Closed loop stimulation reduces the incidence of atrial high-rate episodes compared with conventional rate-adaptive pacing in patients with sinus node dysfunctions.

AIMS: Subclinical atrial fibrillation (AF) is associated with increased risk of progression to clinical AF, stroke, and cardiovascular death. We hypothesized that in pacemaker patients requiring dual-chamber rate-adaptive (DDDR) pacing, closed loop stimulation (CLS) integrated into the circulatory control system through intra-cardiac impedance monitoring would reduce the occurrence of atrial high-rate episodes (AHREs) compared with conventional DDDR pacing. METHODS AND RESULTS: Patients with sinus node dysfunctions (SNDs) and an implanted pacemaker or defibrillator were randomly allocated to dual-chamber CLS (n = 612) or accelerometer-based DDDR pacing (n = 598) and followed for 3 years. The primary endpoint was time to the composite endpoint of the first AHRE lasting ≥6 min, stroke, or transient ischaemic attack (TIA). All AHREs were independently adjudicated using intra-cardiac electrograms. The incidence of the primary endpoint was lower in the CLS arm (50.6%) than in the DDDR arm (55.7%), primarily due to the reduction in AHREs lasting between 6 h and 7 days. Unadjusted site-stratified hazard ratio (HR) for CLS vs. DDDR was 0.84 [95% confidence interval (CI), 0.72-0.99; P = 0.035]. After adjusting for CHA2DS2-VASc score, the HR remained 0.84 (95% CI, 0.71-0.99; P = 0.033). In subgroup analyses of AHRE incidence, the incremental benefit of CLS was greatest in patients without atrioventricular block (HR, 0.77; P = 0.008) and in patients without AF history (HR, 0.73; P = 0.009). The contribution of stroke/TIA to the primary endpoint (1.3%) was low and not statistically different between study arms. CONCLUSION: Dual-chamber CLS in patients with SND is associated with a significantly lower AHRE incidence than conventional DDDR pacing.

The point on the treatment of arrhythmic storm.

Arrhythmic storm is a clinical emergency associated with high mortality, which requires multi-disciplinary management. Reprogramming of the implantable cardiac defibrillator (ICD) aimed at reducing shocks, adrenergic blockade using beta-blockers, sedation/anxiolysis, and blockade of the stellate ganglion represent the first simple and effective manoeuvres, but further suppression of arrhythmias with antiarrhythmics is often required. A low-risk patient (e.g. monomorphic ventricular tachycardia, functioning ICD, and haemodynamically stable) should be managed with a beta-blocker (possibly non-selective) plus amiodarone, in addition to sedation with a benzodiazepine or dexmedetomidine; in patients at greater risk (high burden and haemodynamic instability), autonomic modulation with blockade of the stellate ganglion and the addition of a second antiarrhythmic (lidocaine) should be considered. In patients refractory to these measures, with advanced heart failure, general anaesthesia with intubation and the establishment of a haemodynamic circulatory support should be considered. Ablation, performed early, appears to be superior in terms of mortality and reduction of future shocks compared with titration of antiarrhythmics.