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Biomedical subjects

Shiro Kamakura

Publications and source records attributed to Shiro Kamakura.

At least 73 records · Page 4Linked to original sources
PubMed2003

Investigation of the optimal treatment strategy for atrial fibrillation in Japan.

The Japanese Rhythm Management Trial for Atrial Fibrillation (J-RHYTHM study) is a randomized comparative evaluation of rate control and rhythm control, both combined with antithrombotic therapy, as therapeutic strategies for the treatment of atrial fibrillation (AF). This study differs from the earlier AFFIRM and RACE studies in that it has a composite primary end-point representing mortality and also physical/psychological disablement (total mortality, symptomatic cerebral infarction, systemic embolism, major bleeding, hospitalization for heart failure requiring intravenous administration of diuretics, and patient disablement). Patients' will to change the therapeutic strategy to the other is also considered as an end-point representing disablement under the assigned strategy. The secondary end-point includes quality of life scores and the efficacy and safety of drugs used in treating AF. The J-RHYTHM study emphasizes patient-reported experience and perception of AF-specific disablement, and the safety of antiarrhythmics available in Japan; it will follow 2600 patients treated at more than 150 sites in Japan for a 3-year period.

Anti-Arrhythmia Agents↗
PubMed2003

Intravenous administration of nifekalant hydrochloride for the prevention of ischemia-induced ventricular tachyarrhythmia in patients with renal failure undergoing hemodialysis.

Excretion in the urine is an important pathway for the elimination of nifekalant hydrochloride (NIF), a novel class III antiarrhythmic agent. Three patients with renal failure were undergoing hemodialysis and receiving NIF for the prevention of ischemia-induced ventricular tachyarrhythmia. Because NIF is not dialyzed, dose adjustment at relatively low concentrations was required, with monitoring of the QT interval.

Aged↗
PubMed2003

Shifting of puncture site in the fossa ovalis during radiofrequency catheter ablation: intracardiac echocardiography-guided transseptal left heart catheterization.

Intracardiac echocardiography (ICE) serves as an adjunct to fluoroscopy for electrophysiological procedures by identifying critical anatomic landmarks and confirming catheter-endocardial contact. In the present study, we investigated the usefulness of ICE for radiofrequency catheter ablation. ICE was utilized to guide transseptal puncture in 19 patients undergoing radiofrequency catheter ablation. The fossa ovalis, which was one critical anatomic landmark, had an average vertical diameter of 18.5 +/- 6.9 mm and an average horizontal diameter of 10.0 +/- 2.4 mm, as measured by ICE and fluoroscopy. Although there was only a small shift of the puncture site in the horizontal direction, the puncture site shifted towards the upper edge of the fossa ovalis for 17 patients (89%). Furthermore, we could verify that the distance between the apex of the tent-shape formed by the pressure of the puncture needle in the fossa ovalis and the left atrial wall opposing it was sufficient to carry out the procedure safely. Confirming the puncture site using ICE is useful in carrying out transseptal left heart catheterization safely.

Atrial Fibrillation↗
PubMed2003

Three novel single nucleotide polymorphisms in UGT1A9.

Three novel single nucleotide polymorphisms (SNPs) were found in the UDP-glucuronosyltransferase (UGT) 1A9 gene from 97 Japanese subjects (47 cancer patients and 50 cardiovascular disease patients). The detected SNPs were as follows: 1) SNP, MPJ6_U1A006; GENE NAME, UGT1A9; ACCESSION NUMBER, AF297093; LENGTH, 25 bases; 5'-AATTCTCTTAGGG/TTTCTCAGATGCC-3'. 2) SNP, MPJ6_U1A007; GENE NAME, UGT1A9; ACCESSION NUMBER, AF297093; LENGTH, 25 bases; 5'-TGTTACGGAGTAT/GGATCTCTACAGC-3'. 3) SNP, MPJ6_U1A031; GENE NAME, UGT1A9; ACCESSION NUMBER, AF297093; LENGTH, 25 bases; 5'-ACTCATTCTCAGG/AGGGCATGAGGTG-3'. All three SNPs were located in exon 1 with frequencies of 0.036 for MPJ6_U1A006, and 0.005 for MPJ6_U1A007 and MPJ6_U1A031. SNP MPJ6_U1A007 (726T>G) results in formation of a termination codon TAG (Y242X). The other two SNPs, MPJ6_U1A006 (588G>T) and MPJ6_U1A031 (153G>A), result in synonymous changes (G196G and R51R, respectively).

Journal Article↗
PubMed2002

ST-segment elevation and ventricular fibrillation without coronary spasm by intracoronary injection of acetylcholine and/or ergonovine maleate in patients with Brugada syndrome.

OBJECTIVES: The study examined whether patients with Brugada syndrome are sensitive to vagal stimulation or ischemia. BACKGROUND: Experimental studies have suggested that a prominent transient outward current (I(to))-mediated action potential notch and a subsequent loss of the action potential dome in the epicardium, but not in the endocardium, give rise to ST-segment elevation and subsequent ventricular fibrillation (VF). METHODS: We evaluated the frequency of coronary spasm, augmentation (> or =0.1 mV) of ST-segment elevation in leads V(1) to V(3), and induction of VF by intracoronary injection of acetylcholine (ACh) and/or ergonovine maleate (EM) in 27 symptomatic patients with Brugada syndrome and 30 control subjects. RESULTS: The coronary spasm was induced in 3 (11%) of the 27 patients with Brugada syndrome and in 13 (43%) of the 30 control subjects. ST-segment elevation was augmented by 11 (33%) of the 33 right coronary injections (ACh: 6/11 [55%]; EM: 5/22 [23%]), without coronary spasm, but not by any of the left coronary injections in patients with Brugada syndrome. Ventricular fibrillation was induced by 3 (9%) of the 33 right coronary injections (ACh: 2/11 [18%]; EM: 1/22 [5%]), but not by any of the left coronary injections. In contrast, neither ST-segment elevation nor VF was observed in any of the control subjects. CONCLUSIONS: Our results support the hypothesis that mild ischemia and vagal influences act additively or synergistically with the substrate responsible for the Brugada syndrome to elevate the ST-segment and precipitate VF. These observations suggest that Brugada patients may be at a higher risk for ischemia-related sudden death.

Acetylcholine↗
PubMed2002

The electrophysiologic mechanism of ST-segment elevation in Brugada syndrome.

OBJECTIVES: We sought to demonstrate the electrophysiologic (EP) mechanism of the ST-T change in Brugada syndrome. BACKGROUND: Brugada syndrome is characterized by various electrocardiographic manifestations (e.g., right bundle branch block, ST-segment elevation, and terminal T-wave inversion in the right precordial leads) and sudden cardiac death caused by ventricular fibrillation. Direct evidence in support of the EP mechanism underlying this intriguing syndrome has been lacking. METHODS: Monophasic action potentials (MAPs) were obtained from three patients with the coved-type ST-segment elevation (Brugada patients) and five control patients using the contact electrode method. Epicardial MAPs were recorded during open-chest surgery in all patients. RESULTS: A spike-and-dome configuration was documented from epicardial sites of the right ventricular (RV) outflow tract in all Brugada patients but not in control patients. Monophasic action potential recordings from the endocardium with special focus on the RV outflow tract could not demonstrate any morphological abnormalities in three Brugada patients. CONCLUSIONS: The presence of a deeply notched action potential in the RV epicardium, but not in endocardium, would be expected to induce a transmural current that would contribute to elevation of the ST-segment in the right precordial leads. The spike-and-dome configuration may also prolong the epicardial action potential, thus contributing to a rapid reversal of the transmural gradients and inscription of an inverted T-wave.

Aged↗
PubMed2002

Differential effects of beta-blockade on dispersion of repolarization in the absence and presence of sympathetic stimulation between the LQT1 and LQT2 forms of congenital long QT syndrome.

OBJECTIVES: This study compared the effects of beta-blockade on transmural and spatial dispersion of repolarization (TDR and SDR, respectively) between the LQT1 and LQT2 forms of congenital long QT syndrome (LQTS). BACKGROUND: The LQT1 form is more sensitive to sympathetic stimulation and more responsive to beta-blockers than either the LQT2 or LQT3 forms. METHODS: Eighty-seven-lead, body-surface electrocardiograms (ECGs) were recorded before and after epinephrine infusion (0.1 microg/kg body weight per min) in the absence and presence of oral propranolol (0.5-2.0 mg/kg per day) in 11 LQT1 patients and 11 LQT2 patients. The Q-T(end) interval, the Q-T(peak) interval and the interval between T(peak) and T(end) (T(p-e)), representing TDR, were measured and averaged from 87-lead ECGs and corrected by Bazett's method (corrected Q-T(end) interval [cQT(e)], corrected Q-T(peak) interval [cQT(p)] and corrected interval between T(peak) and T(end) [cT(p-e)]). The dispersion of cQT(e) (cQT(e)-D) was obtained among 87 leads and was defined as the interval between the maximum and minimum values of cQT(e). RESULTS: Propranolol in the absence of epinephrine significantly prolonged the mean cQT(p) value but not the mean cQT(e) value, thus decreasing the mean cT(p-e) value in both LQT1 and LQT2 patients; the differences with propranolol were significantly larger in LQT1 than in LQT2 (p < 0.05). The maximum cQT(e), minimum cQT(e) and cQT(e)-D were not changed with propranolol. Propranolol completely suppressed the influence of epinephrine in prolonging the mean cQT(e), maximum cQT(e) and minimum cQT(e) values, as well as increasing the mean cT(p-e) and cQT(e)-D values in both groups. CONCLUSIONS: Beta-blockade under normal sympathetic tone produces a greater decrease in TDR in the LQT1 form than in the LQT2 form, explaining the superior effectiveness of beta-blockers in LQT1 versus LQT2. Beta-blockers also suppress the influence of sympathetic stimulation in increasing TDR and SDR equally in LQT1 and LQT2 syndrome.

Adolescent↗
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

Change in morphology of reentrant atrial arrhythmias without termination following radiofrequency catheter ablation.

A 60-year-old woman who had previously undergone an atrial septal defect repair and had type I atrial flutter underwent electrophysiological study. After radiofrequency (RF) ablation to the isthmus between the inferior vena cava and the tricuspid annulus, type I atrial flutter was changed to atrial tachycardia following atriotomy without termination. This atrial tachycardia was eliminated by single-site RF ablation of a small lesion below the caudal end of the atriotomy scar, where continuous and fragmented potentials were recorded during tachycardia. We experienced a rare case in which RF energy changed tachycardia circuits.

Atrial Flutter↗
PubMed2002

Macroreentrant atrial flutter around a common atrioventricular canal in an infant with complicated congenital heart anomaly.

This report describes a 2-year-old male infant after repair of complicated congenital heart anomalies including common atrioventricular canal (CAVC), in which macroreentrant atrial flutter around the CAVC was demonstrated by electroanatomic mapping (CARTO) using a single catheter. Radiofrequency catheter ablation at the isthmus between the CAVC and the inferior vena cava eliminated the atrial flutter successfully.

Atrial Flutter↗
PubMed2002

Detection of spatial repolarization abnormalities in patients with LQT1 and LQT2 forms of congenital long-QT syndrome.

The aim of this study is to detect the spatial current dispersion that appears in the T-wave of patients with congenital long-QT syndrome (LQTS). To observe this dispersion, magnetocardiograms (MCGs)--which have a high spatial resolution--of LQT1 patients (n = 7), LQT2 patients (n = 9) and a control group (n = 33) were recorded. The dispersion was evaluated by plotting current-arrow maps (CAMs) calculated from the MCG signals. In the case of LQT1, abnormal current arrows in the CAMs appeared above the inferior part of the heart in two LQT1 patients with a long corrected QT interval (QTc) (>0.6), and the current direction was from the left (origin side) to the right ventricular muscle (110 degrees). In six out of nine LQT2 patients, abnormal current arrows with angles below 20 degrees were observed above the right inferior part or lower septum; the current direction was from the right (origin side) to the left ventricular muscle. However, in the case of the LQT2 patients, the QTc values did not correlate with the abnormal current. These findings suggest that the origin of abnormal repolarization in LQT1 is the left ventricular muscle and the origin of that in LQT2 is the right ventricular muscle or lower septum. The estimation of the origin in LQTS patients can provide important information such as the risk factor of sudden death.

Adolescent↗
PubMed2002

Lack of interaction between amiodarone and mexiletine in cardiac arrhythmia patients.

Amiodarone has pharmacokinetic interactions with various therapeutic agents, including phenytoin, flecainide, and cyclosporine. Mexiletine is metabolized by CYP2D6 and CYP1A2. The objective of this study is to evaluate the effect of amiodarone on the pharmacokinetics of mexiletine through its inhibition of various cytochrome P450 (CYP) subtypes. In a series of 181 inpatients with supraventricular tachyarrhythmias, 26 inpatients received mexiletine and amiodarone therapy (MEX + AMD group), and the others received mexiletine therapy (MEX group). In 10 inpatients of the MEX + AMD group, the mexiletine clearance (CL(MEX)/F) before and after coadministration of amiodarone was compared. CL(MEX)/F was also compared in the MEX and MEX + AMD groups after the start of amiodarone therapy. Serum mexiletine, amiodarone, and desethylamiodarone concentrations were measured by an HPLC method. The CL(MEX)/F was estimated by the Bayesian method using population pharmacokinetic analysis. There was no significant difference in CL(MEX)/F before and after 1-month coadministration of amiodarone in 10 inpatients of the MEX + AMD group. Although serum amiodarone and desethylamiodarone concentrations gradually increased with time after the start of amiodarone therapy in these patients, CL(MEX)/F showed no change at 3 and 5 months after the start of amiodarone therapy. There was no significant difference in CL(MEX)/F of the MEX group and the MEX + AMD group. The results suggest that the pharmacokinetics of mexiletine is not affected by amiodarone in patients with cardiac arrhythmias.

Aged↗
PubMed2002

Long-term efficacy of empirical chronic amiodarone therapy in patients with sustained ventricular tachyarrhythmia and structural heart disease.

The efficacy of empirical chronic oral amiodarone therapy in 129 patients with sustained ventricular tachyarrhythmia (VTNVF) and structural heart disease is evaluated. Twenty-nine patients were treated with class I drugs and monitored by electrophysiological study (EPS) and Holter electrocardiogram (ECG) (class I). The remaining 100 non-responders to the class I drugs were treated with oral amiodarone, of whom 70 were tolerant (AMD+) and 30 were intolerant (AMD-). Patients were followed up to 36 months. The primary and secondary end-points were recurrence of VT/VF and hypothetical death, respectively; whereby, hypothetical death was defined as actual death and the event of rapid VT.VF (heart rate >240beats/min) in patients with an implantable cardioverter defibrillator. Class I and AMD+ patients showed a better prognosis than AMD- patients. The VT/VF event free at 36 months in class I (64.8%) and AMD+ (56.1%) patients were significantly higher than that in AMD- (27.2%) (p<0.01) patients. Hypothetical survival rates in class I (92.0%) and AMD+ (83.6%) patients were significantly higher than that in AMD- (57.0%) (p<0.001) patients, but there were no significant differences in the actual survival rate among the 3 patient groups. The independent clinical factors suppressing the recurrence of VT/VF (Cox hazard) were treatment with amiodarone (p=0.02, 95% confidence interval (CI) =0.19-0.86) and EPS/Holter ECG-guided Class I drugs (p=0.04, 95% CI=0.14-0.94). The results demonstrate that empirical amiodarone has a substantial long-term benefit that is comparable to EPS/Holter ECG-guided class I drugs in the treatment of high-risk patients with VT/VF and structural heart disease.

Amiodarone↗
PubMed2002

Evaluation of mexiletine clearance in a Japanese population.

OBJECTIVE: To evaluate mexiletine clearance in a Japanese population and to clarify the roles of CYP2D6 and CYP1A2 in mexiletine disposition. METHODS: Concentrations of serum and urinary mexiletine and its metabolites were determined and mexiletine clearances were estimated in 334 inpatients receiving mexiletine therapy. Concentrations of mexiletine and its metabolites in serum and urine samples were determined by HPLC. RESULTS: Although interindividual variation of mexiletine clearance was small, the effect of age on mexiletine clearance was comparatively large. Mexiletine clearance in patients with dilated cardiomyopathy (DCM) was decreased when compared with other diagnoses (Non-DCM). The fractional contents of p-hydroxymexiletine (POH) and 2-hydroxymexiletine (OHMEX) in urine amounted to approximately 50%. Almost all of the POH was conjugated, whereas less than one-third of the OHMEX was conjugated. Although no significant differences in POH and OHMEX were observed between patients with DCM and those without, a trend toward an increase in conjugation pathway of DCM patients was observed. CONCLUSIONS: The interindividual variation of mexiletine clearance was small, while the effect of age on the mexiletine clearance in Non-DCM was comparatively large. A significant difference in mexiletine clearance between patients with DCM and those with Non-DCM was observed. Therefore, when mexiletine is administered to patients with DCM, careful monitoring is needed.

Administration, Oral↗
PubMed2002

Five novel single nucleotide polymorphisms in the CYP2C8 gene, one of which induces a frame-shift.

Five novel single nucleotide polymorphisms (SNPs) were found in exon 3 and introns 1, 3, 7, and 8 in cytochrome P450 (CYP) 2C8 gene from 54 Japanese individuals, who were administered the anti-arrhythmic drug amiodarone. The detected SNPs were as follows: 1) SNP, MPJ6_2C8014; GENE NAME, CYP2C8; ACCESSION NUMBER, NT_008769; LENGTH, 25 bases; 5'-ATTCAGAAATATC/TGAATCTATGTGT-3' 2) SNP, MPJ6_2C8015; GENE NAME, CYP2C8; ACCESSION NUMBER, NM_000770 and NT_008769; LENGTH, 25 bases; 5'-GGAGGAGTTGAGA/-AAAACCAAGGGT-3'. 3) SNP, MPJ6_2C8016; GENE NAME, CYP2C8; ACCESSION NUMBER, NT_008769; LENGTH, 25 bases; 5'-ATTTGTAAGATAT/-TGTTTAAAATTT-3' 4) SNP, MPJ6_2C8017; GENE NAME, CYP2C8; ACCESSION NUMBER, NT_008769; LENGTH, 25 bases; 5'-TTGGTTCCAACCC/TTCTAACAACACA-3' 5) SNP, MPJ6_2C8018; GENE NAME, CYP2C8; ACCESSION NUMBER, NT_008769; LENGTH, 25 bases; 5'-GATAGCAAATATA/GTCTCTTTTTGTA-3' Among these SNPs, MPJ6_2C8015 was expected to cause a frame-shift due to the deletion of adenine 471, resulting in amino acid alterations from codon 159 and an early stop codon at residue 177. Therefore, the variant enzyme is most likely to be inactive since it lacks 64% of the protein structure, including the heme-binding site and 5 out of 6 substrate recognition sites.

Journal Article↗
PubMed2002

Novel single nucleotide polymorphisms in the CYP2D6 gene associated with CYP2D6*2 and/or CYP2D6*10 alleles.

Novel single nucleotide polymorphisms (SNPs) were found in introns 1, 3, 4, 5, and 7 of the gene encoding cytochrome (CYP) 2D6 in 90 Japanese subjects. Some of these SNPs were associated with C2850T and/or C100T, which are key SNPs for CYP2D6(*)2 and CYP2D6(*)10, respectively. The SNPs in the CYP2D6 gene (ACCESSION NUMBER, M33388) were designated as follows: SNP, MPJ6_2D6010 (IVS1-138C>G) associated with C2850T; SNP, MPJ6_2D6012 (IVS1-41T>G) associated with C100T, C2850T and G4180C; SNP, MPJ6_2D6016 (IVS3+32A>G); SNP, MPJ6_2D6017 (IVS4-17C>G); SNP, MPJ6_2D6018 (IVS4-17C>T); SNP, MPJ6_2D6020 (IVS5+46G>A); SNP, MPJ6_2D6021 (IVS5-49T>C); SNP, MPJ6_2D6023 (IVS7+40A>C) associated with both C100T, C2850T and G4180C; SNP, MPJ6_2D6024 (IVS7+64T>C); and SNP, MPJ6_2D6025 (IVS7-9C>T) associated with C2850T. These SNPs are convenient for allele typing and should be further investigated for their potential effects on transcription, such as splicing.

Journal Article↗