Months Of Atrial Fibrillation Research Articles

Coronary Artery Dissection After Surgical Cryoablation Procedure

Cryoablation can be used to treat atrial fibrillation (AF) surgically. We describe a 71-year-old woman who underwent cryoablation after 6 months of AF. Four hours post-surgery, electrocardiographic changes were observed in the circumflex artery territory associated with hemodynamic instability, which responded to inotropic agents. Angiography revealed a diffuse circumflex artery spasm with a heterogeneous aspect of the posterior branch evoking a dissection. Platelet anti-aggregant and trinitrine therapy were started. Recovery was uneventful and the patient was discharged on day 13. Cryoablation-associated circumflex artery dissection is rare. Caution is required when locating the ablation lines to avoid coronary artery injury.

Atrial and ventricular fibrosis induced by atrial fibrillation: Evidence to support early rhythm control

Atrial fibrillation (AF) with poorly controlled ventricular response is known to be detrimental to ventricular function, conversely, heart failure (HF) increases susceptibility to AF. This study sought to examine the electropathological effects of 3 months of atrial fibrillation (AF) in dogs with and without concomitant ventricular dysfunction. Three groups of dogs were studied: dogs with chronic AF induced by rapid pacing and concomitant ventricular dysfunction induced by rapid ventricular response with intact atrioventricular node (AVN), dogs with ablated AVN and AF while the ventricle was paced at 80 beats/min, and normal sham dogs. After 3 months of AF, the first 2 groups underwent direct current cardioversion (DCCV) to normal sinus rhythm and were monitored for 3 months, followed by retesting of AF susceptibility. Tissue fibrosis was assessed at various sites by trichrome staining and quantitative immunohistochemistry. AF was induced within 12 +/- 4 days and 30 +/- 13 days, respectively, in the intact and ablated AVN groups (P <.01). After 3 months of AF, left ventricular ejection fraction was 30.4% +/- 10.1% and 55% +/- 5% in the intact and ablated AVN groups (P <.01), respectively. After 3 months of normal sinus rhythm, AF was reinduced after 4 +/- 2 and 7.2 +/- 2 days, respectively (P = NS). There were no regional differences and an abundance of fibrosis within atria. Atrial fibrosis was significantly increased in intact AVN versus ablated AVN and sham groups, and also was greater in AVN-ablated versus sham dogs. Ventricular fibrosis was increased in intact AVN versus ablated AVN and sham groups and was not significantly different in ablated AVN and sham groups. AF without ventricular dysfunction results in atrial fibrosis and increased susceptibility to AF, suggesting that AF alone causes atrial fibrosis. AF with rapid ventricular response further increases atrial and ventricular fibrosis. Conversion to normal sinus rhythm should be done as early as possible to avoid atrial and ventricular fibrosis and increased susceptibility to AF.

P4-17: Conduction in the atrial free walls after short and long term atrial fibrillation in the goat

We have studied activation patterns during pacing and atrial fibrillation (AF) in goats after short term (2.5 weeks) and long term (6 months) AF. After 2.5 weeks of AF, electrical remodeling is complete. After 6 months of AF, structural remodeling has also become pronounced. At this time point, chemical cardioversion was no longer possible (permanent AF). We have evaluated whether the increased stability of AF is related to changes in conduction properties of the atrial free walls (AFWs).

Atrial and Ventricular Volume and Function in Persistent and Permanent Atrial Fibrillation: A Magnetic Resonance Imaging Study

Left atrial size is independently related to cardiovascular morbidity and mortality, and atrial fibrillation (AF) is strongly associated with atrial size. Our aims were to report atrial and ventricular dimensions in patients with AF evaluated with magnetic resonance imaging (MRI), and to assess the inter-study reproducibility of the measurements. Nineteen healthy volunteers, 19 patients with permanent AF, and 58 patients with persistent AF had cardiac dimensions evaluated by 6-mm cinematographic breath-hold MRI scans using a 1.5 Tesla Siemens Vision Magnetom scanner with a phased array chest coil. Intraobserver variability and inter-study reproducibility of the cardiac volumes and ejection fractions (EF) gave acceptable Bland-Altman plots, good correlations (R2: 0.80-0.99), and low reproducibility coefficients. The mean atrial volumes were similar in the two groups with AF [systolic vol. index (SVI): 75.9-80.3 mL/m2; diastolic vol. index (DVI): 77.4-82.1 mL/m2] and significantly different from the healthy volunteers (SVI: 30.3 mL/m2; DVI: 62.3 mL/m2; p < 0.0001). Mean left ventricular (LV) volumes and EF were significantly different in permanent AF (SVI: 34.2 mL/m2; DVI: 68.3 mL/m2; EF: 50.8%) compared to persistent AF [SVI: 44.0 mL/m2 (p = 0.02); DVI: 77.2 mL/m2 (p = 0.03); EF: 44.9% (p = 0.02)], and closer to the normal values (SVI: 22.4 mL/m2; DVI: 66.5 mL/m2; EF: 67.0%). MRI is a highly reproducible method for measurement of atrial and ventricular dimensions in healthy volunteers and in patients with AF. Our results suggest that atrial dilatation appears within the first months of AF and stays more or less unchanged thereafter. The LV appears to dilate early as a response to AF, but later seems to adapt.

Linear lesions provide protection from atrial fibrillation induction with rapid atrial pacing.

In the animal model, segmentation of the atria with radiofrequency-generated linear lesions (LL) using the loop catheter has been shown to be highly effective in terminating chronic atrial fibrillation (AF). This study addresses the question whether the same lesion set also would prevent reinduction and sustainability of AF. We studied two groups of dogs. The AF group included eight dogs in which the atria were paced until chronic AF was present. After 6 months of sustained AF, the dogs were converted to normal sinus rhythm (NSR) by the creation of LL in both atria. Rapid atrial pacing was restarted 6 months later and continued for 4 weeks. In the NSR group, there were nine dogs in NSR without inducible AF at baseline. LL were created, and after 6 months rapid atrial pacing was applied for 4 weeks. Rhythm status was monitored weekly. Transthoracic echocardiography was performed at baseline, before linear lesion placement, and before pacing/repacing. At the conclusion of the study, the hearts were excised and examined. The lesions were stained, and their quality was assessed. AF was induced in a much shorter interval in the dogs in which AF had previously been present than in NSR dogs (8 +/- 5 days vs 25 +/- 13 days; P < 0.05). LL prevented sustainability of AF induced via rapid pacing once the pacing stimulus was stopped. Incomplete lesions were associated with increased inducibility of atrial tachycardia and AF. In this animal model of AF, LL are not only capable of terminating chronic AF, but also lead to self-termination of AF once the rapid pacing is stopped. Self-termination of AF after induction with rapid pacing was not observed in this AF model in the absence of LL. In the dogs with 6 months of AF, the presence of AF led to increased atrial susceptibility to AF induction by rapid pacing, even with LL and after 6 months of recovery. Incomplete LL allows induction of atrial tachycardia and AF.