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Teruo Inoue

Publications and source records attributed to Teruo Inoue.

18 recordsLinked to original sources
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↗
PubMed2002

A new thrombolytic agent, monteplase, is independent of the plasminogen activator inhibitor in patients with acute myocardial infarction: initial results of the COmbining Monteplase with Angioplasty (COMA) trial.

BACKGROUND: Both thrombolytic therapy and coronary angioplasty have been inconsistent together for primary acute myocardial infarction (AMI) therapy, because conventional thrombolytic agents accelerate plasminogen activator inhibitor-1 (PAI-1) activity. However, combining newly developed mutant tissue-type plasminogen activators with coronary angioplasty should be reconsidered. METHODS: This study was designed to investigate clinical usefulness of such an agent, monteplase, for treatment of AMI in light of PAI-1 kinetics. One hundred fifty-four consecutive patients with AMI were randomly assigned to receive direct coronary angioplasty (Group I) or coronary angioplasty after pretreatment with intravenous monteplase (Group II). In 90 of these patients, total PAI-1 antigen levels were serially measured. RESULTS: Baseline PAI-1 levels at admission were higher in patients with occluded infarct-related arteries than in patients with patent arteries in Group I (39 +/- 4 vs 20 +/- 2 ng/mL, P <.01) and in Group II (36 +/- 3 vs 27 +/- 2 ng/mL, P <.05). In the high PAI-1 level subgroup (> or =27 ng/mL, n = 53), Group II showed a higher patency rate than Group I (56 vs 18%, P <.01). Multiple logistic regression analysis indicated that patency could be predicted by the PAI-1 level in Group I (Wald chi2= 3.94, P =.02, odds ratio 0.924, 95% CI 0.855-0.999), but not in Group II. Serial change patterns in the PAI-1 level were identical in Group I and Group II. CONCLUSION: Because monteplase can be used independently of PAI-1 kinetics, a combination of monteplase administration at a community hospital with prompt transfer to a tertiary center for coronary intervention may be a powerful strategy for AMI.

Angioplasty, Balloon, Coronary↗
PubMed2002

Lipid-lowering therapy with fluvastatin inhibits oxidative modification of low density lipoprotein and improves vascular endothelial function in hypercholesterolemic patients.

This prospective randomized trial was designed to elucidate clinically the effect of fluvastatin on inhibiting oxidation of the low density lipoprotein (LDL) and improving the vascular endothelial function as well as its lipid-lowering effects, in comparison with pravastatin. Of 64 consecutive dyslipidemic patients, 40 patients, whose level of total cholesterol or LDL-cholesterol maintained the criteria of the hypercholesterolemia in spite of 12-week dietary therapy, were randomly assigned to receive either fluvastatin (n=20) or pravastatin (n=20). We assessed the titer of antibody against oxidized LDL (anti-Ox-LDL) as a biomarker for LDL-oxidation, and the forearm blood flow response during reactive hyperemia by venous occlusion plethysmography, which indicates the endothelium-dependent vasodilator capacity. After the 16-week lipid-lowering therapy, the anti-Ox-LDL titer significantly decreased in the fluvastatin group (P<0.01) but did not change in the pravastatin group. The percent increase in the forearm blood flow at the peak reactive hyperemia from the baseline value (%RH) significantly increased in the fluvastatin group (P<0.001) but did not change in the pravastatin group. The ratio of the %RH after the therapy over the baseline value negatively correlated with that of the anti-Ox-LDL titer (R=0.73, P<0.001) in all patients. Fluvastatin may serve as an ideal drug for reducing the risk of atherosclerosis, not only by its cholesterol-lowering effect but also by its unique effects of inhibiting LDL oxidation and improving the vascular endothelial function.

Endothelium, Vascular↗
PubMed2002

The influence of diabetes mellitus on late clinical outcomes following coronary stent implantation.

Diabetic patients have a higher restenosis rate and late morbidity following balloon angioplasty. However, the increased risk of restenosis after coronary stent implantation in diabetic patients is controversial. We compared the quantitative coronary angiographic (QCA) variables between 42 diabetic patients and 71 non-diabetic patients undergoing coronary stent implantation and for 6 months follow-up. Pre-procedural variables were identical in the diabetic and non-diabetic patients. The stent-artery ratio was lower (1.07+/-0.13 vs. 1.13+/-0.13, P=0.020), and acute gain after coronary stenting was lower (1.58+/-0.53 vs. 1.77+/-0.48, P=0.049) in the diabetic patients than in the non-diabetic patients. However, the late lumen loss (0.42+/-0.64 vs. 0.49+/-0.69), loss index (0.28+/-0.49 vs. 0.28+/-0.45), restenosis rate (19 vs. 23%) and target lesion revascularization rate (17 vs. 18%) after 6 months were identical in the diabetic and non-diabetic patients. These results suggest that diabetes itself does not increase stent restenosis.

Aged↗
PubMed2002

The levels of five markers of hemostasis and endothelial status at different stages of normotensive pregnancy.

BACKGROUND: Urinary 11-dehydrothromboxane B(2)/creatinine (11-DTXB(2)/Cr) is a marker for in vivo platelet activation and vascular constriction, blood thrombomodulin (TM) for endothelial damage and associated thrombosis, thrombin-antithrombin complex (TAT) for thrombin formation, and beta-thromboglobulin (beta-TG) and platelet factor 4 (PF-4) for in vivo platelet activation and releasing reaction. Little is known about the quantitative relationship among them during pregnancy. The present study investigated levels of five markers at different stages of normotensive pregnancy. METHODS: Subjects were 17 healthy non-pregnant women (Group 1, control) and 67 women carrying single fetuses in normotensive pregnancy. Of the pregnant women, 17 were in the 20th week of gestation (Group 2), 20 were in their 30th week (Group 3), and 30 were in their 36th week (Group 4). Urinary and circulating blood levels of 11-DTXB(2)/Cr, TM, TAT, beta-TG, and PF-4 were measured simultaneously. RESULTS: The 11-DTXB(2)/Cr and TAT levels showed elevated values at the 20th and 30th weeks of gestation, and markedly elevated values at the 36th week, whereas the TM level remained constant throughout pregnancy. The beta-TG and PF-4 levels maintained stable values at the 20th week, but showed elevated values at the 30th and 36th weeks. CONCLUSIONS: Platelet aggregation, vascular constriction, and thrombin formation (detected by 11-DTXB(2)/Cr and TAT) appear to be enhanced as early as the 20th week of gestation, continuously enhanced by the 30th week, and markedly enhanced by the 36th week. Platelet activation and releasing reaction (determined by beta-TG and PF-4) gradually enhanced from the 30th to 36th weeks. In contrast, endothelial damage and associated thrombosis (detected by TM) were minimal throughout pregnancy. Investigating these markers of hemostasis and endothelial function in normotensive pregnancy may provide insights into related disease states.

Adult↗
PubMed2002

Early recanalization and plasma brain natriuretic peptide as an indicator of left ventricular function after acute myocardial infarction.

BACKGROUND: Although plasma brain natriuretic peptide (BNP) levels have been widely measured in patients with acute myocardial infarction (AMI), it is still uncertain whether the early recanalization modulates the levels and whether the levels can predict chronic stage left ventricular function. This study was designed to elucidate these issues. METHODS: In 80 consecutive patients with AMI, plasma BNP levels were measured at admission and at 4 hours, 24 hours, 48 hours, and 1 month after admission. RESULTS: In 35 of the 80 patients, the infarct-related artery was patent within 6 hours from the onset of MI (6-hour patency group), and in 27 patients, the artery was still occluded after 6 hours (6-hour occlusion group). The remaining 18 patients in whom it was unclear whether recanalization of the infarct-related artery had occurred within 6 hours or not were excluded from the analyses. In the 6-hour patency group, the BNP level gradually increased and reached a maximum value at 24 hours after admission. In the 6-hour occlusion group, the level increased more, with the values at 4 hours, 24 hours, and 48 hours significantly higher than those in the 6-hour patency group (86 +/- 18 pmol/L versus 35 +/- 8 pmol/L; P <.01; 112 +/- 13 pmol/L versus 74 +/- 9 pmol/L; P <.05; 102 +/- 15 pmol/L versus 53 +/- 11 pmol/L; P <.01). Chronic stage left ventricular function was correlated with not only the BNP level at same stage but also that at 24 hours and that at 48 hours after admission. Multiple regression analysis indicated that the BNP level at 24 hours was the most powerful predictor of chronic stage left ventricular function. CONCLUSION: Plasma BNP levels can predict subsequent cardiac function. In addition, the importance of early recanalization may also be supported with BNP kinetics.

Angioplasty, Balloon, Coronary↗
PubMed2002

Randomized comparison of cilostazol versus ticlopidine hydrochloride for antiplatelet therapy after coronary stent implantation for prevention of late restenosis.

BACKGROUND: Cilostazol is a newly developed antiplatelet drug that has been widely applied for clinical use. Its antiplatelet action appears to be mainly related to inhibition of intracellular phosphodiesterase activity. Recently, cilostazol has been used for antiplatelet therapy after coronary stent implantation. However, its evaluation has not been established yet. METHODS: This prospective randomized trial was designed to investigate the efficacy of cilostazol for the prevention of late restenosis and acute or subacute stent thrombosis in comparison with ticlopidine hydrochloride. One hundred thirty consecutive patients, scheduled for elective coronary stenting, were randomly assigned to receive oral aspirin (81 mg/day) plus ticlopidine hydrochloride therapy (200 mg/day; group I) or aspirin plus cilostazol therapy (200 mg/day; group II). These medications were started at least 2 days before coronary intervention and continued until follow-up coronary angiography was performed 6 months later. RESULTS: Subacute stent thrombosis was observed in 2 patients of group I but in no patients of group II. Major cardiac events were similarly present in both groups. Elevated transaminase levels were observed more frequently in group I than in group II (P <.05). Each of the quantitative coronary angiography variables before and immediately after coronary stenting were similar in both groups. At follow-up angiography, however, late lumen loss (0.69 +/- 0.79 mm vs 0.28 +/- 0.40 mm; P <.01) and loss index (0.42 +/- 0.56 vs 0.16 +/- 0.27; P <.01) were smaller in group II than in group I. Restenosis rate (13% vs 31%; P <.05) and target lesion revascularization rate (7% vs 21%; P <.05) were both lower in group II than in group I. CONCLUSION: Aspirin plus cilostazol therapy may be an effective regimen for prevention of not only stent thrombosis but also restenosis.

Aged↗
PubMed2002

Effect of cerivastatin on proteinuria and urinary podocytes in patients with chronic glomerulonephritis.

BACKGROUND: We previously reported urinary podocytes to be a marker of glomerular injury. The aim of the present study was to determine whether cerivastatin, a newly developed, potent synthetic statin, affects proteinuria and urinary podocyte excretion in patients with chronic glomerulonephritis (CGN). METHODS: We randomly assigned 40 normotensive hypercholesterolemic patients with CGN to receive either cerivastatin 0.15 mg/day (n=20) or placebo (n=20). Subjects comprised 24 men and 16 women, with a mean age of 40.8+/-14.4 years; 27 had IgA nephropathy and 13 had non-IgA proliferative glomerulonephritis. Treatment was continued for 6 months. Plasma total cholesterol, HDL-cholesterol, LDL-cholesterol and triglycerides, urinary protein excretion and the number of podocytes were measured before treatment and at 3 and 6 months after treatment. RESULTS: After 6 months, a significant reduction in total cholesterol (P<0.001), LDL-cholesterol (P<0.001) and triglycerides (P<0.05), and a significant increase in HDL-cholesterol (P<0.001) were observed in the group treated with cerivastatin. Urinary protein excretion decreased from 1.8+/-0.6 to 0.8+/-0.4 g/day, (P<0.01) in this group, and urinary podocyte excretion decreased from 1.6+/-0.6 to 0.9+/-0.4 cells/ml (P<0.01). However, placebo showed little effect on these lipid levels, urinary protein excretion and urinary podocyte excretion. The differences between the cerivastatin group and the placebo group were significant (cholesterol, P<0.001; LDL-cholesterol, P<0.001; triglycerides, P<0.05; HDL-cholesterol, P<0.001; urinary protein, P<0.01; and urinary podocytes, P<0.01). CONCLUSION: Statins such as cerivastatin may be beneficial for restoration of injured podocytes in patients with CGN and hypercholesterolaemia.

Adult↗
PubMed2002

Clinical significance of the antibody against oxidized low-density lipoprotein in acute myocardial infarction.

To establish the clinical significance of the antibody against oxidized low-density lipoprotein (anti-Ox-LDL) titer in patients with acute myocardial infarction (AMI), we measured the anti-Ox-LDL titer in 39 patients with AMI and 25 controls. In all AMI patients, the anti-Ox-LDL titer on admission was higher (p < 0.05) than the value in the controls. One month after admission, the titer decreased significantly (p < 0.001) reaching control levels. In patients who underwent thrombolytic therapy, the anti-Ox-LDL titer on admission was identical in patients with occluded infarct-related arteries (IRA) and patients with patent IRA during emergency coronary angiography. In patients who did not undergo thrombolytic therapy, the anti-Ox-LDL titer on admission was higher in patients with occluded IRA than in patients with patent IRA. An increased anti-Ox-LDL titer may be a risk factor for the onset of AMI. Spontaneous recanalization of the IRA may be associated with increased anti-Ox-LDL titers, while thrombolysis-induced recanalization may be independent of it.

Antibodies↗
PubMedDate not supplied

Characterization of five marker levels of the hemostatic system and endothelial status in normotensive pregnancy and pre-eclampsia.

OBJECTIVES: Pre-eclampsia is associated with changes in the hemostatic system and endothelial status. Urinary 11-dehydrothromboxane B2/creatinine (11-DTXB2/Cr) is a marker for platelet activation and vascular constriction, thrombin-antithrombin complex (TAT) for thrombin formation, serum thrombomodulin (TM) for endothelial damage, and beta-thromboglobulin (beta-TG) and platelet factor 4 (PF-4) for platelet activation and releasing reaction. The present study attempted to evaluate these five markers in normotensive pregnancy and pre-eclampsia. METHODS: These five markers were simultaneously measured in urine and blood samples from 25 women who were not pregnant (group 1, controls), 31 women with normotensive pregnancy (group 2, second controls), 22 women with mild pre-eclampsia (group 3), and 21 women with severe pre-eclampsia (group 4). The average gestational age was 36 wk. RESULTS: The 11-DTXB2/Cr, TAT, and beta-TG levels were significantly higher (P < 0.01) in groups 2, 3, and 4 than in group 1. The TM and beta-TG levels were significantly higher (P < 0.05) in group 3 than in group 2. The TM, beta-TG, and PF-4 levels were increased significantly (P < 0.05-0.01) in group 4 compared to those in groups 1, 2, and 3. CONCLUSION: Platelet aggregation, vascular constriction, and thrombin formation (detected by 11-DTXB2/Cr and TAT) may be markedly enhanced even in group 2, but further enhancement may be relatively slight in groups 3 and 4. In contrast, endothelial damage (determined by TM) and platelet release of PF-4 may not increase significantly in group 2, but they may increase in group 4. Platelet-release of beta-TG may be enhanced in groups 2, 3, and 4. Endothelial damage and platelet-releasing reaction (detected by PF-4 and beta-TG) may be significantly more enhanced in group 4 than in group 3.

Adult↗