Objective: The objective of the current study was to determine the clinical factors that were associated with abandonment of a rate-control or a rhythm-control strategy in patients with atrial fibrillation(AF). Backgr...Objective: The objective of the current study was to determine the clinical factors that were associated with abandonment of a rate-control or a rhythm-control strategy in patients with atrial fibrillation(AF). Background: Although the AFFIRM Study demonstrated that outcomes are similar with a primary strategy of rate-control or rhythm-control for AF, there may be clinical or demographic factors associated with abandonment of the initial treatment strategy. Knowledge of these risk factors would be useful so that patients may be given appropriate initial therapy and, as appropriate, switched to alternative treatments earlier. Methods: Patients in the AFFIRM Study were subdivided into those who were maintained on their initial treatment strategy versus those who abandoned initial treatment strategy for alternative therapies. We determined the clinical and demographic factors associated with change in initial treatment strategy. Results: At 5 years the original treatment strategy was maintained in 85%of the patients in the rate-control arm versus 62%of those in the rhythm-control arm(P< .0001). Length of the qualifying episode of AF was associated with abandonment of both rhythm-control and rate-control strategies. Antiarrhythmic drug failure before randomization and a history of thyroid disease also were associated with abandonment of rhythm-control. Patients were more likely to maintain rate-control if they already had an implanted pacemaker or if they were older than 75 years, while an ejection fraction < 30%was associated with abandonment of the rate-control strategy. Conclusions: In patients with AF, rhythm-control strategies are abandoned significantly more often than rate-control strategies. Patients with long durations of AF on presentation or previous antiarrhythmic drug failure might be considered for rate-control as initial treatment.展开更多
Background -Right ventricular apical(RVA) pacing creates abnormal left ventricular contraction, hypertrophy, and reduced pump function. The adverse effects of ventricular desynchronization may explain the association ...Background -Right ventricular apical(RVA) pacing creates abnormal left ventricular contraction, hypertrophy, and reduced pump function. The adverse effects of ventricular desynchronization may explain the association of RVA pacing with an increased risk of heart failure hospitalization(HFH) in clinical trials. Methods and Results -Baseline and postimplantation variables were used to predict HFH in the Mode Selection Trial, a 2010-patient, 6-year trial of dual-chamber(DDDR) versus ventricular(VVIR) pacing in sinus node dysfunction. A Cox model showed that New York Heart Association(NYHA) class at baseline and follow-up predicted HFH(hazard ratio[HR], 3.99; 95%confidence interval[CI], 2.74-5.79 for NYHA class III/IV and HR, 2.17; 95%CI, 1.54-3.04 for NYHA class II versus class I); other predictors were heart failure(HR, 2.30; 95%CI, 1.70-3.11),atrioventricular(AV) block(HR, 1.48;95%CI, 1.11-1.97), and myocardial infarction(MI)(HR, 1.37; 95%CI, 1.00-1.86). Postimplantation predictors were VVIR cumulative percent ventricular pacing(Cum%VP) >80(HR, 3.58; 95%CI, 1.72-7.45),DDDR Cum%VP >40 or VVIR Cum%VP ≤80(HR, 1.81; 95%CI, 0.94-3.50) versus DDDR Cum%VP ≤40; whether QRS duration(QRSd) was paced or spontaneous(HR, 2.21; 95%CI, 1.39-3.54; spontaneous versus paced); and drugs for atrial fibrillation(HR, 1.60; 95%CI, 1.19-2.15). Low baseline ejection fraction(EF) and postimplantation RVA-paced or spontaneous QRSd predicted HFH; the increased risk with QRSd was steeper for normal versus low EF(HR, 1.18; 95%CI, 1.11-1.27; versus HR, 1.08; 95%CI, 1.01-1.15; for a 10-ms increase); at a QRSd of ≈200 ms, normal-and low-EF patients had equivalent risk. HFH risk nearly doubled when VVIR Cum%VP was ≤80 or DDDR Cum%VP was >40 versus DDDR Cum%VP ≤40 and was additive with other risk factors. Conclusions -Differences in HFH risk can be explained by interactions between substrate(atrial fibrillation, AV conduction, heart failure, MI, EF) and pacing promoters(ventricular desynchronization-paced QRSd and Cum%VP, and AV desynchro展开更多
文摘Objective: The objective of the current study was to determine the clinical factors that were associated with abandonment of a rate-control or a rhythm-control strategy in patients with atrial fibrillation(AF). Background: Although the AFFIRM Study demonstrated that outcomes are similar with a primary strategy of rate-control or rhythm-control for AF, there may be clinical or demographic factors associated with abandonment of the initial treatment strategy. Knowledge of these risk factors would be useful so that patients may be given appropriate initial therapy and, as appropriate, switched to alternative treatments earlier. Methods: Patients in the AFFIRM Study were subdivided into those who were maintained on their initial treatment strategy versus those who abandoned initial treatment strategy for alternative therapies. We determined the clinical and demographic factors associated with change in initial treatment strategy. Results: At 5 years the original treatment strategy was maintained in 85%of the patients in the rate-control arm versus 62%of those in the rhythm-control arm(P< .0001). Length of the qualifying episode of AF was associated with abandonment of both rhythm-control and rate-control strategies. Antiarrhythmic drug failure before randomization and a history of thyroid disease also were associated with abandonment of rhythm-control. Patients were more likely to maintain rate-control if they already had an implanted pacemaker or if they were older than 75 years, while an ejection fraction < 30%was associated with abandonment of the rate-control strategy. Conclusions: In patients with AF, rhythm-control strategies are abandoned significantly more often than rate-control strategies. Patients with long durations of AF on presentation or previous antiarrhythmic drug failure might be considered for rate-control as initial treatment.
文摘Background -Right ventricular apical(RVA) pacing creates abnormal left ventricular contraction, hypertrophy, and reduced pump function. The adverse effects of ventricular desynchronization may explain the association of RVA pacing with an increased risk of heart failure hospitalization(HFH) in clinical trials. Methods and Results -Baseline and postimplantation variables were used to predict HFH in the Mode Selection Trial, a 2010-patient, 6-year trial of dual-chamber(DDDR) versus ventricular(VVIR) pacing in sinus node dysfunction. A Cox model showed that New York Heart Association(NYHA) class at baseline and follow-up predicted HFH(hazard ratio[HR], 3.99; 95%confidence interval[CI], 2.74-5.79 for NYHA class III/IV and HR, 2.17; 95%CI, 1.54-3.04 for NYHA class II versus class I); other predictors were heart failure(HR, 2.30; 95%CI, 1.70-3.11),atrioventricular(AV) block(HR, 1.48;95%CI, 1.11-1.97), and myocardial infarction(MI)(HR, 1.37; 95%CI, 1.00-1.86). Postimplantation predictors were VVIR cumulative percent ventricular pacing(Cum%VP) >80(HR, 3.58; 95%CI, 1.72-7.45),DDDR Cum%VP >40 or VVIR Cum%VP ≤80(HR, 1.81; 95%CI, 0.94-3.50) versus DDDR Cum%VP ≤40; whether QRS duration(QRSd) was paced or spontaneous(HR, 2.21; 95%CI, 1.39-3.54; spontaneous versus paced); and drugs for atrial fibrillation(HR, 1.60; 95%CI, 1.19-2.15). Low baseline ejection fraction(EF) and postimplantation RVA-paced or spontaneous QRSd predicted HFH; the increased risk with QRSd was steeper for normal versus low EF(HR, 1.18; 95%CI, 1.11-1.27; versus HR, 1.08; 95%CI, 1.01-1.15; for a 10-ms increase); at a QRSd of ≈200 ms, normal-and low-EF patients had equivalent risk. HFH risk nearly doubled when VVIR Cum%VP was ≤80 or DDDR Cum%VP was >40 versus DDDR Cum%VP ≤40 and was additive with other risk factors. Conclusions -Differences in HFH risk can be explained by interactions between substrate(atrial fibrillation, AV conduction, heart failure, MI, EF) and pacing promoters(ventricular desynchronization-paced QRSd and Cum%VP, and AV desynchro
