Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet-derived microparticles (PDMPs) are produced by platelet activation or physical stimulation under various conditions. To evaluate changes in platelet and chemokine function in patients undergoing percutaneous transluminal coronary angioplasty (PTCA), we measured and compared levels of PDMPs and a C-C chemokine, regulated on activation normally T-cell express and secreted (RANTES), by ELISA. Levels of PDMP and RANTES in patients with acute coronary syndrome were significantly higher than those in the control groups (PDMP: 20.1 +/- 2.9 vs 80.4 +/- 7.3 U/ml, p < 0.001; RANTES: 18.6 +/- 3.7 vs 52.1 +/- 4.6 ng/ml, p < 0.01), but did not differ between the control groups and patients with stable angina. PDMP levels were higher in patients with acute myocardial infarction (AMI) than in patients with unstable angina (PDMP: 115.0 +/- 7.1 vs 63.9 +/- 6.2 U/ml, p < 0.001). There was no difference in the RANTES levels, however, between patients with AMI and patients with unstable angina. PDMP and RANTES levels were significantly decreased after PTCA (PDMP, p < 0.001; RANTES, p < 0.05), but without differences between the two groups. In addition, the level of PDMP was significantly correlated with that of RANTES or soluble CD40 ligand. These findings suggest that PTCA may prevent the development of AMI-associated complications in which activated platelets and RANTES play roles. Our ELISA method appears to be sufficient for monitoring PDMP and RANTES levels after PTCA in patients with acute coronary syndrome.
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PMID:Enzyme immunoassay detection of platelet-derived microparticles and RANTES in acute coronary syndrome. 1262 35

CD40-CD40 ligand interaction is involved in the inflammatory pathogenesis of atherosclerosis but clinical data about its role in stent restenosis are still limited. We investigated the effect of preprocedural CD40 ligand (sCD40L) on stent restenosis. We enrolled 36 patients (mean age 61.4 +/- 8.5 years) with stable angina who underwent successful stent implantation. Control angiograms were performed in all patients after 6 months. Plasma sCD40L and high-sensitive C-reactive protein levels were measured before stent implantation and at 1 and 6 months after the procedure. Angiographically proven restenosis rate was 27.8%. Plasma sCD40L levels were significantly higher (preprocedural 0.74 +/- 0.79) and more prolonged in patients with stent restenosis compared with patients without stent restenosis (0.02 +/- 0.22 ng/ml, p < 0.001). According to receiver-operator characteristic analysis, sCD40L > 0.41 ng/ml was the best distinguished parameter between patients with and without restenosis. At the multivariate logistic regression analysis, preprocedural sCD40L was an independent predictor (RR 39.4, 95% confidence interval 4.05 to 383.8, p = 0.002) of stent restenosis after adjusting for confounding variables, including diabetes, reference vessel diameter, lesion length, stent diameter, stent length, and baseline high-sensitive C-reactive protein. Sensitivity, specificity, and positive and negative predictive values and likelihood ratio of preprocedural sCD40L levels in stent restenosis were 78%, 92%, 78%, 92%, and 9.37%, respectively. In conclusion, enhanced inflammation of plaque (increased sCD40L) before percutaneous coronary intervention may increase the rate of stent restenosis. Increased preprocedural sCD40L level is an independent predictor of stent restenosis. We can use this marker for the assessment of risk stratification before planning stent implantation.
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PMID:Usefulness of preprocedural soluble CD40 ligand for predicting restenosis after percutaneous coronary intervention in patients with stable coronary artery disease. 1644 63

Nontraditional atherosclerotic risk factors have become the focus of attention in recent years. In addition, metabolic syndrome is gaining recognition as another multiplex cardiovascular risk factor. However, to date, no studies have investigated the effect of metabolic syndrome on circulating soluble CD40 ligand (sCD40L), monocyte chemoattractant protein 1, cellular adhesion molecules, and disease severity in patients with symptomatic coronary artery diseases. This study was conducted to address this issue. Patients with stable angina who received percutaneous coronary interventions for significant (> or = 70% diameter stenosis) de novo lesions between January 1999 and January 2004 and had preprocedural serum samples were enrolled. Metabolic syndrome was defined by the National Cholesterol Education Program criteria with waist criterion modified into body mass index of more than 25 kg/m2. The serum samples were thawed and analyzed for circulating sCD40L, monocyte chemoattractant protein 1, adhesion molecules, and high sensitivity C-reactive protein (hs-CRP). Coronary severity was assessed by a modified version of Gensini scoring system. A total of 313 patients, 248 males and 65 females, were studied. Among them, 222 (70.9%, 170 males and 52 females) had metabolic syndrome. Patients with metabolic syndrome had higher serum creatinine level and lower low-density lipoprotein cholesterol despite higher triglyceride concentration. In multivariate analysis, patients with metabolic syndrome had higher sCD40L (6057 +/- 275 vs. 5051 +/- 423 pg/mL, P = .037) and more hs-CRP in higher tertiles (P = .005) than patients without, but similar levels of intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and P selectin. Metabolic syndrome was also significantly associated with multiple coronary vessel involvements with 70% or higher diameter stenosis (36.5% double-vessel and 14% triple-vessel diseases vs 30.8% double-vessel and 5.5% triple-vessel diseases, P = .026) and multiple coronary segment involvements with 50% or higher diameter stenosis (P = .014) in multivariate analysis. In conclusion, the presence of metabolic syndrome is independently associated with elevated sCD40L, hs-CRP, and coronary disease severity in patients with coronary artery disease requiring interventional treatment of stable angina.
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PMID:The presence of metabolic syndrome is independently associated with elevated serum CD40 ligand and disease severity in patients with symptomatic coronary artery disease. 1683 37

Atherothrombosis is the process that links atherosclerotic lesion development with unpredictable and life-threatening ischemic vascular events such as angina, myocardial infarction, transient ischemic attack, and stroke. Atherothrombosis is triggered when an unstable atherosclerotic lesion is ruptured, leading to platelet activation and thrombus formation. Inflammatory mediators are responsible for lesion instability leading to rupture, and in recent years atherothrombosis and its underlying condition of atherosclerosis have come to be recognized as manifestations of inflammatory disease. Inflammatory mediators may therefore serve as early markers of atherothrombosis. Measurement of early markers may be used to predict future ischemic events and improve risk stratification in patients following diagnosis of atherothrombotic disease. In addition, detection of such markers may help to optimize the use of current therapies to manage atherothrombosis. Molecules that may serve as early markers of atherothrombotic disease include C-reactive protein, CD40 ligand, myeloperoxidase, pregnancy-associated plasma protein and plasminogen activator inhibitor-1. Early indications are that levels of these markers are influenced by therapies currently in use in the treatment of atherothrombotic conditions, including antiplatelet agents. Ongoing studies will provide further insight into routine assessment of inflammatory markers as a guide to the management of patients with atherothrombosis.
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PMID:The potential role of antiplatelet agents in modulating inflammatory markers in atherothrombosis. 1696 84

The present study examined the association of myocardial perfusion reserve index (MPRI) in cardiovascular magnetic resonance (CMR) with coronary microvascular dysfunction (CMD) and serum levels of markers of inflammation or endothelial activation. Twelve patients with typical angina pectoris without coronary artery disease were enrolled in this study, and CMR perfusion was analyzed using a steady-state-free-precession sequence with 3 short axis slices per heartbeat during first pass of 0.025 mmol Gadolinium-DTPA/kg body weight. The upslope of myocardial signal intensity curves was used to calculate MPRI. CMD was assessed by intracoronary Doppler flow measurement and biplane angiography. Both MPRI and CMD were assessed during endothelium-independent stimulation with intravenous adenosine and during endothelium-dependent stimulation with intracoronary infusion of acetylcholine. Serum values of soluble CD40 ligand (sCD40L), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), soluble intercellular adhesion molecule-1 (sICAM-1), and C-reactive protein (CRP) were measured. Impaired MPRI correlated significantly with a decrease in coronary blood flow reserve after both endothelium-dependent (p = 0.033) and endothelium-independent (p = 0.022) stimulation. Serum levels above the median of all normal ranged biomarkers sCD40L, TNF-alpha, IL-6, sICAM-1 and CRP were associated with an impaired MPRI for stimulation with adenosine as well as acetylcholine. In multivariable analyses, sCD40L (p < 0.001) and TNF-alpha (p = 0.011) were significantly associated with a decrease in MPRI on adenosine, as were TNF-alpha (p = 0.016) and sICAM-1 (p = 0.022) for a decrease in MPRI on acetylcholine. MPRI on adenosine significantly correlated with MPRI on acetylcholine (p < 0.001). Therefore, the present study demonstrates safety and feasibility of an intracoronary infusion of acetylcholine during CMR perfusion analysis, thus allowing direct assessment of endothelial dependent vasomotor function at the myocardial level by CMR. Furthermore, we show that an impaired myocardial perfusion reserved in CMR is associated with established biomarkers of early atherosclerosis and significantly correlated with CMD. CMR combined with adenosine could be proposed as a non-invasive tool to evaluate CMD.
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PMID:Myocardial perfusion reserve in cardiovascular magnetic resonance: Correlation to coronary microvascular dysfunction. 1706 99

We hypothesized that restenosis after coronary stenting is predicted by elevated levels of markers of thrombus formation and inflammation. Plasma levels of representative markers of inflammation, the thrombin and plasmin activation systems and adhesion molecules were measured in 59 patients with stable angina pectoris before, immediately after and 6 hours (h), 12 h, 24 h, one month and six months after elective stent implantation (radioactive phosphorus-32 stents/RSs/ n = 16, bare-metal stents/BMSs/ n = 43). All patients underwent clinical and angiographic follow-up (FUP) six months after stenting. RSs had significantly higher angiographic severity of restenosis than BMSs (47.1 +/- 20.1% vs. 27.6 +/- 22.0%, p = 0.003). Repeated measures ANOVA revealed significant differences between the BMS and RS groups as regards the increases in plasma levels of vascular cell adhesion molecule-1 (VCAM-1, p = 0.022), plasminogen activator inhibitor-1 (PAI-1, p = 0.047), tissue-type plasminogen activator (tPA, p = 0.047) and CD40 ligand (CD40L, p = 0.038). tPA levels tended to increase immediately after stenting in both groups, whereas the PAI-1 level one month after stenting was elevated significantly only in the RS group. In the RS group, the plasma levels of CD40L were increased at 24 h and six months after stenting, and the VCAM-1 level rose immediately after stenting and remained high during the FUP. Multivariate analysis on pooled laboratory data of both groups revealed elevated levels of VCAM-1 at 12 h and at six months as significant predictors of the severity of stent restenosis. In conclusion, the process of inflammation and thrombosis occurring after coronary interventions seems to be prolonged and enhanced in patients with high-grade restenosis at the follow up.
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PMID:Time course of prothrombotic and proinflammatory substance release after intracoronary stent implantation. 1839 32

Current evidence shows that the CD40-CD40 ligand (CD40-CD40L) system plays a crucial role in the development, progression and outcome of acute coronary syndrome (ACS). The aim of this study is to investigate whether a CD40 gene (-1C/T) single nucleotide polymorphism (SNP) is associated with ACS and CD40 expression. We included controls (n = 163) and patients with either ACS (n = 210) or stable angina (SA, n = 189) in the study. The gene polymorphism was measured using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and identified by sequencing. CD40 expression on platelets was detected by flow cytometry. The results showed that the frequency of the CC genotype of CD40 gene in the ACS group was significantly higher than in the SA and control groups (P < 0.001), while the TT genotype frequency in the ACS group was significantly lower than that of the SA and control groups (P < 0.001). The C-allele frequency of the ACS group was higher than that of the SA and control groups (P < 0.001). The C allele increased the risk of ACS when compared with the SA group (OR = 1.841, 95% CI: 1.390-2.437) and the control groups (OR = 1.877, 95% CI: 1.402-2.515). No significant differences in genotypes or allele frequencies were found between the SA and control groups. CD40 expression on platelets in patients with C-allele carriers was significant higher than in the T-allele carriers in each group. In conclusion, our results suggested that the CD40 gene (-1C/T) polymorphism was associated with ACS in Chinese people. The -1C-allele gene carriers had a higher expression of CD40 and an increased risk of suffering from ACS.
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PMID:Association analysis of CD40 gene polymorphism with acute coronary syndrome. 2012 35

We determined the serum levels of soluble CD40 ligand (sCD40L) in patients with chronic coronary artery disease (CAD) and acute coronary syndrome (ACS). Patients with unstable angina (UA) and myocardial infarction (MI) showed significantly higher levels (P < .001) of sCD40L compared with patients with stable angina (SA) and controls; particularly, high levels occurred in patients with UA (UA: 9.23 +/- 2.92, MI: 7.38 +/- 1.05, SA: 4.42 +/- 1.08; control: 4.01 +/- 0.87 ng/mL). There was no significant difference in sCD40L levels between patients with UA and MI or between patients with SA and controls. Levels of sCD40L did not show any significant correlation with peak creatine kinase (CK), CK-MB isoenzyme activity in patients with MI, troponin T serum levels in patients with UA or with culprit vessel (CV) complexity score (CVCS), type of CV lesion, or vessel score in patients with UA or MI. These results suggest that CD40L plays a pathogenic role in triggering ACS.
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PMID:Levels of sCD40 ligand in chronic and acute coronary syndromes and its relation to angiographic extent of coronary arterial narrowing. 2030 68

Percutaneous coronary intervention (PCI) can be regarded as a model for mechanical induced plaque rupture. The objective of this study was to evaluate the inflammatory response to PCI in stable coronary artery disease (CAD) by analysing plasma levels of a wide range of inflammatory mediators. Consecutively, we included 36 patients with stable angina pectoris after successful revascularization by PCI with implantation of a bare metal stent (BMS) or a drug eluting stent (DES). Patients were followed for 7 days with serial measurements of inflammatory mediators in plasma. C-reactive protein (CRP) and Pentraxin 3 showed a statistical significant early increase after PCI peaking at 3 days and 3 h, respectively. Vascular cell adhesion molecule-1 (VCAM-1) increased significantly with a peak at 3 days, while E-selectin showed a statistical significant gradual decrease. Markers of platelet mediated inflammation showed increasing (CD40 ligand) and decreasing (P-selectin) levels after PCI. While monocyte chemoattractant protein, CCL21 and CXCL16 increased rapidly in response to PCI, Interleukin-8, CCL19 and RANTES decreased. Patients with DES had significantly lower levels of VCAM-1 and RANTES compared to those with BMS. A femoral access site was associated with higher CRP levels than a radial access site. The use of glycoprotein-IIb/IIIa-inhibitors was associated with significantly higher CD40L and RANTES levels. Our findings underscore the complex nature of the inflammatory responses during PCI in stable CAD, and suggest that simultaneous measurements of several markers may be needed to characterize these PCI-related responses. The responses were only in a minor degree influenced by stent type, access site and the use of glycoprotein-IIb/IIIa-inhibitors.
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PMID:Inflammatory response to percutaneous coronary intervention in stable coronary artery disease. 2037 28

Following plaque rupture, activated platelet will induce subsequent inflammatory process including neutrophil recruitment. In vitro study demonstrated an interaction between neutrophils and platelets via a mechanism involving CD40-CD40 ligand. However, whether this mechanism exists in the clinical setting remains unknown. Fifty-four patients with acute myocardial infarction (AMI) and 25 with unstable angina of pain onset of < or = 24 h were enrolled consecutively. Acute myocardial infarction was diagnosed from three diagnostic criteria, i.e., anginal pain, electrocardiogram ST-T changes, and cardiac enzyme elevation. Unstable angina was diagnosed in patients without elevated cardiac enzymes. Peripheral venous blood was drawn at admission for routine blood count and soluble CD40 ligand (sCD40L) measurement. Neutrophil count was determined by an automated blood cell counter. Circulating sCD40L was measured using a standard enzyme-linked immunosorbent assay. Neutrophil count was significantly higher in AMI as compared with unstable angina (P < 0.001), whereas circulating sCD40L did not significantly differ. Despite marked elevation, no correlation was observed between neutrophil count and circulating sCD40L in AMI. Interestingly, we observed a strong and positive significant correlation between neutrophil count and circulating sCD40L level (r = 0.607, P = 0.002) in unstable angina. Circulating sCD40L is associated with neutrophil count and may mediate interaction between neutrophils and platelets in acute coronary syndrome, particularly in unstable angina.
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PMID:Circulating soluble CD40 ligand mediates the interaction between neutrophils and platelets in acute coronary syndrome. 2067 35


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