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• An LET guided cryoballoon ablation carries the risk of a gastroparesis. • Gastroesophageal ETI after a cryoballoon PVI was more frequent in bonus freeze group. • Strict early interruption due to LET without bonus freeze prevented the ETLs. • An additional bonus freeze didn't improve the freedom from AF in the cryoballoon PVI. Second-generation cryoballoon (2G-CB) ablation is highly effective for achieving pulmonary vein isolation (PVI) with a promising clinical outcome. However, the ideal freezing strategy for preventing gastroesophageal excessive transmural injury (ETI) remains under debate. This study aimed to clarify the correlation between gastroesophageal ETI and a bonus-freeze protocol after PVI using 2G-CBs. This study included 100 patients who underwent PVI using 2G-CB followed by an endoscopic examination. The freeze-cycle duration was set at 180 s. In the first 33 patients a 120 s bonus-freeze was applied after successful PVI (bonus group), while in the following 67 the bonus freeze was omitted (non-bonus group). Early freezing interruption was performed when the esophageal temperature reached 25 °C. Gastroesophageal ETI was defined as any injury that resulted from the PVI, including esophageal damage or periesophageal nerve injury. Gastroesophageal ETIs were observed in 9 (27.3%) and 6 (9.0%) patients and were all asymptomatic, esophageal damage in 3 and 0, and periesophageal nerve injury in the remaining 6 and 6 in the bonus group and non-bonus group, respectively (p = 0.033). In the multivariate analysis, the bonus freeze protocol (odds ratio 3.527; 95% confidence interval 1.110–11.208; p = 0.033) was the sole independent predictor of gastroesophageal ETI. During a one-year follow-up 26 of 33 bonus group patients (78.8%) and 52 of 67 (77.6%) non-bonus group patients remained in stable sinus rhythm without any differences between the groups. In the patients with a bonus-freeze protocol using the 2G-CB, gastroesophageal ETIs were detected more often than in those with the non-bonus freeze protocol. In contrast, freedom from atrial fibrillation after the 2G-CB based PVI was comparable when applying either a bonus or non-bonus freeze protocol. [ABSTRACT FROM AUTHOR]

Background An effective catheter ablation strategy, beyond pulmonary vein isolation (PVI), for persistent atrial fibrillation (AF) is necessary. Pulmonary vein (PV)-reconduction also causes recurrent atrial tachyarrhythmias. The effect of the PVI and additional effect of a superior vena cava (SVC) isolation (SVCI) was strictly evaluated. Methods Seventy consecutive patients with persistent AF who underwent a strict sequential ablation strategy targeting the PVs and SVC were included in this study. The initial ablation strategy was a circumferential PVI. A segmental SVCI was only applied as a repeat procedure when patients demonstrated no PV-reconduction. Results After the initial procedure, persistent AF was suppressed in 39 of 70 (55.7%) patients during a median follow-up of 32 months. After multiple procedures, persistent AF was suppressed in 46 (65.7%) and 52 (74.3%) patients after receiving the PVI alone and PVI plus SVCI strategies, respectively. In 6 of 15 (40.0%) patients with persistent AF resistant to PVI, persistent AF was suppressed. The persistent AF duration independently predicted persistent AF recurrences after multiple PVI alone procedures [HR: 1.012 (95% confidence interval: 1.006–1.018); p < 0.001] and PVI plus SVCI strategies [HR: 1.018 (95% confidence interval: 1.011–1.025); p < 0.001]. A receiver-operating-characteristic analysis for recurrent persistent AF indicated an optimal cut-off value of 20 and 32 months for the persistent AF duration using the PVI alone and PVI plus SVCI strategies, respectively. Conclusions The outcomes of the PVI plus SVCI strategy were favorable for patients with shorter persistent AF durations. The initial SVCI had the additional effect of maintaining sinus rhythm in some patients with persistent AF resistant to PVI. [ABSTRACT FROM AUTHOR]

Background There is little information about the relationship between J waves and the occurrence of ventricular fibrillation (VF) in patients with vasospastic angina (VSA). The present study aimed to assess the incidence of J waves and the occurrence of VF in patients with VSA. Methods The subjects consisted of 62 patients with VSA diagnosed by acetylcholine provocation tests in our institution from 2002 to 2014. We investigated the VF events, prevalence of J waves, and relationship between the VF events and J waves. Results J waves were observed in 16 patients (26%) and VF events were documented in 11 (18%). The incidence of VF in the patients with J waves was significantly higher than that in those without J waves (38% vs 11%, p = 0.026). J waves were observed in the inferior leads in 14 patients, lateral leads in 5, and anterior leads in 3. A univariate analysis indicated that the incidence of VF in the inferior leads of J wave positive patients (46% = 6/14) was significantly ( p = 0.01) higher than that in the inferior leads of J wave negative patients (10% = 5/48). The J waves in the anterior and/or lateral leads were not related to the incidence of VF. Notched type and slurred type J waves were not associated with VF. A multivariate analysis revealed that J waves in VSA patients were associated with VF [odds ratio (OR) 6.41, 95% confidence interval (CI) 1.37–29.93, p = 0.02] and organic stenosis (OR 6.98, 95% CI 1.39–35.08, p = 0.02). Further, J waves in the inferior leads were strongly correlated with VF (OR 11.85, 95% CI 2.05–68.42, p = 0.006). Conclusions The results suggest that the existence of J waves, especially in the inferior leads, might be a risk factor for VF in VSA patients. [ABSTRACT FROM AUTHOR]

Background: Ischemia suppresses action potentials (APs) by elevating interstitial K(+) and activating KATP channels and alters cytosolic Ca(2+) transients (CaTs) via metabolic inhibition.Objective: To test the hypothesis that AP and CaT respond to ischemia with different spatiotemporal courses and patterns.Methods: Thirty-four transmural wedges were isolated from canine left ventricular free walls, perfused arterially, and stained with voltage- and Ca(2+)-sensitive dyes. Twenty-eight wedges underwent 15 minutes of arterial occlusion during pacing at a cycle length (PCL) of 300 ms (n = 19) or 600 ms (n = 9). Six other wedges had a sequential reduction of perfusion flow from full to 50%, 25%, and 10% at 300 ms PCL. AP and CaT were recorded on the cut-exposed transmural surfaces with an optical mapping system.Results: Although ischemia suppressed APs, it enhanced CaT to 150% ± 10% (more in the endocardium than in the epicardium) and induced CaT alternans during the first 2 minutes of arterial occlusion and then suppressed CaT (PCL = 300 ms). Enhancement of CaT (to 159% ± 23%) also occurred during low flow (25%) perfusion (PCL = 300 ms). Faster suppression of AP occurred with subepicardial preference as compared to that of CaT. After 15 minutes of arterial occlusion, AP and CaT remained in only small regions during 300 ms PCL but were preserved in most regions during 600 ms PCL.Conclusions: Early ischemia induced a surge and alternans in CaT and caused its dissociation from AP both in time course of suppression and in spatial distribution. These results suggested that there were different cellular regulatory mechanisms of AP and of CaT in responding to ischemia from arterial occlusion. [ABSTRACT FROM AUTHOR]

Background: Ischemia suppresses action potentials (APs) by elevating interstitial K+ and activating KATP channels and alters cytosolic Ca2+ transients (CaTs) via metabolic inhibition. Objective: To test the hypothesis that AP and CaT respond to ischemia with different spatiotemporal courses and patterns. Methods: Thirty-four transmural wedges were isolated from canine left ventricular free walls, perfused arterially, and stained with voltage- and Ca2+-sensitive dyes. Twenty-eight wedges underwent 15 minutes of arterial occlusion during pacing at a cycle length (PCL) of 300 ms (n = 19) or 600 ms (n = 9). Six other wedges had a sequential reduction of perfusion flow from full to 50%, 25%, and 10% at 300 ms PCL. AP and CaT were recorded on the cut-exposed transmural surfaces with an optical mapping system. Results: Although ischemia suppressed APs, it enhanced CaT to 150% ± 10% (more in the endocardium than in the epicardium) and induced CaT alternans during the first 2 minutes of arterial occlusion and then suppressed CaT (PCL = 300 ms). Enhancement of CaT (to 159% ± 23%) also occurred during low flow (25%) perfusion (PCL = 300 ms). Faster suppression of AP occurred with subepicardial preference as compared to that of CaT. After 15 minutes of arterial occlusion, AP and CaT remained in only small regions during 300 ms PCL but were preserved in most regions during 600 ms PCL. Conclusions: Early ischemia induced a surge and alternans in CaT and caused its dissociation from AP both in time course of suppression and in spatial distribution. These results suggested that there were different cellular regulatory mechanisms of AP and of CaT in responding to ischemia from arterial occlusion. [Copyright &y& Elsevier]

Background: Isoproterenol (ISP), a beta-adrenergic agonist, suppresses arrhythmic storm in patients with sporadic Brugada syndrome (BS). However, the influence of ISP and the beta-adrenergic antagonist propranolol (PRO) on the inducibility and frequency of ventricular fibrillation (VF) in BS patients remains unclear. Methods and results: Twenty-seven BS patients with induced VF > 10sin a control state were enrolled. Electrophysiological stimulation (EPS) testing was performed during ISP and after PRO in selected patients. The inducibility and frequency of VF were compared. Dominant frequency (DF) was obtained by Fast Fourier transform from 4-s data (phase) and sequentially every 2 s up to phase 5. ISP prevented induction of VF in 20 of 25 patients (80%). During ISP, 5 patients experienced induction of VF. ISP significantly influenced DF transition compared with the control state. DF gradually increased but was unchanged after the middle phase. PRO had no effect on incidence of induced VF in 5 patients: increased PRO induced VF in 5 (83.3%) of 6 patients who tested negative during ISP. After PRO, 10 patients experienced induction of VF. Thus, PRO significantly influenced DF transition. DF after PRO was higher than that in the corresponding phase in the control state. Conclusion: ISP suppressed induction of VF and the increase of DF with time. PRO aggravated VF and accelerated DF. [ABSTRACT FROM AUTHOR]

Summary: Objective: The purpose of our study was to determine what variables were associated with ventricular fibrillation (VF) induced during electrophysiological stimulation test in patients without apparent organic heart disease. Methods: Our study evaluated 77 patients (51±15 years) who underwent electrophysiological stimulation test, signal averaging, and Na+ channel-blocker challenge test (pilsicainide test). The subjects were divided into two groups, the Brugada group and non-Brugada group. Further, the patients were divided into three subgroups on the base of symptoms (8, 7 symptomatic; 9, 13 syncope; 28, 12 asymptomatic group; in the Brugada and non-Brugada groups, respectively). Multivariate analyses evaluated the association between baseline clinical factors and the induction of VF. Results: The inducibility of VF was significantly (p <0.0001) higher in the Brugada group (n =33, 73%) than the non-Brugada group (n =4, 13%). The multivariate analysis demonstrated that symptoms (odds ratio (OR) 31.6; 95% confidence interval (CI): 2.3–430.6; p <0.01), type 1 electrocardiogram after pilsicainide test (OR 21.3; CI: 1.7–272.2; p <0.02), and syncope (OR 13.5; CI: 1.2–158.8; p <0.05) were strongly associated with the inducibility of VF, but not with family history, type 1 electrocardiogram in control, positive in late potential, maxΔST elevation (≧200μV) after pilsicainide test. Conclusions: The symptoms, syncope, and type 1 electrocardiogram after pilsicainide test were independently associated with the electrophysiological substrate of VF in patients without apparent heart disease. [ABSTRACT FROM AUTHOR]

Abstract: We report a patient with a concealed type of Brugada syndrome. The electrocardiogram in the emergency department revealed atrial fibrillation with an almost normal ST segment. Slight electrocardiogram abnormalities of the J wave and mild ST-segment elevation appeared in the inferolateral leads a few days later. Although the ST segment in the right precordial leads, including that recorded from the high intercostal space recording sites, was completely normal, a drug challenge test using pilsicainide revealed a coved-type ST-segment elevation only in a modified V2 lead placed 1 or 2 intercostal spaces higher. [Copyright &y& Elsevier]