ABSTRACT
Objective Identify the mechanism of induced atrial arrhythmias after pulmonary vein isolation (PVI) in patients with paroxysmal atrial ifbrillation(PAF), and investigate its long-term prognosis. Methods All patients with PAF undergoing PVI and induction test afterwards between Feburary 2010 and October 2010 were included. The induction protocol was rapid pacing initiated at cycle length of 250 ms with progressive shortening in a decrement of 10 ms down to 180 ms or refractoriness. Isoproterenol of 2-4μg/min was administrated as well. Inducibility was deifned as induction of atrial arrhythmia lasting >1 min. The mechanism of induced tachycardia was identiifed by activation mapping and entrainment mapping under the guidance of CARTO system. All patients were followed up by 36 months. Results Forty-nine atrial tachycardia were induced in 39 (19.7%) patients, including 35 organized atrial tachycardia (OAT) and 14 atrial ifbrillation (AF). The LA diameter was signiifcantly larger in inducible group than non-inducible group (39.5±6.6 mm vs. 36.7±5.2 mm, P=0.004). Macroreentry was the most common mechanism in induced OATs (28, 80.0%), and mitral isthmus was the most common critical site (20, 40.8%), followed by cavo-tricuspid isthmus (12, 24.5%), PV (6, 12.2%), LA septum (4, 8.2%), superior vena cava (3, 6.1%) and LA roof (1, 2.0%). Conclusions The most common mechanism of induced tachycardia by IV isoproterenol and rapid pacing is MI and CTI dependent after PVI in PAF patients, which can be succssefully eliminated by liner ablation, not increasing long-term recurrence rate.
ABSTRACT
Objective: To explore the effect of valsartan on inflammatory cytokines in patients with hypertension combining paroxysmal atrial ifbrillation (PAF). Methods:A total of 60 patients with hypertension combining PAF converted to sinus rhythm were studied and the patients were divided into 2 groups. Control group, the patients received felodipine and Valsartan group. n=30 in each group, all patients were treated for 6 months. In addition, there was a Normal group including 30 healthy subjects. The levels of high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6) and left atrial diastolic diameter (LADd), the sinus rhythm maintenance rate were examined and compared before and after treatment among different groups. Results: Compared with Normal group, the levels of hs-CRP, IL-6 and LADd were obviously higher in patients at both Control group and Valsartan group, all P Conclusion: Valsartan may inhibit inflammatory response and improve atrial structure remodeling, therefore better maintain the converted sinus rhythm in patients with hypertension combining PAF. The anti-inlfammatory effect of valsartan might be independent from its anti-hypertension effect.