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Biomedical subjects

H Kasanuki

Publications and source records attributed to H Kasanuki.

At least 37 records · Page 2Linked to original sources
PubMed2000

Recurrent pulmonary adenoid cystic carcinoma presenting as a cardiac tumor.

A 58-year-old patient is presented who had a pulmonary adenoid cystic carcinoma which recurred 10 years after sleeve left pneumonectomy. The patient developed acute heart failure because the lesion obstructed blood flow by compressing the left atrium. Transesophageal echocardiography and magnetic resonance imaging demonstrated a solid mass arising from the pericardium which displaced the posterior wall of the left atrium. The mass was resected. Postoperative radiation was not performed.

Carcinoma, Adenoid Cystic↗
PubMed2000

Regional cardiac sympathetic reinnervation in transplanted human hearts detected by 123I-MIBG SPECT imaging.

The purpose of this study was to assess the regional cardiac sympathetic reinnervation late (> or = 1 year) after heart transplantation (HTX) by means of 123I-MIBG (MIBG) scintigraphy. Eight patients with a pretransplantation diagnosis of idiopathic dilated cardiomyopathy underwent MIBG scintigraphy more than one year after HTX. The presence or absence of regional MIBG uptake was evaluated in each SPECT image, and global MIBG uptake was semi-quantitatively assessed by the heart to mediastinum ratio (H/M). Five of 8 patients had visible MIBG uptake in both planar and SPECT images (PU group), whereas 3 of 8 patients had no uptake, 2 of them after a period of 2 years, and one of them as long as 5 years after HTX, respectively (NU group). Positive regional MIBG uptake involved the basal anterior region in all 5 patients, the basal septal region in 4 patients, the basal lateral region in 3 patients and the basal posterior region in 1 patient. The H/M value was 1.24+/-0.10 in the PU group and 1.09+/-0.03 in the NU group. In conclusion, MIBG SPECT can detect regional sympathetic reinnervation, indicating that basal septal and lateral regions next to the basal anterior are more likely to be reinnervated, but reinnervation is much less likely to occur in the midventricular and apical regions.

3-Iodobenzylguanidine↗
PubMed2000

Optimal therapeutic range for oral anticoagulants in Japanese patients with prosthetic heart valves: a preliminary report from a single institution using conversion from thrombotest to PT-INR.

The thrombotest (TT) technique has been widely used in Japan for monitoring oral anticoagulant therapy (OAT). The therapeutic range was originally recommended to be 10%-25%. However, the International Committee for Standardization in Hematology/International Committee on Thrombosis and Hemostasis (ICSH/ICTH) recommended using the international normalized ratio of prothrombin time (PT-INR) for monitoring OAT. It is necessarv to use a universal standard measure for monitoring OAT in accordance with the ICSH/ISTH recommendation. We simultaneously measured TT and PT in blood samples from 1,157 patients on long-term warfarin therapy, and studied the correlation between TT and PT-INR. An excellent linear correlation was obtained between TT-INR and PT-INR with the regression equation PT-INR = 1.0420 TT-INR - 0.0987 (r = 0.905, P < 0.001). We also examined the correlation between the incidence of thromboembolism in 170 patients receiving warfarin therapy after prosthetic valve replacement; 50.5% received concomitant antiplatelet therapy. Thromboembolism occurred in 9 of 170 patients during a mean follow-up period of 2.44 years. The average TT values in patients with and without thromboembolism were 26.4% (PT-INR: 1.53) and 21.1% (1.73), respectively (P < 0.01). The incidence of thromboembolism did not differ significantly between patients on warfarin alone (average TT: 22.2%) and those on warfarin and antiplatelet agent (average TT: 20.9%). Our results suggest that the incidence of thromboembolism is low in Japan despite a less intensive regimen having been adopted.

Administration, Oral↗
PubMed2000

Plasma brain natriuretic peptide as a parameter to assess efficacy of continuous intravenous infusion of prostacyclin (epoprostenol) to treat severe primary pulmonary hypertension: a case report.

Continuous intravenous infusion of prostacyclin (epoprostenol) as a treatment for primary pulmonary hypertension (PPH) definitely improves the patient's quality of life, but few accurate parameters have been found to evaluate the efficacy of the treatment. We observed a patient with severe PPH whose plasma brain natriuretic peptide (BNP) level changed significantly as her condition and symptoms changed. Plasma BNP may be considered as one of the parameters for assessing the efficacy of prostacyclin treatment.

Adolescent↗
PubMed2000

Effect of cimetidine and probenecid on pilsicainide renal clearance in humans.

OBJECTIVE: To investigate the effect of cimetidine and probenecid on the renal clearance of pilsicainide in healthy subjects. METHODS: Nine healthy men (age range, 21 to 38 years) were given oral doses of 50 mg pilsicainide hydrochloride alone, with coadministration of 800 mg oral cimetidine, or with coadministration of 1,500 mg oral probenecid on three occasions in a Latin-square order. Urine and venous blood samples were collected on a timely basis. The concentration of pilsicainide in plasma and urine were determined by an HPLC method. RESULTS: Concomitant administration of cimetidine significantly increased the area under the plasma concentration-time curve of pilsicainide by a mean of 33%, prolonged elimination half-life by a mean of 24% (from 5 to 6.2 hours), reduced apparent oral clearance by a mean of 26% (from 14.7 +/- 0.1 to 10.8 +/- 0.8 L/h) and reduced renal clearance by a mean of 28% (from 196.8 +/- 53.9 to 141.8 +/- 25.9 mL/min). The net renal clearance by tubular secretion was significantly reduced by a mean value of 38%, from 151.4 +/- 62.9 to 93.0 +/- 31.1 mL/min. Coadministration of probenecid did not show any changes in plasma concentrations of pilsicainide, pharmacokinetics, or the net renal clearance by tubular secretion of pilsicainide. CONCLUSIONS: Pilsicainide appeared to be secreted by the active transport system for organic bases in the proximal tubule, and the excretion of pilsicainide was inhibited by cimetidine.

Adult↗
PubMed2000

Diagnostic accuracy of KL-6 as a marker of amiodarone-induced pulmonary toxicity.

The diagnostic accuracy of KL-6 as an indicator of amiodarone-induced pulmonary toxicity was studied in 14 men (mean age = 62 +/- 12, range 33-76 years) treated with amiodarone. The indications for amiodarone were sustained ventricular tachycardia in 13 patients and atrial fibrillation in 1 patient with refractory heart failure. The KL-6 cut-off level was set at 520 U/mL. Group A consisted of two patients with amiodarone-induced pulmonary toxicity, group B of five patients with other pulmonary disorders, and group C of seven patients without pulmonary disease. KL-6 levels, percent diffusing capacity for carbon monoxide (%DLCO), and other laboratory markers were compared among these three groups. KL-6 levels were significantly higher in group A than in group B and C (2550 +/- 36, 252 +/- 99, 198 +/- 82 U/mL, respectively; P < 0.0001). KL-6 levels in group B were below the cutoff value. %DLCO, C-reactive protein (CRP), and lactic dehydrogenase (LDH) were abnormal in group A. The abnormal rates of CRP and LDH in group B were 80% and 40%, respectively. Of the seven patients with pulmonary disease, three patients (43%) could not undergo %DLCO testing because of poor physical condition. In one patient with amiodarone-induced pulmonary toxicity, the KL-6 level increased from 695 to 2,100 U/mL at a time of progression of interstitial changes. KL-6 may be a useful marker of amiodarone-induced pulmonary toxicity.

Adult↗
PubMed2000

Congestive heart failure after peripheral blood stem cell transplantation: role of cytokines.

A 32-year-old woman was admitted with the diagnosis of congestive heart failure (CHF) without organic heart disease after peripheral blood stem cell transplantation (PBSCT) for malignant lymphoma. Various cytokines have been reported to be released from stem cells after PBSCT and some have a suppressive effect on myocardial contractility; elevated levels of cytokines have been reported in dilated cardiomyopathy (DCM) and/or CHF patients. In the present case, elevated levels of interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-alpha) were observed, and there was a parallel relationship between the recovery of cardiac function and the decrease of these cytokines, strongly suggesting that the release of IL-6 and TNF-alpha after PBSCT might have been important in the pathogenesis of the CHF.

Adult↗
PubMed2000

Apoptotic cell death in arrhythmogenic right ventricular cardiomyopathy: a comparative study with idiopathic sustained ventricular tachycardia.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a specific heart muscle disease of unknown etiology characterized by fatty and fibrofatty replacement of the right ventricular myocardium. It often manifests life-threatened ventricular arrhythmias. Previous studies have hypothesized that myocyte apoptosis contributes to the myocyte cell loss and fatty change in ARVC and may be induced by recurrent ventricular tachycardia (VT). We examined whether these progressive pathological changes result from apoptotic cell death in both autopsied and biopsied right ventricular myocardium from 35 patients with ARVC by using in situ terminal deoxynucleotidyl transferase assay (TUNEL) and agarose gel electrophoresis. We also studied the biopsied myocardium from 30 patients with idiopathic sustained VT whose origin was the outflow tract of the right ventricle. TUNEL-positive cells indicating DNA fragments were observed in some cardiomyocytes and fibroblasts in ARVC, but the numbers of TUNEL-positive myocytes were very low in idiopathic VT. DNA laddering was confirmed in two autopsied cases in ARVC, but not in a non-cardiac case who died. These results suggest that at least some cardiomyocytes and fibroblasts are subjected to apoptosis in ARVC, leading to the loss of myocardium with characteristic pathological changes and subsequently progressive cardiomyopathy. Furthermore, the apoptotic process may not result from myocardial ischemia due to repetitive VT.

Adolescent↗
PubMed2000

[Significance of the time course of ST segment elevation just after reperfusion therapy for acute myocardial infarction].

The significance of the time course of ST segment elevation just after reperfusion therapy for acute myocardial infarction was investigated in 25 consecutive patients with acute myocardial infarction and ST elevation. The most elevated ST lead from the standard electrocardiogram on admission was continuously monitored as the ST trend for 72 hr including during the reperfusion procedure. The culprit artery was totally occluded and reperfused without flow delay. Left ventriculograms were obtained after reperfusion and 3-4 weeks later. The most elevated ST level before reperfusion was measured as the maximal level and the ST level 30 min after reperfusion as the reperfused level. The patients were divided into 2 groups, group ST > or = 50% (n = 12) with a decrease of less than 50% of the maximal ST level and group ST < 50% (n = 13) with a decrease of 50% or over 50%. Regional left ventricular wall motion of infarct site, end-diastolic left ventricular volume and ejection fraction were compared between the acute and chronic phase left ventriculograms in each group. In group ST > or = 50%, no significant change was detected in both regional and global ejection fraction, whereas end-diastolic left ventricular volume enlarged significantly in the chronic phase (acute 80 +/- 25 ml/m2 to chronic 95 +/- 17 ml/m2, p < 0.01). In group ST < 50%, regional and global ejection fraction both improved significantly (SD/chord: acute -2.2 +/- 1.5 to chronic -1.4 +/- 0.4, p < 0.001; ejection fraction: acute 50 +/- 14% to chronic 57 +/- 13%, p < 0.01) but end-diastolic left ventricular volume remained the same in the chronic phase. The peak creatine kinase level and the frequency of ST re-elevation at reperfusion were significantly higher in group ST > or = 50% than in group ST < 50% (creatine kinase: group ST > or = 50% 5,496 +/- 2,219 IU/l, group ST < 50% 1,913 +/- 1,180 IU/l, p < 0.0001; ST re-elevation: group ST > or = 50% 83%, group ST < 50% 38%, p < 0.05), although the time from onset of myocardial infarction to reperfusion, the maximal ST level, the degree of collateral development, and the frequency of pre-infarction angina were not different between the 2 groups. Rapid resolution of ST elevation after reperfusion is a useful marker of the improvement of left ventricular function in acute myocardial infarction.

Creatine Kinase↗
PubMed2000

[Diagnostic usefulness of KL-6 measurements in patients with pulmonary complications after administration of amiodarone].

Amiodarone-induced pulmonary toxicity is one of the major complications in patients receiving administration of amiodarone. KL-6 is a useful indicator to evaluate the activity of interstitial pneumonitis. We studied the clinical utility of KL-6 as a marker for amiodarone-induced pulmonary toxicity. We investigated 6 patients in whom chest radiography revealed abnormal consolidations after administration of amiodarone from 1997 to 1999. All patients were male aged 56 to 76 years (mean 66 +/- 7 years). The indications for amiodarone included sustained ventricular tachycardia in 5 patients and atrial fibrillation in one patient with refractory heart failure. The mean left ventricular ejection fraction was 31 +/- 12% (22-52%). KL-6 levels were measured by a sandwich type enzyme immunoassay using a murine monoclonal antibody (KL-6 antibody), and the cutoff level was determined at 520 U/ml. Complications occurred from 17 days to 45 months after treatment with amiodarone. The KL-6 levels were abnormally high (2,100 and 3,000 U/ml) in 2 patients with amiodarone-induced pneumonitis but under the cutoff level in the non-pneumonitis patients. In one patient with amiodarone-induced pneumonitis, the KL-6 level increased from 695 to 2,100 U/ml concurrently with worsening interstitial changes shown by high resolution computed tomography. We conclude that KL-6 has practical uses as a marker for the detection and evaluation of amiodarone-induced pulmonary toxicity.

Aged↗
PubMed2000

[Risk factors and effect of reperfusion therapy on left ventricular free wall rupture following acute myocardial infarction].

Reperfusion therapy is one of the most effective treatments for acute myocardial infarction, but the effect on left ventricular free wall rupture remains to be determined. This study tried to clarify the risk factors and effect of reperfusion therapy on the risk of free wall rupture following acute myocardial infarction. 2,671 consecutive patients with acute myocardial infarction admitted to our hospital were examined. Incidence of free wall rupture showed no degenerative change(0 to 5.8%; mean 2.1%). The 1,269 consecutive patients from 1985 to 1995 were examined closely to evaluate risk factors and the effect of reperfusion therapy on the risk of free wall rupture. Fourteen patients who underwent emergent coronary artery bypass surgery were excluded. Free wall rupture was found in 25 patients (2.0%). Multivariate analysis confirmed that high age(> or = 70 years) and first acute myocardial infarction were independent risk factors of free wall rupture (odds ratio 3.62, p = 0.003; odds ratio 7.69, p = 0.046, respectively). The incidence of free wall rupture in the conservative therapy group(n = 799) was 2.1%, successful reperfusion group(n = 373) was 0.5%, and unsuccessful reperfusion group(n = 83) was 7.2% with significant statistical differences(p < 0.01). There was no statistical difference between the direct percutaneous transluminal coronary angioplasty group(n = 84, 3.6%) and the thrombolysis group(n = 372, 1.3%). Successful reperfusion was the only independent factor in the reperfusion therapy group that reduced the incidence of free wall rupture(odds ratio = 0.07, p = 0.001). We conclude that reperfusion of the infarct-related artery and more intensive management of unsuccessful reperfusion is important to prevent free wall rupture following acute myocardial infarction.

Age Factors↗
PubMed2000

[Efficacy of continuous intravenous drip infusion of disopyramide in hypertrophic obstructive cardiomyopathy during cardiogenic shock: a case report].

A 54-year-old woman was admitted to our hospital complaining of dyspnea due to hypertrophic obstructive cardiomyopathy. On admission, she was treated with 4 antiarrhythmic drugs and 2 beta-blockers. After 4 of these 6 drugs were withdrawn, the left ventricular outflow pressure gradient markedly increased and then she fell into cardiogenic shock. Therefore, disopyramide(600 mg/day) was administered by continuous intravenous drip infusion to reduce the left ventricular outflow pressure gradient. After intravenous administration of disopyramide, the left ventricular outflow pressure gradient markedly decreased from 100 to 16 mmHg and the cardiogenic shock could be improved. Continuous intravenous drip infusion of disopyramide is effective for the treatment of cardiogenic shock due to severe left ventricular outflow obstruction in patients with hypertrophic obstructive cardiomyopathy.

Anti-Arrhythmia Agents↗
PubMed2000

[Long-term outcome of pharmacological and nonpharmacological treatment for ventricular arrhythmias].

Recent advances of nonpharmacological therapy such as catheter ablation and implantable cardioverter defibrillator and lessons from the Cardiac Arrhythmia Suppression Trial(CAST) have changed the strategy for ventricular arrhythmias. The safety and efficacy of radiofrequency catheter ablation of symptomatic sustained monomorphic ventricular tachycardia without structural heart disease has made ablation the firstline curative therapy. In idiopathic ventricular fibrillation such as Brugada syndrome, an implantable cardioverter defibrillator is the most effective treatment to prevent sudden cardiac death. In patients with asymptomatic ventricular tachyarrhythmias in heart failure, class I antiarrhythmic drugs should be avoided due to proarrhythmic and negative inotropic effects that may be responsible for increased mortality in some trials. In such patients, amiodarone and beta-blocker may reduce sudden cardiac death. For patients with sustained ventricular tachycardia or ventricular fibrillation in heart failure, amiodarone or implantable cardioverter defibrillator should be considered. In comparison with amiodarone, implantable cardioverter defibrillator markedly reduced sudden death in ventricular tachycardia and ventricular fibrillation survivors in Antiarrhythmics Versus Implantable Defibriltors(AVID). Although better patient selection and clarification of mapping criteria improved the successful ablation rate in patients with structural heart disease, candidates of ablation are few. In patients with extensive structural heart disease, multiple ventricular tachycardias are often present. Catheter ablation of a single ventricular tachycardia may be only palliative. Therefore, implantable cardioverter defibrillator is the most effective treatment to prevent sudden cardiac death, with amiodarone and ablation as the adjunctive therapy to prevent frequent ventricular tachycardia. Furthermore, an implantable cardioverter defibrillator improved survival in selected patients with depressed ventricular function after myocardial infarction, who also have nonsustained and inducible sustained ventricular tachycardia in Multicenter Automatic Defibrillator Implantation Trial(MADIT) and Multicenter Unsustained Tachycardia Trial(MUSTT).

Adrenergic beta-Antagonists↗
PubMed2000

[Myocardial involvement in rheumatic diseases].

The rheumatic diseases share many features. Clinically, they are often systemic diseases affecting multiple organs. Pathologically, these diseases share in common a diffuse vasculitis with an inflammatory process. Involvement of myocardium is also pathologically a common finding in rheumatic diseases, especially systemic sclerosis and dermatopolymyositis. Although clinical symptoms are often silent, potentially life-threatening manifestations are well known. Non invasive techniques such as nuclear imaging and echocardiography are useful to detect occult cardiac lesions. Clinically overt cardiac involvement portends an unfavorable prognosis. Early detection of subclinical involvement of myocardium is essential to improve prognosis.

Cardiomyopathies↗
PubMed2000

Malfunction of a Hancock bioprosthesis in the mitral position 24 years after initial implantation.

BACKGROUND AND AIMS OF THE STUDY: Although many types of cardiac bioprosthetic valves are currently available, the major disadvantage of their use is limited durability due to progressive structural valve deterioration. Few such valves function beyond 20 years. METHODS: A 61-year-old man was admitted urgently to our institute with acute mitral insufficiency, 24 years after undergoing mitral valve replacement with a 25-mm standard Hancock porcine bioprosthesis for mitral stenosis. RESULTS: Mitral valve reoperation was performed successfully with a mechanical valve. The explanted bioprosthesis showed leaflet perforations and a commissural tear, moderate calcification on the commissures, and pannus overgrowth. CONCLUSION: The findings in this case suggest that individual patient variables, as well as the design and the construction of the valve are major determining factors in the rate of valve failure.

Bioprosthesis↗
PubMed1999

Clinical potential of intravascular ultrasound for physiological assessment of coronary stenosis: relationship between quantitative ultrasound tomography and pressure-derived fractional flow reserve.

BACKGROUND: Little is known regarding intravascular ultrasound (IVUS) criteria to determine the functional severity of coronary stenosis. Recently, fractional flow reserve (FFR) has emerged as a lesion-specific index of the functional severity of a coronary stenosis that is independent of systemic hemodynamic variability. The present study was undertaken to determine the IVUS parameters for the physiological severity of coronary stenosis. METHODS AND RESULTS: Fifty-one lesions in 42 patients were evaluated by means of quantitative coronary angiogram, IVUS, and intracoronary pressure measurements. The FFR was calculated as the ratio of the distal coronary pressure divided by the proximal coronary pressure under hyperemia. We considered a value of the FFR <0.75 as significant in determining inducible ischemia, according to the previous studies. The minimal luminal area (MLA) and the area stenosis were measured by IVUS. By regression analysis, the MLA showed a positive correlation with the FFR value (r(2)=0.62, P<0.0001). The area stenosis had a significant inverse correlation with the value of FFR (r(2)=0.60, P<0.0001). The IVUS thresholds that maximized the sensitivity and specificity were MLA <3.0 mm(2) (sensitivity, 83.0%; specificity, 92.3%) and area stenosis >0.6 (sensitivity, 92.0%; specificity, 88.5%). The combination of both criteria (MLA <3.0 mm(2) and area stenosis <0.6) without exception met a value of the FFR <0.75. CONCLUSIONS: Anatomic parameters obtained by IVUS showed a significant correlation to the FFR values. The present study demonstrated that the combination of the MLA and area stenosis measured by IVUS can be an anatomic predictor for the physiological impact of coronary epicardial stenosis.

Coronary Angiography↗
PubMed1999

Novel mechanism associated with an inherited cardiac arrhythmia: defective protein trafficking by the mutant HERG (G601S) potassium channel.

BACKGROUND: The congenital long-QT syndrome (LQTS) is an inherited disorder characterized by a prolonged cardiac action potential and a QT interval that leads to arrhythmia. Mutations in the human ether-a-go-go-related gene (HERG), which encodes the rapidly activating component of the delayed rectifier current (IKr), cause chromosome 7-linked LQTS (LQT2). Studies of mutant HERG channels in heterologous systems indicate that the mechanisms mediating LQT2 are varied and include mutant subunits that form channels with altered kinetic properties or nonfunctional mutant subunits. We recently reported a novel missense mutation of HERG (G601S) in an LQTS family that we have characterized in the present work. METHODS AND RESULTS: To elucidate the electrophysiological properties of the G601S mutant channels, we expressed these channels in mammalian cells and Xenopus oocytes. The G601S mutant produced less current than wild-type channels but exhibited no change in kinetic properties or dominant-negative suppression when coexpressed with wild-type subunits. To examine the cellular trafficking of mutant HERG channel subunits, enhanced green fluorescent protein tagging and Western blot analyses were performed. These showed deficient protein trafficking of the G601S mutant to the plasma membrane. CONCLUSIONS: Our results from both the Xenopus oocyte and HEK293 cell expression systems and green fluorescent protein tagging and Western blot analyses support the conclusion that the G601S mutant is a hypomorphic mutation, resulting in a reduced current amplitude. Thus, it represents a novel mechanism underlying LQT2.

Animals↗