Statin for atrial fibrillation

In the long term effects of simvastatin on protectingagainst atrial fibrillation in patients with acute myocardialinfarction, in this issue of the Journal of GeriatricCardiology, Chi et al. presented interesting data regard-ing the positive beneficial effects of simvastatin in the re-duction of the frequency of atrial fibrillation in a selectedgroup of patients. There have been occasional reports sug-gestive of mild antiarrhythmic properties of simvastatin,but these were more observational in nature. What isthought provoking about this report is that the group re-ceiving simvastatin actually received less beta blockertherapy than the control group. It remains unclear as tohow simvastatin actually reduces dispersion of tissuerefractoriness, the basis of most arrhythmias. It also re-     

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.     

Left atrial dimension and atrial fibrillation in surgical heart disease patients

Objective The effect of left atrial (LA) dimension on the occurrence of atrial fibrillation (AF) has been examined in some small studies.Less is known about the relationship of LA dimension,hemodynamic with AF during echocardiographic evaluation,especially,the flow dynamics in LA poorly described.The objective of this study was to investigate the relationship between LA dimension and the occurrence of AE Methods Two hundred and forty-five consecutive patients with heart disease scheduled to undergo open heart surgery were prospectively enrolled in the study.Patients were divided into 2 groups according to atrial fibrillation:AF group (n=148,99 men and 49 women,with a mean age 59.3+8.4 years),and no-AF group (n= 97,60 men and 37 womem).Echocardiography was performed before surgery.All measurements were performed following the American Society of Echocardiography recommendations.Results There were more patients with congestive heart failure in AF group than in no-AF group (45.9% vs 39.1%,P ＜0.05).The mean LA volume was 49.2±12.2 ml/m2 in AF group and 33.1±10.8 ml/m2 in no-AF group.There were also significant differences between two groups in left atrial end systolic dimension (LAESD) (50±13mm vs 27±14mm),left atrial end diastolic dimension (LAEDD) (79±17mm vs 53±13mm),PA pressure ( 41.3+11.6 mmHg vs 37.5±10.4 mmHg),and ratio of mitral E velocity and septal mitral annulus motion velocity (E/E') .The percentage of abnormal diastolic function grades (DGF) was also higher in AF than in no-AF group (89.9% versus 59.8% );.Conclusion Atrial fibrillation is associated more frequently with an increased LA dimension and more severe atrial hemodynamics disorder.(J Geriatr Cardiol 2008;5:11-4)     

C-reactive protein and atrial fibrillation. Is inflammation a consequence or a cause of atrial fibrillation?

To clarify whether inflammation is a cause or consequence of atrial fibrillation (AF), we measured high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) before and after pharmacological cardioversion in 15 patients with paroxysmal AF. Levels of hs-CRP, IL-6, and TNF-alpha after cardioversion were significantly higher than those in controls (P < 0.05). Furthermore, the levels of these indices did not differ significantly even at 24 hours and 2 weeks after cardioversion. These results suggest that inflammation is a causative agent of paroxymal AF.     

Can we ablate permanent atrial fibrillation?

There is growing evidence of the benefit of ablation in the treatment of drug refractory atrial fibrillation.     

Does atrial overdrive pacing prevent paroxysmal atrial fibrillation in paced patients?

The role of atrial overdrive pacing for the suppression of paroxysmal atrial fibrillation remains unclear. To investigate this we have performed a randomised study evaluating the role of an increased atrial base rate in suppressing this arrhythmia in patients implanted with a permanent pacemaker (Chorum ELA) for sick sinus syndrome with previous documented paroxysmal atrial fibrillation. Twenty-seven patients (mean age, 69; 15 female) were randomised to two 3-month single-blinded crossover periods of DDDR pacing. The pacemaker was set with a base rate of 60 bpm (normal) during one period and at 10 bpm (overdrive) above the average heart rate during the other, mean (S.D.) 75+/-7 beats/min (range, 70-96). The fallback algorithm of the pacemaker was activated to record the number and duration of paroxysmal atrial fibrillation episodes. During the overdrive period there was a significant increase in the total duration of atrial pacing (normal 60+/-26% vs. overdrive 72+/-28%, P<0.001). However there was no significant difference in the number of paroxysmal atrial fibrillation episodes (normal 43+/-109 vs. overdrive 43+/-106, P=ns), or their total duration (normal 42+/-108 h vs. overdrive 99+/-254 h, P=ns). In conclusion, atrial overdrive pacing, achieved by increasing the atrial base rate, has no incremental benefit in the suppression of paroxysmal atrial fibrillation when compared to rate responsive pacing with a base rate of 60 bpm.     

Electrophysiological remodeling induced by atrial fibrillation. An experimental curiosity or major factor in atrial fibrillation in man?

Atrial fibrillation usually progresses from a paroxysmal to a permanent arrhythmia, even in the absence of underlying cardiac disease. The treatment is more difficult when the arrhythmia is chronic. This progression may be explained by the aggravation of underlying cardiac disease with time. Another explanation is that the arrhythmia induces functional and structural changes of the atrial tissues (remodelling) which promote the perpetuation of the arrhythmia and which make treatment less effective. Although the electrophysiological changes predisposing to atrial fibrillation have been known for over 15 years, it was only in 1995 that experimental studies showed the presence of atrial electrophysiological remodelling induced by the arrhythmia. This process of long term adaptation of the atrial myocytes to the tachycardia comprises marked changes of the parameters which sustain the arrhythmia: changes in refractory period (decreased duration, inadaptation to the heart rate, increased dispersion), reduced conduction speed and sinus dysfunction. Atrial remodelling also affects the contractile function by the structural changes. The calcium currents play a major role in its development. This mechanism has not yet been completely defined in the clinical setting and its importance in sustaining the arrhythmia has not been clearly evaluated. Atrial fibrillation remains one of the most difficult arrhythmias to treat. A better understanding of cellular mechanisms of remodelling could open up new therapeutic approaches to limit the natural history of the arrhythmia with progression to chronicity and structural changes responsible for the degradation of atrial contractility.