BackgroundA drug provocation test using a sodium channel blocker (SCB) can unmask a type 1 ECG pattern in patients with Brugada syndrome. However, the prognostic value of the results of an SCB challenge is limited in patients with non–type 1 ECG. We investigated the associations of future risk for ventricular fibrillation with SCB‐induced ECG changes and ventricular tachyarrhythmias (VTAs).Methods and ResultsWe administered intravenous pilsicainide to 245 consecutive patients with Brugada syndrome (181 patients with spontaneous type 1 ECG, 64 patients with non–type 1 ECG). ECG parameters before and after the test and occurrence of drug‐induced VTAs were evaluated. During a mean follow‐up period of 113±57 months, fatal VTA events occurred in 31 patients (sudden death: n=3, ventricular tachycardia/ventricular fibrillation: n=28). Symptomatic patients and spontaneous type 1 ECG were associated with future fatal arrhythmic events. Univariable analysis of ECG parameters after the test showed that long PQ and QRS intervals, high ST level, and SCB‐induced VTAs were associated with later VTA events during follow‐up. Multivariable analysis showed that symptomatic patients, high ST level (V1) ≥0.3 mV after the test, and SCB‐induced VTAs were independent predictors for future fatal arrhythmic events (hazard ratios: 3.28, 2.80, and 3.62, 95% confidence intervals: 1.54–7.47, 1.32–6.35, and 1.64–7.75, respectively; P<0.05).Conclusions
SCB‐induced VTAs and ST‐segment augmentation are associated with an increased risk of the development of ventricular tachycardia/ventricular fibrillation events during follow‐up in patients with Brugada syndrome.
This study investigated the effect of fractional flow reserve (FFR) after stent implantation on clinical outcomes. Pressurewire measurements and follow-up data were obtained after stent implantation. Regarding the end point, target lesion revascularization (TLR) occurred in 11 patients (15.9%). Patients with TLR had higher frequencies of multiple stenting (54.5 vs. 19.0%, p = 0.01), lower post-interventional FFRs (0.84 vs. 0.88, p = 0.01), and longer stent lengths (42.20 vs. 27.69 mm, p = 0.01) than patients without TLR. The post-interventional FFR cutoff for TLR was 0.79, although this value had a weak discriminatory ability. However, multivariate analysis did not show any significant independent predictors of TLR (odds ratio 6.33; confidence interval 0.75-53.4, p = 0.09). Post-interventional FFR values were not significantly associated with TLR when a sub-analysis was performed in patients who underwent only drug-eluting stent (DES) implantation. It was difficult to achieve post-interventional FFRs of 0.9 or greater. DES implantation eliminated the effect of post-interventional FFR on TLR. Post-interventional FFR was not able to predict TLR in the present study.
1734UEOKA A et al.
Circulation JournalOfficial Journal of the Japanese Circulation Society http://www. j-circ.or.jp ity is also an important finding in patients with BrS. 5,8,12,13 Elimination of VF attacks and normalization of ST elevation by radiofrequency catheter ablation directly targeting the abnormal potentials at the RVOT epicardium have demonstrated that the abnormal electrical substrate that initiates the ventricular tachyarrhythmias exists in the epicardium of the RVOT. 6 The electrophysiological abnormality in the RVOT epicardium should contribute to the initiation of ventricular tachyarrhythmia. Both the mechanism of maintenance and polymorphic QRS change of the ventricular arrhythmias are still unknown because it is difficult to map electrical activation during ventricular tachyarrhythmias that immediately cause collapse of the patient's hemodynamics.he right ventricular outflow tract (RVOT) has an important role in the initiation of ventricular fibrillation (VF) in patients with Brugada syndrome (BrS). The characteristic type 1 ST elevation 1,2 represents an electrophysiological abnormality in the RVOT, 3 and delayed potential has been frequently recorded in this area. 4-6 Moreover, premature ventricular contractions followed by VF frequently originate from this area. 7, 8 Although the mechanisms of ST elevation and occurrence of ventricular tachyarrhythmias in BrS are controversial, experimental studies have shown that epicardial repolarization abnormality at the RVOT causes ST elevation and promotes VF.
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