Objectives. Evaluate the effects of a 6-month High Intensity Interval Training (HIIT) program on (1) functional capacity and health-related quality of life, (2) multiple blood biomarkers, (3) echocardiographic parameters, and (4) exercise performance, in patients in cardiac resynchronization therapy (CRT) stratified by the presence of atrial fibrillation (AF), targeting the following questions: (1) Does CRT provide similar benefits in patients in AF and sinus rhythm (SR)?; and (2) Does HIIT provides similar benefits in patients in AF and SR? Design. Estimates were available at baseline and 6 months after CRT implantation in 37 patients with heart failure. Patients were randomized after CRT to a 24-week HIIT group or to a usual care group (CON). In this sub-analysis, HIIT (AF ¼ 7; SR ¼ 11) and CON (AF ¼ 9; SR ¼ 10) were stratified by the presence of AF. Results. Patients in AF benefitted to a lesser degree from CRT in functional status than patients in SR (23.8-46.0%). However, HIIT induced superior improvements in patients in AF compared to CON (23.9-61.0%). Decreases in TNF-a (8.5-42.9%), BNP (15.3-34.6%) and left ventricular mass (9.6-26.2%) were only observed in patients in SR, whereas increases in peak oxygen uptake were only observed in patients in . HIIT improved exercise capacity (8.8-59.4%) in patients in SR. Conclusions. Patients in AF or SR undergoing CRT demonstrated distinct benefits from device implantation and from HIIT as an adjunctive therapeutic strategy. This suggests that both mainstay and adjunctive therapeutics may need to be managed differently in patients in AF and SR. ARTICLE HISTORY

Purpose Recurrence of atrial fibrillation (AF) after catheter ablation is common, being clinically relevant to identify predictors of recurrence. The left atrial appendage (LAA) role as an AF trigger is scarcely explored. Our aim was to identify if LAA volume is an independent predictor of AF recurrence after catheter ablation. Methods We analysed 52 patients (aged 54 ± 10 years, 58% male) with paroxysmal and persistent AF who underwent a first AF catheter ablation and had performed contrast-enhanced cardiac computed tomography (CT) prior to the procedure. Results The mean left atrial and LAA volumes measured by cardiac CT were 98.9 ± 31.8 and 9.3 ± 3.5 mL, respectively. All patients received successful pulmonary vein isolation and were followed up for 24 months. AF recurrence occurred in 17 patients (33%). LAA volume was significantly greater in patients with AF recurrence than in those without recurrence (11.3 ± 2.9 vs. 8.2 ± 3.4 mL; p = 0.002). Multivariable analysis using Cox regression revealed that LAA volume (hazard ratio 1.32; 95% confidence interval 1.12-1.55; p = 0.001) and persistent AF (hazard ratio 4.22; 95% confidence interval 1.48-12.07; p = 0.007) were independent predictors for AF recurrence. An LAA volume greater than 8.825 mL predicted AF recurrence with 94% sensitivity and 66% specificity. The Kaplan-Meier analysis showed a lower rate free from AF recurrence in the group with an LAA volume >8.825 mL (p < 0.001).Conclusions Larger LAA volume was associated with AF recurrence after catheter ablation in patients with paroxysmal and persistent AF.

Slowed atrial conduction may contribute to reentry circuits and vulnerability for atrial fibrillation (AF). The autonomic nervous system (ANS) has modulating effects on electrophysiological properties. However, complex interactions of the ANS with the arrhythmogenic substrate make it difficult to understand the mechanisms underlying induction and maintenance of AF. Aim: To determine the effect of acute ANS modulation in atrial activation times in patients (P) with paroxysmal AF (PAF). Methods and results: 16P (9 men; 59 ± 14 years) with PAF, who underwent electrophysiological study before AF ablation, and 15P (7 men; 58 ± 11 years) with atrioventricular nodal reentry tachycardia, without documentation or induction of AF (control group). Each group included 7P with arterial hypertension but without underlying structural heart disease. The study was performed while off drugs. Multipolar catheters were placed at the high right atrium (HRA), right atrial appendage (RAA), coronary sinus (CS) and His bundle area (His). At baseline and with HRA pacing (600 ms, shortest propagated S2) we measured: i) intraatrial conduction time (IACT, between RAA and atrial deflection in the distal His), ii) inter-atrial conduction time (interACT, between RAA and distal CS), iii) left atrial activation time (LAAT, between atrial deflection in the distal His and distal CS), iv) bipolar electrogram duration at four atrial sites (RAA, His, proximal and distal CS). In the PAF group, measurements were also determined during handgrip and carotid sinus massage (CSM), and after pharmacological blockade of the ANS (ANSB). AF was induced by HRA programmed stimulation in 56% (self-limited -6; sustained -3), 68.8% (self-limited -6; sustained -5), and 50% (selflimited -5; sustained -3) of the P, in basal, during ANS maneuvers, and after ANSB, respectively (p = NS). IACT, interACT and LAAT significantly lengthened during HRA pacing in both groups (600 ms, S2). P with PAF have longer IACT (p b 0.05), a higher increase in both IACT, interACT (p b 0.01) and electrograms duration (p b 0.05) with S2, and more fragmented activity, compared with the control group. Atrial conduction times and electrograms duration were not significantly changed during ANS stimulation. Nevertheless, ANS maneuvers increased heterogeneity of the local electrograms duration. Also, P with sustained AF showed longer interACT and LAAT during CSM. Conclusion: Atrial conduction times, electrograms duration and fractionated activity are increased in PAF, suggesting a role for conduction delays in the arrhythmogenic substrate. Acute vagal stimulation is associated with prolonged interACT and LAAT in P with inducible sustained AF and ANS modulation may influence the heterogeneity of atrial electrograms duration.

Complete atrioventricular block conferred a worse outcome during hospitalisation, including a higher incidence of cardiogenic shock, ventricular arrhythmias and death.