Biomedical subjects

Hiroshi Furushima

Publications and source records attributed to Hiroshi Furushima.

At least 19 recordsLinked to original sources

PubMed2006

Ventricular tachycardia late after repair of congenital heart disease: efficacy of combination therapy with radiofrequency catheter ablation and class III antiarrhythmic agents and long-term outcome.

OBJECTIVE: This study investigated the treatment of ventricular tachycardia (VT) after repair of tetralogy of Fallot or double outlet of the right ventricle. BACKGROUND: The ideal antiarrhythmic therapy for VT in patients after repair of congenital heart disease, especially without left ventricular dysfunction, has not yet been established. METHODS: Seven consecutive patients (2 women and 5 men) with stable monomorphic sustained VT were investigated. The mean age was 25 +/- 7 years (range, 16-35 years). Four patients had undergone surgical repair of tetralogy of Fallot, and 3 had surgical correction of double outlet of the right ventricle at the mean age of 18 +/- 7 years (range, 9-27 years) before documentation of the arrhythmia. RESULTS: The mean ejection fraction of the left ventricle was 60% +/- 8% (range, 50-72). Fourteen sustained monomorphic VTs were induced in 7 patients using programmed electrical stimulation. The mean cycle length of tachycardia was 346 +/- 77 milliseconds (range, 260-480 seconds). The site of the surgical correction of the right ventricle was associated with the origin of VT in all patients. Radiofrequency catheter ablation was attempted in 8 VTs in 7 patients: 7 clinical and 1 nonclinical VTs. In 6 patients, class III antarrhythmic agents were added because VT remained inducible after ablation. During a follow-up of 61 +/- 29 months (range, 15-110 months), there were no recurrences of VT. CONCLUSION: In patients with drug-refractory VT originating from the right ventricle late after congenital heart disease, and when their left ventricular function do not deteriorate, combined therapy for radiofrequency catheter ablation with class III antiarrhythmic agents might effective and should be considered as a therapeutic option.

Adolescent↗

PubMed2006

Role of autonomic nervous activity in the antiarrhythmic effects of magnesium sulfate in a canine model of polymorphic ventricular tachyarrhythmia associated with prolonged QT interval.

This study was performed to examine the role played by the autonomic nervous system in the antiarrhythmic effects of magnesium sulfate (Mg) in a canine model of polymorphic ventricular tachyarrhythmia facilitated by anthopleurin-A and a slower heart rate induced QT interval prolongation. In 6 experiments, complete atrioventricular block was created to control the heart rate and bradycardia at 800- to 1500-ms cycle lengths was applied for 60 sec before and after drug-induced autonomic block. Transmural unipolar electrograms were recorded from multipolar needle electrodes, and activation-recovery intervals (ARI) were measured. Before drug-induced autonomic block, polymorphic ventricular tachyarrhythmia developed in all 6 experiments during bradycardia before but not after the administration of Mg (0.2 ml/kg intravenous bolus). During drug-induced autonomic block, triggered premature activity decreased without significant changes in underlying dispersion of repolarization and polymorphic ventricular tachyarrhythmia developed during bradycardia in 1 experiment. Administration of Mg during drug-induced autonomic block eliminated premature activity and polymorphic ventricular tachyarrhythmia during bradycardia. The distribution of left ventricular (LV) and right ventricular repolarization and dispersion of transmural repolarization were analyzed before and 60 sec after Mg administration during ventricular pacing at 80 bpm. Mg caused a modest shortening of ARI at all sites before and after drug-induced autonomic block. Since ARI shortening was greater at the mid-myocardial sites than at other LV sites, Mg decreased transmural ARI dispersion from 77 +/- 16 to 46 +/- 21 ms before drug-induced autonomic block and from 79 +/- 7 to 51 +/- 16 ms after drug-induced autonomic block. The antiarrhythmic effects of Mg in this model of long QT syndrome were attributable to its direct pharmacological properties and not to changes in ambient autonomic nervous activity. The blockade of sympathetic activity decreased the incidence of premature events and partially suppressed polymorphic ventricular tachyarrhythmia in this model.

Animals↗

PubMed2006

Multiple premature beats triggered ventricular arrhythmias during pilsicainide infusion in a patient with inferior ST-segment elevation.

A 17-year-old man was referred to our hospital for treatment of common paroxysmal atrial flutter. His electrocardiogram at rest showed subtle ST-segment elevation in leads II, III, and aV(F). Intravenous pilsicainide caused further ST-segment elevation in the inferior leads, new ST-segment depression in leads V2-V6, two distinct forms of premature ventricular complexes (PVCs) triggering short runs of polymorphic ventricular tachycardia (VT). An infusion of isoproterenol suppressed these arrhythmias and normalized the ST-segment. Pilsicainide may induce PVCs and polymorphic VT in atypical Brugada syndrome.

Adolescent↗

PubMed2006

Japanese randomized trial for investigation of a combined therapy of amiodarone and implantable cardioverter defibrillator in patients with ventricular tachycardia and fibrillation: the Nippon ICD Plus Pharmachologic Option Necessity study design.

BACKGROUND: Implantable cardioverter-defibrillators (ICDs) are the most effective therapy in reducing the mortality of patients with life-threatening ventricular tachyarrhythmias. However, the ICD cannot prevent the recurrence of tachycarida attacks and that limits the clinical usefulness of them. The Nippon ICD Plus Pharmachologic Option Necessity (NIPPON) trial was designed as the first prospective randomized study to test the hypothesis whether amiodarone could improve the patient's clinical outcome by reducing the amount of ICD therapy in the Japanese patient population. METHODS AND RESULTS: Approximately 400 patients with organic heart disease and spontaneous episode(s) of sustained ventricular tachycardia/fibrillation (VT/VF) will be randomly assigned to one of 2 groups; the amiodarone group and non-amiodarone group. Both groups of patients will be followed at least for 24 months. The end-point committee will adjudicate events in a blinded fashion. The primary end-points of this study are determination of the appropriate therapy from the ICD and alteration of the assigned treatment because of its harmful effects and/or frequent ICD therapies. CONCLUSION: The NIPPON study is expected to confirm our understanding of the prognostic and therapeutic usefulness of adjuvant amiodarone therapy for patients with an ICD and with a history of sustained VT/VF.

Amiodarone↗

PubMed2006

Comparison of efficacy of sotalol and nifekalant for ventricular tachyarrhythmias.

BACKGROUND: Suppression of implantable defibrillator discharges associated with ventricular tachyarrhythmia (VTA) has been reported for sotalol. This study aimed to investigate the efficacy of intravenous nifekalant hydrochloride in predicting the effects of oral sotalol. METHODS AND RESULTS: The present study included 14 patients who had sustained VTA associated with structural heart disease. All patients also had inducible VTA. To compare the effects of nifekalant and sotalol, programmed electrical stimulation was performed, in the basal state, after nifekalant administration, and after sotalol administration. Nifekalant and sotalol similarly prolonged the corrected QT interval and ventricular effective refractory periods, but the heart rate was slowed by sotalol only. In 4 of 5 patients whose VTA became non-inducible by nifekalant, subsequent treatment with sotalol also suppressed the inducible VTA. In all of the 9 patients non-responding to nifekalant, VTA remained inducible during sotalol treatment. Nifekalant accurately predicted the response to sotalol during electrophysiologic study in 13 of 14 patients. Of 11 patients who remained on sotalol, VTA recurred in 3 non-responders during a follow-up of 46 +/- 11 months. CONCLUSIONS: Nifekalant and sotalol had similar effects on inducible VTA. The response of inducible VTA to nifekalant may predict the clinical efficacy of sotalol.

Adult↗

PubMed2006

Decrease in amplitude of intracardiac ventricular electrogram and inappropriate therapy in patients with an implantable cardioverter defibrillator.

Intracardiac electrograms are important for discrimination of tachyarrhythmia by implantable cardioverter defibrillators (ICD). A low R-wave can cause not only undersensing of ventricular tachyarrhythmia but also inappropriate discharges due to oversensing of unexpected signals because of its characteristic sensing algorithm. Therefore, this study aimed to investigate adverse events associated with R-wave amplitude. We included 115 consecutive patients followed-up over one year after implantation of a transvenous ICD system. The status of the ICD was checked every 3 months and intracardiac ventricular electrograms were analyzed. The decrease in R-wave amplitude was high in arrhythmogenic hypertrophy cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (ARVC), and sarcoidosis. Low R-waves (< 5.0 mV) were observed in 13 patients at a follow-up of 15 +/- 16 months after implantation, and the mean R-wave was 3.0 +/- 0.8 mV. The frequency of low R-waves was high in ARVC (38%), sarcoidosis (33%), and dilated cardiomyopathy (17%). All of the dilated cardiomyopathy patients with low R-waves had severe left ventricular dysfunction. Inappropriate ICD therapy resulting from T-wave oversensing occurred in 7 patients and the R-wave was < 5.0 mV in 6 of the patients. The frequency of inappropriate therapy was high in patients with sarcoidosis. In 3 patients, inappropriate therapy caused ventricular tachyarrhythmia. In conclusion, decreases in R-wave amplitude occurred in some progressive cardiac disorders and caused inappropriate ICD discharges having arrhythmogenicity. Physicians should attempt to obtain a high R-wave amplitude during ICD implantation and careful follow-up is required, especially in patients with ARVC or sarcoidosis.

Adult↗

PubMed2005

Elimination of late potentials by quinidine in a patient with Brugada syndrome.

The beneficial effects of quinidine on ST-segment elevation, inducible ventricular tachyarrhythmias, and episodes of ventricular tachyarrhythmia have been reported in Brugada syndrome. This is the first report describing quinidine-induced elimination of the late potential, which is considered one of the parameters for an arrhythmic event, in a patient with Brugada syndrome.

Anti-Arrhythmia Agents↗

PubMed2005

Similarities between Brugada syndrome and ischemia-induced ST-segment elevation. Clinical correlation and synergy.

Vasospastic angina (VSA) and Brugada syndrome (BS) are classified into different categories of cardiac disease, but both can be causes of sudden cardiac death from ventricular fibrillation (VF). The coexistence of VSA and BS in the same patient is possible, and this raises several questions: (1) what is the incidence of the coexistence of BS and VSA in the same patient? (2) is susceptibility to VF enhanced by the coexistence of the 2 diseases? and (3) is there any possibility of Ca-antagonists being used for the treatment of VSA-aggravated BS? In our institution, VSA coexisted in 5 of the 38 patients with BS (13.1%). Anginal episodes were confirmed clinically in 4 of the 5 patients, and syncope attack occurred after the symptom of chest pain in 2 patients. However, VF did not develop during the coronary vasospasm in any of the patients. Treatment with Ca-antagonist was effective for VSA, and neither aggravation of Brugada-type electrocardiographic abnormality nor an increase in the incidence of syncope attack was observed. Although the coexistence of BS and VSA in the same patient is not rare, neither enhanced susceptibility to VF nor the proarrhythmic effect of Ca-antagonist has been confirmed in our experience. However, careful attention is required in such patients because the influence of myocardial ischemia and/or the effect of Ca-antagonist may be different in each patient with BS.

Aged↗

PubMed2005

Unsuccessful internal defibrillation in Brugada syndrome: focus on refractoriness and ventricular fibrillation cycle length.

INTRODUCTION: In patients with Brugada syndrome, implantable cardioverter defibrillator (ICD) is the only reliable treatment to prevent sudden death though, in some cases, internal defibrillation may be unsuccessful. The aim of this study was to examine the determinants of defibrillation failure, with a focus on electrophysiologic characteristics. METHODS: The study included 51 patients treated with ICD: 22 with Brugada syndrome and 29 with structural heart disease (SHD). The prevalence of defibrillation energy requirement precluding the programming of a 10-J safety margin, the mean right ventricular effective refractory period (ERP), and mean induced ventricular fibrillation cycle length (VFCL) from the stored ICD electrograms, were compared between the two patient groups. RESULTS: High defibrillation requirements were observed in 18% of patients with Brugada syndrome versus 0% of patients with SHD. However, the patients with SHD had larger heart size than those with Brugada syndrome. Mean VFCL and mean ERP were both significantly shorter in patients with Brugada syndrome than in patients with SHD, and ERP and VFCL were significantly correlated. CONCLUSION: Patients with Brugada syndrome have a high prevalence of high defibrillation energy requirement, and short ventricular ERP and VFCL.

Bundle-Branch Block↗

PubMed2005

Effects of intravenous magnesium in a prolonged QT interval model of polymorphic ventricular tachycardia focus on transmural ventricular repolarization.

BACKGROUND: This study was performed to clarify the antiarrhythmic effects of magnesium sulfate (Mg(++)) in a prolonged QT interval canine model of polymorphic ventricular tachyarrhythmia (VTA). METHODS: In six experiments in a canine model of prolonged QT by anthopleurin-A, Mg(++) was administered in boluses of 0.2 mL/kg during repetitive episodes of self-terminating polymorphic VTA or frequent premature ventricular complexes (PVCs). The distribution of ventricular repolarization across the left ventricular(LV) wall and dispersion of transmural repolarization were analyzed before, and 30 and 120 seconds after Mg(++) administration, during ventricular pacing at 100 bpm. Transmural unipolar electrograms were recorded from multipolar needle electrodes, and local activation-recovery intervals (ARI) were measured. RESULTS: Mg(++) rapidly eliminated self-terminating polymorphic VTA and all isolated PVCs. During ventricular pacing at 100 bpm, Mg(++) caused modest shortening of ARI at all recording sites. Since the magnitude of ARI shortening was greater at mid-myocardial sites than at other ventricular sites, mean transmural ARI dispersion decreased from 80 +/- 22 to 45 +/- 18 ms within 30 seconds after Mg(++) injection. However, this effect was transient, and, at 120 seconds after Mg(++) administration, ARI had increased all sites and transmural ARI dispersion lengthened to 65 +/- 18 ms. Besides suppression of triggered premature activity, homogenization of transmural ventricular repolarization was associated with the antiarrhythmic effects of intravenous Mg(++) in this model. CONCLUSION: Since these effects were transient, a continuous intravenous infusion of Mg(++) is preferred to prevent recurrences of VTA.

Analysis of Variance↗

PubMed2005

Electrophysiologic study-guided therapy with sotalol for life-threatening ventricular tachyarrhythmias.

The aim of this study was to investigate the long-term efficacy and safety of electrophysiologic study (EPS)-guided sotalol administration combined with implantable cardioverter defibrillators (ICD) for ventricular tachyarrhythmias (VTA). This study enrolled 92 patients with both structural heart disease and sustained VTA. Sotalol was administered to 57 patients, and its efficacy was assessed by EPS. Long-term treatment was continued in combination with ICD in 31 patients (57%) whose VTA was no longer inducible (responder group) and in 16 patients whose VTA remained inducible (nonresponder group). The long-term outcomes were compared among the responder group, the nonresponder group, and 35 ICD recipients untreated with antiarrhythmic drugs (ICD-only group). During a mean follow-up of 44 +/- 33 months, the recurrence of VTA was not significantly different between all patients treated with sotalol (30%) and patients in the ICD-only group (46%). However, the recurrence of VTA was significantly lower in the responder (13%) than in the nonresponder (63%) or the ICD-only groups (46%). There was no significant difference in VTA recurrence between the nonresponder and the ICD-only groups. One patient each in the responder and the ICD-only groups died suddenly, and all-cause mortality was similar in the three groups. The incidence of inappropriate ICD discharges was less in the sotalol than in the ICD-only groups. No patient had to discontinue long-term sotalol treatment because of the adverse effects. In conclusion, sotalol reduced VTA recurrence in the responding patients and inappropriate ICD discharge. EPS may predict the efficacy of sotalol for VTA recurrence.

Aged↗

PubMed2005

Variable electrocardiographic effects of short-term quinidine sulfate administration in Brugada syndrome.

Quinidine, a class I antiarrhythmic agent with blocking property of transient outward current, is a possible candidate for the suppression of ventricular fibrillation in patients with Brugada syndrome; although there is a concern that its ability to these effects may be proarrhythmic. Therefore, we evaluated the effect of quinidine sulfate on ST-segment elevation in Brugada syndrome. In 8 patients with Brugada syndrome, the magnitude of ST-elevation at the J-point (ST(J)), and the ST-segment configuration in leads V1-V3, were compared before and on day 2 after the initiation of quinidine administration. In 3 patients, quinidine attenuated ST(J) by > or = 0.1 mV. Of these 3 patients, ST-segment elevation was normalized in 2 patients, while the ST-segment configuration was unchanged in another. In another 3 patients, quinidine augmented ST(J) by > or = 0.1 mV without any change of ST-segment configuration, and the augmentation was returned to baseline after the discontinuation of quinidine. Quinidine exhibited no effect on the ST-segment in the remaining 2 patients. The favorable effects of quinidine on the ST-segment tended to be more pronounced in patients with prominent ST-elevation at baseline. In 1 patient, quinidine was effective in eliminating both ST-segment elevation and repetitive tachyarrhythmia episodes. In conclusion, the effects of quinidine on ST-segment elevation were variable. Quinidine may potentially augment the ST-segment elevation in some patients with Brugada syndrome.

Adult↗

PubMed2005

Relationship between dominant prolongation of the filtered QRS duration in the right precordial leads and clinical characteristics in Brugada syndrome.

BACKGROUND: Electrical abnormalities in the RVOT may be involved in Brugada syndrome. OBJECTIVES: We investigated the relationship between the signal-averaged ECG (SAECG) and electrophysiologic study (EPS), especially focusing on conduction delay in the outflow tract of the right ventricle (RVOT) and its contribution to clinical characteristics. METHODS: Twenty-four patients with Brugada syndrome (23 men and 1 woman; 61 +/- 16 years old) were studied. We assessed the presence of late potential (LP) in SAECG and the filtered QRS duration in the right precordial leads (V1 or V2; RfQRS) and in the left precordial leads (V5 or V6; LfQRS) and the difference between them. In 18 patients, SAECG was evaluated for an LP on three separate occasions. RESULTS: SAECG was positive for LP in 15 patients at least once; and in 7 patients, SAECG was positive for an LP on multiple occasions, and 6 of 7 patients (86%) had a history of cardiac arrest. The difference between RfQRS and LfQRS was significantly greater in patients with cardiac arrest than in patients with syncope or in asymptomatic patients; 29 +/- 10, 14 +/- 11 (P < 0.01), and 7 +/- 5 msec (P < 0.001), respectively. All patients were alive and one patient with cardiac arrest had an appropriate VF therapy delivered by the ICD. CONCLUSIONS: The dominant prolongation of the filtered QRS duration in the right precordial leads may be related to the risk of arrhythmic event in Brugada syndrome.

Adult↗

PubMed2005

Nifekalant hydrochloride suppresses severe electrical storm in patients with malignant ventricular tachyarrhythmias.

BACKGROUND: Some patients with an implantable cardioverter-defibrillator (ICD) suffer from burst of inappropriate multiple discharges (severe electrical storm), and because the current therapeutic options are limited, the effect of nifekalant hydrochloride, a new class III drug, on severe electrical storm was investigated in the present study. METHODS AND RESULTS: Ninety-one consecutive patients treated with ICD were included in the study (M 70; mean age 58 years; left ventricular ejection fraction 45+/-15%). Severe electrical storm was defined as more than 10 ICD discharges within 1 h. During a mean follow-up period of 30+/-13 months, 41/91 (45%) patients had appropriate ICD therapy for arrhythmias and severe electrical storm occurred in 11 of them (12%) at 20+/-18 months after ICD implantation. The mean number of ICD discharges/h during severe electrical storm was 18+/-12. In 4 of 10 patients, severe electrical storm was successfully suppressed by a combination of deep sedation and beta-blocking agent; 6 other patients were refractory to this treatment, but severe electrical storm was successfully suppressed by intravenous administration of nifekalant hydrochloride with no adverse effects. CONCLUSIONS: Nifekalant hydrochloride is an effective and safe treatment for severe electrical storm.

Adolescent↗

PubMed2005

Inappropriate discharges of intravenous implantable cardioverter defibrillators owing to lead failure.

We describe here the case of a 58-year-old female patient who experienced inappropriate shocks from her implantable cardioverter-defibrillator (ICD). Stored electrograms from her ICD showed high frequency noise preceding the shock. Although the pacing threshold was normal and lead fracture was not found in chest X-rays, pacing lead impedance decreased to 480 omega. Moreover, such high frequency noise was observed by electrogram telemetry, but not by routine evaluation every 3 months. ICD lead dysfunction was suspected, so we elected to replace the ICD lead system. At the time of the operation, lead impedance was 410 omega and pacing threshold was the same as it was at the time of the ICD implantation, and no lead insulation disturbances were observed in the generator pocket. However, manipulation of the lead system produced high frequency noise reproducibly. Since some of the ICD lead dysfunction initially was clinically silent at rest, dysfunction was difficult to detect before serious problems occurred. Therefore, more careful evaluation of the ICD lead system is needed during long-term follow-up of ICD implants.

Defibrillators, Implantable↗

PubMed2004

Ventricular tachyarrhythmia associated with cardiac sarcoidosis: its mechanisms and outcome.

BACKGROUND: Cardiac sarcoidosis is increasingly recognized and is associated with poor prognosis. Ventricular tachycardia (VT) associated with cardiac sarcoidosis is the most likely cause of sudden death in most patients, but the mechanism has not been well established. HYPOTHESIS: This study investigated the mechanisms and outcome of VT associated with cardiac sarcoidosis. METHODS: The study included eight consecutive patients (five men, three women, aged 54 +/- 19 years) who had sustained monomorphic VT associated with cardiac sarcoidosis in our hospital. RESULTS: The average ejection fraction was 43 +/- 11%. Twenty-two VTs were observed in these patients, and mean heart rate during VT was 192 +/- 29 beats/min (range 144-259). The phenomenon of transient entrainment was documented in 10 of 22 (45%) VTs by ventricular pacing (eight in the active phase). Another five (23%) VTs could not be entrained, but could be initiated by programmed stimulation and terminated by rapid pacing, reproducibly. In 3 of the 22 (14%) VTs, cardioversion was required urgently because of the fast rate, while the remaining 4 (18%) could be induced during electrophysiologic study. CONCLUSIONS: In this study, there was a high possibility that the mechanism of 15 (68%) VTs was reentry. Reentrant substrate is formed not only in association with the healing of cardiac granulomas in the inactive phase of cardiac sarcoidosis but also in the active phase. Ventricular tachycardia with cardiac sarcoidosis, even if this mechanism is reentry, has different inducibility between the active and inactive phases in an electrophysiologic study. This makes the therapy for cardiac sarcoidosis (e.g., corticosteroids, antiarrhythmic agents, and catheter ablation) difficult. The implantable cardioverter-defibrillator is an effective treatment for ventricular tachyarrythmia with cardiac sarcoidosis.

Adult↗

PubMed2004

Radiofrequency catheter ablation for incessant atrioventricular nodal reentrant tachycardia normalized H-V block associated with tachycardia-induced cardiomyopathy.

A 30-year-old man was admitted for treatment of tachycardia-induced cardiomyopathy caused by incessant atrioventricular nodal reentrant tachycardia (AVNRT). An echocardiogram revealed dilatation of all cardiac chambers with severe globally depressed biventricular systolic function. During an electrophysiologic study, HV interval was prolonged to 118 ms by atrial extrastimulus and 2:1 HV block was documented during AVNRT. Four weeks after catheter ablation for AVNRT, an echocardiogram demonstrated regression of the wall motion abnormality of both ventricles and of their dimensions. In the electrophysiologic study, the HV conduction disturbance disappeared. So far, this is the first case in which tachycardia-induced cardiomyopathy was accompanied by transient His-Purkinje conduction abnormality.

Adult↗

PubMed2004

Postprandial variations in ST-segment in a patient with Brugada syndrome and partial gastrectomy.

A 74-year-old man with a history of partial gastrectomy presented with an electrocardiogram consistent with Brugada syndrome and marked meal related fluctuations in the ST segment. ST-segment elevation was prominently attenuated at 30 minutes and increased at 120 minutes after meals. Analysis of heart rate variability revealed a relationship between postprandial heightened parasympathetic activity and increase in Brugada-type ECG abnormality. A rapid postprandial increase in blood glucose may initially stimulate sympathetic nervous activity and secondarily increase parasympathetic tone. Food intake can be associated with fluctuations in ST-segment elevation in patients with the Brugada syndrome.

Aged↗