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Katsusuke Yano

Publications and source records attributed to Katsusuke Yano.

88 records · Page 5Linked to original sources

[Significance of acute-phase inflammatory reactants as an indicator of prognosis after acute myocardial infarction: which is the most useful predictor?].

OBJECTIVES: To investigate the relationship between representative acute-phase inflammatory reactants [highly sensitive C-reactive protein (hsCRP), serum amyloid A protein (SAA) and interleukin-6 (IL-6)] and the severity of acute myocardial infarction and patient prognosis, and to identify the most useful predictor of the three. METHODS: This study investigated 132 consecutive patients admitted within 8 hr of onset of first acute myocardial infarction and successfully reperfused with primary percutaneous coronary intervention. Acute-phase (= 24 hr from onset) blood samples were taken for evaluation of inflammatory reactants (hsCRP, SAA and IL-6), and peak creatine phosphokinase levels were measured every 4 hr after admission for 48 hr to assess myocardial infarction infarct size. Left ventriculography was performed in the chronic stage (20 +/- 9 days post-admission) to analyze left ventricular ejection fraction and regional wall motion, using Killip's classification to determine acute myocardial infarction severity. Logistic regression analysis was used to quantify the usefulness of the reactants as predictors of patient prognosis. RESULTS: Both hsCRP and SAA showed significant positive correlations with peak creatine phosphokinase. hsCRP and SAA showed significant inverse correlations with left ventricular ejection fraction and regional wall motion in the chronic stage. Multivariate analysis identified SAA as the best predictor of severe heart failure (Killip's classification III, IV). SAA was the best predictor of a major cardiac event (shock, cardiac death). CONCLUSIONS: These results suggest a strong correlation between acute-phase SAA and the clinical course of patient outcomes after acute myocardial infarction, such as cardiac function, heart failure and cardiac death. SAA may be the most useful acute-phase inflammatory reactant for predicting the prognosis after acute myocardial infarction.

Acute-Phase Proteins↗

Clinical significance of acute-phase brain natriuretic peptide in acute myocardial infarction treated with direct coronary angioplasty.

OBJECTIVES: To investigate the relationship between brain natriuretic peptide (BNP) plasma concentration levels and the clinical course, mortality and success of left ventricular remodeling by direct percutaneous coronary intervention (PCI) in patients with acute myocardial infarction. METHODS: One hundred thirty consecutive first-acute myocardial infarction patients were successfully reperfused by direct PCI. BNP plasma concentration levels were assessed at 24 hr from onset, and patients were divided into the high (> or = 290 pg/ml) plasma BNP group (H-BNP group; n = 65) or low (< 290 pg/ml) plasma BNP subset (L-BNP group; n = 65). Left ventriculography was performed in both the acute (following reperfusion therapy) and chronic (20 +/- 8 days after onset) stages to evaluate left ventricular ejection fraction (LVEF), left ventricular end-diastolic volume index (LVEDVI) and regional wall motion (RWM). Differences between the parameters at the two stages (chronic stage--acute stage) were expressed as delta LVEF, delta LVEDVI, and delta RWM. RESULTS: There were significantly more major complications in the H-BNP group than in the L-BNP group. There was significantly higher mortality in the H-BNP group (p < 0.01). Multivariate analysis identified only BNP plasma concentration as an independent predictor of mortality (p < 0.05). There were no significant differences in left ventricular function in the acute stage between the groups, but LVEF, LVEDVI, and RWM were all significantly worse in the chronic stage in the H-BNP group compared with the L-BNP group. Moreover, delta LVEF (p < 0.001), delta LVEDVI (p < 0.05), and delta RWM (p < 0.01) were also significantly worse in the H-BNP group. CONCLUSIONS: Early-phase BNP plasma concentrations after successful PCI in patients with acute myocardial infarction may be correlated closely with major complications, and may be of prognostic importance. BNP plasma concentration may also be an indicator of left ventricular remodelling.

Aged↗

Overexpression of calreticulin modulates protein kinase B/Akt signaling to promote apoptosis during cardiac differentiation of cardiomyoblast H9c2 cells.

Calreticulin is a Ca(2+)-binding molecular chaperone of the lumen of the endoplasmic reticulum. Calreticulin has been shown to be essential for cardiac and neural development in mice, but the mechanism by which it functions in cell differentiation is not fully understood. To examine the role of calreticulin in cardiac differentiation, the calreticulin gene was introduced into rat cardiomyoblast H9c2 cells, and the effect of calreticulin overexpression on cardiac differentiation was examined. Upon culture in a differentiation medium containing fetal calf serum (1%) and retinoic acid (10 nm), cells transfected with the calreticulin gene were highly susceptible to apoptosis compared with controls. In the gene-transfected cells, protein kinase B/Akt signaling was significantly suppressed during differentiation. Furthermore, protein phosphatase 2A, a Ser/Thr protein phosphatase, was significantly up-regulated, implying suppression of Akt signaling due to dephosphorylation of Akt by the up-regulated protein phosphatase 2A via regulation of Ca(2+) homeostasis. Thus, overexpression of calreticulin promotes differentiation-dependent apoptosis in H9c2 cells by suppressing the Akt signaling pathway. These findings indicate a novel mechanism by which cytoplasmic Akt signaling is modulated to cause apoptosis by a resident protein of the endoplasmic reticulum, calreticulin.

Androstadienes↗

Electrophysiological abnormalities of the atrial muscle in patients with paroxysmal atrial fibrillation associated with hyperthyroidism.

OBJECTIVE: Atrial fibrillation (AF) is common in patients with hyperthyroidism. Although the choice of an antiarrhythmic agent should be based on its electrophysiological effects and the electrophysiological properties of the arrhythmia in question, the atrial electrophysiological features of AF associated with hyperthyroidism are unknown. The purposes of this study are to clarify the atrial electrophysiological abnormalities of AF with hyperthyroidism, and to propose effective therapies for AF in patients with hyperthyroidism. SUBJECTS AND DESIGN: This study included 117 patients who underwent electrophysiological study and were evaluated for thyroid function: 29 patients without AF or hyperthyroidism (Group I), 78 patients with lone paroxysmal AF (Group II), and 10 patients with paroxysmal AF and hyperthyroidism (Group III). The following electrophysiological parameters were assessed and measured quantitatively: (1) the incidence of abnormal right atrial electrograms during sinus rhythm, indicating areas of altered anatomy and conduction where AF is likely to develop; (2) the atrial effective refractory period (ERP); and (3) the atrial conduction delay (CD), which is induced by early atrial premature beats close to the atrial ERP and is thought to facilitate the occurrence of AF. RESULTS: The incidence of abnormal right atrial electrograms during sinus rhythm was significantly higher in Group II (67.1%) than in Group I (20.0%, P < 0.001) and Group III (22.2%, P = 0.009). The atrial ERP was significantly shorter in Group III (187 +/- 7 ms) than in Group I (215 +/- 36 ms, P = 0.019) and Group II (208 +/- 28 ms, P = 0.022). The atrial CD was observed in Group III as well as in Group II. CONCLUSIONS: Our data indicate that the electrophysiological features of paroxysmal AF associated with hyperthyroidism are essentially different from those of lone paroxysmal AF. In patients with paroxysmal AF and hyperthyroidism, a shortening of the refractory period in association with a facilitation of the atrial CD could be expected to increase the propensity for AF, and a pre-existent arrhythmogenic substrate might not be essential to the genesis of AF. These findings suggest that the agents that prolong the atrial ERP are effective against AF in patients with hyperthyroidism.

Adolescent↗

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↗

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↗

The influence of tumor size on the electrocardiographic changes in patients with left atrial myxoma.

The authors assessed the usefulness of the electrocardiography in patients with left atrial myxoma. The authors retrospectively reviewed the records of 15 patients with left atrial myxoma before and after tumor excision. The 12-lead electrocardiogram presented the P-wave abnormality shown by a broad P wave in lead II (PDII) and/or a deep and broad negative P terminal force in lead V1 (PTFV1). These abnormal findings were shown in the 13 patients whose tumor weight was 16 g or more. However, the other 2 patients whose tumor weight were 7 g or less did not have a prolonged PDII or an increased PTFV1. Both PDII and PTFV1 were correlated not only with the tumor size but also with the left atrial dimension and/or the left atrial pressure. These P-wave abnormalities were markedly improved or disappeared, and the left atrial dimension and pressure decreased immediately after tumor excision. The increasing size of the tumor brings about the P-wave abnormalities, which may result from enlargement of the left atrial cavity. It is suggested that while not specific the 12-lead ECG findings of PDII and PTFV1 may be useful for detecting a myxoma weighting 16 g or more, but was an insensitive technique for smaller ones.

Adult↗

Norepinephrine enhances fibrosis mediated by TGF-beta in cardiac fibroblasts.

Cardiac fibrosis results from proliferation of interstitial fibroblasts and concomitant increased biosynthesis of extracellular matrix (ECM) components and is often complicated by cardiac hypertrophy. This study was conducted to investigate whether norepinephrine (NE) potentiates transforming growth factor-beta (TGF-beta)-induced cardiac fibrosis. The expression of the cardiac ECM proteins, plasminogen activator inhibitor-1 (PAI-1), fibronectin, and collagen type I, was examined by Western blotting using extracts from neonatal rat primary cardiac fibroblasts. In cardiac fibroblasts, treatment with a combination of NE and TGF-beta1 increased cell proliferation and ECM expression. Luciferase assays were conducted to clarify the effect of NE on TGF-beta signaling. TGF-beta1 (1 ng/mL) increased the specific signaling activity 2-fold, whereas the combination of NE (10 micro mol/L) and TGF-beta1 (1 ng/mL) resulted in an approximate 10-fold increase in specific signaling activity. We confirmed that treatment with NE markedly enhances TGF-beta-induced phosphorylation of activating transcription factor 2 (ATF-2). These results indicated that NE has a synergistic effect on TGF-beta signaling. To determine whether this activation by NE was mediated by the TGF-beta1 receptor, we used a dominant negative vector of the TGF-beta1 type II receptor, and the synergistic effects were inhibited. Furthermore, this synergistic effect was attenuated by a specific inhibitor of p38, SB203680. These data indicate that NE enhances cardiac fibrosis through TGF-beta1 post-receptor signaling, predominantly via the p38 MAP kinase pathway.

Activating Transcription Factor 2↗

A histone deacetylase inhibitor enhances killing of undifferentiated thyroid carcinoma cells by p53 gene therapy.

Mutation of the p53 tumor suppressor gene is recognized to be a key event in the development of the highly aggressive behavior of undifferentiated or anaplastic thyroid carcinomas. Attempts to treat these carcinomas with p53 gene therapy have, however, been largely unsuccessful. Since epigenetic changes such as histone deacetylation are associated with loss of thyroid differentiation, we have evaluated the potential of combining p53 gene therapy with exposure to the histone deacetylase inhibitor (HDAC-1), depsipeptide. We used two carcinoma cell lines: FRO cells that express very low levels of p53 and WRO cells producing a dominant negative p53. A p53 response element luciferase assay showed that stimulation of p53 transcriptional activity by the combined treatment with the HDAC-1 and p53 was 10 to 100 times greater than with p53 alone. Western blot analysis demonstrated that the HDAC-1 increased the expression of acetylated histones, as well as of p21(cip1/waf1), but did not affect levels of total histone and endogenous p53. The combined treatment was much more effective than either treatment alone in inhibiting the growth of both cell lines, and flow cytometric analysis suggested that this was due to an increase in the sub-G1 apoptotic population. Our findings indicate that HDAC-1 enhances apoptotic killing by p53 transfer, and suggest that this combination strategy may be useful in treating undifferentiated thyroid carcinomas.

Acetylation↗

Coronary arteriovenous fistula presenting as chronic pericardial effusion.

In August 1998, the patient, a 75-year-old woman, was diagnosed with pericardial effusion (PE) during an investigation of cardiomegaly. The PE disappeared after the administration of diuretics, but in February 1999, shortness of breath and general fatigue developed, and PE was again present. Diagnostic pericardiocentesis revealed bloody fluid. Chest computed tomography revealed a markedly expanded and tortuous right coronary artery (RCA). Coronary angiography (CAG) confirmed a RCA-coronary sinus fistula, and there was a significant step-up of O2 saturation at the right atrium. Cardiac tamponade developed soon after CAG, so the patient underwent surgical closure of the CAVF. Although a bleeding point was not identified, the PE was disappeared after operation. Histopathologically, parts of the wall of the fistula were quite thin and erythrocytes and lymphocytes had infiltrated the pericardial space. The clinical course and the findings indicate that the CAVF caused chronic PE.

Aged↗

Six-month follow-up of takotsubo cardiomyopathy with I-123-beta-metyl-iodophenyl pentadecanoic acid and I-123-meta-iodobenzyl-guanidine myocardial scintigraphy.

A 69-year-old man with a history of transient chest pain was diagnosed takotsubo cardiomyopathy. In I-123-beta-metyl-iodophenyl pentadecanoic acid myocardial scintigraphy, decreased uptake of apex was seen in the acute phase, and it recovered in 3 months. In I-123-meta-iodobenzyl-guanidine myocardial scintigraphy, decreased uptake of apex persisted for 6 months, and there was a discrepancy between apical and total washout rate in the acute phase and after 3 months, which disappeared after 6 months. We speculate that the discrepancy of sympathetic innervation between the apical and basal region is the cause of the characteristic left ventricular apical akinesia of takotsubo cardiomyopathy.

3-Iodobenzylguanidine↗

[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↗

[Clinical evaluation of the cause of left ventricular dysfunction in type 2 diabetes without significant cardiac disease].

OBJECTIVES: The relationship between left ventricular dysfunction and hypertension or proteinuria was evaluated in type 2 diabetic patients without significant cardiac disease to investigate the cause of diabetic cardiac dysfunction. METHODS: Twenty-one patients with type 2 diabetes mellitus (mean age 63.8 +/- 7.4 years) underwent left ventriculography and Doppler echocardiography to calculate the ejection fraction and E/A ratio (E/A). RESULTS: Thirteen patients had hypertension (61.9%) and six patients had proteinuria (28.6%). The E/A was 0.82 +/- 0.21 in all patients. The E/A in patients with hypertension or proteinuria was significantly less than in those without these diseases (0.74 +/- 0.18 vs 0.97 +/- 0.18, p = 0.011; 0.65 +/- 0.10 vs 0.89 +/- 0.20, p = 0.010, respectively). The ejection fraction was 73.3 +/- 7.2% in all patients. The ejection fraction in patients with proteinuria was significantly less than in those without proteinuria (67.6 +/- 10.0% vs 75.5 +/- 4.4%, p = 0.019), but there was no significant difference in ejection fraction between patients with and without hypertension. The duration of diabetes was significantly related to the ejection fraction (r = -0.436, p = 0.048) but not to the E/A. CONCLUSIONS: In patients with type 2 diabetes without significant cardiac disease, left ventricular diastolic function may be related to both hypertension and proteinuria and left ventricular systolic function may be related to proteinuria and duration of diabetes. Therefore, in addition to hypertension, complications of nephropathy or long duration of diabetes may be related to the cause of the diabetic cardiac dysfunction.

Diabetes Mellitus, Type 2↗

Left cervical aortic arch associated with aortic aneurysm, aortic coarctation, and branch artery aneurysm--a case report and review.

Cervical aortic arch (CAA) is a rare congenital aortic anomaly. Although, in CAA, other cardiovascular abnormalities including aortic aneurysm and aortic coarctation are occasionally accompanied, coexistence of those 2 aortic abnormalities on the same patient is rare, and moreover, association of the aneurysm of branching artery has not been reported. The authors present here the first patient with CAA who had both an aneurysm and a coarctation in the aortic arch, and further, another aneurysm in the left subclavian artery. Clinical characteristics of CAA with either aortic aneurysm or aortic coarctation are reviewed.

Aneurysm↗

Relationship between adrenomedullin and left-ventricular systolic function and mortality in acute myocardial infarction.

The purpose of this study was to investigate the relationship between plasma adrenomedullin concentration levels and left-ventricular systolic function in patients with acute myocardial infarction (AMI), and to assess whether these findings can be used to predict clinical outcomes, including mortality. One hundred twenty-four consecutive first AMI attack subjects were successfully reperfused with primary percutaneous coronary intervention therapy. Plasma adrenomedullin concentrations were evaluated at 24 hours from onset. Left ventriculograms of all patients taken in the acute (soon after reperfusion therapy) and subacute (21 +/-9 days after onset) phases were used to evaluate left-ventricular ejection fraction (LVEF), and the difference in LVEF (delta-LVEF) between the two stages calculated. There were significantly more patients with cardiogenic shock in the H-Adm group (above the median value of plasma adrenomedullin concentrations > or =3.5 Fmol/mL) than in the L-Adm (< 3.5 Fmol/mL) group (p<0.0001). There was significantly higher mortality in the H-Adm group (p<0.01). Multivariate analysis identified plasma adrenomedullin concentrations alone as an independent predictor of mortality (p<0.05). There were no significant differences in acute-stage LVEF between the groups. LVEF in the subacute stage was, however, significantly lower in the H-Adm group than in the L-Adm group (52 +/-12% vs 59 +/-11%, p<0.05). Also, delta-LVEF was significantly lower in the H-Adm group than in the L-Adm group (1.9 +/-9.7% vs 6.3 +/-10.3%, p<0.01). Plasma adrenomedullin concentrations in the early phase of AMI correlate closely with the severity of heart failure, and may offer important prognostic information about the risk of mortality. Our data suggest that plasma adrenomedullin concentrations may be an independent predictor of the deterioration of left-ventricular systolic function.

Adrenomedullin↗