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Kiyotaka Matsuo

Publications and source records attributed to Kiyotaka Matsuo.

11 recordsLinked to original sources
PubMed2006

Angiotensin-converting enzyme inhibitor suppresses the incidence of prolonged and fractionated right atrial electrograms.

INTRODUCTION: Although prolonged and fractionated right atrial electrograms have been reported as predictors of the development of chronic atrial fibrillation in patients with paroxysmal atrial fibrillation (PAF), the effects of angiotensin-converting enzyme inhibitor (ACEI) on these electrophysiologic abnormalities remain unknown. The purpose of this study was to evaluate whether ACEI influences these electrophysiologic abnormalities of atrial muscle in patients with PAF. METHODS: While taking oral ACEI for hypertension, 12 patients (ACEI group) with PAF underwent electrophysiologic study (EPS). Catheter mapping of 12 right atrial sites and right atrial extrastimulation were performed during sinus rhythm. Twenty-four age-matched patients with PAF but not taking oral ACEI were included as a control group. RESULTS: The longest duration of the right atrial electrogram was significantly shorter and the maximum number of fragmented deflections per patient was significantly lower in the ACEI group than in the control group (79 +/- 15 ms vs 100 +/- 15 ms, P < 0.005; 5.5 +/- 1.9 vs 7.9 +/- 2.4, P < 0.001, respectively). The number of abnormal atrial electrograms per patient was significantly lower in the ACEI group than in the control group (0.5 +/- 1.4 vs 2.1 +/- 1.8, P < 0.05). The percentage of patients with at least one abnormal atrial electrogram was significantly lower in the ACEI group than in the control group (16.7% vs 79.2%, P < 0.0005). CONCLUSIONS: ACEI use is associated with a decrease in the incidence of prolonged and fractionated right atrial electrograms in patients with PAF. In addition, we suggest that ACEI may help prevent PAF from becoming chronic.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

Value of electrocardiographic parameters and ajmaline test in the diagnosis of Brugada syndrome caused by SCN5A mutations.

BACKGROUND: The Brugada syndrome is an arrhythmogenic disease caused in part by mutations in the cardiac sodium channel gene, SCN5A. The electrocardiographic pattern characteristic of the syndrome is dynamic and is often absent in affected individuals. Sodium channel blockers are effective in unmasking carriers of the disease. However, the value of the test remains controversial. METHODS AND RESULTS: We studied 147 individuals representing 4 large families with SCN5A mutations. Of these, 104 were determined to be at possible risk for Brugada syndrome and underwent both electrocardiographic and genetic evaluation. Twenty-four individuals displayed an ECG diagnostic of Brugada syndrome at baseline. Of the remaining, 71 received intravenous ajmaline. Of the 35 genetic carriers who received ajmaline, 28 had a positive test and 7 a negative ajmaline test. The sensitivity, specificity, and positive and negative predictive values of the drug challenge were 80% (28:35), 94.4% (34:36), 93.3% (28:30), and 82.9% (34:41), respectively. Penetrance of the disease phenotype increased from 32.7% to 78.6% with the use of sodium channel blockers. In the absence of ST-segment elevation under baseline conditions, a prolonged P-R interval, but not incomplete right bundle-branch block or early repolarization patterns, indicates a high probability of an SCN5A mutation carrier. CONCLUSIONS: In families with Brugada syndrome, the data suggest that ajmaline testing is valuable in the diagnosis of SCN5A carriers. In the absence of ST-segment elevation at baseline, family members with first-degree atrioventricular block should be suspected of carrying the mutation. An ajmaline test is often the key to making the proper diagnosis in these patients.

Ajmaline↗
PubMed2004

Clinical characteristics of subjects with the Brugada-type electrocardiogram:.

INTRODUCTION: The Brugada-type ECG, a terminal r' wave accompanied by ST segment elevation in the right precordial leads, is not a very rare condition. Most of the cases are men in Japan and elsewhere; however, information about the clinical features of these cases is lacking. The aim of this study was to determine the clinical characteristics of subjects with the Brugada-type ECG, specifically Japanese men. METHODS AND RESULTS: We extracted male Brugada-type ECG cases from 3,374 men followed biennially from 1958 through 2001 in Nagasaki, Japan, and compared the clinical characteristics at diagnosis between these cases and four age-matched male controls for each case. A total of 34 cases with the Brugada-type ECG were observed during follow-up. Body mass index (BMI) at diagnosis was significantly lower in Brugada-type ECG cases than in 136 controls (20.2 +/- 2.1 kg/m(2) vs 21.8 +/- 2.8 kg/m(2), P = 0.003). The BMI trend in cases was always lower than that in controls throughout the 8-year observation period (from 4 years before diagnosis to 4 years after diagnosis). Pulse rate at diagnosis was also somewhat lower in Brugada-type ECG cases than in controls (68.9 +/- 7.7 beats/min vs 72.7 +/- 11.1 beats/min, P = 0.038). The significance disappeared after controlling for BMI (P = 0.131) or body weight (P = 0.153). CONCLUSION: The cases with the Brugada-type ECG had lower BMI than controls, leading to a clue to possible basic mechanisms of the Brugada-type ECG with a focus on this association.

Adult↗
PubMed2004

Abnormal right atrial electrograms predict the transition to chronic atrial fibrillation in paced patients with sick sinus syndrome.

Although pacing therapy for sick sinus syndrome (SSS) is established, the risk of developing chronic atrial fibrillation (CAF) makes pacing therapy infeasible in some patients. We evaluated whether electrophysiological characteristics of atrial muscle can serve as predictors of the transition to CAF after pacemaker implantation in patients with SSS. Eighty-nine patients with SSS underwent electrophysiological study before pacing therapy. Catheter mapping of 12 right atrial sites was performed during sinus rhythm during electrophysiological. An abnormal atrial electrogram was defined as having a duration of 100 ms or longer, or eight or more fragmented deflections, or both. Right atrial extrastimulation was also performed for atrial vulnerability. After electrophysiological study, all patients underwent pacemaker implantation and were followed up. During the follow-up period of 85 +/- 50 months, development of CAF was observed in 12 patients (group A). The remaining 77 patients remained in sinus rhythm (group B). There were significantly more abnormal atrial electrograms in group A than group B (2.7 +/- 2.3 vs 0.8 +/- 1.2; P < 0.001). The distribution of abnormal atrial electrograms was also greater in group A; patients in group A had more abnormal atrial electrograms than patients in group B in both the high and middle right atrium (P < 0.005 and P < 0.01, respectively). Kaplan-Meier analysis showed that almost 50% of the paced patients with abnormal atrial electrograms (n = 42) developed CAF (P < 0.005). Our data suggest that the existence of abnormal atrial electrograms is predictive of the transition to CAF in paced patients with SSS.

Aged↗
PubMed2003

Sudden death associated with short-QT syndrome linked to mutations in HERG.

BACKGROUND: Sudden cardiac death takes the lives of more than 300 000 Americans annually. Malignant ventricular arrhythmias occurring in individuals with structurally normal hearts account for a subgroup of these sudden deaths. The present study describes the genetic basis for a new clinical entity characterized by sudden death and short-QT intervals in the ECG. METHODS AND RESULTS: Three families with hereditary short-QT syndrome and a high incidence of ventricular arrhythmias and sudden cardiac death were studied. In 2 of them, we identified 2 different missense mutations resulting in the same amino acid change (N588K) in the S5-P loop region of the cardiac IKr channel HERG (KCNH2). The mutations dramatically increase IKr, leading to heterogeneous abbreviation of action potential duration and refractoriness, and reduce the affinity of the channels to IKr blockers. CONCLUSIONS: We demonstrate a novel genetic and biophysical mechanism responsible for sudden death in infants, children, and young adults caused by mutations in KCNH2. The occurrence of sudden cardiac death in the first 12 months of life in 2 patients suggests the possibility of a link between KCNH2 gain of function mutations and sudden infant death syndrome. KCNH2 is the binding target for a wide spectrum of cardiac and noncardiac pharmacological compounds. Our findings may provide better understanding of drug interaction with KCNH2 and have implications for diagnosis and therapy of this and other arrhythmogenic diseases.

Adult↗
PubMed2002

Electrophysiologic characteristics and implications of induced ventricular fibrillation in symptomatic patients with Brugada syndrome.

OBJECTIVES: The study examined the electrocardiographic and electrophysiologic characteristics in relation to programmed ventricular stimulation (PVS)-induced ventricular fibrillation (VF), as well as the implications of PVS-induced VF on the recurrence of cardiac events in symptomatic Brugada syndrome. BACKGROUND: Brugada syndrome is characterized by ST-segment elevation in the right precordial leads (V(1)-V(3)) and an episode of VF. METHODS: Thirty-four symptomatic patients with Brugada syndrome (33 men and 1 woman; 44 +/- 12 years old) were classified into two groups according to the inducibility of VF with PVS: 22 patients with induced VF requiring direct cardioversion for termination (Induced VF group) and 12 patients without induced VF (Noninduced VF group). RESULTS: The induced VF group showed a longer QRS duration, a higher incidence of right bundle branch block and late potentials detected on the signal-averaged electrocardiogram, longer His-ventricular intervals and a longer conduction time from the RVOT to the left ventricle at extrastimulation than those in the non-induced VF group. However, there was no significant difference in the recurrence of cardiac events (VF documented by an implantable cardioverter-defibrillator and sudden cardiac death) between the two groups (8 [36%] of 22 patients vs. 7 [58%] of 12 patients) during long-term follow-up (range 1 to 149 months; mean 38). CONCLUSIONS: Our data suggest that induction of VF by PVS depends on the severity of depolarization abnormalities but does not predict the recurrence of cardiac events in symptomatic Brugada syndrome, indicating that both depolarization and repolarization abnormalities are important in the development of VF.

Adult↗
PubMed2002

Simultaneous atrial and ventricular pacing to facilitate mapping of concealed left-sided accessory pathways.

Several local electrogram characteristics have been proposed as criteria to predict successful ablation. However, poor specificity due to obscuration of the retrograde atrial electrogram by the ventricular electrogram is problematic. The aim of this study was to analyze local electrograms obtained by simultaneous pacing to identify quantitative criteria that may predict successful ablation sites for concealed left free-wall accessory pathways. Twenty-four local electrograms from 10 successful and 14 unsuccessful ablation sites in ten patients were analyzed. Retrograde atrial electrograms were confirmed by the simultaneous pacing method. The intervals between the retrograde atrial electrogram of the coronary sinus and the ablation site, the initiation of the ventricular electrogram and the retrograde atrial electrogram, and the stimulus and retrograde atrial electrogram were analyzed. All retrograde atrial electrograms could be confirmed clearly by the simultaneous pacing method. The interval between the retrograde atrial electrogram of the coronary sinus and that of the ablation site was shorter at successful sites than at unsuccessful sites (-7.0 +/- 9.2 ms vs 5.7 +/- 2.7 ms; 95% confidence interval, -18 to -7; P < 0.0001). An interval of < or = 0 ms resulted in 100% sensitivity and 92.7% specificity for success. The other two interval measurements at successful sites did not differ significantly from those at unsuccessful sites. The authors propose an interval of < or = 0 ms between the retrograde atrial electrogram of the coronary sinus and that of the ablation site confirmed by the simultaneous pacing method as a quantitative criterion to identify the successful ablation site for concealed left free-wall accessory pathways. Application of this criterion may reduce the number of unnecessary ablations.

Adolescent↗
PubMed2002

Extended distribution of prolonged and fractionated right atrial electrograms predicts development of chronic atrial fibrillation in patients with idiopathic paroxysmal atrial fibrillation.

INTRODUCTION: This study evaluates whether electrophysiologic abnormalities in patients with idiopathic paroxysmal atrial fibrillation (PAF) predict the transition to chronic atrial fibrillation (CAF). METHODS AND RESULTS: Ninety-six patients with idiopathic PAF underwent electrophysiologic study and were followed up. During electrophysiologic study, endocardial mapping was performed at 12 sites in the right atrium (four aspects of the high, middle, and low right atrium). During follow-up of 60 to 130 months, conversion from PAF to CAF was observed in 17 patients (CAF group). The remaining 79 patients remained in sinus rhythm (PAF group). Although a high frequency of abnormal atrial electrograms was observed in the high right atrium in both groups, the frequency of those recorded from the middle right atrium was significantly higher in the CAF group than in the PAF group (70.6% vs 13.9%, P < 0.0005). Kaplan-Meier analysis showed that >50% of the patients with abnormal atrial electrograms in the middle right atrium developed CAF after 10 years, whereas only 7% of patients without those developed CAF (P < 0.0001). CONCLUSION: Our data suggest that extended distribution of abnormal atrial electrograms from the high to middle right atrium is predictive of the development of CAF in patients with idiopathic PAF.

Adult↗
PubMed2002

[Brugada syndrome].

Brugada syndrome is characterized by an ECG pattern of right bundle branch block and ST-segment elevation in right precordial leads, and sudden death caused by ventricular fibrillation(VF). The cellular basis for the syndrome is thought to be due to an outward shift in the ionic current active during phase 1 of the right ventricular epicardial action potential. Mutations of the cardiac sodium channel gene, SCN5A, have been identified as the genesis of the syndrome. This ECG pattern, which appears intermittently in most patients, is accentuated just before and after episodes of VF and is unmasked by class IA and IC antiarrhythmic agents. Development of VF is associated with an increase in vagal activity, and it occurs frequently during sleep. Implantable-cardioverter defibrillator is the effective therapy for prevention from sudden death.

Bundle-Branch Block↗