Left atrial “stunning” following radiofrequency catheter ablation of chronic atrial flutter

Objectives. This study examined the effect of radiofrequency ablation (RFA) on left atrial (LA) and left atrial appendage (LAA) function in humans with chronic atrial flutter (AFL).Background. Atrial stunning and the development of spontaneous echocardiographic contrast (SEC) is a consequence of electrical cardioversion of AFL to sinus rhythm. This phenomenon has been termed “stunning” and is associated with thrombus formation and embolic stroke. Radiofrequency ablation is now considered to be definitive treatment for chronic AFL, but whether this procedure is complicated by LA stunning is unknown.Methods. Fifteen patients with chronic AFL undergoing curative RFA underwent transesophageal echocardiography to evaluate LA and LAA function and SEC before and immediately, 30 minutes and 3 weeks after RFA. To control for possible direct effects of RFA on atrial function, seven patients undergoing RFA for paroxysmal AFL were also studied. In this group, RF energy was delivered in sinus rhythm and echocardiographic parameters were assessed before and immediately and 30 minutes following RFA.Results. Chronic AFL: Mean arrhythmia duration was 17.2 ± 13.3 months. Twelve patients (80%) developed SEC following RF energy application and reversion to sinus rhythm. LAA velocities decreased significantly from 54.0 ± 14.2 cm/s in AFL to 18.0 ± 7.1 cm/s in sinus rhythm after arrhythmia termination (p < 0.01). These changes persisted for 30 minutes. Following 3 weeks of sustained sinus rhythm, significant improvements in LAA velocities (68.9 ± 23.6 vs. 18.0 ± 7.1 cm/s, p < 0.01) and mitral A-wave velocities (49.8 ± 10.3 vs. 13.4 ± 11.2 cm/s, p < 0.01) were evident and SEC had resolved in all patients. Paroxysmal AFL: Radiofrequency energy delivered in sinus rhythm had no significant effect on any of the above indexes of LA or LAA function and no patient developed SEC following RFA.Conclusions. Radiofrequency ablation of chronic AFL is associated with significant LA stunning and the development of SEC. Left atrial stunning is not secondary to the RF energy application itself. Sustained sinus rhythm for 3 weeks leads to resolution of these acute phenomena. Left atrial stunning occurs in the absence of direct current shock or antiarrhythmic drugs, suggesting that its mechanism may be a function of the preceding arrhythmia rather than the mode of reversion.     

Histopathological substrate of the atrial myocardium in the progression of obstructive sleep apnoea–related atrial fibrillation

Sleep and Breathing - Obstructive sleep apnoea (OSA) is closely related to atrial fibrillation (AF), and OSA-induced atrial structural remodelling is the basis of AF maintenance. However, the...     

Impact of pulmonary vein isolation on atrial vagal activity and atrial electrical remodeling

Objective Mechanisms of pulmonary vein isolation (PVI) for atrial fibrillation remain controversy.This study aimed to investigate the impact of PVI on vagal modulation to atria.Methods Eighteen adult mongrel dogs under general anesthesia were randomly divided into two groups.Bilateral cervical sympathovagal trunks were decentralized and sympathetic effects was blocked by metoprolol administration.Atrial electrical remodeling (AER) was established by rapid right atrial pacing at the rate of 600 bpm for 30 minutes.PVI was performed in group A.Atrial effective refractory period (ERP),vulnerability window (VW) of atrial fibrillation,and sinus rhythm cycle length (SCL) were measured at baseline and during vagal stimulation before and after atrial rapid pacing with and without PVI at fight atrial appendage (RAA),left atrial appendage (LAA),distal coronary sinus (CSd) and proximal coronary sinus (CSp).Results (1) Effects of PVI on vagal modulation:Shortening of SCL during vagal stimulation decreased significantly after PVI compared with that before PVI in group A (P＜0.001).Shortening of ERP during vagal stimulation decreaseed significantly after PVI compared with that before PVI (P＜0.05).VW of atrial fibrillation during vagal stimulation decreased significantly after PVI compared with that before PVI (P＜0.05).(2) Effects of PVI on AER:shortening of ERP before and after atrial rapid pacing increased significantly at baseline and vagal stimulation in group B compared with that in group A (P＜0.05).VW during vagal stimulation increased significantly after atrial rapid pacing in group B (P＜0.05).Conclusion PVI attenuates the vagal modulation to the atria,thereby decreases the susceptibility to atrial fibrillation mediated by vagal activity.PVI releases AER,which maybe contributes to the vagal denervation.Our study indicates that PVI not only can eradicate triggered foci but also modify substrates for AF.(J Geriatr Cardiol 2008;5:28-32)     

Is left atrial fibrosis an independent determinant of atrial fibrillation in mitral stenosis?

We prospectively studied whether left atrial (LA) fibrosis is a determinant of atrial fibrillation (AF) in mitral stenosis in patients who underwent balloon mitral valvotomy. There were 2 groups: Group A (n = 16), with AF and Group B (n = 27), without AF. Fibrosis was assessed by MRI. Patients underwent cardioversion before MRI. There were 27 females and 16 males, aged 29 ± 6 years. The LA areas in Groups A and B were 54.3 ± 4.4 mm² and 39.4 ± 2.3 mm² (p < 0.05) and the LA volume index was 46.2 ± 2.9 ml/m² vs 33 ± 3 ml/m² respectively (p < 0.0001). The presence of LA scarring was not statistically different in the two groups.     

Is time to first recurrence of atrial fibrillation correlated with atrial fibrillation burden?

The time to the first recurrence of atrial fibrillation (AF) and the AF burden have commonly been used as end points for AF therapy. We conducted a retrospective analysis of data from a large pacemaker registry to assess the relation between the time to the first recurrence and the AF burden. Although a statistical association exists, the small correlation coefficients limit the clinical value of the time to first recurrence as an indicator of AF burden.     

Transesophageal echocardiography before cardioversion of recurrent atrial fibrillation: does absence of previous atrial thrombi preclude the need of a repeat test?

Background

Atrial fibrillation (AF) is a recurrent problem that frequently requires repeat cardioversion. Transesophageal echocardiography (TEE) is indicated before cardioversion in patients who are underanticoagulated (warfarin therapy <3 weeks or international normalized ratio [INR] <2.0). It remains uncertain if TEE should be repeated in underanticoagulated patients who had no atrial thrombi detected by previous TEE.

Methods and results

From January 1996 to June 2001, 76 patients (43 men, 33 women; mean age, 68.8 ± 10.4 years) who were underanticoagulated and had no atrial thrombi in previous TEE underwent repeat TEE before cardioversion of recurrent AF. The duration of recurrent AF at the time of the second TEE was 5.1 ± 9.3 months (1 day to 4 years). The underlying diseases included coronary artery disease (n = 30), hypertension (n = 22), valvular heart diseases (n = 8), dilated cardiomyopathy (n = 4), hypertrophic cardiomyopathy (n = 2), and others (n = 10). Eight (10.5%) patients (2 men, 6 women; mean age, 68.6 ± 6.6 years) were found to have intra-atrial thrombi on the second TEE. Of these 8 patients, 3 had coronary artery disease, 1 had hypertension, 2 had dilated cardiomyopathy, 1 had hypertrophic cardiomyopathy, and 1 had AF of unknown cause. The duration of recurrent AF in patients with and without thrombi was not significantly different (3.6 ± 4.7 versus 5.3 ± 9.7 months, P = .22). Of the 8 patients with intra-atrial thrombi on the second TEE, 5 had been taking warfarin for 3 to 4 weeks but had subtherapeutic INR and 3 were taking aspirin only. Compared with patients without intra-atrial thrombi, patients with intra-atrial thrombi had lower ejection fraction (32.5% ± 18.1% versus 49.9% ± 14.1%, P = .015), slower left atrial appendage empty velocity (0.22 ± 0.08 versus 0.41 ± 0.17 m/s, P < .01), and higher prevalence of spontaneous echo contrast (87.5%) than in patients without intra-atrial thrombi (19.1%, P < .05) but similar left atrial size (49.5 ± 5.3 versus 47.3 ± 7.1 mm, P = .15). Cardioversion was cancelled in all patients with atrial thrombi.

Conclusions

In underanticoagulated patients, repeat TEE is necessary before cardioversion of recurrent AF even if the previous TEE showed no atrial thrombi.     

Is left atrial appendage occlusion useful for prevention of stroke or embolism in atrial fibrillation?

Since in atrial fibrillation more than 90% of the thrombi are located in the left atrial appendage, an "elimination" of the left atrial appendage, either by resection or occlusion, seems an attractive alternative to oral anticoagulation. Although frequently regarded as an useless appendage, data from animal and human investigations show that the left atrial appendage may play an important role in the maintenance and regulation of the cardiac function, especially in arterial hypertension, atrial fibrillation, coronary heart disease, valvular heart disease and heart failure. Elimination of the left atrial appendage may impede thirst in hypovolemia, deteriorate hemodynamic responses to volume or pressure overload, decrease cardiac output and promote heart failure. Instead of preventing stroke, the consequences of left atrial appendage elimination may create new risk factors for stroke and thus might induce more harm than benefit to patients with atrial fibrillation. As long as the physiologic and pathophysiologic role of the left atrial appendage is not fully understood, left atrial appendage elimination should not be an alternative to oral anticoagulation.     

Can we predict the occurrence of atrial fibrillation?

Atrial fibrillation (AF) is a complex disease with increasing prevalence in an aging population and longer survival with cardiovascular diseases. Whereas most clinical efforts have been aimed at predicting risk of AF sequelae such as stroke and heart failure, little is known on primary prevention. AF risk assessment is complicated by the existence of distinct subtypes of AF, such as lone AF or postoperative AF, in contrast to common AF in the elderly. Due to its often intermittent nature, diagnosing AF can be a challenge. Risk prediction becomes reasonable when specific interventions arise. Due to our limited understanding of AF pathophysiology and substantial lack of specific preventive strategies in the population, modification of the general cardiovascular risk profile has largely remained the only option. Initial attempts at combining established risk factors for AF such as age, sex, hypertension, body mass index, electrocardiographic characteristics, and cardiovascular disease in a risk-prediction instrument have produced a robust algorithm. However, known risk factors only explain a fraction of the population-attributable risk of AF, and the search for novel risk indicators is ongoing. More efficient monitoring for electrocardiographic precursors of AF and the field of genomics are evolving areas of AF risk factor research. A better understanding of the underlying substrate of AF will provide targets for prevention. In the future, clinical trials will be needed to establish risk categories, interventions, and their efficacy. Despite a relevant public-health impact, knowledge on risk prediction and primary prevention of AF is still limited today. There are no conflicts of interest to disclose.