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Biomedical subjects

Teruo Inoue

Publications and source records attributed to Teruo Inoue.

At least 19 recordsLinked to original sources
PubMed2006

Effect of pitavastatin on urinary liver-type fatty-acid-binding protein in patients with nondiabetic mild chronic kidney disease.

BACKGROUND/AIM: Urinary liver-type fatty-acid-binding protein (L-FABP) is a useful clinical marker in the monitoring of chronic kidney disease (CKD) associated with tubulointerstitial damage. Statins have been shown to be effective in the treatment of renal disease. The aim of the present study was to determine whether pitavastatin, a newly developed statin, modulates the urinary L-FABP levels in normolipidemic patients with CKD. METHODS: Thirty normolipidemic mild CKD patients (18 males and 12 females, mean age 40 years, mean serum creatinine level 1.0 mg/dl) were randomly assigned to two groups: (1) pitavastatin (1 mg/day, n = 15) and (2) placebo (n = 15). Urinary protein and urinary L-FABP levels were measured before the initiation of treatment and 3 and 6 months thereafter. Twenty age-matched healthy subjects were also studied as controls. RESULTS: Before treatment, the urinary L-FABP levels in 30 CKD patients (84.0 +/- 68.5 microg/g creatinine) were significantly higher than those of healthy subjects (6.4 +/- 4.2 mug/g creatinine; p < 0.001). Pitavastatin slightly reduced serum total cholesterol and triglyceride levels, but this was not statistically significant. However, pitavastatin reduced the urinary protein excretion from 1.8 to 1.0 g/day (p < 0.01), while the urinary L-FABP levels fell from 88.5 +/- 70.5 to 28.0 +/- 16.5 mug/g creatinine (p < 0.01). CONCLUSION: The present data suggest that pitavastatin ameliorates tubulointerstitial damage in CKD patients independent of the lipid-lowering effect.

Adult↗
PubMed2005

An appropriate indication for the initiation of beta-blocker therapy in dilated cardiomyopathy.

BACKGROUND: Although long-term treatment with beta-blockers has been shown to improve morbidity and mortality in dilated cardiomyopathy (DCM), patient responses are heterogeneous. METHODS: To establish the appropriate indication for the initiation of beta-blocker therapy, we retrospectively analyzed 38 DCM patients treated with beta-blockers (metoprolol or carvedilol) and examined differences in baseline profiles between patients who could continue the therapy (responders) and those who could not (non-responders). RESULTS: In 13 non-responders, the duration from onset of symptoms to beta-blocker initiation was longer (p < 0.05), systolic blood pressure was lower (p < 0.001), serum sodium concentration was lower (p < 0.05), left ventricular posterior wall thickness was thinner (p < 0.05), left ventricular end-diastolic pressure was higher (p < 0.05) and left ventricular wall stress was lower (p < 0.05) than in 25 responders. In 19 patients receiving carvedilol, 5 non-responders showed higher levels of human atrial natriuretic peptide (p < 0.05) and brain natriuretic peptide (p < 0.01) than 13 responders. Discriminant analysis with a linear discriminant function showed the following equation predicted response to beta-blocker therapy: h = 0.004 x systolic blood pressure - 0.002 x brain natriuretic peptide + 0.667 (R2 = 0.67, p < 0.001). The probability of predicting the response was 94.1% with h > or = 0.5. CONCLUSION: We conclude that h > or = 0.5 is the appropriate indication for the initiation of beta-blocker therapy in DCM.

Adrenergic beta-Antagonists↗
PubMed2005

Local release of C-reactive protein from vulnerable plaque or coronary arterial wall injured by stenting.

OBJECTIVES: The purpose of this study was to assess local release of C-reactive protein (CRP) from atherosclerotic plaques or the vessel wall injured by stenting. BACKGROUND: Recent research has focused on the local production of CRP, especially in inflammatory atherosclerotic plaques. METHODS: The study consisted of two separate protocols. In protocol 1, we measured serum high-sensitivity-CRP (hs-CRP) levels in coronary arterial blood sampled just distal and proximal to the culprit lesions in 36 patients with stable angina and 13 patients with unstable angina. In protocol 2, we measured serial serum hs-CRP levels and activated Mac-1 on the surface of neutrophils in both coronary sinus and peripheral blood in 20 patients undergoing coronary stenting. RESULTS: In protocol 1, CRP was higher in distal blood than proximal blood in both stable (p < 0.05) and unstable angina (p < 0.01). The translesional CRP gradient (distal CRP minus proximal CRP, p < 0.05) as well as the proximal CRP (p < 0.05) and distal CRP (p < 0.05) was higher in unstable angina than in stable angina. In protocol 2, the transcardiac CRP gradient (coronary sinus minus peripheral blood) and activated Mac-1 increased gradually after stenting, reaching a maximum at 48 h (p < 0.001 vs. baseline for both). There was a positive correlation between the transcardiac CRP gradient and activated Mac-1 at 48 h (r = 0.45, p < 0.01). CONCLUSIONS: C-reactive protein is an excellent marker for plaque instability or poststent inflammatory status, and its source might be the inflammation site of the plaque or the coronary arterial wall injured by stenting.

Aged↗
PubMed2005

Long-term benefits of monteplase before coronary angioplasty in acute myocardial infarction.

Patients with acute myocardial infarction were randomly assigned to receive direct percutaneous coronary intervention (PCI) or pretreatment with intravenous monteplase followed by PCI. Although the combination of monteplase and PCI did not alter mortality compared with direct PCI, there was a dramatic reduction in the cardiac event rate over a 2-year follow-up compared with direct PCI.

Angioplasty, Balloon, Coronary↗
PubMed2005

Therapeutic potential of monteplase in acute myocardial infarction.

Thrombolysis with conventional thrombolytic agents prior to percutaneous coronary intervention (PCI) has had no impact on the treatment of acute myocardial infarction (AMI). However, the development of mutant tissue type plasminogen activators (mt-PA) has prompted us to reassess the combination of thrombolysis and PCI. Monteplase is a newly developed mt-PA that can be administered as a single intravenous bolus injection. The results of the COMA (COmbining Monteplase with Angioplasty) trial, suggest that monteplase administration prior to emergent PCI in AMI improves 6-month outcomes and possibly the long-term prognosis of myocardial infarction. Combining monteplase administration on presentation at a community hospital with prompt transfer to a tertiary center for PCI would be an ideal strategy for the treatment of AMI.

Acute Disease↗
PubMed2004

Cilostazol inhibits leukocyte integrin Mac-1, leading to a potential reduction in restenosis after coronary stent implantation.

OBJECTIVES: The aim of this study was to confirm clinically a hypothesis that cilostazol inhibits leukocyte Mac-1, leading to prevention of post-stent restenosis. BACKGROUND: The platelet phosphodiesterase III inhibitor called cilostazol also inhibits alpha-granule release of P-selectin in platelets. The P-selectin-mediated platelet-leukocyte interaction promotes activation and upregulation of leukocyte Mac-1 after coronary stenting, which plays a key role on the mechanism of restenosis. Thus, cilostazol's potential inhibition of this process may lead to prevention of restenosis. METHODS: Using flow cytometric analysis of whole blood obtained from the coronary sinus, the expression of platelet membrane glycoproteins and neutrophil adhesion molecules was observed in 70 consecutive patients undergoing coronary stenting. The patients were randomly assigned to either a cilostazol or ticlopidine group before stent placement. RESULTS: The restenosis rate was lower (15% vs. 31%, p < 0.05) in the cilostazol group (n = 34) than in the ticlopidine group (n = 32). A stent-induced increase in platelet P-selectin (CD62P) expression and an increase in neutrophil Mac-1 (CD11b) expression were suppressed in the cilostazol group compared with the ticlopidine group. Angiographic late lumen loss was correlated with the relative changes in platelet P-selectin and neutrophil Mac-1 at 48 h after coronary stenting. CONCLUSIONS: Cilostazol may have effects on suppression of P-selectin-mediated platelet activation, platelet-leukocyte interaction, and subsequent Mac-1-mediated leukocyte activation, which might lead to a reduced restenosis rate after coronary stent implantation.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2004

Therapeutic potential of monteplase in acute myocardial infarction as a powerful thrombolytic agent for pretreatment of coronary intervention.

Thrombolysis with conventional thrombolytic agents followed by percutaneous coronary intervention (PCI) had no impact on the treatment of acute myocardial infarction (AMI). However, the development of mutant type plasminogen activator (mt-PA) has prompted us to reassess the combination of thrombolysis and PCI. Monteplase (Eisai, Co. Ltd., Tokyo, Japan) is a newly developed mt-PA that can be administrated as a single intravenous bolus injection. We initiated a clinical trial [Combining Monteplase with Angioplasty (COMA)] to evaluate the effectiveness of monteplase followed by PCI. The AMI patients were randomly assigned to receive PCI following pretreatment with a single bolus intravenous injection of monteplase or direct PCI without monteplase. The initial coronary angiography prior to PCI showed that 36.2% of patients in the monteplase group achieved Thrombolysis in Myocardial Infarction (TIMI) 3 flow in the infarct-related artery, compared with in only 7.9% of patients in the direct PCI group (P < 0.0001). During 24 months following PCI, major cardiac events occurred in 27.7% of patients in the monteplase + PCI group, and in 46.7% of patients in the direct PCI group without monteplase (P < 0.05). Thus, the ideal strategy for the treatment of AMI is the administration of monteplase upon arrival at a community hospital with a prompt transfer to a tertiary center for PCI.

Acute Disease↗
PubMed2004

Results of blood inflammatory markers are associated more strongly with toe-brachial index than with ankle-brachial index in patients with type 2 diabetes.

OBJECTIVE: Three blood markers of inflammation (high-sensitivity C-reactive protein [hsCRP], interleukin [IL]-6, and fibrinogen) were compared with markers of atherosclerotic cardiovascular disease (CVD) (history of stroke or cardiac ischemia and measured toe-brachial index [TBI]) to determine whether inflammatory markers are associated with atherosclerosis in patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: Of 103 patients with type 2 diabetes, 26 had CVD. TBI was plethysmographically determined in both great toes. Serum hsCRP was immunonephelometrically determined. Plasma IL-6 was measured by an enzyme immunoassay. RESULTS: Both ABI and TBI were lower in diabetic patients with CVD than in those without CVD (1.05 +/- 0.19 vs. 1.14 +/- 0.09, P < 0.05, and 0.75 +/- 0.20 vs. 0.95 +/- 0.21, P < 0.001, respectively). By linear regression, right TBI but not right ABI showed a significant negative correlation with serum hsCRP (r = -0.372, P < 0.01) and plasma fibrinogen (r = -0.224, P < 0.05). Serum hsCRP was also negatively correlated with lower TBI, but not lower ABI. We found no significant correlation between plasma IL-6 and ABI or TBI. CONCLUSIONS: TBI was strongly associated with CVD, serum hsCRP, and plasma fibrinogen. Of these inflammatory markers, serum hsCRP may be the most promising marker for vascular inflammation.

Aged↗
PubMed2004

[Primary malignant pericardial mesothelioma temporarily reduced by radiation therapy: a case report].

A 47-year-old woman was referred to our hospital because of cardiomegaly and pericardial effusion. She complained of a cough. Computed tomography, echocardiography, and magnetic resonance imaging showed a mass on the pericardium. Exploratory surgery revealed a solid tumor invading the pericardium over the aortic arch and main pulmonary artery. Histological examination indicated primary malignant pericardial mesothelioma. After 58 Gy radiation, the size of the tumor was temporarily reduced and the patient's symptoms disappeared. However, the tumor enlarged and her symptoms reappeared 7 months after temporary improvement. Eighteen months after the development of cough, the patient died suddenly.

Female↗
PubMed2003

Circulating matrix metalloproteinase-1 and -3 in patients with an acute coronary syndrome.

To elucidate the diagnostic value of serum matrix metalloproteinase (MMP) levels, we measured MMP-1 and MMP-3 by a 1-step sandwich enzyme immunoassay. The transcardiac gradients of both MMPs were greater in patients with unstable angina and acute myocardial infarction than in patients with stable effort angina or control patients. Serum MMP levels appear to be a marker of plaque instability in patients with acute coronary syndrome.

Angina Pectoris↗
PubMed2003

Stent-induced expression and activation of the leukocyte integrin Mac-1 is associated with neointimal thickening and restenosis.

BACKGROUND: Increased expression of the beta2 integrin Mac-1 (CD11b/CD18, alphaMbeta2), which is responsible for firm leukocyte adhesion to platelets and fibrinogen at injured vessels, is found in association with neointimal hyperplasia after coronary interventions. The role of Mac-1 in the pathophysiology of restenosis is incompletely defined. To clarify further the role of Mac-1, we determined whether coronary stenting induced activation of Mac-1, which is required for high-affinity receptor-ligand interactions. METHODS AND RESULTS: Expression of CD11b (alpha-subunit of Mac-1) and binding of 8B2 (monoclonal antibody against an activation-dependent neoepitope of Mac-1) on the surface of polymorphonuclear leukocytes were analyzed in 62 patients undergoing coronary stenting using flow cytometric analysis of whole blood obtained from the coronary sinus and femoral vein. Transcardiac CD11b expression increased significantly at 24 hours and maximally at 48 hours after stenting; 8B2 began to increase at 10 minutes and was maximally increased at 48 hours after stenting. These changes were more prominent in patients with subsequent restenosis. Multiple regression analysis showed that the late lumen loss by quantitative coronary angiographic analysis was independently correlated with the CD11b increase (R=0.42, P<0.01) and the 8B2 increase (R=0.55, P<0.001) 48 hours after the procedure. Mac-1 activation, as assessed by 8B2 binding, was the most powerful predictor of late lumen loss. CONCLUSIONS: Coronary stenting produced upregulation and early activation of the leukocyte integrin Mac-1, which is associated with late lumen loss and restenosis. These data support a role for inflammation in neointimal thickening and suggest the validity of targeting leukocyte recruitment for preventing clinical restenosis.

Angioplasty, Balloon, Coronary↗
PubMed2003

Accelerated plasminogen activator inhibitor may prevent late restenosis after coronary stenting in acute myocardial infarction.

BACKGROUND: Although acceleration of plasma plasminogen activator inhibitor-1 (PA-1) level after emergent coronary angioplasty in acute myocardial infarction (AMI) has been documented, its pathophysiologic role is still unknown. HYPOTHESIS: This study was designed to elucidate the role of PAI-1 in the development of restenosis after primary coronary stenting in AMI. METHODS: We selected for this study 66 patients with AMI, who underwent primary coronary stenting for infarct-related coronary artery lesions in an emergent situation. In all patients, plasma PAI-1 level was measured at admission, and at 3 h, 24 h, 48 h, and 1 month after coronary stenting. RESULTS: At admission, the PAI-1 level was equivalent in 24 patients who experienced restenosis and in 42 patients without restenosis (28 +/- 4 vs. 29 +/- 4 ng/ml). In patients with restenosis, the levels did not change during the course after coronary stenting. In patients without restenosis, however, the level significantly increased at 3 h (48 +/- 9 ng/ml, p < 0.001), 24 h (42 +/- 9, p < 0.01), and 48 h (38 +/- 7, p < 0.05) after coronary stenting, and was restored to the level equivalent to that at admission (27 +/- 2 ng/ml) I month aftercoronary stenting. The PA-1 level at 3 h after coronary stenting in patients without restenosis was significantly higher (p < 0.05) than the level (33 +/- 6 ng/ml) in patients with restenosis. Multiple logistic regression analysis indicated that the PAI-1 level 3 h after coronary stenting was an independent predictor of restenosis (Wald chi2 = 3.826, p = 0.019, odds ratio 0.921, 95% confidence interval 0.866-0.961). CONCLUSION: Accelerated PAI-1 after coronary stenting in patients with AMI may protect against the development of late restenosis.

Angioplasty, Balloon, Coronary↗
PubMed2003

Fluvastatin attenuates nitrate tolerance in patients with ischemic heart disease complicating hypercholesterolemia.

BACKGROUND: Long-term administration of nitrates results in the development of tolerance. Nitrate tolerance is considered to occur in association with oxidative stress, although its underlying mechanisms are multi-factorial. Fluvastatin, a newly developed statin, is considered to have not only a cholesterol-lowering effect but also anti-oxidative properties. METHODS: In this study, the effect of fluvastatin on nitrate tolerance was investigated in 12 dyslipidemic patients (nine men and three women, aged 63.5+/-6.7 years), who were complicated with ischemic heart disease and had received organic nitrates for a long period. RESULTS: Four months after fluvastatin therapy, symptoms of angina were significantly reduced. Consumption of sublingual nitrates over 2 weeks significantly decreased (14.4+/-11.2 to 2.3+/-2.5 tablets, P<0.01). In exercise stress testing, exercise duration was significantly prolonged (275+/-73 to 360+/-86 s, P<0.01) and the blood pressure-heart rate products significantly increased (16368+/-2246 to 18381+/-1772, P<0.01). Both the percent change in forearm blood flow with reactive hyperemia (232+/-83 to 282+/-104%, P<0.05) and that after sublingual nitroglycerine (2.5+/-4.7 to 5.8+/-4.7%, P<0.05) were increased. Although the levels of total cholesterol, triglyceride, HDL-cholesterol, and LDL-cholesterol were unchanged, the serum anti-Ox-LDL titer (16.7+/-6.3 to 13.4+/-5.4 AcU/ml, P<0.05) and 8-OHdG level (1.11+/-0.34 to 0.73+/-0.34 ng/ml, P<0.05) decreased. CONCLUSIONS: Fluvastatin attenuated nitrate tolerance in dyslipidemic patients complicated with ischemic heart disease who had been receiving organic nitrates over long period. The anti-oxidative effect of fluvastatin may attenuate nitrate tolerance.

Anticholesteremic Agents↗
PubMed2003

Hemoperfusion with polymyxin B-immobilized fiber in septic patients with methicillin-resistant Staphylococcus aureus-associated glomerulonephritis.

BACKGROUND/AIMS: We investigated whether urinary podocytes are present in septic patients with methicillin-resistant Staphylococcus aureus (MRSA)-associated glomerulonephritis and whether polymyxin B-immobilized fiber (PMX-F) treatment affects proteinuria and urinary podocyte excretion in these patients. METHODS: Twenty septic patients with MRSA-associated glomerulonephritis (mean age: 63.7 years) and 80 septic patients whose MRSA infection was not followed by glomerulonephritis (mean age: 60.5 years) were included in this study. All septic patients were treated with fosfomycin sodium, beta-lactams, arbekacin sulfate, and teicoplanin, or a combination of these. Twenty septic patients with MRSA-associated glomerulonephritis were randomly assigned to one of two treatments: PMX-F treatment (group A, n = 10) and conventional treatment (group B, n = 10). PMX-F treatment was repeated twice. RESULTS: Urinary podocytes and urinary protein excretion were not detected in MRSA septic patients without glomerulonephritis. However, urinary podocytes (1.7 +/- 0.6 cells/ml) and proteinuria (2.6 +/- 0.6 g/d) were detected in the 20 septic patients with MRSA-associated glomerulonephritis. Plasma endotoxin levels were decreased from 13.6 +/- 4.6 pg/ml to 6.6 +/- 2.2 pg/ml (p < 0.05) in group A. Levels in group B, however, showed little difference after treatment. Urinary podocytes were reduced in group A (from 1.8 +/- 0.6 cells/ml to 0.4 +/- 0.2 cells/ml, p < 0.01) as was urinary protein excretion (from 3.0 +/- 0.5 g/d to 0.8 +/- 0.4 g/d, p < 0.01) but urinary podocytes and protein excretion levels showed little difference after treatment in group B. CONCLUSION: PMX-F treatment may be effective in reducing urinary protein and urinary podocyte excretion in septic patients with MRSA-associated glomerulonephritis.

Endotoxins↗
PubMed2002

Possible relationship between insulin resistance and remnant-like lipoprotein particles in coronary endothelial dysfunction.

BACKGROUND: High insulin resistance and elevated remnant lipoprotein levels both correlate with impaired coronary vascular endothelial function. Hyperinsulinemia induces abnormalities of lipid metabolism. However, the correlation among insulin resistance, remnant lipoproteins, and endothelial function has not been clinically elucidated. HYPOTHESIS: This study was designed to elucidate the correlation among insulin resistance, remnant lipoproteins, and acetylcholine (ACh)-induced coronary artery response. METHODS: Forty-nine patients suspected of having ischemic heart disease, but without angiographically significant atherosclerotic coronary artery disease, underwent an ACh provocation test. Fasting venous blood was taken early in the morning on the day coronary angiography was performed. The insulin resistance index (IR) was determined from fasting plasma glucose and insulin concentrations, using the homeostasis model assessment (HOMA). Serum levels of remnant-like lipoprotein particle cholesterol (RLP-C) were measured. RESULTS: Homeostasis model assessment IR was significantly higher (3.65 +/- 1.38 vs. 0.75 +/- 0.14, p < 0.05) and log-transformed HOMA (Log HOMA) was even more significantly higher (0.20 +/- 0.12 vs. -0.29 +/- 0.08, p < 0.001) in the ACh-positive group (n = 23) than in the ACh-negative group (n = 26). The serum RLP-C level was also higher in the ACh-positive group than in the ACh-negative group (4.37 +/- 0.63 vs. 2.52 +/- 0.18 mg/dl, p < 0.01). Log HOMA and RLP-C levels correlated with each other (R = 0.54, p < 0.001). Multiple regression analysis indicated that only the RLP-C level was a dependent predictor of Log HOMA in various lipid profiles. CONCLUSIONS: Both high insulin resistance and elevated remnant lipoprotein levels correlated and might have a crucial role in the impairment of coronary vascular endothelial function, even in patients without angiographically significant coronary artery disease.

Acetylcholine↗