manual contouring (intra- and inter-observer), and subject repositioning and reacquisition of data, both within the same session (same-day scan–rescan), and over time (interval scan). Within-subject coefficients of variation (CV) and bootstrapped 95% CIs were calculated and compared. Results Same-day scan–rescan CVs were 6% for peak velocity, 5% for mean velocity, 7% for vorticity, 9% for vortex volume, and 10% for stasis, and were similar between SR and AF subjects (all p > 0.05). Interval-scan variability was similar to same-day scan–rescan variability for peak velocity, vorticity, and vortex volume (all p > 0.05), and higher for stasis and mean velocity (interval scan CVs of 14% and 8%, respectively, both p < 0.05). Longitudinal changes in heart rate and blood pressure at the interval scan in the same subjects were associated with significantly higher variability for LA stasis (p = 0.024), but not for the remaining flow parameters (all p > 0.05). SR subjects showed significantly greater interval-scan variability than AF patients for mean velocity, vortex volume, and stasis (all p < 0.05), but not peak velocity or vorticity (both p > 0.05). Conclusions LA peak velocity and vorticity are the most reproducible and temporally stable novel LA 4D flow biomarkers, and are robust to changes in heart rate, blood pressure, and differences in heart rhythm.

Aims  Altered left atrial (LA) blood flow characteristics account for an increase in cardioembolic stroke risk in atrial fibrillation (AF). Here, we aimed to assess whether exposure to stroke risk factors is sufficient to alter LA blood flow even in the presence of sinus rhythm (SR). Methods and results  We investigated 95 individuals: 37 patients with persistent AF, who were studied before and after cardioversion [Group 1; median CHA2DS2-VASc = 2.0 (1.5–3.5)]; 35 individuals with no history of AF but similar stroke risk to Group 1 [Group 2; median CHA2DS2-VASc = 3.0 (2.0–4.0)]; and 23 low-risk individuals in SR [Group 3; median CHA2DS2-VASc = 0.0 (0.0–0.0)]. Cardiac function and LA flow characteristics were evaluated using cardiac magnetic resonance. Before cardioversion, Group 1 displayed impaired left ventricular (LV) and LA function, reduced LA flow velocities and vorticity, and a higher normalized vortex volume (all P &lt; 0.001 vs. Groups 2 and 3). After restoration of SR at ≥4-week post-cardioversion, LV systolic function and LA flow parameters improved significantly (all P &lt; 0.001 vs. pre-cardioversion) and were no longer different from those in Group 2. However, in the presence of SR, LA flow peak and mean velocity, and vorticity were lower in Groups 1 and 2 vs. Group 3 (all P &lt; 0.01), and were associated with impaired LA emptying fraction (LAEF) and LV diastolic dysfunction. Conclusion  Patients at moderate-to-high stroke risk display altered LA flow characteristics in SR in association with an LA myopathic phenotype and LV diastolic dysfunction, regardless of a history of AF.

Background Obesity is associated with left atrial (LA) remodeling (ie, dilatation and dysfunction) which is an independent determinant of future cardiovascular events. We aimed to assess whether LA remodeling is present in obesity even in individuals without established cardiovascular disease and whether it can be improved by intentional weight loss. Methods and Results Forty‐five individuals with severe obesity without established cardiovascular disease (age, 45±11 years; body mass index; 39.1±6.7 kg/m 2 ; excess body weight, 51±18 kg) underwent cardiac magnetic resonance for quantification of LA and left ventricular size and function before and at a median of 373 days following either a low glycemic index diet (n=28) or bariatric surgery (n=17). Results were compared with those obtained in 27 normal‐weight controls with similar age and sex. At baseline, individuals with obesity displayed reduced LA reservoir function (a marker of atrial distensibility), and a higher mass and LA maximum volume (all P <0.05 controls) but normal LA emptying fraction. On average, weight loss led to a significant reduction of LA maximum volume and left ventricular mass (both P <0.01); however, significant improvement of the LA reservoir function was only observed in those at the upper tertile of weight loss (≥47% excess body weight loss). Following weight loss, we found an average residual increase in left ventricular mass compared with controls but no residual significant differences in LA maximum volume and strain function (all P >0.05). Conclusions Obesity is linked to subtle LA myopathy in the absence of overt cardiovascular disease. Only larger volumes of weight loss can completely reverse the LA myopathic phenotype.