[Role of atrial stimulation in the treatment of paroxysmal atrial fibrillation]. / Place de la stimulation auriculaire dans le traitement de la fibrillation auriculaire paroxystique.

Preventive treatments for atrial fibrillation by stimulation have been developed for several years now, mainly due to the relative failure of anti-arrhythmic treatments. They are based on the hypothetical effects of stimulation by controlling cardiac frequency, abolishing bradycardia-dependent extrasystoles, by the inhibition of atrial automatic foci with "overdrive", and by the modification of intra- or inter-atrial conduction delays as well as by remodelling the arrhythmogenic substrate. It is clear that an undeniable effect exists for the prevention of atrial fibrillation, even for the risk of cerebral vascular accident, by physiological stimulation (DDD/DDDR) compared to pure ventricular stimulation (VVI/VVIR) in a heterogenous global population of stimulated patients. For the moment, there is not sufficient proof of a positive effect for the emerging sites of cardiac stimulation, either atrial mono-site or double site in the populations at high risk of atrial fibrillation, with or without associated bradycardia. Some new prevention algorithms by "overdrive" are under development but for the moment only a few preliminary studies seem to show a slight benefit. It is clear that at present stimulation should be reserved only for cases of atrial fibrillation associated with a classic indication for implantation. In these patients it is recommended to position the probes in an optimal manner in order to counteract conduction disorders, choosing an adapted double chamber stimulator with prevention algorithms. That said, the patient should be clearly warned that the long term success rate is no more than 50%.

Altered baroreflex gain during voluntary breathing in chronic heart failure.

BACKGROUND: We assessed the behavior of the baroreflex (BR) gain in chronic heart failure (CHF) patients using the spectral analysis method during application of a forcing stimulus, i.e. respiration. METHODS: Simultaneous RR interval and arterial pressure fluctuation recordings were obtained during two random-order periods of voluntary paced-breathing (0.15 Hz and 0.25 Hz) in seven patients with moderate CHF (NYHA class II/III; EF, 30+/-9%; peak VO(2), 18+/-5 ml kg(-1) min(-1)) and six age-matched controls. BR gain was assessed in the time (sequential method) and frequency (cross-spectral gain in the low and high frequency) domains. RESULTS: Slower breathing was associated with a BR gain decrease in CHF patients whereas a BR gain increase was evidenced in controls (BR gain: 6+/-5 ms mmHg(-1) at 0.25 Hz vs. 4+/-3 ms mmHg(-1) at 0.15 Hz, P<0.05 in CHF; BR gain: 12+/-7 ms mmHg(-1) at 0.25 Hz vs. 15+/-7 ms mmHg(-1) at 0.15 Hz, P<0.05 in controls). CONCLUSIONS: Voluntary breathing, which involves cortical centers in the brain, had major effects on cardiovascular system controller gain in CHF patients, indicating an impairment of the central neural regulation of the autonomic outflow.