Left‐Sided Atrial Flutter Originating in the Coronary Sinus after Radiofrequency Ablation of Atrial Fibrillation

We describe a case of atypical atrial flutter presenting 1 year after radiofrequency ablation for atrial fibrillation (AF). Electrophysiologic study showed a reentry circuit involving the inferolateral aspect of the mitral annulus and the coronary sinus (CS); however, a mitral isthmus line did not terminate the arrhythmia. Participation of the proximal CS musculature in the circuit suggested a possible target for ablation. Radiofrequency energy applications from within the CS terminated the tachycardia. Mapping and ablation within the CS should be considered in patients with post‐AF ablation arrhythmias, particularly when the mitral annulus appears to be involved in the tachycardia circuit. (PACE 2010; 33:e96–e99)     

Inhibition of the Renin‐Angiotensin System for Prevention of Atrial Fibrillation

Atrial fibrillation (AF) is a source of considerable morbidity and mortality. There has been compelling evidence supporting the role of renin‐angiotensin system (RAS) in the genesis and perpetuation of AF through atrial remodeling, and experimental studies have validated the utilization of RAS inhibition for AF prevention. This article reviews clinical trials on the use of angiotensin‐converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) for the prevention of AF. Results have been variable, depending on the clinical background of treated patients. ACEIs and ARBs appear beneficial for primary prevention of AF in patients with heart failure, whereas they are not equally effective in hypertensive patients with normal left ventricular function. Furthermore, the use of ACEIs or ARBs for secondary prevention of AF has been found beneficial only after electrical cardioversion. Additional data are needed to establish the potential clinical role of renin‐angiotensin inhibition for prevention of AF. (PACE 2010; 33:1270–1285)     

Atrial High Rate Episodes in Patients with Dual‐Chamber Cardiac Implantable Electronic Devices: Unmasking Silent Atrial Fibrillation

Assessment of the prevalence of silent paroxysmal atrial fibrillation (AF) represents a challenge, since the arrhythmia may be brief, completely asymptomatic, and difficult to detect. Lack of symptoms from AF should not be equated to lack of risk of thromboembolic complications. Today's cardiac implantable electronic devices (CIED) diagnostics include system diagnostics accurately revealing asymptomatic cardiac arrhythmias as atrial high rate episodes (AHRE). The presence of AHRE has been related to increased risk of stroke and systemic embolism. The application of anticoagulation therapy in patients with device‐detected AHRE is yet unclear and challenging in the absence of randomized studies. Until further studies are available, anticoagulation therapy should be individualized and promoted attending to the CHADS₂ score. Future guidelines should deal with this peculiar AF scenario to make professionals who routinely perform CIED follow‐ups aware of these relevant episodes and their clinical implications.     

Atrial Refractory Periods after Atrial Premature Beats in Patients with Paroxysmal Atrial Fibrillation

To study the effects of an atrial premature beat on atrial refractory periods, we investigated 11 patients (group A) who were the control group, 12 patients suffering from paroxysmal atrial fibrillation (group B), and 10 patients (group C) without arrhythmias but with cardiopathy or cardiomyopathy. At every eighth complex of a constant atrial electrostimulated rhythm a fixed premature extrastimulus was introduced, and effective and functional refractory periods (ERP and FRP) were measured in three different sites of the right atrium, before and after introduction of this extrastimulus. Average ERP and FRP shortened respectively in group A, from 220.28 ± 25.68 msec and 281.17 ± 28.15 msec before extrastimulation, to 190.58 ± 22.74 msec and 245.88 ± 19.86 msec after; in group B, from 219.44 ± 27.38 msec and 284 ± 30.06 msec to 191.66 ± 28.72 msec and 253.23 ± 34.01 msec; and in group C from 229.03 ± 29.65 msec and 289.67 ± 51.62 msec to 194.19 ± 24.6 msec and 237.74 ± 39.59 msec. The average dispersions of ERP and FRP in group A were, respectively: 41.81 ± 21.36 msec and 36.36 ± 18.04 msec before extrastimulation, 28.18 ± 18.14 msec and 35.45 ± 15.72 msec after. In group B: 26.66 ± 19.46 msec and 41.66 ± 16.96 msec versus 45.83 ± 23.91 msec and 45 ± 34.77 msec and in group C: 27 ±11.59 msec and 45 ± 29.15 msec versus 29 ± 18.52 and 27 ± 18.88. It is concluded that an atrial premature beat tends to shorten the dispersion of atrial refractory periods when patients are free of arrhythmias, and to lengthen them when paroxysmal atrial fibrillation are documented.