![]() Atrial flutter: clinical risk factors and adverse outcomes in the Framingham Heart Study. Rahman F, Wang N, Yin X, Ellinor PT, Lubitz SA, LeLorier PA, et al. ![]() Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. 2002 113(5):359–64.īenjamin EJ, Wolf PA, D'Agostino RB, Silbershatz H, Kannel WB, Levy D. A population-based study of the long-term risks associated with atrial fibrillation: 20-year follow-up of the Renfrew/Paisley study. Stewart S, Hart CL, Hole DJ, McMurray JJ. 2012 focused update of the ESC Guidelines for the management of atrial fibrillation: an update of the 2010 ESC Guidelines for the management of atrial fibrillation. doi: 10.1016/j.ccl.2015.12.002Ĭamm AJ, Lip GY, De Caterina R, Savelieva I, Atar D, Hohnloser SH, et al. The epidemiology of atrial fibrillation and stroke. Pistoia F, Sacco S, Tiseo C, Degan D, Ornello R, Carolei A. More trials at low risk of bias and low risk of random errors assessing the clinical effects of digoxin are needed. The long-term effect of digoxin is unclear, as no trials reported long-term follow-up. Digoxin seems to be superior compared with placebo in reducing the heart rate, but inferior compared with beta blockers. The clinical effects of digoxin on all-cause mortality, serious adverse events, quality of life, heart failure, and stroke are unclear based on current evidence. Meta-analysis on acute conversion to sinus rhythm showed that digoxin compared with amiodarone reduced the probability of converting atrial fibrillation to sinus rhythm, but TSA showed that we lacked information (RR, 0.54 TSA-adjusted CI, 0.13 to 2.21 I2 = 0%). Meta-analyses on acute heart rate control showed that digoxin was inferior compared with both calcium antagonists (MD, 21.0 bpm TSA-adjusted CI, -30.3 to 72.3) and with amiodarone (MD, 14.7 bpm TSA-adjusted CI, -0.58 to 30.0 I2 = 42%), but in both comparisons TSAs showed that we lacked information. Our analyses on acute heart rate control (within 6 hours of treatment onset) showed firm evidence of digoxin being superior compared with placebo (mean difference (MD), -12.0 beats per minute (bpm) TSA-adjusted CI, -17.2 to -6.76 I2 = 0%) and inferior compared with beta blockers (MD, 20.7 bpm TSA-adjusted CI, 14.2 to 27.2 I2 = 0%). ![]() When digoxin was compared with all control interventions in one analysis, we found no evidence of a difference on all-cause mortality (risk ratio (RR), 0.82 TSA-adjusted confidence interval (CI), 0.02 to 31.2 I2 = 0%) serious adverse events (RR, 1.65 TSA-adjusted CI, 0.24 to 11.5 I2 = 0%) quality of life heart failure (RR, 1.05 TSA-adjusted CI, 0.00 to 1141.8 I2 = 51%) and stroke (RR, 2.27 TSA-adjusted CI, 0.00 to 7887.3 I2 = 17%). All were at high risk of bias and reported only short-term follow-up. We used GRADE to assess the quality of the body of evidence.Ģ8 trials (n = 2223 participants) were included. We used Trial Sequential Analysis (TSA) to control for random errors. We performed both random-effects and fixed-effect meta-analyses and chose the more conservative result as our primary result. ![]() Our secondary outcomes were heart failure, stroke, heart rate control, and conversion to sinus rhythm. Our primary outcomes were all-cause mortality, serious adverse events, and quality of life. We searched CENTRAL, MEDLINE, Embase, LILACS, SCI-Expanded, BIOSIS for eligible trials comparing digoxin versus placebo, no intervention, or other medical interventions in patients with atrial fibrillation or atrial flutter in October 2016. Our objective was to assess the benefits and harms of digoxin for atrial fibrillation and atrial flutter based on randomized clinical trials. During recent years, systematic reviews of observational studies have compared digoxin to no digoxin in patients with atrial fibrillation or atrial flutter, and the results of these reviews suggested that digoxin seems to increase the risk of all-cause mortality regardless of concomitant heart failure.
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