BACKGROUND Ventricular arrhythmias are known to originate from the aortic sinus of Valsalva. OBJECTIVE The purpose of this study was to identify the characteristics associated with ventricular arrhythmias originating from the right coronary cusp-left coronary cusp (RCC-LCC) commissure.METHODS Thirty-seven consecutive patients with ventricular arrhythmias originating from the aortic cusp region were studied. Intracardiac echocardiography and electroanatomic mapping were used to define coronary cusp anatomy and catheter position. Ventricular arrhythmias from the RCC-LCC commissure were compared with ventricular arrhythmias originating from other sites in the aortic cusp region.RESULTS Nineteen (51%) ventricular arrhythmias had an anatomic origin at the RCC-LCC commissure. Eighteen ventricular arrhythmias originated from other aortic cusp sites (4 right cusp, 7 left cusp, 3 left ventricular endocardium, 4 left ventricular epicardium anterior to aortic valve). A QS morphology in lead V(1) with notching on the downward deflection was present in 15 of 19 ventricular arrhythmias originating from the RCC-LCC commissure compared to 2 of 18 ventricular arrhythmias from other aortic cusp sites (P <.01). At the site of earliest activation, 13 of 19 patients with RCC-LCC ventricular arrhythmias had late potentials in sinus rhythm compared to 1 of 18 ventricular arrhythmias from other aortic cusp sites (P <.01). The site of successful ablation was confirmed to be above the aortic valve plane in 15 (79%) of 19 patients with RCC-LCC ventricular arrhythmias.CONCLUSION RCC-LCC aortic cusp ventricular arrhythmias are common and have a QS morphology in lead V(1) with notching on the downward deflection with precordial transition at lead V(3). In the majority of cases, the site of successful ablation has late potentials in sinus rhythm.

Background : While many patients (pts) remain free of atrial fibrillation (AF) without anti-arrhythmic drug(AAD) therapy after ablation, some pts require re-initiation of medications to control AF long-term. Factors associated with need for reinstituting AAD have not been identified. Methods: A total of 578 pts who underwent AF ablation and demonstrated AF control for at least 12months were included in this study. The ablation included proximal pulmonary vein (PV) isolation with entry and exit block and elimination of non PV triggers. AAD were reinitiated if with ECG documented AF recurrence after the 2 month blanking period. Confirmation of AF control was based on symptoms and transtelephonic ECG monitoring at 6 mos, 12 mos, and with symptoms. Clinical variables were compared between each group by univariate analysis to determine if significant differences existed. Significant parameters were included in a multivariate analysis to determine interaction between variables. Results: Table 1 delineates clinical parameters included in the analysis, with unadjusted P values for each variable. Multivariate analysis with forward and backward regression identified larger LA size and advancing age as only factors which correlated with the need for AAD therapy after ablation to maintain AF control. Conclusions: Increased LA size and advancing age are clinical parameters which suggest progressive fibrosis of the LA. In our analysis, these two variables strongly predicted the need to restart AAD therapy after proximal PV ablation and elimination of non PV triggers in order to maintain long-term control of AF. Table 1