Francesco Biscione

n-3 Polyunsaturated fatty acids for the prevention of arrhythmia recurrence after electrical cardioversion of chronic persistent atrial fibrillation: a randomized, double-blind, multicentre study

AIMS Persistent atrial fibrillation (AF) often recurs after direct current electrical cardioversion (ECV). As several experimental and clinical studies suggest that n-3 polyunsaturated fatty acids (PUFAs) may have antiarrhythmic properties even at the atrial level, we aimed to evaluate whether oral supplementation with PUFAs, in addition to conventional antiarrhythmic drugs, could reduce the recurrence rate of the arrhythmia after ECV of persistent AF. METHODS AND RESULTS Two hundred and four patients (mean age 69.3 years, 33% females) with persistent AF were randomly assigned to receive 3 g/day of PUFAs until ECV and 2 g/day thereafter (104 patients) or placebo (100 patients) for 6 months, beginning at least 1 week before ECV. Selection of conventional antiarrhythmic prophylaxis was left to local medical advice. The cardiac rhythm was assessed by both trans-telephonic monitoring and clinical visits. Primary end-point was the recurrence rate of AF. Sinus rhythm was restored, either spontaneously or after ECV, in 187 patients (91.7%); 95 patients (91.4%) on PUFAs and 92 patients (92.0%) on placebo (P=not significant). AF relapsed in 56 (58.9%) of the PUFAs patients and in 47 (51.1%) of the placebo patients (P=0.28). The mean time to AF recurrence was 83±8 days in the PUFAs group and 106±9 days in the placebo group (P=0.29). CONCLUSION Our results do not support the hypothesis that, in patients undergoing ECV of chronic persistent AF, supplementation with PUFAs in addition to the usual antiarrhythmic treatment reduces recurrent AF.

Cardiovascular Effects of Omega-3 Free Fatty Acids.

Omega-3 fatty acids are essential substances for the development and function of human organism. They cannot be synthesized in humans, and consequently have to be acquired from food, almost exclusively from fish. Omega-3 fatty acids exert potent anti-inflammatory and anti-atherosclerotic actions by interfering with the metabolism of arachidonic acid, modifying lipid composition (mainly lowering triglycerides), improving hemodynamics and reducing cardiac hypertrophy. Recently, clinical and experimental studies demonstrated an anti-arrhythmic effect and a significant impact on survival after myocardial infarction (MI). It follows that omega-3 fatty acids have been widely accepted for clinical use in patients with dyslipidemia or with atherosclerotic disease and in survivors of acute MI. This review briefly explores the metabolic mechanisms and the clinical effects of this class of substances and considers their use in patients with cardiovascular disease.

Electrograms for identification of the atrial ablation site during catheter ablation of accessory pathways.

Background: Catheter ablation of accessory pathways using radiofrequency current has been shown to be effective in patients with Wolff‐Parkinson‐White syndrome, by using either the ventricular or atrial approach. However, the unipolar electrogram criteria for identifying a successful ablation at the atrial site are not well established. Methods and Results: One hundred patients with Wolff‐Parkinson‐White were treated by delivering radiofrequency energy at the atrial site. Attempts were considered successful when ablation (disappearance of the delta wave) occurred in < 10 seconds. In eight patients with concealed pathway, the accessory pathway location was obtained by measuring the shortest V‐A interval either during ventricular pacing or spontaneous or induced reciprocating tachycardia. In 92 patients both atrioventricular valve annuli were mapped during sinus rhythm, in order to identify the accessory pathway (K) potential before starting the ablation procedure. When a stable filtered (30–250 Hz) “unipolar” electrogram was recorded, the following time intervals were measured: (1) from the onset of the atrial to the onset of the K potential (A‐K); (2) from the onset of the delta wave to the onset of the K potential (delta‐K); and (3) from the onset of the K potential to the onset of the ventricular deflection (K‐ V). During unsuccessful versus successful attempts, A‐K (51 ± 11 ms vs 28 ± 8 ms, P < 0.0001 for left pathways [LPs]; and 44 ± 8 ms vs 31 ± 8 ms, P < 0.02 for right pathways [RPs]) and delta‐K intervals (2 ± 9 ms vs ‐18 ± 10 ms, P < 0.0001 for LPs; and 13 ± 7 ms vs 5 ± 8 ms, P < 0.02 ms for RPs) were significantly longer. Conclusions: Short A‐K interval (< 40 ms), and a negative delta‐K interval recorded from the catheter positioned in the atrium are strong predictors of successful ablation of LPs and RPs. Therefore, the identification of the K potential appears to be of paramount importance for positioning of the ablation catheter, followed by analysis of A‐K and delta‐K unipolar electrogram intervals. However, it appears that the mere recording of K potential is not, per se, predictive of successful outcome, but rather the A‐K and delta‐K interval.

Electrophysiologic effects of amlodipine vs. dilitazem in patients with coronary artery disease and beta-blocking therapy

SummaryThis study compares the electrophysiologic effects of amlodipine and diltiazem in patients with coronary artery disease concomitantly treated with background beta-blocking therapy. Thirty patients were included in an open-label parallel study in two phases. During phase 1, patients were screened and placed on maintenance atenolol therapy at 50 or 100 mg/day, while phase 2 consisted of right-sided catheterization and randomization of patients to either amlodipine (10 mg IV) or diltiazem (10 mg IV). Following treatment with amlodipine, no significant alteration in markers of electrophysiological activity was observed. Treatment with diltiazem resulted in a significant lengthening of sinus cycle length (SCL, p<0.04), AH interval (p<0.02), and Wenckebach CL (WCL, p<0.001), and a trend towards an increase in sinus node recovery time (SNRT, p=0.057). No effects were observed with regard to HV interval and corrected SNRT. The results of this study indicate that 10 mg intravenous amlodipine has no significant electrophysiological action on sinus or AV node function in patients receiving beta-blocker therapy with atenolol, suggesting that amlodipine can be added to beta-blockers to treat patients with myocardial ischemia and/or hypertension without any significant increase in the risk of bradyarrhythmias.