Longitudinal myocardial systolic function assessed by STE, which is a sensitive marker of subclinical ventricular dysfunction is impaired in BD. Increased NT-proBNP levels may be a sign of subclinical ventricular dysfunction in these patients.

This study showed that interatrial and intra-atrial electromechanical delay and PWD were prolonged in patients with moderate-to-severe OSA. LA dilatation, hypoxemia, and the severity of the disease may contribute a prolongation in interatrial electromechanical delay via atrial structural and electrical alterations, which may predict the risk of future AF development in patients with moderate-to-severe OSA.

BackgroundIvabradine is a novel specific heart rate (HR)-lowering agent that improves event-free survival in patients with heart failure (HF).ObjectivesWe aimed to evaluate the effect of ivabradine on time domain indices of heart rate variability (HRV) in patients with HF.MethodsForty-eight patients with compensated HF of nonischemic origin were included. Ivabradine treatment was initiated according to the latest HF guidelines. For HRV analysis, 24-h Holter recording was obtained from each patient before and after 8 weeks of treatment with ivabradine.ResultsThe mean RR interval, standard deviation of all normal to normal RR intervals (SDNN), the standard deviation of 5-min mean RR intervals (SDANN), the mean of the standard deviation of all normal-to-normal RR intervals for all 5-min segments (SDNN index), the percentage of successive normal RR intervals exceeding 50 ms (pNN50), and the square root of the mean of the squares of the differences between successive normal to normal RR intervals (RMSSD) were low at baseline before treatment with ivabradine. After 8 weeks of treatment with ivabradine, the mean HR (83.6 ± 8.0 and 64.6 ± 5.8, p < 0.0001), mean RR interval (713 ± 74 and 943 ± 101 ms, p < 0.0001), SDNN (56.2 ± 15.7 and 87.9 ± 19.4 ms, p < 0.0001), SDANN (49.5 ± 14.7 and 76.4 ± 19.5 ms, p < 0.0001), SDNN index (24.7 ± 8.8 and 38.3 ± 13.1 ms, p < 0.0001), pNN50 (2.4 ± 1.6 and 3.2 ± 2.2 %, p < 0.0001), and RMSSD (13.5 ± 4.6 and 17.8 ± 5.4 ms, p < 0.0001) substantially improved, which sustained during both when awake and while asleep.ConclusionOur findings suggest that treatment with ivabradine improves HRV in nonischemic patients with HF.

Our aim was to evaluate whether atrial electromechanical delay measured by tissue Doppler imaging (TDI), which is an early predictor of atrial fibrillation (AF) development, is prolonged in obese subjects. A total of 40 obese and 40 normal-weight subjects with normal coronary angiograms were included in this study. P-wave dispersion (PWD) was calculated on the 12-lead electrocardiogram (ECG). Systolic and diastolic left ventricular (LV) functions, inter-and intra-atrial electromechanical delay were measured by TDI and conventional echocardiography. Inter-and intra-atrial electromechanical delay were significantly longer in the obese subjects compared with the controls (44.08 ± 10.06 vs. 19.35 ± 5.94 ms and 23.63 ± 6.41 vs. 5.13 ± 2.67 ms, P < 0.0001 for both, respectively). PWD was higher in obese subjects (53.40 ± 5.49 vs. 35.95 ± 5.93 ms, P < 0.0001). Left atrial (LA) diameter, LA volume index and LV diastolic parameters were significantly different between the groups. Interatrial electromechanical delay was correlated with PWD (r = 0.409, P = 0.009), high-sensitivity C-reactive protein (hsCRP) levels (r = 0.588, P < 0.0001). Interatrial electromechanical delay was positively correlated with LA diameter, LA volume index, and LV diastolic function parameters consisting of mitral early wave (E) deceleration time (DT) and isovolumetric relaxation time (IVRT; r = 0.323, P = 0.042; r = 0.387, P = 0.014; r = 0.339, P = 0.033; r = 0.325, P = 0.041; respectively) and, negatively correlated with mitral early (E) to late (A) wave ratio (E/A) (r = −0.380, P = 0.016) and myocardial early-to-late diastolic wave ratio (E m /A m ) (r = −0.326, P = 0.040). This study showed that atrial electromechanical delay is prolonged in obese subjects. Prolonged atrial electromechanical delay is due to provoked low-grade inflammation as well as LA enlargement and early LV diastolic dysfunction in obese subjects.

Our study has shown that LA mechanical functions and volumes are impaired in BD. These results may be an early form of subclinical cardiac involvement in patients with BD who have no clinical evidence for cardiovascular disease.