[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%.

Local delivery of nadroparin for the prevention of neointimal hyperplasia following stent implantation: results of the IMPRESS trial. A multicentre, randomized, clinical, angiographic and intravascular ultrasound study.

BACKGROUND: We hypothesized that intramural delivery of nadroparin, a low molecular weight heparin, would prevent in-stent restenosis by inhibiting neointimal hyperplasia in an angioplasty model free of arterial remodelling. METHODS AND RESULTS: In a prospective randomized multicentre trial, 250 patients submitted to balloon angioplasty followed by stent implantation were randomized into control group (no local drug delivery) or intramural delivery of nadroparin (2 ml of 2500 anti-Xa-units/ml with a microporous catheter). An ancillary intravascular ultrasound substudy was performed to supplement angiographic data with specific measurements of in-stent neointimal hyperplasia. The primary end-point was the late loss in minimal luminal diameter on the 6 month follow-up angiogram. Secondary end-points included feasibility and safety of local nadroparin delivery, and major adverse cardiac events at 8 weeks and 6 months follow-up. Local delivery of nadroparin was successful in 124 patients (99.2% success rate) and was not associated with an increase in stent thrombosis, coronary artery dissection, side branch occlusion, distal embolization or abrupt arterial closure. At angiographic follow-up, the late loss in lumen diameter was 0.84 +/- 0.62 mm in the control group compared to 0.88 +/- 0.63 mm in the nadroparin group (P=0.56). Angiographic restenosis rate (defined as a >50% diameter stenosis) did not differ in the control group (20%) compared to the nadroparin group (24%). The average area of neointimal tissue within the stent was 2.86 +/- 0.64 mm(2) vs 2.90 +/- 0.53 mm(2) (P=0.57), control vs nadroparin groups. There was no difference in major adverse cardiac events at any time (88.8% vs 89.6% event free survival at 6 months, control vs nadroparin). CONCLUSION: Intramural delivery of nadroparin with a microporous catheter after stent deployment was feasible and safe but had no effect in reducing restenosis or the occurrence of major adverse clinical events over 6 months.

Time-course of changes in plasma levels of trace elements after thrombolysis during the acute phase of myocardial infarction in humans.

It has been suggested that the injury induced by reperfusion of the ischemic myocardium could result, in part, from the cytotoxic effects of oxygen free radicals. Since various trace elements are involved in several of the reactions leading to free radical production, we have measured plasma levels of copper, zinc, selenium, and iron: 1. In 18 patients (mean age 60 yr old) subjected to thrombolytic therapy within 6 h after the onset of a myocardial infarction (G1); 2. In 16 patients with coronary artery disease, but without a history of a previous myocardial infarction (MI) (mean age 50 yr old, G2); and 3. In 50 healthy volunteers divided into two subgroups according to age (mean age 33 yr old, G3 and 55 yr old, G4). Plasma myosin levels were used to estimate quantitatively the extent of the infarcted mass. Plasma trace element levels were measured in blood samples following centrifugation and storage at -80 degrees C. The main results were as followed: In G1 patients who have been subjected to thrombolysis, an important release of myosin was measured in plasma, with a peak at D6 (1678 vs 95 microU/L at H0). In those G1 patients after MI: 1. A significant increase in plasma copper levels was observed from day 4 to day 10 postinfarction (x1.15 in reference to the baseline data at H0); 2. A decrease in plasma zinc levels was observed and was maximum 12 h after the onset of the thrombolytic treatment; 3. A decrease in selenium concentration was observed in G1, as well as in G2 patients, compared to the control groups (80% of G3 and G4 values); and 4. A significant decrease in plasma iron levels was observed in G1 (67.8% of G3 and G4 control values) and was significant from H0 to day 7 (p < 0.01). In conclusion, this study underlined the time-course evolution of plasma trace element levels in the followup of patients who have been subjected to thrombolysis following a MI and the potential prognostic implication of such variations.