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Articles by W Shimizu
Total Records ( 3 ) for W Shimizu
  S Kamakura , T Ohe , K Nakazawa , Y Aizawa , A Shimizu , M Horie , S Ogawa , K Okumura , K Tsuchihashi , K Sugi , N Makita , N Hagiwara , H Inoue , H Atarashi , N Aihara , W Shimizu , T Kurita , K Suyama , T Noda , K Satomi , H Okamura , H Tomoike and for the Brugada Syndrome Investigators in Japan
 

Background— The prognosis of patients with saddleback or noncoved type (non–type 1) ST-elevation in Brugada syndrome is unknown. The purpose of this study was to clarify the long-term prognosis of probands with non–type 1 ECG and those with coved (type 1) Brugada-pattern ECG.

Methods and Results— A total of 330 (123 symptomatic, 207 asymptomatic) probands with a coved or saddleback ST-elevation ≥1 mm in leads V1–V3 were divided into 2 ECG groups—type 1 (245 probands) and non–type 1 (85 probands)—and were prospectively followed for 48.7±15.0 months. The absence of type 1 ECG was confirmed by drug provocation test and multiple recordings. The ratio of individuals with a family history of sudden cardiac death (14%) was lower than previous studies. Clinical profiles and outcomes were not notably different between the 2 groups (annual arrhythmic event rate of probands with ventricular fibrillation; type 1: 10.2%, non–type 1: 10.6%, probands with syncope; type 1: 0.6%, non–type 1: 1.2%, and asymptomatic probands; type 1: 0.5%, non–type 1: 0%). Family history of sudden cardiac death at age <45 years and coexistence of inferolateral early repolarization with Brugada-pattern ECG were independent predictors of fatal arrhythmic events (hazard ratio, 3.28; 95% confidence interval, 1.42 to 7.60; P=0.005; hazard ratio, 2.66; 95% confidence interval, 1.06 to 6.71; P=0.03, respectively, by multivariate analysis), although spontaneous type 1 ECG and ventricular fibrillation inducibility by electrophysiological study were not reliable parameters.

Conclusions— The long-term prognosis of probands in non–type 1 group was similar to that of type 1 group. Family history of sudden cardiac death and the presence of early repolarization were predictors of poor outcome in this study, which included only probands with Brugada-pattern ST-elevation.

  H Horigome , M Nagashima , N Sumitomo , M Yoshinaga , H Ushinohama , M Iwamoto , J Shiono , K Ichihashi , S Hasegawa , T Yoshikawa , T Matsunaga , H Goto , K Waki , M Arima , H Takasugi , Y Tanaka , N Tauchi , M Ikoma , N Inamura , H Takahashi , W Shimizu and M. Horie
 

Background— Data on the clinical presentation and genotype-phenotype correlation of patients with congenital long-QT syndrome (LQTS) diagnosed at perinatal through infantile period are limited. A nationwide survey was conducted to characterize how LQTS detected during those periods is different from that in childhood or adolescence.

Methods and Results— Using questionnaires, 58 cases were registered from 33 institutions. Diagnosis (or suspicion) of LQTS was made during fetal life (n=18), the neonatal period (n=31, 18 of them at 0 to 2 days of life), and beyond the neonatal period (n=9). Clinical presentation of LQTS included sinus bradycardia (n=37), ventricular tachycardia/torsades de pointes (n=27), atrioventricular block (n=23), family history of LQTS (n=21), sudden cardiac death/aborted cardiac arrest (n=14), convulsion (n=5), syncope (n=5), and others. Genetic testing was available in 41 (71%) cases, and the genotype was confirmed in 29 (71%) cases, consisting of LQT1 (n=11), LQT2 (n=11), LQT3 (n=6), and LQT8 (n=1). Ventricular tachycardia/torsades de pointes and atrioventricular block were almost exclusively observed in patients with LQT2, LQT3, and LQT8, as well as in those with no known mutation. In LQT1 patients, clues to diagnosis were mostly sinus bradycardia or family history of LQTS. Sudden cardiac death/aborted cardiac arrest (n=14) was noted in 4 cases with no known mutations as well as in 4 genotyped cases, although the remaining 6 did not undergo genotyping. Their subsequent clinical course after aborted cardiac arrest was favorable with administration of β-blockers and mexiletine and with pacemaker implantation/implantable cardioverter-defibrillator.

Conclusions— Patients with LQTS who showed life-threatening arrhythmias at perinatal periods were mostly those with LQT2, LQT3, or no known mutations. Independent of the genotype, aggressive intervention resulted in effective suppression of arrhythmias, with only 7 deaths recorded.

  T. a Matsuyama , T Kurita , K Suyama , H Okamura , T Noda , K Satomi , W Shimizu , N Aihara , Y Ikeda , S Inoue , S Kamakura and H. Ishibashi Ueda
 

A 68-year-old woman with idiopathic dilated cardiomyopathy suffered from drug-resistant monomorphic ventricular tachycardia (VT). Electrophysiological study revealed a re-entrant VT circuit located just beneath the inferior mitral valve annulus. The VT was considered to be related to the mitral valve isthmus and was abolished by radiofrequency ablation. The patient died 2 years after the ablation due to worsening of heart failure and an autopsy was performed. Pathological examination revealed ablation scar tissue on the localized myocardial bundle running parallel to the mitral valve annulus. Therefore, this bundle appeared to comprise the slow conduction area of the re-entrant VT in this case.

 
 
 
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