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Journal of Cardiology 03/2013; · 1.28 Impact Factor
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ABSTRACT: 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.
Twenty-seven BS patients with induced VF>10s in 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 2s 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.
ISP suppressed induction of VF and the increase of DF with time. PRO aggravated VF and accelerated DF.
Journal of Cardiology 03/2012; 60(1):47-54. · 1.28 Impact Factor
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ABSTRACT: Limited information is available on the ventricular fibrillation (VF) spectrum in Brugada syndrome (BS) patients. We clarified differences in the VF cycle length (CL) using fast-Fourier transformation (FFT) analysis in symptomatic and asymptomatic BS patients.
VF was induced by pacing from the right ventricular (RV) apex and/or RV outflow tract (RVOT) for >8s. A 4096-point FFT analysis of results from 28 male BS patients (51.1 ± 13.7 years old) was performed. Dominant frequency (DF) from phases 1 (4s) to 6 was obtained at 2-s intervals. The average DF from surface and intracardiac electrograms (ECG: DF(ECG); ICE: DF(ICE,), respectively) was compared between symptomatic and asymptomatic patients. Symptomatic patients had a significantly shorter effective refractory period at a CL of 600 ms at the RVOT than asymptomatic patients. DF(ECG) significantly increased with phase (5.64 ± 0.32 Hz in phase 1 to 6.16 ± 0.52 Hz in phase 6) and was significantly higher in symptomatic patients than in asymptomatic patients. DF(ICE) had the same characteristics as DF(ECG).
Induced VF in BS patients can be characterized using FFT analysis. Our data support the hypothesis that symptomatic patients have a significantly shorter VF CL than asymptomatic patients.
Circulation Journal 02/2012; 76(3):624-33. · 3.77 Impact Factor
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Shigeki Kobayashi,
Takehisa Susa,
Takeo Tanaka,
Yasuaki Wada,
Shinichi Okuda,
Masahiro Doi,
Tomoko Nao, Yasuhiro Yoshiga,
Jutaro Yamada,
Takayuki Okamura,
Takeshi Ueyama,
Syuji Kawamura,
Masafumi Yano,
Masunori Matsuzaki
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ABSTRACT: Oxidative stress is known to play a crucial role in the pathogenesis of heart failure (HF). We investigated whether urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), a product of oxidative DNA damage, is a clinically useful biomarker of the severity of chronic heart failure (CHF) and oxidative stress levels in failing hearts.
We measured 8-OHdG in the serum obtained from the coronary sinus (CS) and aortic root (Ao) in small groups of control subjects and CHF patients. We then measured urinary 8-OHdG and other biomarkers (brain natriuretic peptide, 8-isoplastane, high-sensitivity C-reactive protein, interleukin-6, and tumour necrosis factor-α) in 31 control subjects and 194 patients with CHF [left-ventricular ejection fraction (LVEF): 28.3 ± 8.1%]. Serum 8-OHdG was significantly higher in the CS than the Ao in CHF patients only. Urinary 8-OHdG was also significantly higher in CHF patients than in control subjects, and urinary 8-OHdG became higher as New York Heart Association class increased. Moreover, there was a significant correlation between urinary 8-OHdG and LVEF (r = -0.27), pulmonary capillary wedge pressure (r = 0.31), or left-ventricular end-diastolic volume index (r = 0.22). In contrast, there was poor correlation between the severity of CHF and the other neurohumoral biomarkers.
In HF, urinary 8-OHdG seems to reflect the level of oxidative stress and various parameters related to symptomatic status and functional severity of CHF.
European Journal of Heart Failure 10/2010; 13(1):29-36. · 4.90 Impact Factor
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ABSTRACT: 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.
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.
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, maxDeltaST elevation (>==200microV) after pilsicainide test.
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.
Journal of Cardiology 03/2010; 56(1):35-43. · 1.28 Impact Factor
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ABSTRACT: To investigate the activation patterns and conduction velocity (CV) in the posterolateral right atrial (RA) wall during typical counterclockwise atrial flutter (AFL) using an electroanatomic mapping system.
During typical AFL in 25 patients, the transverse conduction pattern and CV were classified and calculated. The line blocking transverse conduction was defined by the conduction pattern and double potentials recorded during mapping. There were 3 types (including 2 subtypes) of transverse conduction pattern based on the conduction blocks across the posterolateral RA in a line between the superior and inferior venae cava. Trans-cristal conduction activation in a horizontal direction was seen in all but 4 patients. The CV in the gap area was 0.59+/-0.21 m/s.
Three types of transverse conduction pattern were observed during trans-ctristal conduction and the trans-ctristal CV was relatively slower than that in other parts of the RA, except for the isthmus.
Circulation Journal 04/2008; 72(3):384-91. · 3.77 Impact Factor
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ABSTRACT: The patient was a 50-year-old male in 2002, who was first suspected of having a Brugada-type electrocardiogram (ECG). A drug challenge test using pilsicainide was performed and unmasked a typical coved type ST elevation followed by ventricular arrhythmias (VAs) manifesting a QRS pattern with a right bundle branch block and left axis deviation. Three years later, he was transferred to the emergency room due to a wide QRS tachycardia with the same QRS morphology as the VA that previously occurred in the drug challenge test. An ECG just after the recorded termination of the tachycardia exhibited a typical Brugada-type ECG. In an electrophysiological study, ventricular fibrillation could be easily induced with reproducibility. Since the clinical tachycardia could not be sustained by an isoproterenol infusion, mapping and catheter ablation targeting the pilsicainide-induced VAs was performed. The successful ablation site was the left mid-lower septal wall where a Purkinje potential was recorded and a false tendon was attached just to it.
Europace 02/2008; 10(1):86-90. · 1.98 Impact Factor
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Nippon rinsho. Japanese journal of clinical medicine 09/2007; Suppl 4:338-41.
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Takeshi Ueyama,
Akihiko Shimizu,
Toshihiko Yamagata,
Masahiro Esato,
Masato Ohmura, Yasuhiro Yoshiga,
Masashi Kanemoto,
Ryousuke Kametani,
Akira Sawa,
Shinsuke Suzuki,
Naoki Sugi,
Masunori Matsuzaki
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ABSTRACT: The response of the ST-segment in the right precordial leads to Na+ channel blockers in patients without structural heart disease and a typical Brugada-type ECG has not been fully elucidated.
A pilsicainide challenge test was performed in 161 patients and according to recently established ECG criteria and an organized computer algorithm, the ST morphology was classified and the maximum increase in the J wave amplitude (maxDeltaJ) from the standard and high right precordial leads V1-3 was examined. Before the test, subjects exhibiting type 1 ECG in the standard leads were excluded. After administering pilsicainide, type 1 ECGs in the standard leads were observed in 31 cases and a maxDeltaJ of >or=200 microV was observed in 29 cases (23 type 1, 2 type 2/3 and 4 normal ECGs). In the additional higher right precordial leads, type 1 ECGs were observed in 55 cases and a maxDeltaJ of >or=200 microV was observed in 45 cases (42 type 1 and 3 type 2/3 ECGs).
A maxDeltaJ>or=200 microV induced by pilsicainide, including that measured in the high right precordial leads, was associated with a change mainly to a type 1 ECG.
Circulation Journal 01/2007; 71(1):57-62. · 3.77 Impact Factor
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Masashi Kanemoto,
Akihiko Shimizu,
Toshihiko Yamagata,
Masahiro Esato,
Takeshi Ueyama, Yasuhiro Yoshiga,
Hiroyuki Kakugawa,
Ryousuke Kametani,
Noriko Inoue,
Akira Sawa,
Masunori Matsuzaki
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ABSTRACT: The purpose of this study was to identify the difference between the pure Na channel blocker, pilsicainide and Ic-antiarrhythmic drug, flecainide, on the atrial electrophysiological characteristics.
The subjects consisted of 24 patients (48 +/- 12 years-old: P-group) in whom pilsicainide was administrated intravenously (1 mg/kg/10 min) and 31 patients (47 +/- 15 years-old: F-group) in whom flecainide was administrated intravenously (2 mg/kg/10 min). The atrial effective refractory period (ERP-A), intra-atrial conduction time (CT), max intra-atrial conduction delay (Max CD), repetitive atrial firing zone (RAFZ), fragmented atrial activity zone (FAZ) and intra-atrial conduction delay zone (CDZ) were measured before and after the drugs.
Pilsicainide and flecainide significantly prolonged the ERP-A (211 +/- 27 msec to 246 +/- 39 msec; p < 0.001, 217 +/- 25 msec to 244 +/- 33 msec; p < 0.001, respectively) and CT (121 +/- 33 msec to 149 +/- 43 msec; p < 0.001, 122 +/- 22 msec to 153 +/- 27 msec; p < 0.001, respectively) to the same degree. However, the Max CD was shortened by pilsicainide, but not by flecainide. The RAFZ, FAZ and CDZ decreased in the P-group (21 +/- 25 msec to 4 +/- 10 msec; p < 0.01, 24 +/- 24 msec to 14 +/- 18 msec; p < 0.05, 56 +/- 29 msec to 43 +/- 32 msec, p < 0.05, respectively), but not in the F-group.
The effects of atrial conduction delays may differ between pilsicainide and flecainide. Further examination will be needed to explain this mechanism.
Cardiovascular Drugs and Therapy 07/2004; 18(4):295-303. · 3.13 Impact Factor
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ABSTRACT: Atrial electrograms were recorded from the high right atrium, coronary sinus, and right lateral wall in 15 patients with induced atrial fibrillation (AF). Intravenous cibenzoline terminated AF in 8 patients (T group), but not in 7 patients (non-T group). The cycle length of the AF (AFCL) obtained by the autocorrelation function was measured every 5 s during the 30 s prior to the cibenzoline administration, and just before the termination of AF or at the end of the cibenzoline infusion in the non-T group. The mean AFCL, and spatial and temporal dispersion of the AFCL were then compared between the 2 groups (dispersion = standard deviation x 100 /mean AFCL). Cibenzoline significantly increased the mean AFCL and decreased the spatial dispersion in both groups. No significant difference in either the mean AFCL or temporal dispersion before or after cibenzoline was observed between the 2 groups. In addition, no significant difference in the spatial dispersion before the cibenzoline was observed, but the spatial dispersion after the cibenzoline was significantly smaller in the T group than in the non-T group. The mean AFCL, and the spatial and temporal dispersion before the cibenzoline did not predict the termination of AF. The decrease in the spatial dispersion may be the most important mechanism by which intravenous cibenzoline terminates AF.
Circulation Journal 11/2003; 67(10):810-5. · 3.77 Impact Factor
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Yasuhiro Yoshiga,
Akihiko Shimizu,
Toshihiko Yamagata,
Masahiro Esato,
Takeshi Ueyama,
Masato Ohmura,
Kazuo Itagaki,
Masayasu Kimura,
Hiroyuki Kakugawa,
Masahiro Doi,
Masunori Matsuzaki
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ABSTRACT: The aims of this study were to evaluate the changes in the electrophysiological characteristics of the right atrium after the administration of flecainide and to clarify whether flecainide has a selective effect on human atrial tissue. Electrophysiological measurements were made in 38 patients, before and after intravenous administration of flecainide (2 mg/kg per 10 min). The effective refractory period of the right atrium (ERP-A), maximum conduction delay (Max.CD), repetitive atrial firing zone (RAFZ), fragmented atrial activity zone (FAAZ), and conduction delay zone (CDZ) were studied in the patients who were divided into 2 groups based on whether repetitive atrial firing (RAF) was induced in the baseline study. Flecainide significantly prolonged the ERP-A (202+/-22 to 238+/-33 ms, p<0.001) and shortened Max.CD (77+/-17 to 63+/-32 ms, p<0.05) in the patients with RAF, but not in those without RAF in the baseline study. After flecainide administration, there were significant reductions in the RAFZ (43+/-22 to 13+/-19 ms, p<0.0001), FAAZ (51+/-22 to 28+/-26 ms, p<0.001) and CDZ (70+/-21 to 48+/-30 ms, p<0.01) in the patients with RAF. However, atrial fibrillation (AF) was induced by stimulation after flecainide in 2 patients without RAF in the baseline study. There was a significant negative correlation between the ERP-A in the baseline study and the change in the ERP-A upon flecainide administration (r=0.45, p<0.01). Flecainide may preferentially activate the substrate for AF and RAF, but that action is mainly based on the electrophysiological characteristics found in the baseline study.
Circulation Journal 05/2003; 67(5):437-42. · 3.77 Impact Factor
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Tomoko Nao,
Tomoko Ohkusa,
Yuji Hisamatsu,
Noriko Inoue,
Tomo Matsumoto,
Jutaro Yamada,
Akihiko Shimizu, Yasuhiro Yoshiga,
Toshihiko Yamagata,
Shigeki Kobayashi,
Masafumi Yano,
Kimikazu Hamano,
Masunori Matsuzaki
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ABSTRACT: An abnormal distribution of the gap junction occurs in chronic atrial fibrillation (AF). There are conflicting data regarding changes in connexins (Cxs) in experimental models of AF. We examined whether patients with chronic AF have alterations in atrial Cxs. We analyzed the expression of Cx40 and Cx43 in the right atrial myocardium from 10 patients with mitral valvular disease (MVD) who had AF (MVD/AF), 10 patients with MVD who were in normal sinus rhythm (MVD/NSR), and 10 control patients in NSR (tissue obtained during coronary artery bypass surgery). Hemodynamic and echocardiographic data were obtained before surgery, and an electrophysiologic examination was performed during the operation. An immunohistochemical study was performed on atrial tissue. The relative expression level of Cx40 protein was significantly lower in MVD/AF patients (6.5 +/- 4.6) than in either MVD/NSR patients (17.7 +/- 8.9, p <0.05) or controls (24.7 +/- 11.1, p <0.01). The relative expression level of Cx40 messenger ribonucleic acid was also significantly lower in MVD/AF patients (0.23 +/- 0.13) than in MVD/NSR patients (0.47 +/- 0.26, p <0.01) or controls (0.47 +/- 0.17, p <0.01). For Cx43 protein and messenger ribonucleic acid, there was no significant difference in relative expression levels among the 3 groups. Interestingly, the level of serine-phosphorylated Cx40 was approximately 52% greater in MVD/AF patients than in controls. In MVD/AF patients, the immunoreactive signal of Cx40 was significantly lower than in controls. There was no significant difference in the connective tissue-volume fraction among the groups. Thus, downregulation of Cx40 and abnormal phosphorylation of Cx40 may result in abnormal cell-to-cell communication and alteration in the electrophysiologic properties of the atrium, leading to the initiation and/or perpetuation of AF.
The American Journal of Cardiology 04/2003; 91(6):678-83. · 3.37 Impact Factor
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ABSTRACT: Bepridil is effective for intractable cardiac arrhythmia, but in rare cases will induce torsades de pointes (TdP) associated with QT interval prolongation. Beta-blockers will effectively prevent TdP in some clinical settings, so the effect of beta-blocker on the change in QT interval, QT dispersion and transmural dispersion of repolarization (TDR) induced by bepridil was investigated in 10 patients (7 male, 3 female; 62+/-6 years old) with intractable paroxysmal atrial fibrillation. The QTc interval, QTc dispersion and TDR were measured before and after 1 month of administration of bepridil, and then a beta-blocker was added and the QTc interval, QTc dispersion and TDR re-measured 1 month later. Bepridil significantly prolonged the QTc interval (0.42+/-0.05 to 0.50+/-0.08; p<0.01), and increased both the QT dispersion (0.07+/-0.05 to 0.14+/-0.08; p<0.01) and TDR (0.10+/-0.04 to 0.16+/-0.05; p<0.01). The addition of a beta-blocker decreased the QTc interval (0.50+/-0.08 to 0.47+/-0.04; p=0.09) and significantly decreased both the QTc dispersion (0.14 +/-0.08 to 0.06+/-0.02; p<0.01) and TDR (0.16+/-0.05 to 0.11+/-0.04; p<0.001). Compared with the control, the combination therapy significantly prolonged the QTc interval, but did not increase either QTc dispersion or TDR, and so was effective in all patients with intractable AF. The findings suggest that beta-blocker reduces the increase in QT dispersion and TDR induced by bepridil, and combined therapy with bepridil and beta-blocker might thus be useful for intractable atrial fibrillation.
Circulation Journal 12/2002; 66(11):1024-8. · 3.77 Impact Factor
