BackgroundAtrial fibrillation is associated with higher mortality. Identification of causes of death and contemporary risk factors for all‐cause mortality may guide interventions.Methods and ResultsIn the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF) study, patients with nonvalvular atrial fibrillation were randomized to rivaroxaban or dose‐adjusted warfarin. Cox proportional hazards regression with backward elimination identified factors at randomization that were independently associated with all‐cause mortality in the 14 171 participants in the intention‐to‐treat population. The median age was 73 years, and the mean CHADS 2 score was 3.5. Over 1.9 years of median follow‐up, 1214 (8.6%) patients died. Kaplan–Meier mortality rates were 4.2% at 1 year and 8.9% at 2 years. The majority of classified deaths (1081) were cardiovascular (72%), whereas only 6% were nonhemorrhagic stroke or systemic embolism. No significant difference in all‐cause mortality was observed between the rivaroxaban and warfarin arms (P=0.15). Heart failure (hazard ratio 1.51, 95% CI 1.33–1.70, P<0.0001) and age ≥75 years (hazard ratio 1.69, 95% CI 1.51–1.90, P<0.0001) were associated with higher all‐cause mortality. Multiple additional characteristics were independently associated with higher mortality, with decreasing creatinine clearance, chronic obstructive pulmonary disease, male sex, peripheral vascular disease, and diabetes being among the most strongly associated (model C‐index 0.677).ConclusionsIn a large population of patients anticoagulated for nonvalvular atrial fibrillation, ≈7 in 10 deaths were cardiovascular, whereas <1 in 10 deaths were caused by nonhemorrhagic stroke or systemic embolism. Optimal prevention and treatment of heart failure, renal impairment, chronic obstructive pulmonary disease, and diabetes may improve survival.Clinical Trial Registration URL: https://www.clinicaltrials.gov/. Unique identifier: NCT00403767.
Echocardiographic guidance of this procedure is essential. Which approach will be preferred will depend on the development of these two methods.
Abstract:Background: Since the late 1990s, a growing number of clinical studies have indicated that long-term permanent right ventricular (RV) apical pacing will induce severe complications such as development of heart failure, increased burden of atrial fi brillation leading to decreased quality of life. Aim of the study: To investigate whether cardiac resynchronization therapy (CRT) using biventricular (BiV) pacing can prevent the development of left ventricular (LV) dysfunction, LV remodelling, worsening of the clinical status and quality of life in chronically RV paced patients with normal LV ejection fraction (EF). Methods and results:A total of 127 patients with Class I indication for permanent cardiac pacing and without established indication for CRT were subjected to 6 months of RV and BiV pacing in a patient-blinded, randomized crossover trial. Treatment effects of BiV pacing were evaluated for LV function, LV remodelling and clinical status. Conclusion: BiV pacing, compared to RV pacing, did not change LV function and quality of life in patients with the absence of LV dysfunction or remodelling, standard bradycardia pacing indications in a pilot phase (12-month follow-up) of the TUGENDHAT trial. The fi nal report will be published after 60-month follow-up termination (Tab. 5, Fig. 3, Ref. 30). Full Text in PDF www.elis.sk. Key words: BiV and RV pacing, LV remodelling, heart failure, atrial fi brillation, quality of life. Results of several trials have supported the fact that right ventricular (RV) apical pacing might lead to adverse clinical outcomes in patients with standard pacing indications. Nevertheless, RV apical pacing continues to be practiced by many physicians because of its easy accessibility and relative stability over time (1, 2). The optimal mode and site of pacing remain undefi ned.The detrimental effect of RV pacing is probably most important in patients with pre-existing left ventricular (LV) dysfunction and may lead to worsening of heart failure (3, 4). In RV pacing, the sequence of electrical activation resembles the activation pattern in left bundle branch block (LBBB). This asynchronous electrical pattern is accompanied by abnormal dyssynchronous mechanical interactions within the LV (5). Experimental data suggested that biventricular (BiV) pacing might preserve myocardial performance better than RV apical pacing in patients with atrioventricular (AV) block and normal systolic function (6). The underlying mechanism may be a signifi cant reduction in LV systolic dyssynchrony, as shown by Cojoc et al (7). In the majority of patients with severe LV dysfunction and severe clinical heart failure associated with either LBBB-or RV pacing-induced dyssynchrony, BiV pacing improves clinical status, reduces mortality and morbidity, reduces heart failure (HF) hospitalizations, reverses LV remodelling and improves LV function (8, 9). Therefore, BiV pacing is nowadays recommended in patients with ventricular dyssynchrony (QRS > 120 ms), severe LV dysfunction [LV ejection fraction (LVEF) < 0.35] ...
Aims To assess the reproducibility of tissue Doppler myocardial velocities in patients with dilated ventricles and markedly reduced systolic function (ejection fraction ,35%). Methods and results Forty-one patients referred for cardiac resynchronization therapy (CRT) were evaluated using tissue Doppler echocardiography. The inter and intra-individual reproducibility of peak systolic myocardial velocities and the intra-ventricular delay in three apical projections was assessed by repeated evaluation of each registered data set. Variability (measured by the coefficient of variation) ranged between 18 and 56% for the peak systolic velocities and between 32 and 117% for the time intervals. Conclusion The reproducibility of the tissue Doppler echocardiography parameters (peak systolic myocardial velocity and intra-ventricular delay) was poor in our set of patients with dilated left ventricles and low ejection fraction. The most probable causes of our poor results are discussed including the missing standardization of the TDI measurements.
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