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Biomedical subjects

Michihiro Yoshimura

Publications and source records attributed to Michihiro Yoshimura.

At least 19 recordsLinked to original sources
PubMed2007

The effects of long-term smoking on endothelial nitric oxide synthase mRNA expression in human platelets as detected with real-time quantitative RT-PCR.

Endothelium-derived nitric oxide (NO) plays an important role in the prevention of platelet aggregation and adhesion to the vascular wall. Endothelial nitric oxide synthase (eNOS) and L-arginine/NO pathway are both present in human platelets. Platelet-derived NO inhibits excessive activation and aggregation of platelets. However, the expression level of the eNOS gene in human platelets has yet to be elucidated. The current study investigates the individual expression level of platelet eNOS mRNA using the real-time reverse transcriptase-polymerase chain reaction (RT-PCR) detection method. eNOS mRNA expression was examined in platelets isolated from 50 subjects: 11 male smokers, 15 male nonsmokers, and 24 female non-smokers. After extraction of platelet total RNA, eNOS (target) and GAPDH (internal control) mRNA expression levels were quantitated using real-time RT-PCR. The expression levels of eNOS mRNA (relative copy numbers) were significantly lower in male smokers (59+/-17) than in male nonsmokers (195+/-71, P < .03), and higher in female nonsmokers (285+/-60) than in the male nonsmokers (195+/-71, P < .03). By multiple linear regression analysis, cigarette smoking (P = .008) and diabetes mellitus (P = .047) were found to be significantly negative predictors, and antioxidant (vitamin E) treatment (P = .01) was a significantly positive predictor of platelet eNOS mRNA expression. Age, other medications, and other risk factors for coronary artery disease were not significant. Using this method, eNOS mRNA abundance in human platelets was detected and quantitated in real-time. The intraplatelet eNOS mRNA expression levels were significantly decreased in cigarette smokers. Low platelet NO synthesis in smokers may result in the augmentation of platelet aggregation and thrombus formation, developing into acute coronary syndromes.

Adult↗
PubMed2006

Future adverse cardiac events can be predicted by persistently low plasma adiponectin concentrations in men and marked reductions of adiponectin in women after acute myocardial infarction.

There is conflicting information about whether mortality after AMI is higher in women than men. We investigated the significance of plasma adiponectin concentrations on major adverse cardiac events (MACE) after acute myocardial infarction (AMI) to delineate any differences between men and women. The study patients consisted of 114 men and 42 women with AMI. The incidence of MACE was significantly higher in women than men during the entire follow-up period (p<0.05). Compared with men for post-AMI MACE, the hazard ratio for women was 5.6 after adjustment for prognostic factors. Killip class (p<0.001) and sex differences (p<0.05) were independent predictors of MACE at 1 year post-AMI. Plasma adiponectin levels in women were significantly higher than men on admission (8.66 microg/mL [range: 6.6-14.08] versus 4.71 microg/mL [range: 3.47-7.27], p<0.0001) and during the post-AMI course (all p<0.0001). Multivariate analysis identified plasma adiponectin level on admission as an independent predictor of MACE in men (p<0.001) and the difference between plasma adiponectin levels at discharge and on admission in women (p<0.05). Patterns of serial changes in plasma adiponectin concentrations are different between men and women and plasma adiponectin concentrations can be used to predict future adverse cardiac events in AMI patients.

Acute Disease↗
PubMed2006

Plasma adiponectin levels are associated with coronary lesion complexity in men with coronary artery disease.

OBJECTIVES: We sought to assess whether plasma adiponectin levels correlate with angiographic coronary lesion complexity in patients with coronary artery disease (CAD). BACKGROUND: Metabolic disorders, including diabetes mellitus and metabolic syndrome, are important risk factors for acute cardiovascular events, and adiponectin is a key molecule of metabolic disorders, with anti-atherogenic properties. Low plasma adiponectin levels are associated with CAD and future incidence of myocardial infarction. The involvement of adiponectin in coronary plaque vulnerability, which may be reflected by angiographic complex lesions, remains to be elucidated. METHODS: We measured plasma adiponectin levels in 207 men (152 with stable CAD and 55 with acute coronary syndromes [ACS]). Coronary lesions were classified as of simple or complex appearance. RESULTS: Plasma adiponectin levels were significantly lower in stable CAD patients with complex coronary lesions (n = 60) than in those with simple lesions (n = 92) (4.14 [range 2.95 to 6.02] vs. 5.27 [range 3.67 to 8.12] microg/ml, p = 0.006). Multiple logistic regression analysis demonstrated that adiponectin level was independently associated with complex lesions (odds ratio 0.514, 95% confidence interval 0.278 to 0.951; p = 0.034). Polytomous logistic regression revealed that adiponectin correlated independently with both single and multiple complex lesions. Among patients with ACS, who had lower adiponectin levels than stable CAD patients, those with multiple complex lesions had significantly lower adiponectin than those with a single complex lesion (3.26 [range 2.26 to 4.46] vs. 4.21 [range 3.36 to 5.41] microg/ml, p = 0.032). CONCLUSIONS: Plasma adiponectin levels are significantly associated with coronary lesion complexity in men with CAD. Low adiponectin levels may contribute to coronary plaque vulnerability.

Acute Disease↗
PubMed2006

Elevated levels of remnant lipoproteins are associated with plasma platelet microparticles in patients with type-2 diabetes mellitus without obstructive coronary artery disease.

AIMS: Platelets participate in the pathogenesis of arterial thrombosis and it has been demonstrated that enhanced platelet activation occurs in patients with diabetes mellitus (DM). Dyslipidaemia is a common feature of diabetes. We investigated the association between certain lipid fractions and plasma platelet-derived microparticle (PMP) levels in patients with type-2 DM. METHODS AND RESULTS: We measured fasting serum levels of remnant-like lipoprotein particles-cholesterol (RLP-cholesterol) and assessed in vivo platelet activation by quantifying the number of PMP in the plasma detected as CD42b-positive microparticles by flow cytometry in Japanese type-2 DM patients without obstructive coronary artery disease who were more slender when compared with Western diabetic patients. The levels of total cholesterol, triglycerides, RLP-cholesterol, and plasma glucose were significantly higher in patients with type-2 DM (n = 105) than in non-diabetic patients (n = 92). The plasma levels of PMP were elevated significantly in type-2 DM patients when compared with non-diabetic control subjects [7.41(5.39-10.50) x 10(6) vs. 3.44(2.43-4.41)x10(6), P < 0.001]. We found that RLP-cholesterol levels were the best predictor of PMP in multivariable linear regression analyses (beta = 0.375, P < 0.001). Lipid-lowering medication with bezafibrate successfully reduced levels of both RLP-cholesterol and PMP in patients with type-2 DM (P < 0.05). CONCLUSIONS: RLP-cholesterol and platelet microparticles are both elevated in type-2 DM patients when compared with controls. RLP-cholesterol is the primary and only predictor of platelet microparticles in the multivariable analysis, which include several standard atherosclerosis risk factors. This suggested that reducing elevated RLP-cholesterol with lipid-lowering therapy may be an effective strategy to prevent thrombogenic vascular complications in type-2 DM.

Angina Pectoris↗
PubMed2006

Relation between platelet microaggregates and ankle brachial index in patients with peripheral arterial disease.

INTRODUCTION: Peripheral arterial disease is one of the systemic atherosclerotic diseases, and patients with the disorder are classified in the high risk group of coronary artery disease. A lower ankle brachial index is a frequent finding in peripheral arterial disease. While platelet microaggregates are a significant predictor of adverse clinical outcome in coronary artery disease, the significance of platelet aggregability in peripheral arterial disease has not been elucidated. MATERIALS AND METHODS: Small platelet aggregates measured using laser-light scattering and ankle brachial index were determined in 42 patients with both coronary artery disease and peripheral arterial disease (peripheral group), 56 patients with only coronary artery disease (coronary group) and 32 patients without both (control group). RESULTS: The level of small platelet aggregates was increased significantly in the peripheral group (4.3 x 10(4) [range 2.2 x 10(4) to 7.4 x 10(4)]) compared with both the coronary (1.1 x 10(4) [range 0.3 x 10(4) to 5.0 x 10(4)]) and control groups (0.5 x 10(4) [range 0.1 x 10(4) to 0.9 x 10(4)]). There was a significant inverse correlation between log small platelet aggregates and ankle brachial index (n=130, r=-0.422, p<0.001). Multivariate logistic regression analysis revealed that a lower ankle brachial index (<0.90) was an independent determinant of increased levels of small platelet aggregates. CONCLUSIONS: Platelet aggregability was increased in patients with peripheral arterial disease with the degree of platelet aggregation being closely associated with ankle brachial index. It is possible that this change in platelet activity may be one mechanism to explain why a lower ankle brachial index is a predictor of poor prognosis in patients with peripheral arterial disease.

Aged↗
PubMed2006

A -786T>C polymorphism in the endothelial nitric oxide synthase gene reduces serum nitrite/nitrate levels from the heart due to an intracoronary injection of acetylcholine.

We identified a -786T>C polymorphism in the eNOS gene, and this polymorphism was strongly associated with coronary spasm. The present study aimed to elucidate whether the -786T>C polymorphism or acetylcholine (ACh)-induced coronary spasm affects serum nitrite/nitrate (NOx) levels. The study population comprised three groups: (i) 26 patients without coronary spasm in the left anterior descending coronary artery (LAD) with the T/T genotype (group A); (ii) 20 patients with coronary spasm in the LAD with the T/T genotype (group B); and (iii) 16 patients with coronary spasm in the LAD with the C/T genotype (group C). Paired blood samples were obtained from the coronary sinus (CS) and the aortic tract (Ao) before and after an intracoronary injection of ACh. Serum NOx and plasma lactate levels were measured. The delta NOx level was calculated as the serum concentration of NOx in the CS minus that in the Ao. We compared lactate extraction ratios (LERs) and delta NOx levels between the three groups. The LERs after the provocation test in groups A, B and C were 18.9+/-2.4%, -0.5+/-3.9% and -13.5+/-4.2%, respectively. The LER in group C was significantly lower than in group B. The delta NOx levels after the provocation test in groups A, B and C were 11.5+/-1.7 micromol/l, 10.4+/-3.5 micromol/l and -2.1+/-4.8 micromol/l, respectively. The delta NOx levels in group C were significantly lower (P<0.05). Although the NOx level was significantly increased after the provocation test in group A (P<0.05), the NOx level was significantly decreased after the provocation test in group C (P=0.001). In group B, the provocation test did not significantly change the delta NOx level. In conclusion, the -786T>C polymorphism reduces the NOx level from the heart due to an intracoronary injection of ACh, and thereby predisposes the patients to severe coronary spasm.

Acetylcholine↗
PubMed2006

Low-grade inflammation, thrombogenicity, and atherogenic lipid profile in cigarette smokers.

BACKGROUND: Cigarette smoking is one of the major risk factors for atherosclerotic coronary disease, but the precise mechanism(s) by which cigarette smoking promotes atherosclerosis remains unknown. As there is now increasing evidence that atherosclerosis is an inflammatory condition, the present study investigated whether inflammation exists in smokers. METHODS AND RESULTS: The inflammatory markers and lipid profiles were compared among a current-smoker group (210 patients, mean age 61.8 +/- 11.0 years), past-smoker group (115 patients, 67.1 +/- 9.0 years) and never-smoked group (113 patients, 68.2 +/- 10.7 years), all of whom had no apparent signs of inflammation. The respective levels of blood leukocytes, platelets, C-reactive protein and fibrinogen were significantly higher in current-smokers than in the never-smoked group (6,600 +/- 1,723 /microl vs 5,638 +/- 1,313 /microl p<0.01; 22.7 +/- 6.8 x 10(4) /microl vs 18.7 +/- 7.4 x 10(4) /microl, p<0.01; 3.50+/-4.91 mg/L vs 1.92+/-3.02 mg/L, p<0.01; 334.2 +/- 90.9 mg/dl vs 314.7 +/- 80.2 mg/dl, p<0.05). The respective levels of plasma triglycerides, remnant-like particle cholesterol and apolipoprotein-B were significantly higher and that of high-density lipoprotein cholesterol significantly lower in the current-smokers than in the never-smoked group (152.4 +/- 96.2 mg/dl vs 120.5 +/- 58.1 mg/dl, p<0.01; 5.4+/-6.3 mg/dl vs 3.8 +/- 2.0 mg/dl, p<0.05; 101.6 +/- 23.7 mg/dl vs 95.0 +/- 21.2 mg/dl, p<0.05; 45.2 +/- 12.3 mg/dl vs 50.6 +/- 15.6 mg/dl, p<0.01). Past smokers had intermediate values between those of current-smokers and never-smoked. CONCLUSIONS: Low-grade inflammation, atherogenic dyslipidemia, and hypercoagulability are present in smokers compared with those who have never smoked among subjects without apparent inflammation who underwent coronary angiography on suspicion of coronary artery disease.

Aged↗
PubMed2006

Long-term efficacy of edaravone in patients with acute myocardial infarction.

BACKGROUND: The effect of edaravone, a free radical scavenger, on long-term prognosis and its efficacy with regards to scavenging injurious free radicals in patients with acute myocardial infarction (AMI) was examined. METHODS AND RESULTS: One hundred and one initial AMI patients were randomly assigned to receive 30 mg edaravone (n = 50) or a placebo (n = 51) intravenously just before reperfusion. The infarct size, using serum biomarkers and Q-wave formations, and the incidence of reperfusion arrhythmia between the groups were compared. Cardiovascular event-free curves were estimated by using the Kaplan - Meier method. In addition, the serum thioredoxin levels, an oxidative stress marker, to assess the antioxidant effect of edaravone was determined. In all cases, successful reperfusion was obtained within 6 h after the onset of symptoms. Infarct size and reperfusion arrhythmia were significantly attenuated in the edaravone group compared with the placebo group (p = 0.035 and p = 0.031). The cumulative event-free rate was significantly higher in the edaravone group than in the placebo group (p = 0.045). Serum thioredoxin levels were significantly lower in the edaravone group than in the placebo group throughout the acute phase. CONCLUSIONS: The present study suggests that the edaravone administration just prior to reperfusion might reduce oxidative stress and improve the long-term clinical outcomes of AMI patients.

Acute Disease↗
PubMed2006

Elevated plasma osteopontin levels were associated with osteopontin expression of CD4+ T cells in patients with unstable angina.

BACKGROUND: Plaque instability in patients with unstable angina (UA) is associated with stimulated CD4+ T cells, so the present study investigated whether there is a relationship among plaque instability, osteopontin and CD4+ T cells. METHODS AND RESULTS: Peripheral blood mononuclear cells were collected from 51 consecutive patients with UA, 60 patients with stable angina (SA), and 39 patients with chest pain syndrome (CPS). Osteopontin-producing CD4+ T cells were quantified by flow cytometry. Plasma osteopontin levels (ng/ml) were measured by ELISA and were higher in patients with UA (792.0 +/- 316.7) than in those with SA (626.0 +/- 195.0, p < 0.005) or CPS (594.7 +/- 239.4, p < 0.005). The frequency (%) of osteopontin-producing CD4+ T cells was higher in patients with UA (26.7 +/- 13.3) than in those with SA (19.5 +/- 11.1, p < 0.05) or CPS (16.6 +/- 9.0, p < 0.005). Furthermore, the plasma osteopontin level correlated with the frequency of osteopontin-producing CD4+ T cells (r = 0.327, p = 0.0004), as did the high-sensitivity C-reactive protein level (r = 0.360, p = 0.0002). CONCLUSIONS: The plasma osteopontin levels are elevated in patients with UA, accompanied by an increase in the number of osteopontin-production of circulating CD4+ T cells. Circulating CD4+ T cells may play a role through osteopontin in the pathophysiology of UA.

Aged↗
PubMed2006

Acute myocardial infarction induced by cisplatin-based combination chemotherapy for malignant melanoma: a case report.

A 61-year-old woman with stage IV malignant melanoma suffered acute myocardial infarction during the third course of chemotherapy with cisplatin, dacarbazine, nimustine hydrochloride and tamoxifen citrate, despite no serious problem occurring during the first and second courses of chemotherapy. Since this patient, excluding menopause, had no significant risk factor for coronary heart disease before the start of chemotherapy, the infarction was likely to be attributable to the chemotherapy regimen. Chemotherapy should be used cautiously in patients with coronary risk factors before treatment is begun.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2006

[Cardiac aldosterone].

In heart failure, the heart carries out compensation of its functional deterioration using various hormonal actions. Many hormones are recently found to be synthesized and secreted from the failing or hypertensive heart. We have reported that the steroid synthesis is present in the heart; aldosterone but not dehydroepiandrosterone (DHEA) is secreted from the failing heart and contrarily DHEA but not aldosterone is secreted from the normal heart. Furthermore, we reported that adrenocorticotropic hormone (ACTH) is also secreted from the failing or hypertensive heart, suggesting that the hormones composing the hypothalamus-pituitary-adrenal(HPA) axis as well as the RAA system would be present in the heart.

Aldosterone↗
PubMed2005

Direct effects of aldosterone on cardiomyocytes in the presence of normal and elevated extracellular sodium.

It is now recognized that aldosterone is potentially cardiotoxic, although its local effects in the heart are not well understood. We examined the effects of aldosterone on cultured neonatal rat cardiomyocytes in the presence of normal and elevated extracellular Na+ ([Na+]o). We evaluated the intracellular volume of cardiomyocytes in the presence of normal (141 mEq/liter) and elevated (146 mEq/liter) [Na+]o by measuring cell size. Intracellular Na+ was measured using sodium-binding-benzofuran-isophthalate as a fluorescent sodium indicator, and cardiac hypertrophy was assessed using B-type natriuretic peptide transcription and (3)H-leucine incorporation. Cardiomyocytes shrank in the presence of 146 mEq/liter Na+ due to the increased extracellular osmolarity at early phase. Aldosterone (10(-7) mol/liter) mitigated the shrinkage by stimulating Na+ uptake by the cells. This effect of aldosterone was blocked by SM 20220, a Na+/H+ exchanger 1 (NHE1) inhibitor, but not by eplerenone, a mineralocorticoid receptor blocker. Seventy-two hours of exposure to aldosterone in the presence of 146 mEq/liter Na+ led to increases in cardiomyocyte size, 3H-leucine incorporation, and B-type natriuretic peptide and NHE1 transcription that were significantly greater than were seen in the presence of 141 mEq/liter Na+. All but the last were blocked by either eplerenone or SM 20220; the increase in NHE1 transcription was blocked only by eplerenone. Aldosterone exerts a beneficial effect via NHE1 to block cardiomyocyte shrinkage in the presence of elevated [Na+]o at early phase, but long-time exposure to aldosterone in the presence of elevated [Na+]o leads to cardiomyocyte hypertrophy via genomic effects mediated by the mineralocorticoid receptor.

Aldosterone↗
PubMed2005

Stabilization of carotid atheroma assessed by quantitative ultrasound analysis in nonhypercholesterolemic patients with coronary artery disease.

OBJECTIVES: This study examined whether intensive cholesterol-lowering therapy with statins in nonhypercholesterolemic patients is effective in improving echolucency of vulnerable plaques assessed by ultrasound with integrated backscatter (IBS) analysis. BACKGROUND: Atherosclerotic plaque stabilization is a promising clinical strategy to prevent cardiovascular events in patients with coronary artery disease (CAD). There is a correlation between coronary and carotid plaque instability, and echolucent plaques are recognized as vulnerable plaques. METHODS: Consecutive nonhypercholesterolemic patients with CAD were randomly assigned Adult Treatment Panel-III diet therapy (diet group; n = 30) or pravastatin (statin group; n = 30). Echolucent carotid plaques were monitored by measuring intima-media thickness (IMT) and echogenicity by IBS for six months. RESULTS: Total cholesterol, low-density lipoprotein cholesterol (LDL-C), and high-sensitivity C-reactive protein were significantly decreased in the statin group (from 197 +/- 15 mg/dl to 170 +/- 18 mg/dl [p < 0.001]; from 131 +/- 14 mg/dl to 99 +/- 14 mg/dl [p < 0.001]; and from 0.11 [0.04 to 0.22] mg/dl to 0.06 [0.04 to 0.11] mg/dl [p < 0.05]; respectively), whereas only total cholesterol was moderately reduced (from 193 +/- 24 mg/dl to 185 +/- 22 mg/dl [p < 0.05]) and LDL-C and triglycerides insignificantly reduced in the diet group. Significant increases of echogenicity of carotid plaques were noted in the statin group but not in the diet group (from -18.5 +/- 4.1 dB to -15.9 +/- 3.7 dB [p < 0.001] and from -18.2 +/- 4.0 dB to -18.9 +/- 3.5 dB [p = 0.13]; respectively) without significant regression of plaque-IMT values in both groups. CONCLUSIONS: Statin therapy is rapidly effective in increasing echogenicity of vulnerable plaques without regression of plaque size in nonhypercholesterolemic patients with CAD. Quantitative assessment of carotid plaque quality by ultrasound with IBS is clinically useful for monitoring atherosclerotic lesions by evaluating vulnerability of atheroma.

Atherosclerosis↗
PubMed2005

Id1 gene transfer confers angiogenic property on fully differentiated endothelial cells and contributes to therapeutic angiogenesis.

BACKGROUND: Transplantation of endothelial progenitor cells has been proposed as a potential strategy for therapeutic revascularization. However, the limited endogenous cell pool and the related technical difficulties constitute clinically important disadvantages to autologous transplantation. In this study we investigated whether fully differentiated endothelial cells (ECs) modified with gene transfer of Id1, a helix-loop-helix transcription factor involved in angiogenesis, have the potential to contribute to therapeutic angiogenesis. METHODS AND RESULTS: The Id1 gene was transferred into human umbilical vein ECs (HUVECs) via a Sendai virus vector. Id1 stimulated migration, proliferation, and capillary-like tube/cord formation of HUVECs. In addition, Id1 reduced serum deprivation-induced HUVEC apoptosis, as shown by FACS analysis with annexin V and TUNEL staining. Transplantation of Id1-overexpressing HUVECs accelerated recovery of blood flow as evaluated by laser-Doppler perfusion imaging, increased capillary density, and improved the rate of limb salvage compared with the transplantation of control HUVECs. Histochemical analysis revealed that the regenerated vascular networks of limbs transplanted with Id1-overexpressing HUVECs contained numerous HUVECs, some of which were in a proliferative state. Untransfected HUVECs were also incorporated with Id1-transfected HUVECs, suggesting the noncell autonomous effect of Id1. Finally, angiopoietin-1 was upregulated in Id1-overexpressing HUVECs and functionally contributed to the in vitro angiogenic effect of Id1. CONCLUSIONS: Id1 gene transfer conferred HUVECs with an angiogenic property, contributing to neovascularization after transplantation into ischemic lesions. Transplantation of Id1-overexpressing mature ECs may serve as a novel and useful strategy for therapeutic angiogenesis.

3' Untranslated Regions↗
PubMed2005

Usefulness of preprocedural platelet aggregation to predict restenosis after percutaneous coronary intervention.

We investigated whether the assessment of small platelet aggregates before percutaneous coronary intervention (PCI) could predict restenosis after PCI. This was a prospective cohort study that enrolled 189 consecutive patients who had coronary artery disease. In multiple logistic regression analysis, higher levels of preprocedural small platelet aggregates were independently associated with restenosis after PCI. Measurement of small platelet aggregates may serve as a useful clinical variable for stratifying patients who present for PCI.

Aged↗
PubMed2005

Elevated levels of VE-cadherin-positive endothelial microparticles in patients with type 2 diabetes mellitus and coronary artery disease.

OBJECTIVES: The purpose of this study was to examine whether CD144-EMP (endothelium-derived microparticles) is useful as a specific marker of endothelial cell (EC) dysfunction and to determine whether plasma levels of circulating CD144-EMP predicted coronary artery disease (CAD) in patients with type 2 diabetes mellitus (DM). BACKGROUND: Endothelial cell dysfunction is involved in atherogenesis; however, the quantitative assessment of EC dysfunction has yet to be established clinically. Endothelium-derived microparticles are small, membrane-shed vesicles that are generated from the EC surface in response to cellular dysfunction and/or injury. Diabetes mellitus is known to be associated with EC dysfunction and accelerated atherosclerosis. METHODS: We characterized EMP using anti-CD144 (VE-Cadherin) antibody in various atherosclerosis-related cells and investigated the association between the levels of CD144-positive microparticles and hydrogen-peroxide-induced EC injury and acetylcholine-induced coronary vasomotion. Furthermore, we evaluated plasma CD144-EMP levels in patients with and without DM. RESULTS: We demonstrated that CD144-positive microparticles were derived selectively from human EC. The levels of CD144-EMP reflected the degree of in vitro hydrogen-peroxide-induced EC injury and impairment of in vivo endothelium-dependent coronary vasodilation (p < 0.01). Plasma CD144-EMP levels were increased significantly in DM patients compared with patients without DM (p < 0.001). In DM patients, the elevated levels of CD144-EMP were the most significant risk factor for CAD relative to all other traditional risk factors (odds ratio [OR] 3.5, 95% confidence interval [CI] 1.8 to 6.9, p < 0.001). Notably, plasma CD144-EMP identified a subpopulation of established CAD patients in DM subjects without typical anginal symptoms (OR 10.6, 95% CI 3.9 to 29.5, p < 0.001). CONCLUSIONS: The CD144-positive EMP exist in human plasma, and plasma CD144-EMP levels can be a clinically specific and quantitative marker of EC dysfunction and/or injury. Measurement of CD144-EMP, by providing a quantitative assessment of EC dysfunction, may be useful for identifying DM patients with increased risk of CAD.

Aged↗
PubMed2005

Plasma thioredoxin levels in patients with unstable angina.

Plasma levels of human thioredoxin are indicative of the responses against oxidative stress. We measured the plasma thioredoxin levels in patients with unstable angina in order to examine the relationships between subsequent clinical course and plasma thioredoxin levels before and after treatment for unstable angina. Blood was sampled both on admission and after treatment in 44 patients with unstable angina. In addition, blood samples were obtained from 41 patients with stable exertional angina and 41 patients with chest pain syndrome after admission. The plasma levels of thioredoxin were the highest in the unstable angina group among three groups (p<0.001). Treatment of unstable angina decreased the plasma thioredoxin levels (p<0.01). We divided the patients with unstable angina into two groups according to the plasma thioredoxin levels on admission and after treatment. There was a significant difference in Braunwald's classification between the high thioredoxin and the low thioredoxin group on admission, as analyzed by the chi2 test with Yates's correction (p<0.05). Moreover, there was a significant difference in incidence of recurrent anginal attacks at rest between the high thioredoxin and the low thioredoxin group after treatment, as analyzed by the chi2 test with Yates's correction (p<0.001). The present study demonstrated that plasma thioredoxin levels are significantly increased in patients with unstable angina compared to those with stable exertional angina and chest pain syndrome. Thioredoxin levels were associated with recurrent myocardial ischemia in patients with unstable angina.

Aged↗