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Satoshi Ogawa - One of the best experts on this subject based on the ideXlab platform.
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Electropharmacologic effects of Pilsicainide, a pure sodium channel blocker, on the remodeled atrium subjected to chronic rapid pacing.
Journal of Cardiovascular Pharmacology, 2001Co-Authors: Toshiaki Sato, Hideo Mitamura, Yasuo Kurita, Akiko Takeshita, Kaori Shinagawa, Shunichiro Miyoshi, Hideaki Kanki, Motoki Hara, Satoshi OgawaAbstract:Clinical experience suggests that sodium channel blockers are effective in converting atrial fibrillation of recent onset but not chronic atrial fibrillation. We investigated changes in the electrophysiologic effects of Pilsicainide, a pure sodium channel blocker, on the canine atrium during chronic rapid pacing (400/min). Three pairs of bipolar electrodes were sutured to the right atrial appendage in six dogs. Five days later, rapid atrial pacing was started after baseline measurements of the effective refractory period (ERP), the intra-atrial conduction velocity, the atrial wavelength, and the inducibility of atrial fibrillation. These studies were repeated at 2, 7, and 14 days of pacing, both before and after Pilsicainide administration. Before pacing, Pilsicainide increased ERP more than it decreased conduction velocity, causing an increase of wavelength, particularly at faster rates. However, this use-dependent prolongation of ERP disappeared after 2 days of pacing. Thus, Pilsicainide failed to prolong ERP during chronic pacing, allowing progressive shortening of wavelength in the remodeled atrium. The effect of sodium channel blockers on atrial refractoriness may decline as rapid atrial excitation persists, limiting the usefulness of these agents for the treatment of chronic atrial fibrillation.
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Determination of refractory periods and conduction velocity during atrial fibrillation using atrial capture in dogs: direct assessment of the wavelength and its modulation by a sodium channel blocker, Pilsicainide.
Journal of the American College of Cardiology, 2000Co-Authors: Kaori Shinagawa, Toshiaki Sato, Hideo Mitamura, Akiko Takeshita, Hideaki Kanki, Seiji Takatsuki, Satoshi OgawaAbstract:Abstract OBJECTIVES The purposes of this study were to measure the atrial refractory period and the conduction velocity (CV) during atrial fibrillation (AF) and to explore the antiarrhythmic mechanism of a sodium channel blocker, Pilsicainide, during AF. BACKGROUND Sodium channel blockers not only decrease the CV, but also prolong the atrial refractory period, particularly during rapid excitation. Because these effects on the wavelength are counteractive and rate dependent, it is critical to measure these parameters during AF. METHODS In eight dogs, after AF was induced under vagal stimulation, a single extra-stimulus was repeatedly introduced from the left atrium and its capture was statistically determined for each coupling interval. The local CV was also measured during constant capture of the fibrillating atrium by rapid pacing. The same procedure was repeated after Pilsicainide administration. RESULTS Pilsicainide significantly increased the mode of AF intervals from 81 ± 10 to 107 ± 16 ms (p CONCLUSIONS During AF, whereas the sodium channel blocker Pilsicainide decreases CV, it lengthens the wavelength by increasing the refractory period, an action that is likely to contribute to the drug’s ability to terminate the arrhythmia. The direct measurement of refractoriness and CV during AF may provide new insights into the determinations of the arrhythmia and antiarrhythmic drug action.
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Profiles of Aprindine, Cibenzoline, Pilsicainide and Pirmenol in the Framework of the Sicilian Gambit
Japanese circulation journal, 1999Co-Authors: Itsuo Kodama, Hideo Mitamura, Satoshi Ogawa, Hiroshi Kasanuki, Hiroshi Inoue, Masayasu Hiraoka, Takao Kato, Tsuneaki SugimotoAbstract:The Vaughan Williams classification has been used widely by clinicians, cardiologists and researchers engaged in antiarrhythmic drug development and testing in many countries throughout the world since its initial proposal in the early 1970s. However, a major criticism of the Vaughan Williams system arose from the extent to which the categorization of drugs into classes I-IV led to oversimplified views of both shared and divergent actions. The Sicilian Gambit proposed a two-dimensional tabular framework for display of drug actions to solve these problems. From April to December 1996, members of the Guideline Committee met to discuss pharmacologic profiles of 4 antiarrhythmic drugs (aprindine, cibenzoline, Pilsicainide, and pirmenol) that were not included in the original spreadsheet but are used widely in clinical practice in Japan. The discussion aimed to fit the drug profiles into the Gambit framework based on all the important literature published to date regarding the actions of the 4 drugs. This report is a summary of that deliberation. (Jpn Circ J 1999; 63: 1 - 12)
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Postrepolarization refractoriness as a potential anti-atrial fibrillation mechanism of Pilsicainide, a pure sodium channel blocker with slow recovery kinetics.
Cardiovascular Drugs and Therapy, 1998Co-Authors: Hideaki Kanki, Toshiaki Sato, Hideo Mitamura, Kaori Shinagawa, Seiji Takatsuki, Kouichiro Sueyoshi, Satoshi OgawaAbstract:The antifibrillatory effect of Pilsicainide, a sodium channel blocker with slow recovery kinetics, was investigated in a canine model of atrial fibrillation. Prolonging the atrial effective refractory period is an important mechanism for pharmacological termination of atrial fibrillation. However, the effectiveness of potassium channel blockers has been questioned because of their reverse-use–dependent property. In eight open-chest dogs, the duration of the atrial endocardial monophasic action potential and the atrial effective refractory period were determined using a Franz catheter. Conduction velocity was obtained from a 96-channel mapping electrode at multiple cycle lengths. Inducibility of sustained atrial fibrillation (>30 minutes) was confirmed by atrial burst pacing during bilateral vagal stimulation, and local fibrillation cycle lengths were measured. Five minutes after restarting fibrillation, Pilsicainide (0.6 mg/kg + 0.04 mg/kg/min) was administered. After fibrillation was terminated, measurements were repeated. Pilsicainide successfully terminated atrial fibrillation in 7 of 8 dogs after the median time of 5.1 minutes. The conduction velocity decreased significantly. Although Pilsicainide did not affect monophasic action potential duration, it caused use-dependent prolongation of the atrial effective refractory period (P < 0.05), creating postrepolarization refractoriness. Accordingly, Pilsicainide prolonged the atrial fibrillation cycle length from 80.6 to 113.8 ms (P < 0.05) before termination of fibrillation. Sodium channel blockers with slow recovery kinetics can prolong the atrial effective refractory period without affecting monophasic action potential duration. Unlike potassium channel blockers, these sodium channel blockers maintain postrepolarization refract
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ischemia enhances use dependent sodium channel blockade by Pilsicainide a class ic antiarrhythmic agent
Journal of the American College of Cardiology, 1994Co-Authors: Tsuneaki Sadanaga, Satoshi OgawaAbstract:Abstract Objectives . The aim of this study was to elucidate whether the electrophysiologic properties of Pilsicainide, a novel class IC drug with slow kinetic properties, could be altered in the presence of acute myocardial ischemia. Background . An increase in the rate of sudden death in patients taking flecainide and encainide has been reported by the Cardiac Arrhythmia Suppression Trial (CAST), implying a proarrhythmic effect that may be due to the interaction between ischemia and class IC antiarrhythmic drugs. Methods . Thirty-five patients and 16 age-matched control patients performed a treadmill exercise test and were assigned to four study groups: group A = 16 control patients; group B = 15 patients with ischemic ST segment depression; group C = 11 patients receiving Pilsicainide without ST segment depression; and group D = 9 patients receiving Pilsicainide with ischemic ST segment depression. The QRS duration was measured at rest and at heart rates of 80, 100 and 120 beats/min. Results . There were no changes in the QRS duration as heart rates increased to 120 beats/min in the control patients. Ischemia, however, independently caused a significant increase in QRS duration at a heart rate of 120 beats/min. Pilsicainide produced a rate-dependent prolongation of the QRS duration in patients without ST segment depression as the heart rate increased to 100 beats/min. The combination of ischemia and Pilsicainide led to a much greater rate-dependent prolongation of the QRS duration. Conclusions . Combination of a class IC drag and acute ischemia could lead to additive rate-pendent ventricular conduction slowing. This may be one plausible mechanism for the induction of proarrhythimias noted ta the CAST study.
Tohru Ohe - One of the best experts on this subject based on the ideXlab platform.
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longer repolarization in the epicardium at the right ventricular outflow tract causes type 1 electrocardiogram in patients with brugada syndrome
Journal of the American College of Cardiology, 2008Co-Authors: Satoshi Nagase, Hiroshi Morita, Atsuyuki Watanabe, Nobuhiro Nishii, Kimikazu Banba, Kazufumi Nakamura, Kengo Kusano, Shigeki Hiramatsu, Satoru Sakuragi, Tohru OheAbstract:Objectives We examined the relationship between repolarization abnormality and coved-type ST-segment elevation with terminal inverted T-wave (type 1 electrocardiogram [ECG]) in patients with Brugada syndrome (BrS). Background Recent experimental studies have suggested that accentuation of the right ventricular action potential (AP) notch preferentially prolongs epicardial AP causing inversion of the T-wave. Methods In 19 patients with BrS and 3 control subjects, activation-recovery intervals (ARIs) and repolarization times (RTs) in the epicardium and endocardium were directly examined with the use of local unipolar electrograms at the right ventricular outflow tract. Surface ECG, ARI, and RT were examined before and after administration of Pilsicainide. Results Type 1 ECG was observed in 10 of the 19 BrS patients before the administration of Pilsicainide and in all of the 19 patients after the administration of Pilsicainide. We found that ARI and RT in the epicardium were shorter than those in the endocardium in all 9 BrS patients without type 1 ECG under baseline conditions and in all control subjects regardless of Pilsicainide administration. However, longer epicardial ARI than endocardial ARI was observed in 8 of the 10 BrS patients manifesting type 1 ECG under baseline conditions and in all of the BrS patients after the administration of Pilsicainide. Also, epicardial RT was longer than endocardial RT in all patients manifesting type 1 ECG regardless of Pilsicainide administration. Conclusions Our data provide support for the hypothesis that the negative T-wave associated with type 1 BrS ECG is due to a preferential prolongation of the epicardial AP secondary to accentuation of the AP notch in the region of the right ventricular outflow tract.
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clinical significance of macroscopic t wave alternans after sodium channel blocker administration in patients with brugada syndrome
Journal of Cardiovascular Electrophysiology, 2007Co-Authors: Takeshi Tada, Hiroshi Morita, Atsuyuki Watanabe, Nobuhiro Nishii, Satoshi Nagase, Kimikazu Banba, Kazufumi Nakamura, Kengo Kusano, Daiji Miura, Tohru OheAbstract:Introduction: Macroscopic T-wave alternans (TWA) is sometimes observed after sodium channel blocker administration in patients with Brugada syndrome (BS), but little is known about the association between occurrence of TWA and clinical characteristics in BS patients. We investigated the association between spontaneous ventricular fibrillation (VF) occurrence and TWA after Pilsicainide, a sodium channel blocker administration in BS patients. Methods and Results: We administered Pilsicainide at a dose of 1 mg/kg to 77 BS patients (76 males and one female; mean age, 48.4 years) and examined the association between TWA after Pilsicainide administration and clinical characteristics, including age, spontaneous VF, syncope, family history of sudden death, spontaneous coved ST elevation, late potentials (LP), induction of VF by programmed electrical stimulation, and SCN5A mutation. None of the patients had TWA before Pilsicainide administration, but TWA became apparent in 17 (22.1%) of the patients after Pilsicainide administration. Patients with TWA had a significantly higher incidence of spontaneous VF (52.9% vs 8.3%, P < 0.001) and syncope (58.8% vs 26.7%, P < 0.05) than did patients without TWA. Then, we focused on the association between spontaneous VF and clinical characteristics. Patients with spontaneous VF had a significantly higher incidence of TWA (64.3% vs 12.7%, P < 0.001) and LP positive (92.9% vs 56.5%, P < 0.01) than did patients without spontaneous VF. In multivariate analysis, TWA (P = 0.001) and LP (P = 0.047) appeared as the independent predictor for spontaneous VF. Conclusion: TWA after Pilsicainide administration is associated with a high risk of clinical VF in patients with BS.
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effect of Pilsicainide a pure sodium channel blocker on spiral waves during atrial fibrillation theoretical analysis by numerical simulation
Journal of Electrocardiology, 1999Co-Authors: Tsunetoyo Namba, Takashi Ashihara, Kazuo Nakazawa, Tohru OheAbstract:Abstract This study investigated the effects of a particular type of sodium channel blocker, Pilsicainide, on spiral waves, which are a possible mechanism of atrial fibrillation, by using numerical simulation. A meandering spiral wave was induced on a two-dimensional matrix corresponding to the isolated atrial myocardium. The model attempted to simulate the changes caused by Pilsicainide. The conductivity was depressed and the refractory period was prolonged with little change in the action potential duration. The dynamic change in the refractory period depended on the preceding coupling interval. A blockline occurred and changed gradually because of the change in the refractory period. The spiral wave became a stable reentry rotating around the blockline, decreasing the excitation frequency in the matrix before rushing out of the matrix. The electrocardiogram showed a slow coarse wave, as well as a real electrocardiographic change by Pilsicainide. This might, in part, explain how Pilsicainide acts on atrial fibrillation.
Hiroshi Morita - One of the best experts on this subject based on the ideXlab platform.
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longer repolarization in the epicardium at the right ventricular outflow tract causes type 1 electrocardiogram in patients with brugada syndrome
Journal of the American College of Cardiology, 2008Co-Authors: Satoshi Nagase, Hiroshi Morita, Atsuyuki Watanabe, Nobuhiro Nishii, Kimikazu Banba, Kazufumi Nakamura, Kengo Kusano, Shigeki Hiramatsu, Satoru Sakuragi, Tohru OheAbstract:Objectives We examined the relationship between repolarization abnormality and coved-type ST-segment elevation with terminal inverted T-wave (type 1 electrocardiogram [ECG]) in patients with Brugada syndrome (BrS). Background Recent experimental studies have suggested that accentuation of the right ventricular action potential (AP) notch preferentially prolongs epicardial AP causing inversion of the T-wave. Methods In 19 patients with BrS and 3 control subjects, activation-recovery intervals (ARIs) and repolarization times (RTs) in the epicardium and endocardium were directly examined with the use of local unipolar electrograms at the right ventricular outflow tract. Surface ECG, ARI, and RT were examined before and after administration of Pilsicainide. Results Type 1 ECG was observed in 10 of the 19 BrS patients before the administration of Pilsicainide and in all of the 19 patients after the administration of Pilsicainide. We found that ARI and RT in the epicardium were shorter than those in the endocardium in all 9 BrS patients without type 1 ECG under baseline conditions and in all control subjects regardless of Pilsicainide administration. However, longer epicardial ARI than endocardial ARI was observed in 8 of the 10 BrS patients manifesting type 1 ECG under baseline conditions and in all of the BrS patients after the administration of Pilsicainide. Also, epicardial RT was longer than endocardial RT in all patients manifesting type 1 ECG regardless of Pilsicainide administration. Conclusions Our data provide support for the hypothesis that the negative T-wave associated with type 1 BrS ECG is due to a preferential prolongation of the epicardial AP secondary to accentuation of the AP notch in the region of the right ventricular outflow tract.
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clinical significance of macroscopic t wave alternans after sodium channel blocker administration in patients with brugada syndrome
Journal of Cardiovascular Electrophysiology, 2007Co-Authors: Takeshi Tada, Hiroshi Morita, Atsuyuki Watanabe, Nobuhiro Nishii, Satoshi Nagase, Kimikazu Banba, Kazufumi Nakamura, Kengo Kusano, Daiji Miura, Tohru OheAbstract:Introduction: Macroscopic T-wave alternans (TWA) is sometimes observed after sodium channel blocker administration in patients with Brugada syndrome (BS), but little is known about the association between occurrence of TWA and clinical characteristics in BS patients. We investigated the association between spontaneous ventricular fibrillation (VF) occurrence and TWA after Pilsicainide, a sodium channel blocker administration in BS patients. Methods and Results: We administered Pilsicainide at a dose of 1 mg/kg to 77 BS patients (76 males and one female; mean age, 48.4 years) and examined the association between TWA after Pilsicainide administration and clinical characteristics, including age, spontaneous VF, syncope, family history of sudden death, spontaneous coved ST elevation, late potentials (LP), induction of VF by programmed electrical stimulation, and SCN5A mutation. None of the patients had TWA before Pilsicainide administration, but TWA became apparent in 17 (22.1%) of the patients after Pilsicainide administration. Patients with TWA had a significantly higher incidence of spontaneous VF (52.9% vs 8.3%, P < 0.001) and syncope (58.8% vs 26.7%, P < 0.05) than did patients without TWA. Then, we focused on the association between spontaneous VF and clinical characteristics. Patients with spontaneous VF had a significantly higher incidence of TWA (64.3% vs 12.7%, P < 0.001) and LP positive (92.9% vs 56.5%, P < 0.01) than did patients without spontaneous VF. In multivariate analysis, TWA (P = 0.001) and LP (P = 0.047) appeared as the independent predictor for spontaneous VF. Conclusion: TWA after Pilsicainide administration is associated with a high risk of clinical VF in patients with BS.
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Ventricular arrhythmia induced by sodium channel blocker in patients with Brugada syndrome
Journal of the American College of Cardiology, 2003Co-Authors: Hiroshi Morita, Atsuyuki Watanabe, Nobuhiro Nishii, Shiho Takenaka Morita, Satoshi Nagase, Kimikazu Banba, Yoshinori Tani, Kazufumi Nakamura, Kengo Kusano, Tetsuro EmoriAbstract:OBJECTIVES We administered Pilsicainide chloride, a class Ic pure sodium channel blocker, to patients with Brugada syndrome (BS) and evaluated the occurrence of ventricular arrhythmia (VA) and T-wave alternans (TWA). BACKGROUND Ventricular arrhythmia and TWA are sometimes induced by a sodium channel blocker challenge test in BS patients, but the significance of the induced VA and TWA is not known. METHODS Pilsicainide was administered to 65 patients with BS (10 symptomatic and 55 asymptomatic patients), and the occurrence of VA, TWA, and change of electrocardiogram were evaluated. Electrophysiologic study was performed in 57 patients, and the induction of VA by programmed electrical stimulation (PES) was evaluated. RESULTS Ventricular arrhythmia was not induced by administration of Pilsicainide in 55 patients (no-VA group). Administration of Pilsicainide-induced VA in 10 patients (Pil-VA group) and polymorphic ventricular tachycardia in four patients. Pilsicainide-induced VA in 60% of the symptomatic patients but in only 7% of asymptomatic patients (p < 0.01). ST level, QTc, and indexes of cardiac conduction in the Pil-VA group were not different from those in the no-VA group. Ventricular fibrillation was induced by PES in 67% of the patients in the Pil-VA group and in 33% of the patients in the no-VA group. In six cases, macroscopic TWA occurred in association with Pilsicainide-induced VA, but TWA occurred in only one patient without Pilsicainide-induced arrhythmia. CONCLUSIONS Administration of a sodium channel blocker results in induction of not only ST-elevation but also VA and TWA in patients with BS.
Satoshi Nagase - One of the best experts on this subject based on the ideXlab platform.
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longer repolarization in the epicardium at the right ventricular outflow tract causes type 1 electrocardiogram in patients with brugada syndrome
Journal of the American College of Cardiology, 2008Co-Authors: Satoshi Nagase, Hiroshi Morita, Atsuyuki Watanabe, Nobuhiro Nishii, Kimikazu Banba, Kazufumi Nakamura, Kengo Kusano, Shigeki Hiramatsu, Satoru Sakuragi, Tohru OheAbstract:Objectives We examined the relationship between repolarization abnormality and coved-type ST-segment elevation with terminal inverted T-wave (type 1 electrocardiogram [ECG]) in patients with Brugada syndrome (BrS). Background Recent experimental studies have suggested that accentuation of the right ventricular action potential (AP) notch preferentially prolongs epicardial AP causing inversion of the T-wave. Methods In 19 patients with BrS and 3 control subjects, activation-recovery intervals (ARIs) and repolarization times (RTs) in the epicardium and endocardium were directly examined with the use of local unipolar electrograms at the right ventricular outflow tract. Surface ECG, ARI, and RT were examined before and after administration of Pilsicainide. Results Type 1 ECG was observed in 10 of the 19 BrS patients before the administration of Pilsicainide and in all of the 19 patients after the administration of Pilsicainide. We found that ARI and RT in the epicardium were shorter than those in the endocardium in all 9 BrS patients without type 1 ECG under baseline conditions and in all control subjects regardless of Pilsicainide administration. However, longer epicardial ARI than endocardial ARI was observed in 8 of the 10 BrS patients manifesting type 1 ECG under baseline conditions and in all of the BrS patients after the administration of Pilsicainide. Also, epicardial RT was longer than endocardial RT in all patients manifesting type 1 ECG regardless of Pilsicainide administration. Conclusions Our data provide support for the hypothesis that the negative T-wave associated with type 1 BrS ECG is due to a preferential prolongation of the epicardial AP secondary to accentuation of the AP notch in the region of the right ventricular outflow tract.
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clinical significance of macroscopic t wave alternans after sodium channel blocker administration in patients with brugada syndrome
Journal of Cardiovascular Electrophysiology, 2007Co-Authors: Takeshi Tada, Hiroshi Morita, Atsuyuki Watanabe, Nobuhiro Nishii, Satoshi Nagase, Kimikazu Banba, Kazufumi Nakamura, Kengo Kusano, Daiji Miura, Tohru OheAbstract:Introduction: Macroscopic T-wave alternans (TWA) is sometimes observed after sodium channel blocker administration in patients with Brugada syndrome (BS), but little is known about the association between occurrence of TWA and clinical characteristics in BS patients. We investigated the association between spontaneous ventricular fibrillation (VF) occurrence and TWA after Pilsicainide, a sodium channel blocker administration in BS patients. Methods and Results: We administered Pilsicainide at a dose of 1 mg/kg to 77 BS patients (76 males and one female; mean age, 48.4 years) and examined the association between TWA after Pilsicainide administration and clinical characteristics, including age, spontaneous VF, syncope, family history of sudden death, spontaneous coved ST elevation, late potentials (LP), induction of VF by programmed electrical stimulation, and SCN5A mutation. None of the patients had TWA before Pilsicainide administration, but TWA became apparent in 17 (22.1%) of the patients after Pilsicainide administration. Patients with TWA had a significantly higher incidence of spontaneous VF (52.9% vs 8.3%, P < 0.001) and syncope (58.8% vs 26.7%, P < 0.05) than did patients without TWA. Then, we focused on the association between spontaneous VF and clinical characteristics. Patients with spontaneous VF had a significantly higher incidence of TWA (64.3% vs 12.7%, P < 0.001) and LP positive (92.9% vs 56.5%, P < 0.01) than did patients without spontaneous VF. In multivariate analysis, TWA (P = 0.001) and LP (P = 0.047) appeared as the independent predictor for spontaneous VF. Conclusion: TWA after Pilsicainide administration is associated with a high risk of clinical VF in patients with BS.
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Ventricular arrhythmia induced by sodium channel blocker in patients with Brugada syndrome
Journal of the American College of Cardiology, 2003Co-Authors: Hiroshi Morita, Atsuyuki Watanabe, Nobuhiro Nishii, Shiho Takenaka Morita, Satoshi Nagase, Kimikazu Banba, Yoshinori Tani, Kazufumi Nakamura, Kengo Kusano, Tetsuro EmoriAbstract:OBJECTIVES We administered Pilsicainide chloride, a class Ic pure sodium channel blocker, to patients with Brugada syndrome (BS) and evaluated the occurrence of ventricular arrhythmia (VA) and T-wave alternans (TWA). BACKGROUND Ventricular arrhythmia and TWA are sometimes induced by a sodium channel blocker challenge test in BS patients, but the significance of the induced VA and TWA is not known. METHODS Pilsicainide was administered to 65 patients with BS (10 symptomatic and 55 asymptomatic patients), and the occurrence of VA, TWA, and change of electrocardiogram were evaluated. Electrophysiologic study was performed in 57 patients, and the induction of VA by programmed electrical stimulation (PES) was evaluated. RESULTS Ventricular arrhythmia was not induced by administration of Pilsicainide in 55 patients (no-VA group). Administration of Pilsicainide-induced VA in 10 patients (Pil-VA group) and polymorphic ventricular tachycardia in four patients. Pilsicainide-induced VA in 60% of the symptomatic patients but in only 7% of asymptomatic patients (p < 0.01). ST level, QTc, and indexes of cardiac conduction in the Pil-VA group were not different from those in the no-VA group. Ventricular fibrillation was induced by PES in 67% of the patients in the Pil-VA group and in 33% of the patients in the no-VA group. In six cases, macroscopic TWA occurred in association with Pilsicainide-induced VA, but TWA occurred in only one patient without Pilsicainide-induced arrhythmia. CONCLUSIONS Administration of a sodium channel blocker results in induction of not only ST-elevation but also VA and TWA in patients with BS.
Nobuhiro Nishii - One of the best experts on this subject based on the ideXlab platform.
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longer repolarization in the epicardium at the right ventricular outflow tract causes type 1 electrocardiogram in patients with brugada syndrome
Journal of the American College of Cardiology, 2008Co-Authors: Satoshi Nagase, Hiroshi Morita, Atsuyuki Watanabe, Nobuhiro Nishii, Kimikazu Banba, Kazufumi Nakamura, Kengo Kusano, Shigeki Hiramatsu, Satoru Sakuragi, Tohru OheAbstract:Objectives We examined the relationship between repolarization abnormality and coved-type ST-segment elevation with terminal inverted T-wave (type 1 electrocardiogram [ECG]) in patients with Brugada syndrome (BrS). Background Recent experimental studies have suggested that accentuation of the right ventricular action potential (AP) notch preferentially prolongs epicardial AP causing inversion of the T-wave. Methods In 19 patients with BrS and 3 control subjects, activation-recovery intervals (ARIs) and repolarization times (RTs) in the epicardium and endocardium were directly examined with the use of local unipolar electrograms at the right ventricular outflow tract. Surface ECG, ARI, and RT were examined before and after administration of Pilsicainide. Results Type 1 ECG was observed in 10 of the 19 BrS patients before the administration of Pilsicainide and in all of the 19 patients after the administration of Pilsicainide. We found that ARI and RT in the epicardium were shorter than those in the endocardium in all 9 BrS patients without type 1 ECG under baseline conditions and in all control subjects regardless of Pilsicainide administration. However, longer epicardial ARI than endocardial ARI was observed in 8 of the 10 BrS patients manifesting type 1 ECG under baseline conditions and in all of the BrS patients after the administration of Pilsicainide. Also, epicardial RT was longer than endocardial RT in all patients manifesting type 1 ECG regardless of Pilsicainide administration. Conclusions Our data provide support for the hypothesis that the negative T-wave associated with type 1 BrS ECG is due to a preferential prolongation of the epicardial AP secondary to accentuation of the AP notch in the region of the right ventricular outflow tract.
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clinical significance of macroscopic t wave alternans after sodium channel blocker administration in patients with brugada syndrome
Journal of Cardiovascular Electrophysiology, 2007Co-Authors: Takeshi Tada, Hiroshi Morita, Atsuyuki Watanabe, Nobuhiro Nishii, Satoshi Nagase, Kimikazu Banba, Kazufumi Nakamura, Kengo Kusano, Daiji Miura, Tohru OheAbstract:Introduction: Macroscopic T-wave alternans (TWA) is sometimes observed after sodium channel blocker administration in patients with Brugada syndrome (BS), but little is known about the association between occurrence of TWA and clinical characteristics in BS patients. We investigated the association between spontaneous ventricular fibrillation (VF) occurrence and TWA after Pilsicainide, a sodium channel blocker administration in BS patients. Methods and Results: We administered Pilsicainide at a dose of 1 mg/kg to 77 BS patients (76 males and one female; mean age, 48.4 years) and examined the association between TWA after Pilsicainide administration and clinical characteristics, including age, spontaneous VF, syncope, family history of sudden death, spontaneous coved ST elevation, late potentials (LP), induction of VF by programmed electrical stimulation, and SCN5A mutation. None of the patients had TWA before Pilsicainide administration, but TWA became apparent in 17 (22.1%) of the patients after Pilsicainide administration. Patients with TWA had a significantly higher incidence of spontaneous VF (52.9% vs 8.3%, P < 0.001) and syncope (58.8% vs 26.7%, P < 0.05) than did patients without TWA. Then, we focused on the association between spontaneous VF and clinical characteristics. Patients with spontaneous VF had a significantly higher incidence of TWA (64.3% vs 12.7%, P < 0.001) and LP positive (92.9% vs 56.5%, P < 0.01) than did patients without spontaneous VF. In multivariate analysis, TWA (P = 0.001) and LP (P = 0.047) appeared as the independent predictor for spontaneous VF. Conclusion: TWA after Pilsicainide administration is associated with a high risk of clinical VF in patients with BS.
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Ventricular arrhythmia induced by sodium channel blocker in patients with Brugada syndrome
Journal of the American College of Cardiology, 2003Co-Authors: Hiroshi Morita, Atsuyuki Watanabe, Nobuhiro Nishii, Shiho Takenaka Morita, Satoshi Nagase, Kimikazu Banba, Yoshinori Tani, Kazufumi Nakamura, Kengo Kusano, Tetsuro EmoriAbstract:OBJECTIVES We administered Pilsicainide chloride, a class Ic pure sodium channel blocker, to patients with Brugada syndrome (BS) and evaluated the occurrence of ventricular arrhythmia (VA) and T-wave alternans (TWA). BACKGROUND Ventricular arrhythmia and TWA are sometimes induced by a sodium channel blocker challenge test in BS patients, but the significance of the induced VA and TWA is not known. METHODS Pilsicainide was administered to 65 patients with BS (10 symptomatic and 55 asymptomatic patients), and the occurrence of VA, TWA, and change of electrocardiogram were evaluated. Electrophysiologic study was performed in 57 patients, and the induction of VA by programmed electrical stimulation (PES) was evaluated. RESULTS Ventricular arrhythmia was not induced by administration of Pilsicainide in 55 patients (no-VA group). Administration of Pilsicainide-induced VA in 10 patients (Pil-VA group) and polymorphic ventricular tachycardia in four patients. Pilsicainide-induced VA in 60% of the symptomatic patients but in only 7% of asymptomatic patients (p < 0.01). ST level, QTc, and indexes of cardiac conduction in the Pil-VA group were not different from those in the no-VA group. Ventricular fibrillation was induced by PES in 67% of the patients in the Pil-VA group and in 33% of the patients in the no-VA group. In six cases, macroscopic TWA occurred in association with Pilsicainide-induced VA, but TWA occurred in only one patient without Pilsicainide-induced arrhythmia. CONCLUSIONS Administration of a sodium channel blocker results in induction of not only ST-elevation but also VA and TWA in patients with BS.