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Biomedical subjects

Teruo Takano

Publications and source records attributed to Teruo Takano.

At least 55 records · Page 3Linked to original sources
PubMed2005

Emergency treatment with nifekalant, a novel class III anti-arrhythmic agent, for life-threatening refractory ventricular tachyarrhythmias: post-marketing special investigation.

BACKGROUND: Because class I anti-arrhythmic drugs sometimes suppress cardiac function caused by their negative inotropic effects, they are not adequate for use in patients with severe heart failure, even as emergency treatment for life-threatening ventricular tachyarrhythmias (ventricular tachycardia (VT)/ventricular fibrillation (VF)). METHODS AND RESULTS: An objective evaluation committee re-evaluated the effect of nifekalant in 191 patients with refractory VT/VF. The attack termination was achieved in 45 out of 93 patients (48.4%). Nifekalant was administered to 39 patients with direct-current (DC) shock-resistant VT/VF and directly terminated VT/VF in 9 patients. In 15 of the remaining 29 patients (51.7%), VT/VF was successfully cardioverted by additional DC shock after nifekalant administration. Prevention of recurrence was achieved in 60 out of 99 patients (60.6%). Corrected QT interval (QTc) was significantly prolonged after initial administration of nifekalant (0.463+/-0.056 to 0.504 +/-0.072), and during maintenance infusion (0.470 +/-0.056 to 0.547+/-0.070). As an adverse reaction, excess prolongation of QTc was noted in 11 patients including 3 patients with torsades de pointes. Hemodynamic parameters tended to improve after maintenance infusion of nifekalant. CONCLUSION: Nifekalant is effective and useful for life-threatening refractory ventricular tachyarrhythmias, although careful observation of the QT interval is required.

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PubMed2005

A rapid bedside D-dimer assay (cardiac D-dimer) for screening of clinically suspected acute aortic dissection.

BACKGROUND: A rapid laboratory test for diagnosis of acute aortic dissection (AAD) has not been available. We performed this prospective study to determine the utility of a rapid bedside D-dimer (DD) assay for detection of AAD. METHODS AND RESULTS: Patients with suspected AAD were recruited and their DD levels were measured by rapid bedside assay. They were divided into 2 groups according to enhanced computed tomography findings: an AAD group (n = 30) and a non-AAD group (n = 48). The median DD level was higher in the AAD group (1.80 microg/ml) than in the non-AAD group (0.42 microg/ml) (p = 0.000). The rapid bedside DD assay showed 100% sensitivity, 54% specificity, 58% positive predictive value and 100% negative predictive value for detection of AAD with a normal DD level of up to 0.5 microg/ml. The combination of DD level >0.5 microg/ml and systolic blood pressure > or = 180 mmHg showed 86% positive predictive value for detection of AAD. Conclusions We conclude that the rapid bedside DD assay is a highly sensitive method for early exclusion of AAD in patients with chest and/or back pain suggestive of AAD. Acute aortic dissection is highly probable if a rapid DD assay shows the elevated DD level with systolic blood pressure > or = 180 mmHg on admission.

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PubMed2005

Clinical implication of T-wave morphology analysis as a new repolarization descriptor.

BACKGROUND: T-wave morphology analysis (TMA) quantifies irregularities of ventricular repolarization based on singular value decomposition of the 12-lead electrocardiogram (ECG). Furthermore, TMA is useful for risk stratification of patients with myocardial infarction (MI), although gender differences in TMA and the relationship between TMA and heart diseases are unknown. The aim of this study was to evaluate the significance of TMA in healthy individuals and patients with heart diseases. METHODS AND RESULTS: Patients with heart disease and either with or without an implanted cardioverter defibrillator (ICD, n = 33, 57+/-16 years; non-ICD, n = 50, 67+/-10 years) were studied. Normal control ECGs (n = 114) were selected from Marquette's database (NC, 33+/-13 years) and the TMA descriptors, including T-wave morphology dispersion (TMD) and percentage of the loop area (PL), were calculated. TMD was significantly lower in group NC males than in the group NC females (11+/-5.9 vs 22+/-16, p < 0.0001). PL was significantly higher in group NC than in the ICD and non-ICD groups (0.63+/-0.12 vs 0.53+/-0.15, p < 0.0001). TMD of group NC was significantly lower than that of the ICD and non-ICD groups (14+/-11 vs 47+/-27, p < 0.0001). CONCLUSION: There are gender differences in TMD. Abnormal values for TMA could reflect abnormalities of ventricular repolarization.

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PubMed2005

Angiotensin-converting enzyme inhibitor therapy inhibits the progression from paroxysmal atrial fibrillation to chronic atrial fibrillation.

BACKGROUND: Atrial fibrillation is a progressive disease, which in the paroxysmal form (PAF) becomes more frequent and finally becomes chronic (CAF). A retrospective analysis of patients with PAF was conducted to examine the hypothesis that angiotensin-converting enzyme inhibitors (ACEI) will prevent the progression to CAF. METHODS AND RESULTS: On the basis of their treatment, 95 patients with PAF were divided into 2 groups: 42 patients treated with ACEI for hypertension throughout the period of treatment and follow-up (ACEI group) and 53 patients not given ACEI (non-ACEI group). Cardiac rhythms were assessed either from the medical records or the electrocardiograms recorded every 2-4 weeks at follow-up visits. The mean follow-up time was 8.3+/-3.5 years. There was no significant difference in the use of antiarrhythmic drugs, left atrial diameter or left ventricular ejection fraction between the 2 groups. The Kaplan-Meier curve for the time to occurrence of CAF showed a lower incidence of CAF in the ACEI group and demonstrated that the 5-year probability for persistence of PAF without progression to CAF was 88.3%, but 47.5% in the non-ACEI group. CONCLUSIONS: These results indicate that ACEI will prevent progression from PAF to CAF.

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PubMed2005

Impact of the revised criteria for acute myocardial infarction using cardiac troponins in a Japanese population with acute coronary syndromes.

BACKGROUND: The clinical implications of applying the new criteria of acute myocardial infarction (AMI) with cardiac troponins in terms of their diagnostic and prognostic impact in patients with suspected acute coronary syndromes (ACS) have not been well evaluated. METHODS AND RESULTS: The study group comprised 973 consecutive patients who were diagnosed as having ACS with or without ST elevation (STE). They were divided into 3 groups: unstable angina (UA) group (n=195) representing patients with no significant elevations of creatine kinase (CK) and troponin T (TnT); TnT-myocardial infarction (MI) group (n=170) with TnT elevation and no CK elevation (additionally detected AMI by the new criteria); CK-MI group (n=608) with significant elevation of CK (AMI by the old criteria). In the TnT-MI group, 140 (76%) patients had non-STE ACS. In-hospital mortality rates for STE ACS were 0%, 2.5% and 9.7% in the UA, TnT-MI and CK-MI groups, respectively. The corresponding values for non-STE ACS were 1.8%, 4.6%, and 16.5%, respectively (p<0.0001), suggesting a pivotal role of TnT. In multiple logistic regression analysis, significant CK elevation was selected as an independent predictor of in-hospital death in concurrence with age > or =75 years, prior MI, shock and low left ventricular ejection fraction in non-STE ACS. CONCLUSIONS: The new criteria result in a substantial increase in the diagnosis of AMI from non-STE ACS in particular. They assist greatly in detailed risk stratification of ACS patients, notably in cooperation with the old CK criteria.

Acute Disease↗
PubMed2005

Hemodynamic features of advanced cirrhosis due to chronic bile duct ligation.

AIM: The aim of the present study was to compare the hemodynamic features of portal hypertension in rats with early cirrhosis with those of rats with advanced cirrhosis following common bile duct ligation (CBDL). METHODS: A total of 53 male Sprague-Dawley rats were used. Hemodynamics were evaluated under conscious and unrestrained conditions 4 weeks and 8 weeks after CBDL, and 4 weeks after a sham operation. Arterial pressure and portal pressure were measured directly via catheters placed in the right femoral artery and main portal vein, respectively. The cardiac index and organ (splanchninc organs, brain, kidneys and lungs) blood flow were determined by the reference sample method using (141)Ce-labeled microspheres (15 mum in diameter). Arterial levels of endothelin-1 and nitrate/nitrite, as well as liver function variables, were also determined. RESULTS: Portal pressure was significantly higher 8 weeks after CBDL (15.8+/-2.1, n=8) than 4 weeks after CBDL (13.9+/-2.1 mmHg, n=12, p<0.05), and the hyperdynamic circulation of the early period was attenuated (p<0.05). Although hepatic artery blood flow 4 and 8 weeks after CBDL was higher than that after sham operation (p<0.05), portal territory blood flow was not increased. There was a significant positive correlation between portal pressure and portal territory blood flow 8 weeks after CBDL (r=0.822, n=8, p=0.012). In rats with anemia 4 weeks after CBDL, the hemoglobin concentration was negatively correlated with portal territory blood flow (r=-0.597, n=12, p=0.040). CONCLUSION: Portal pressure was higher 8 weeks after CBDL than 4 weeks after CBDL and increased with portal territory blood flow, suggesting that portal hypertension is maintained by a mechanism consistent with the forward flow theory. Anemia might exacerbate the hyperdynamic systemic circulation 4 weeks after CBDL.

Animals↗
PubMed2005

Association of limited scleroderma and pulmonary hypertension in a patient with primary biliary cirrhosis.

We report a male patient with primary biliary cirrhosis (PBC) who developed limited scleroderma (l-SSc) and pulmonary hypertension (PHT). He had noticed shortness of breath seven months earlier, which slowly progressed before admission. Sclerodactyly and telagiectasia of the fingers and chest wall were found. Chest X-ray and Doppler echocardiography suggested the presence of PHT. Histologic examination of the liver (needle biopsy) revealed stage two PBC, and histologic findings of the skin (obtained from the dorsum of right finger IV) were compatible with l-SSc. Direct measurement of pulmonary arterial pressure revealed PHT with normal capillary wedge pressure during right heart catheterization. A striking increment of plasma thromboxane B(2) across the lungs was found, which suggested that thromboxane A(2) (precursor of thromboxane B(2)) contributed considerably to a rise in pulmonary vascular resistance leading to PHT.

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PubMed2005

Sudden death in a case of cardiac amyloidosis immediately after pacemaker implantation for complete atrioventricular block.

We report a patient with cardiac involvement associated with primary amyloidosis presenting marked left ventricular (LV) wall thickening, severely decreased systolic and diastolic function, and complete atrioventricular block (CAVB), who died suddenly of cardiac arrest caused by electro-mechanical uncoupling occurring immediately after permanent pacemaker implantation. Post mortem examination showed no procedural complications such as cardiac or venous perforation. The heart was densely infiltrated with amyloid fibrils, especially in the extracellular tissues surrounding the papillary vessels.

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PubMed2005

Recent advances in interventional radiology for acute massive pulmonary thromboembolism.

Acute massive pulmonary thromboembolism is life-threatening and requires vigorous treatment. Anticoagulation is the most traditional treatment for pulmonary thromboembolism, but may not be sufficient for massive thromboemboli. Systemic thrombolytic therapy and surgical thrombectomy are the traditional therapeutic options in this situation. Catheter-directed thrombolysis, percutaneous embolectomy and, more recently, percutaneous thrombus fragmentation techniques using specialized devices are now available to treat the most severe cases of massive pulmonary thromboembolism. The success of these techniques depends on a thorough understanding of the mechanism of action of each of the devices and familiarity with the relevant catheterization techniques. We present a review of currently available equipment and techniques, and describe our work with hybrid treatment using a combination of mechanical fragmentation, localized fibrinolysis and clot aspiration.

Acute Disease↗
PubMed2005

Pharmacological preconditioning with bradykinin affords myocardial protection through NO-dependent mechanisms.

Bradykinin (BK) is one of the triggers of ischemic preconditioning. Protein kinase C (PKC) and mitochondrial ATP-dependent potassium (K(ATP)) channels are central factors in cardioprotection afforded by BK. However, the role of nitric oxide (NO) in the early phase protection of preconditioning with BK is not well understood. We assessed the signaling pathway of the early phase protection of pharmacological preconditioning afforded by BK. Isolated perfused rat hearts (n = 8/group) were subjected to 30-minute global ischemia and 50-minute reperfusion. Left ventricular systolic pressure (LVSP) was recorded prior to the global ischemia and at the end of reperfusion. Preconditioning with BK was induced by two cycles of 5-minute infusion of BK (0.5 micromol/L) and 5-minute washout prior to the global ischemia. To examine participants in the signaling pathway, 5-hydroxydecanoate (5-HD, 200 micromol/L), chelerythrine (CH, 5 micromol/L), or N(omega)-nitro-L-arginine methyl ester (L-NAME, 50 mmol/L) was added to the perfusate for 5 minutes prior to the infusion of BK. Pharmacological preconditioning by BK improved postischemic recovery of LVSP (+ 45.1% versus control, P < 0.01). Protection by BK was abolished by coadministration of CH, 5-HD, or L-NAME. BK affords myocardial protection in the early phase of pharmacological preconditioning through a pathway that includes endogenous NO, PKC, and mitochondrial K(ATP) channels.

Alkaloids↗
PubMed2004

Application of NT-proBNP and BNP measurements in cardiac care: a more discerning marker for the detection and evaluation of heart failure.

BACKGROUND: Measurement of brain natriuretic peptide (BNP) has become a potent diagnostic aid as a means of identifying patients with systolic or diastolic dysfunction. Due to better stability in circulating blood, we reasoned that measurement of N-terminal proBNP (NT-proBNP) may be a more discerning marker for the detection and evaluation of chronic heart failure. METHODS: The relationships between plasma concentrations of NT-proBNP and BNP, and aetiology, New York Heart Association (NYHA) classification, and left ventricular ejection fraction (LVEF) were analyzed in 105 patients with chronic heart failure. Sixty-seven healthy volunteers were studied as the controls. RESULTS: Both NT-proBNP and BNP showed progressive increases (P<0.001) in proportion to the NYHA classification; the increment of NT-proBNP was larger than that of BNP. Elevated NT-proBNP significantly correlated with BNP (r=0.737, P<0.001). Receiver operating characteristics analysis to detect LVEF<40% showed similar values (area under the curve, AUC: NT-proBNP 0.754 vs. BNP 0.770), however, AUC to detect LVEF<50% tended to be greater for NT-proBNP than that for BNP (NT-proBNP 0.820 vs. BNP 0.794). CONCLUSION: NT-proBNP may be a more discerning marker for the detection and evaluation of heart failure than BNP.

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PubMed2004

Elevated troponin T levels and lesion characteristics in non-ST-elevation acute coronary syndromes.

BACKGROUND: Elevated troponin T levels in non-ST-elevation acute coronary syndromes (NSTE-ACS) have been shown to predict an adverse outcome. Furthermore, it has been reported that troponin T could help improve the effectiveness of such new antithrombotic drugs as platelet GPIIb/IIIa antagonists and low-molecular-weight heparins. We hypothesized that such elevated troponin T levels in NSTE-ACS indicate the presence of thrombus at culprit lesions, and this hypothesis was verified through the use of coronary angioscopy. METHODS AND RESULTS: We studied 57 consecutive patients with NSTE-ACS who underwent preinterventional angioscopy. Before catheterization, we obtained blood samples to determine troponin positivity, and the patients were then classified as either troponin-positive or troponin-negative groups (diagnostic threshold, 0.1 ng/mL). Using angioscopy at the culprit lesions, we examined the presence of coronary thrombus, yellow plaque, and complex plaque. Moreover, we compared the preinterventional angiographic parameters (thrombus and complexity of the culprit lesion, and TIMI flow) between the two groups. Twenty-two patients were troponin-positive and 35 patients were troponin-negative. Univariate analyses indicated that the TIMI flow and the incidence of coronary thrombus detected with angioscopy correlate with the elevated troponin T levels. A multivariate logistic regression analysis showed the presence of coronary thrombus detected with angioscopy to be the only independent factor associated with elevated troponin T levels in patients with NSTE-ACS (odds ratio, 22.1; 95% CI, 2.59 to 188.42; P=0.0046). CONCLUSIONS: Using angioscopy, the elevated troponin T levels in NSTE-ACS were confirmed to be strongly associated with the presence of coronary thrombus.

Acute Disease↗
PubMed2004

Effects of the patent false lumen on the long-term outcome of type B acute aortic dissection.

OBJECTIVE: To determine the most effective treatment, we performed a detailed comparative study of the clinical course of patients with type B aortic dissection with a patent or thrombosed false lumen who did not undergo surgery in the acute period. We examined the effect of patency of the false lumen on outcome. METHODS: Computed tomography scans of 138 patients with type B acute aortic dissection were reviewed. Of 138 patients, 110 were medically treated and survived the acute period. We focused on the outcome of these 110 patients, 62 with medically treated thrombosed false lumen (thrombosed group) and 48 with medically treated patent false lumen (patent group). We investigated factors influencing outcome among the 110 patients. The follow-up period was up to 10 years after the onset of aortic dissection. The three study endpoints were death from any cause, dissection-related death (aortic rupture, perioperative death, or death due to organ ischemia), and a dissection-related event (aortic rupture or surgery). In the patent group, we investigated factors influencing long-term outcome. RESULTS: Patency of the false lumen was an independent risk factor for dissection-related death (P = 0.038, hazard ratio=5.6, confidence interval=1.1-28) and for a dissection-related event (P = 0.000, hazard ratio=7.6, confidence interval=2.7-22) but not for death from any cause (P = 0.769, hazard ratio=1.2, confidence interval=0.45-2.91). In the patent group, location of the most dilated aortic segment at the distal arch was an independent risk factor for dissection-related death (P = 0.026, hazard ratio=13.6, confidence interval=1.4-135) and for a dissection-related event (P = 0.048, hazard ratio=2.6, confidence interval=1.0-6.9). CONCLUSIONS: Patency of the false lumen is a strong independent prognostic factor for type B aortic dissection. Location of the most dilated aortic segment at the distal arch is a significant risk factor in the patients with a patent false lumen.

Acute Disease↗
PubMed2004

Impaired baroreflex as a cause of chronotropic incompetence during exercise via autonomic mechanism in patients with heart disease.

PURPOSE: It is thought that the mechanisms responsible for impaired chronotropic response to exercise are related to disturbance of cardiovascular autonomic regulation such as the baroreflex. However, it is still unclear whether the baroreflex mechanisms modulate heart rate (HR) responses to exercise via vagal and/or sympathetic alteration. We therefore investigated the effects of baroreflex sensitivity (BRS) on the exercise HR response in the early phase of vagal deactivation and in the later phase of sympathetic excitation via metabolic stimulation. METHODS: Twenty-four patients (18 males and 6 females, age 59+/-9 years) with heart disease underwent symptom-limited treadmill exercise testing according to the Bruce protocol, and BRS was measured utilizing the phenylephrine method. Subjects were grouped by their resting BRS value: 12 with normal BRS (> or =6 ms/mmHg) and 12 with depressed BRS (<6 ms/mmHg). The HR response to exercise was assessed using two parameters: the increment in HR during exercise and the ratio of HR response to the metabolic reserve (chronotropic index). RESULTS: (1) In the patients with depressed BRS, the HR responses within 1 min after the start of exercise and from 1 min to peak exercise were attenuated compared with those having a normal BRS (15+/-8 vs. 24+/-8 bpm and 36+/-9 vs. 47+/-15 bpm, respectively). (2) The chronotropic index in the patients with depressed BRS was lower than in those with normal BRS (0.50+/-0.14 vs. 0.64+/-0.08). CONCLUSION: These findings suggest that impaired BRS modulates both the parasympathetic influence in early exercise and sympathetic effects in the later phase on HR response to exercise.

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