One-Year Landmark Analysis of the Effect of Beta-Blocker Dose on Survival After Acute Myocardial Infarction.

Background Although beta-blockers are recommended following myocardial infarction (MI), the benefits of long-term treatment have not been established. The study's aim was to evaluate beta-blocker efficacy by dose in 1-year post-MI survivors. Methods and Results The OBTAIN (Outcomes of Beta-Blocker Therapy After Myocardial Infarction) registry included 7057 patients with acute MI, with 6077 one-year survivors. For this landmark analysis, beta-blocker dose status was available in 3004 patients and analyzed by use (binary) and dose at 1 year after MI. Doses were classified as no beta-blocker and >0% to 12.5%, >12.5% to 25%, >25% to 50%, and >50% of target doses used in randomized clinical trials. Age was 63 to 64 years, and approximately two thirds were men. Median follow-up duration was 1.05 years (interquartile range, 0.98-1.22). When analyzed dichotomously, beta-blocker therapy was not associated with improved survival. When analyzed by dose, propensity score analysis showed significantly increased mortality in the no-beta-blocker group (hazard ratio,1.997; 95% CI, 1.118-3.568; P<0.02), the >0% to 12.5% group (hazard ratio, 1.817; 95% CI, 1.094-3.016; P<0.02), and the >25% to 50% group (hazard ratio, 1.764; 95% CI, 1.105-2.815; P<0.02), compared with the >12.5% to 25% dose group. The mortality in the full-dose group was not significantly higher (hazard ratio, 1.196; 95% CI, 0.687-2.083). In subgroup analyses, only history of congestive heart failure demonstrated significant interaction with beta-blocker effects on survival. Conclusions This analysis suggests that patients treated with >12.5% to 25% of the target dose used in prior randomized clinical trials beyond 1 year after MI may have enhanced survival compared with no beta-blocker and other beta-blocker doses. A new paradigm for post-MI beta-blocker therapy is needed that addresses which patients should be treated, for how long, and at what dose.

Reduction of RV pacing by continuous optimization of the AV interval.

BACKGROUND: In patients requiring permanent pacing, preservation of intrinsic ventricular activation is preferred whenever possible. The Search AV+ (SAV+) algorithm in Medtronic EnPulsetrade mark dual-chamber pacemakers can increase atrioventricular (AV) intervals to 320 ms in patients with intact or intermittent AV conduction. This prospective, multicenter study compared the percentage of ventricular pacing with and without AV interval extension. METHODS: Among 197 patients enrolled in the study, the percentage of ventricular-paced beats was evaluated via device diagnostics at the 1-month follow-up. Patient cohorts were defined by clinician assessment of conduction via a 1:1 AV conduction test at the 2-week follow-up. The observed percentage of ventricular pacing with SAV + ON and the predicted percentage of ventricular pacing with SAV + OFF were determined from the SAV + histogram data for the period between the 2-week and 1-month follow-up visits. RESULTS: Of 197 patients, 110 (55.8%) had intact 1:1 AV conduction, of which 109 had 1-month data. SAV + remained ON in 99/109 patients; 10 patients had intrinsic A-V conduction intervals beyond SAV + nominal and therefore SAV + disabled. The mean percentage of ventricular pacing in the 109 patients was SAV+ ON = 23.1% (median 3.7%) versus SAV + OFF = 97.2% (median 99.7%). In 87 patients without 1:1 AV conduction, SAV + was programmed OFF in 6, automatically disabled in 52, and remained ON in 29. In 8 of these patients, 80-100% reduction in ventricular pacing was observed with SAV + ON. CONCLUSION: The Search AV+ algorithm in the EnPulse pacemaker effectively promotes intrinsic ventricular activation and substantially reduces unnecessary ventricular pacing.

Automatic measurement of atrial pacing thresholds in dual-chamber pacemakers: clinical experience with atrial capture management.

BACKGROUND: The Medtronic EnPulse pacemaker incorporates the new atrial capture management (ACM) algorithm to automatically measure atrial capture thresholds and subsequently manage atrial pacing outputs. OBJECTIVES: The purpose of this study was to evaluate the clinical performance of ACM. METHODS: Two hundred patients with an indication for a dual-chamber pacemaker underwent implantation. ACM thresholds and manually measured atrial pacing thresholds were assessed at follow-up visits. Clinical equivalence was defined as the ACM-measured threshold being within -0.25 V to +0.5 V of the manually measured threshold. The clinician analyzed all ACM measurements performed in-office for evidence of proarrhythmia. RESULTS: All 200 implanted patients had a 1-month visit, and validated manual and in-office ACM threshold data were available for 123 patients. The ACM threshold was 0.595 +/- 0.252 V, and the manual threshold was 0.584 +/- 0.233 V. The mean difference was 0.010 V with a 95% confidence interval of (-0.001, 0.021). The mean difference over all visits was 0.011 V. For all patients, the individual threshold differences were within the range of clinical equivalence at all visits. No atrial arrhythmias were observed during 892 ACM tests in 193 patients. CONCLUSION: This study demonstrated that the ACM algorithm is safe, accurate, and reliable over time. ACM was demonstrated to be clinically equivalent to the manual atrial threshold test in all patients at 1 month and over the entire follow-up period of up to 6 months. ACM ensures atrial capture, may save time during follow-up, and can be used to manage atrial pacing outputs.