Ventricular arrhythmias in arrhythmic mitral valve syndrome-a prospective continuous long-term cardiac monitoring study.

AIMS: Arrhythmic mitral valve syndrome is linked to life-threatening ventricular arrhythmias. The incidence, morphology and methods for risk stratification are not well known. This prospective study aimed to describe the incidence and the morphology of ventricular arrhythmia and propose risk stratification in patients with arrhythmic mitral valve syndrome. METHODS: Arrhythmic mitral valve syndrome patients were monitored for ventricular tachyarrhythmias by implantable loop recorders (ILR) and secondary preventive implantable cardioverter-defibrillators (ICD). Severe ventricular arrhythmias included ventricular fibrillation, appropriate or aborted ICD therapy, sustained ventricular tachycardia and non-sustained ventricular tachycardia with symptoms of hemodynamic instability. RESULTS: During 3.1 years of follow-up, severe ventricular arrhythmia was recorded in seven (12%) of 60 patients implanted with ILR [first event incidence rate 4% per person-year, 95% confidence interval (CI) 2-9] and in four (20%) of 20 patients with ICD (re-event incidence rate 8% per person-year, 95% CI 3-21). In the ILR group, severe ventricular arrhythmia was associated with frequent premature ventricular complexes, more non-sustained ventricular tachycardias, greater left ventricular diameter and greater posterolateral mitral annular disjunction distance (all P < 0.02). CONCLUSIONS: The yearly incidence of ventricular arrhythmia was high in arrhythmic mitral valve syndrome patients without previous severe arrhythmias using continuous heart rhythm monitoring. The incidence was even higher in patients with secondary preventive ICD. Frequent premature ventricular complexes, non-sustained ventricular tachycardias, greater left ventricular diameter and greater posterolateral mitral annular disjunction distance were predictors of first severe arrhythmic event.

Effect of continuous positive airway pressure therapy on recurrence of atrial fibrillation after pulmonary vein isolation in patients with obstructive sleep apnea: A randomized controlled trial.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with atrial fibrillation (AF). Whether treatment with continuous positive airway pressure (CPAP) reduces AF recurrence after catheter ablation with pulmonary vein isolation (PVI) is unknown. OBJECTIVE: The purpose of this study was to assess the effect of CPAP treatment on the recurrence and burden of AF after PVI in patients with OSA. METHODS: We randomized patients with paroxysmal AF and an apnea-hypopnea index (AHI) ≥15 events/hour to treatment with CPAP or standard care. Heart rhythm was monitored by an implantable loop recorder. AF recurrence after PVI was defined as any episode of AF lasting >2 minutes after a 3-month blanking period. RESULTS: PVI was performed in 83 patients. Thirty-seven patients were randomized to CPAP treatment and 46 patients to standard care. The AHI was reduced from 26.7 ± 14 events/hour to 1.7 ± 1.3 events/hour at follow-up in the CPAP group (P = .001). A total of 57% of patients in both the CPAP group and the standard care group had at least 1 episode of AF 3-12 months after PVI (P for difference = 1). AF burden after ablation was reduced in both groups, with no between-group difference (P = .69). CONCLUSION: In patients with paroxysmal AF and OSA, treatment with CPAP did not further reduce the risk of AF recurrence after ablation. PVI considerably reduced the burden of AF in OSA patients, without any difference between groups.

A New Era in Epicardial Access for the Ablation of Ventricular Arrhythmias: The Epi-Co2 Registry.

OBJECTIVES: This multicenter registry aimed to assess the reproducibility and safety of intentional coronary vein exit and carbon dioxide insufflation to facilitate subxiphoid epicardial access in the setting of ventricular tachycardia ablation. BACKGROUND: Epicardial ablation for ventricular tachycardia is not a widespread technique due to the significant potential complications associated with subxiphoid puncture. The first experience in 12 patients showed that intentional coronary vein exit and carbon dioxide insufflation was technically feasible. METHODS: A branch of the coronary sinus was cannulated by means of a diagnostic JR4 coronary catheter. Intentional perforation at the distal portion of that branch was performed with a high tip load 0.014-inch angioplasty wire. A microcatheter was advanced over the wire into the pericardial space. Carbon dioxide was then insufflated into the pericardial space, allowing direct visualization of the anterior pericardial space to facilitate subxiphoid puncture. RESULTS: Intentional coronary vein exit was attempted in 102 consecutive patients in 16 different centers and successfully completed in 101 patients. Significant pericardial adhesions were confirmed in 3 patients, preventing carbon dioxide insufflation and epicardial ablation. None of the punctures were complicated with inadvertent right ventricular puncture or damage to a coronary artery. Significant bleeding (>80 ml) due to coronary vein exit occurred in 5 patients, without hemodynamic compromise. None of the patients required surgery. CONCLUSIONS: Coronary vein exit and carbon dioxide insufflation can be safely and reproducibly achieved to facilitate subxiphoid pericardial access in the setting of ventricular tachycardia ablation.

A randomized invasive cardiac electrophysiology study of the combined ion channel blocker AZD1305 in patients after catheter ablation of atrial flutter.

BACKGROUND: This study assessed the cardiac electrophysiological and hemodynamic effects of an intravenous infusion of the combined ion channel blocker AZD1305. METHODS: After successful ablation of atrial flutter, patients were randomized to receive placebo (n = 12) or AZD1305 (n = 38) in 4 ascending dose groups. Electrophysiological and hemodynamic measurements were performed before and commencing 20 minutes after start of infusion. RESULTS: Left atrial effective refractory period increased dose and the primary outcome measure increased dose and plasma concentration dependently, with a mean increase of 55 milliseconds in dose group 3. There was a corresponding increase in right atrial effective refractory period of 84 milliseconds. The right ventricular effective refractory period and the paced QT interval also increased dose and concentration dependently, by 59 and 70 milliseconds, respectively, in dose group 3. There were indications of moderate increases of atrial, atrioventricular nodal, and ventricular conduction times. No consistent changes in intracardiac pressures were observed, but there was a small transient decrease in systolic blood pressure. Adverse events were consistent with the study population and procedure, and there were no signs of proarrhythmia despite marked delay in ventricular repolarization in some individuals. CONCLUSIONS: AZD1305 shows electrophysiological characteristics indicative of potential antiarrhythmic efficacy in atrial fibrillation.

Effects of angiotensin receptor blockade on serial P-wave signal-averaged electrocardiograms after electrical cardioversion of persistent atrial fibrillation.

AIMS: To evaluate the effects of the angiotensin II type 1 receptor blocker candesartan on P-wave signal-averaged electrocardiogram (P-SAECG) after electrical cardioversion in patients with atrial fibrillation (AF). METHODS AND RESULTS: One hundred and seventy-one patients with persistent AF were randomized to receive candesartan 8 mg/day or placebo for 3-6 weeks before and candesartan 16 mg/day or placebo for 6 months after electrical cardioversion. P-SAECG was recorded in 114 patients (57 in each treatment group) after cardioversion and repeated in those with sinus rhythm at 1 and 6 weeks, and 3 and 6 months. Filtered P-wave duration (FPD), root-mean-squared (RMS) voltages of the terminal 40 ms of the filtered P-wave, RMS voltage of the entire filtered P-wave, and the integral of the voltages in the entire PD were analysed. No effects of candesartan were observed on any P-SAECG parameter at baseline. In the subgroup of patients in sinus rhythm after 6 months, FPD was significantly shorter both at baseline (151 +/- 16 vs. 163 +/- 16 ms) and at 6 months (143 +/- 12 vs. 153 +/- 15 ms) in the candesartan (n = 15) compared with the placebo group (n = 21). CONCLUSION: Treatment with candesartan was associated with a shorter FPD in patients remaining in sinus rhythm for 6 months.

The Mitral Annulus Disjunction Arrhythmic Syndrome.

BACKGROUND: Mitral annulus disjunction (MAD) is an abnormal atrial displacement of the mitral valve leaflet hinge point. MAD has been associated with mitral valve prolapse (MVP) and sudden cardiac death. OBJECTIVES: The purpose of this study was to describe the clinical presentation, MAD morphology, association with MVP, and ventricular arrhythmias in patients with MAD. METHODS: The authors clinically examined patients with MAD. By echocardiography, the authors assessed the presence of MVP and measured MAD distance in parasternal long axis. Using cardiac magnetic resonance (CMR), the authors assessed circumferential MAD in the annular plane, longitudinal MAD distance, and myocardial fibrosis. Aborted cardiac arrest and sustained ventricular tachycardia were defined as severe arrhythmic events. RESULTS: The authors included 116 patients with MAD (age 49 ± 15 years; 60% female). Palpitations were the most common symptom (71%). Severe arrhythmic events occurred in 14 (12%) patients. Longitudinal MAD distance measured by CMR was 3.0 mm (interquartile range [IQR]: 0 to 7.0 mm) and circumferential MAD was 150° (IQR: 90° to 210°). Patients with severe arrhythmic events were younger (age 37 ± 13 years vs. 51 ± 14 years; p = 0.001), had lower ejection fraction (51 ± 5% vs. 57 ± 7%; p = 0.002) and had more frequently papillary muscle fibrosis (4 [36%] vs. 6 [9%]; p = 0.03). MVP was evident in 90 (78%) patients and was not associated with ventricular arrhythmia. CONCLUSIONS: Ventricular arrhythmias were frequent in patients with MAD. A total of 26 (22%) patients with MAD did not have MVP, and MVP was not associated with arrhythmic events, indicating MAD itself as an arrhythmogenic entity. MAD was detected around a large part of the mitral annulus circumference and was interspersed with normal tissue.

Lower than expected burden of premature ventricular contractions impairs myocardial function.

AIMS: We aimed to explore the burden of frequent premature ventricular contractions (PVCs) associated with myocardial dysfunction in patients with outflow tract arrhythmia (OTA). We hypothesized that this threshold is lower than the previously suggested threshold of 24 000 PVCs/24 h (24%PVC) when systolic function is assessed by strain echocardiography. Furthermore, we aimed to characterize OTA patients with malignant arrhythmic events. METHODS AND RESULTS: We included 52 patients referred for OTA ablation (46 ± 12 years, 58% female). Left ventricular global longitudinal strain (GLS) and mechanical dispersion were assessed by speckle tracking echocardiography. A subset underwent cardiac magnetic resonance imaging. PVC burden (%PVC) was assessed by Holter recording. Sinus rhythm QRS duration and PVC QRS duration were recorded from electrocardiogram, and the ratio was calculated (PVC QRS duration / sinus rhythm QRS duration). Median %PVC was 7.2 (0.2-60.0%). %PVC correlated with GLS (R = 0.44, P = 0.002) and with mechanical dispersion (R = 0.48, P < 0.001), but not with ejection fraction (R = 0.22, P = 0.12). %PVC was higher in patients with impaired systolic function by GLS (worse than -18%) compared with patients with normal function (22% vs. 5%, P = 0.001). Greater than 8%PVC optimally identified patients with abnormal GLS (area under the curve 0.79). Serious arrhythmic events occurred in 11/52 (21%) patients characterized by high QRS ratios (1.56 vs. 1.91, P < 0.001). CONCLUSIONS: More than 8%PVC was associated with impaired systolic function by GLS, which is a lower threshold than previously reported. Patients with serious arrhythmic events had higher QRS ratios, which may represent a more malignant phenotype of OTA.

Strain echocardiographic assessment of left atrial function predicts recurrence of atrial fibrillation.

AIMS: We evaluated if a dispersed left atrial (LA) contraction pattern was related to atrial fibrillation (AF) in patients with normal left ventricular (LV) function, and normal or mildly enlarged left atrium. METHODS AND RESULTS: We included 61 patients with paroxysmal AF (PAF). Of these, 30 had not while 31 had recurrence of AF after radiofrequency ablation (RFA). Twenty healthy individuals were included for comparison. Echocardiography was performed in patients in sinus rhythm the day before RFA. LA volume was calculated. Peak negative longitudinal strain was assessed in 18 LA segments during atrial systole. Contraction duration in 18 LA segments was measured as the time from peak of the P wave on electrocardiogram to maximum myocardial shortening in each segment. The standard deviation of contraction durations was defined as LA mechanical dispersion (LA MD). LA size was rather preserved in patients with PAF (LA volume 25 ± 10 mL/m(2)). LA MD was more pronounced in patients with recurrence of AF after RFA compared with those without recurrence and controls (38 ± 14 ms vs. 30 ± 12 ms vs. 16 ± 8 ms, both P < 0.001). LA MD was a predictor of PAF [OR 7.84 (95%CI 2.15-28.7), P < 0.01, per 10 ms increase] adjusted for age, LA volume, e', and LA function. LA function by strain was reduced in both patients with and without recurrent AF after RFA compared with controls (-14 ± 4% vs. -16 ± 3% vs. -19 ± 2%, both P < 0.05). CONCLUSION: LA MD was pronounced, and LA deformation was reduced in patients with PAF with apparently normal LV structure and function, and normal or mildly enlarged LA. LA MD may be useful as a predictor of AF recurrence after RFA.

Effects of short-term exercise training on symptoms and quality of life in patients with chronic atrial fibrillation.

BACKGROUND: A randomised study was conducted to determine if short-term exercise training in patients with chronic atrial fibrillation (AF) might improve symptoms and health-related quality of life (HRQoL). METHODS: AF patients (64+/-7 years) were randomised to exercise training (n=15) or a 2-month control period (n=15) followed by an exercise training program (ETP). The ETP consisted of 24 training sessions with aerobic exercise and muscle strengthening. A cycle ergometer test, with recording of perceived exertion on the Borg scale, was performed. The participants completed HRQoL questionnaires, the Short-Form 36 (SF-36) and Symptom and Severity Checklist (SSCL), before and after training. Because there were no changes after two months in the control group, pooled data for all patients are presented before and after training. RESULTS: Four of the eight SF-36 scales improved significantly (p<0.05) following training: physical functioning (82+/-14 pre-ETP, 86+/-10 post-ETP), bodily pain (82+/-17 pre-ETP, 92+/-14 post-ETP), vitality (61+/-14 pre-ETP, 68+/-13 post-ETP) and role-emotional (85+/-28 pre-ETP, 94+/-20 post-ETP). The SF-36 physical component summary scale also increased from 49+/-6 pre-ETP to 52+/-6 post-ETP (p<0.05). Significant improvements were also observed for summary and specific symptom scores of the SSCL. Exercise capacity improved by 41+/-20% and perceived exertion during testing by 1.4 points after training (p<0.05 for both). CONCLUSIONS: The study demonstrates a significant improvement in HRQoL, symptoms during exercise testing and exercise capacity after a short-term exercise training program in patients with chronic AF.

Short-term exercise training in patients with chronic atrial fibrillation: effects on exercise capacity, AV conduction, and quality of life.

PURPOSE: A randomized study was conducted to determine whether short-term exercise training in patients with chronic atrial fibrillation (AF) might improve exercise capacity and quality of life (QOL), and influence atrioventricular conduction. METHODS: Atrial fibrillation patients (age 64 +/- 7 years) were randomized to exercise training (n = 15) or a 2-month control period (n = 15) followed by the training program. Twenty-four training sessions consisted of aerobic exercise and muscle strengthening. A cycle ergometer test and a 15-minute resting high-frequency spectral electrocardiogram analysis were performed and a QOL questionnaire (SF-36) was completed before and after training. Because there were no changes after 2 months in the control group, pooled data for all patients are presented before and after training. RESULTS: Cumulated work at Borg scale 17 increased by 41% +/- 36%. Heart rate at rest and after 10 minutes of exercise decreased from 75 +/- 14 to 68 +/- 14 bpm and 145 +/- 19 to 137 +/- 21 bpm, respectively. HF increased from 81 +/- 17 to 91 +/- 22 milliseconds. Four of the 8 scales and 1 of the 2 summary scales of the Short-Form-36 improved. P <.05 for all results. CONCLUSIONS: Exercise capacity, heart rate variability, and QOL improved after 2 months of exercise training in patients with chronic AF. Heart rates at rest and during exercise decreased.

Effects of ablation, digitalis, and beta-blocker on dual atrioventricular nodal pathways and conduction during atrial fibrillation.

INTRODUCTION: Modification of AV nodal conduction by radiofrequency ablation (RFA) results in a variable reduction in heart rate during atrial fibrillation (AF). Using AF induced in patients with dual AV nodal pathways as a model, we tested the effect of additional treatment with digitalis (ouabain) and beta-blocker (esmolol). METHODS AND RESULTS: Ten patients were randomized to control (group I) and studied only before ablation. AF was induced in 30 patients before and after slow pathway ablation (group II). Mean ventricular cycle lengths (AF CLmean) were recorded. Slow pathway conduction was eliminated after ablation in 10 patients (group IIA), whereas slow pathway conduction was still present in 20 patients (group IIB). Compared to pre-RFA there was a 10% increase in AF CLmean post-RFA (P < 0.01). During isoproterenol infusion the increase was 8% (P = NS). Adding digitalis and beta-blocker during isoproterenol infusion increased AF CLmean by 75% (95% in group IIA) compared to 36% in group I (P < 0.001 II vs I). CONCLUSION: Slow pathway ablation reduces ventricular rate during AF. Addition of digitalis and beta-blocker during isoproterenol infusion significantly decreases ventricular rate after ablation compared to the control group. The finding suggests that beta-blocker has significant effects on fast AV nodal pathway conduction during induced AF with isoproterenol infusion.

Dual AV nodal pathways and conduction during atrial fibrillation.

OBJECTIVE: AV node modification reduces ventricular rate during atrial fibrillation (AF). We induced AF in patients with dual AV nodal pathways before and after radiofrequency ablation (RFA) of AV nodal reentry tachycardia (AVNRT) and examined the role of the two pathways in the transmission of impulses during AF. DESIGN AND RESULTS: AF was induced in 30 patients before and after slow pathway ablation. Before RFA mean (AF CLmean) and shortest (AF CLshort) ventricular cycle lengths correlated significantly to ERPf, ERPs, and antegrade Wenckebach block (r = 0.53-0.67). Ablation eliminated slow pathway conduction completely in 10 patients (group A), whereas in 20 patients some slow pathway conduction was still present (group B). After RFA there was a 10% increase in AF CLmean (20%, p < 0.05 in A and 5%, p = NS in B) and 7% in AF CLshort (11%, p = NS in A and 6%, p = NS in B). During isoproterenol infusion after RFA AF CLmean increased 8% (p < 0.05) (14% in A and 6% in B; p < 0.05 in both groups). The effects of RFA were mainly confined to patients with ERPs less than the median value (13% vs 3% in those above median, respectively; p < 0.05). CONCLUSION: The refractory periods of the AV nodal pathways are the main determinants of ventricular rate during induced AF. Slow pathway ablation reduces ventricular rate during AF. This effect was greatest when slow pathway conduction was completely eliminated. A short ERPs predicted a greater reduction in ventricular rate.