Effects of long-term ω-3 polyunsaturated fatty acid supplementation on paroxysmal atrial tachyarrhythmia burden in patients with implanted pacemakers: results from a prospective randomised study.

BACKGROUND: Sino-atrial node disease and aging increase AF risk. We investigated if long-term fish oil supplementation reduces paroxysmal atrial tachycardia/fibrillation (AT/AF) burden in patients aged ≥60 years with sinoatrial node disease and dual chamber pacemakers. METHODS: Following a run-in period of 6 months (p1) where AT/AF burden was logged,78 patients were randomised to control or fish oil group (total omega-3 6 g/d) and AT/AF burden evaluated after 6 months (p2; 39 controls, 39 fish oil) and 12 months (p3; 39 controls; 18 fish oil). A subset of 21 fish oil patients crossed over to controls in the final 6 months (crossover group). RESULTS: Median AT/AF burden increased significantly in controls (1.5%, 3.2%, 4.3%, P<.001) but not in fish oil patients at 6 months (1.4% to 2%, P=.46) or those continuing for 12 months (1.5%, 0.98%, 1%, P=.16). Time to first episode of AT/AF >1 min was not significantly different between the groups (P=.9). There was a rebound increase in AT/AF burden in p3 in cross over patients (2.2% to 5.8%, P=.01) reaching a level similar to controls (crossover vs. controls, 5.8% vs. 4.3%, P=.63) and higher than those who continued fish oil for 12 months (crossover vs. continued intake 5.8% vs. 1.2%, P=.02). Fish oil patients had shorter duration episodes of AT/AF with no difference in frequency compared to controls. CONCLUSION: Long-term fish oil supplementation did not suppress AT/AF burden but may have attenuated its temporal progression related to aging and sinus node disease.

[Activation of the sympathetic nervous system influences the antifibrillatory effect of class I antiarrhythmic drugs]. / Vliianie aktivatsii simpaticheskoi nervnoi sistemy na protivofibrilliarnoe deistvie antiaritmicheskikh sredstv I klassa.

The experiments with anesthetized rats showed that drugs belonging to various subclasses of class I antiarrhytmic agents (novocainamide, IA; lidocaine, IB; ethacizine, IC) produce a pronounced antifibrillatory and antiarrhythmic action under the conditions of a 7-min occlusion followed by reperfusion of the anterior descending branch of the left coronary artery. In the arrhythmia model with beta-adrenoreceptors stimulated by isoproterenol, novocainamide (IA) and lidocaine (IB) retained their efficacy, in contrast to ethacizine (IC). This difference in the behavior of antiarrhythmic drugs may be related to their different antiarrhythmogenic potentials.

Postural tachycardia syndrome. Reversal of sympathetic hyperresponsiveness and clinical improvement during sodium loading.

A patient with disabling postural tachycardia without postural hypotension had symptoms that included palpitations, weakness, abdominal and leg pain, light-headedness, headache and diaphoresis that occurred only in the upright position. She was shown to have an enhanced sympathetic neural response to standing (exaggerated plasma nor epinephrine response), and her cardiovascular responsiveness to released catecholamines was clearly intact. However, she was unable to maintain normal sodium balance and had a measurably reduced plasma volume while consuming normal amounts (120 mmol daily) of dietary sodium. Sodium loading (240 mmol ingested daily plus administration of fluorohydrocortisone, 0.1 mg daily) largely corrected the hemodynamic abnormalities, prevented postural symptoms and caused the compensatory sympathetic response to revert to normal.