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)

The Epidemiological Study of Myocardial Infarction Study which enrolled 9758 apparently healthy men aged 50-59 years, is a prospective cohort study designed to evaluate markers of coronary risk. Soluble forms of the intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) levels were measured in plasma obtained at baseline from 317 subjects who suffered a coronary event during the 5-year follow-up and in twice the number of control subjects who were matched for center, age and day of inclusion in a nested case-control design. The relative risk associated with the highest compared with the lowest thirds of ICAM-1 (>625 versus <502 ng/ml) was 2.45 (95% CI: 1.64-3.65, P<0.001) without adjustment; it decreased moderately (RR: 2.09; 95% CI: 1.34-3.24, P<0.001) after control for lipid and non-lipid factors and remained significantly elevated after adjustment for C-reactive protein (CRP) (RR: 1.90; 95% CI: 1.21-2.96, P=0.005). Plasma ICAM-1 was essentially associated with the risk of myocardial infarction or coronary death and also with angina pectoris. Subjects with CRP presented elevated coronary risk only if ICAM-1 was high. An elevated level of VCAM-1 was not associated with any risk of future acute coronary event, or with angina pectoris. This data indicates that plasma levels of ICAM-1 may serve as risk markers for future coronary events whatever their clinical presentation and that risk is better defined using simultaneous measurements of ICAM-1 and CRP than any of these levels separately.
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PMID:Circulating soluble adhesion molecules ICAM-1 and VCAM-1 and incident coronary heart disease: the PRIME Study. 1517 38

BACKGROUND: There is growing evidence of the prognostic importance of inflammatory markers in angina pectoris. However, the independent value of high-sensitive C-reactive protein (hsCRP), cardiac troponin T (cTnT), or their combination has not been established in young patients with angina pectoris without ECG changes. Therefore, we assessed the 6-month prognostic values of serum hsCRP and cTnT in young and middle-aged patients who were admitted to the hospital with chest pain but without ECG changes. METHODS: Forty young or middle-aged patients (45+/-10 years old; two females) were included in the study. All had chest pain for the first time without ST-T changes or any other ECG changes and with normal CPK-MB levels. Blood was drawn on admission, separated, and serum was frozen at -80 degrees C for 1 year until thawed and studied as one batch in order to measure hsCRP and cTnT levels. A clinical follow-up was done for 6 months. RESULTS: Our findings showed that the strongest independent marker of an adverse outcome was the hsCRP level on admission (sensitivity 66.7%; specificity 94.1%); cTnT level added a little to the specificity (97.1%), but did not add to the sensitivity that was found by hsCRP level. CONCLUSIONS: hsCRP level on admission could be an independent prognostic marker in young and middle-aged patients with angina pectoris without ECG changes and without CPK-MB elevation.
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PMID:The prognostic value of high-sensitive C-reactive protein and cardiac troponin T in young and middle-aged patients with chest pain without ECG changes. 1367 56

Studies have shown disparate results in relation to the role of plasma concentrations of inflammation markers such as fibrinogen, cytokines, and cell adhesion molecules in acute coronary syndromes. The differentiation of primary versus secondary alterations of these markers in response to acute coronary syndromes is not clear. The aim of this study was to investigate the effect of soluble cell adhesion molecules and some inflammatory markers on coronary plaque instability. The prospective study consisted of 15 patients with stable angina pectoris (SAP), 16 with unstable angina pectoris (UAP), and 16 who had undergone percutaneous transluminal coronary angioplasty (PTCA). Blood samples were obtained from the SAP group on admission, from the UAP group at the early stage of pain onset within 6 h of pain, and again after 12 h of pain. Samples from the PTCA group were collected before, 2, 14 h after the procedure. Soluble vascular cell adhesion molecule-1 (VCAM-1), endothelial selectin, interleukin-1 beta (IL-1 beta) and interleukin-2 (IL-2), and C-reactive protein (CRP) were analyzed by enzyme-linked immunosorbent assay. CRP serum levels gradually increased although IL-2 gradually decreased in patients with UAP and PTCA. In addition, VCAM-1 levels were sharply decreased after the PTCA procedure. However, this value returned back to the preprocedure levels 14 h after PTCA. Both CRP and IL-2 are directly involved in the triggering mechanisms of acute coronary events.
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PMID:The role of inflammation markers in triggering acute coronary events. 1452 Apr 83

Treatment with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) decreases cardiovascular event rates in hypercholesterolemic patients. Whether statins exert effects within 24 hours on the coronary vasculature in patients with endothelial dysfunction has not been elucidated. Twenty-seven patients with stable angina pectoris and average low-density lipoprotein cholesterol concentrations of 138+/-9 mg/dL at baseline were allocated to treatment with placebo (14 patients) or 40 mg/d pravastatin (13 patients) in a randomized, double-blind, prospective trial. Coronary endothelial function was assessed before and 24 hours after single treatment by quantitative coronary angiography during intracoronary infusion of nitroglycerin or increasing concentrations of acetylcholine (0.01, 0.1, and 1 micromol/L). Coronary blood flow reserve was measured by Doppler velocimetry during adenosine infusion. Intracoronary acetylcholine infusion induced abnormal vasoconstriction in both groups before treatment, indicating coronary endothelial dysfunction. Treatment with a single oral 40-mg dose of pravastatin significantly attenuated acetylcholine-mediated vasoconstriction after 24 hours (mean+/-SE decrease in luminal diameter before and after treatment: 0.01 micromol/L, 6.1+/-2.2% versus 3.0+/-1.2%; 0.1 micromol/L, 15.6+/-2.6% versus 7.4+/-1.8%; P<0.05; 1 micromol/L, 22.9+/-2.9% versus 13.2+/-2.6%; P<0.05). There was no significant difference in the response to acetylcholine in the placebo group (8.1+/-2.4% versus 9.7+/-2.4%, 16.1+/-2.9% versus 16.8+/-3.2%, and 21.4+/-3.9% versus 23.3+/-4.2%). The response to nitroglycerin infusion was not altered in both groups. Increase in coronary blood flow in response to adenosine and coronary flow reserve remained unchanged during placebo and statin treatment. Serum concentrations of blood lipids and high-sensitive C-reactive protein were not significantly altered after 24 hours in response to placebo or pravastatin therapy. Statin treatment improves endothelium-dependent coronary vasomotion within 24 hours in the absence of significant cholesterol reduction. The full text of this article is available online at http://www.circresaha.org.
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PMID:Rapid effect of 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibition on coronary endothelial function. 1455 Dec 37

The designation of atherosclerosis as a chronic inflammatory process represents an interesting paradigmatic shift for cardiologists. The plasma concentrations of interleukin-6 and its hepatic byproduct, C-reactive protein, may reflect the intensity of occult plaque inflammation and the vulnerability to rupture. Monocyte chemoattractant protein-1 and interleukin-8 play a crucial role in initiating atherosclerosis by recruiting monocytes/macrophages to the vessel wall, which promotes atherosclerotic lesions and plaque vulnerability. In addition, circulating levels of these proinflammatory cytokines increase in patients with acute myocardial infarction and unstable angina, but not in those with stable angina. Also, the plasma concentrations of these cytokines increase after percutaneous coronary intervention, causing late restenosis after the procedure. Angiotensin II and other atherogenic factors induce these cytokines in the cardiovascular tissues through the activation of transcription factors, such as nuclear factor-kappaB or peroxisome proliferator-activated receptors. Conversely, HMG-CoA reductase inhibitors (statins) can potently inhibit these proinflammatory factors in the vessels. A small GTP-binding protein, Rho, may be a key molecule to explain the anti-inflammatory effects of statins. Interleukin-10 also exerts anti-inflammatory effects on the cardiovascular tissues, possibly by deactivating proinflammatory cytokines and inducible nitric oxide synthase. Gene therapy using interleukin-10 may be a promising means for untreatable or complicated cases of cardiovascular diseases. Thus, therapeutic modulations of these inflammatory cytokines may be useful in the prevention of atherosclerosis and future cardiovascular events.
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PMID:Inflammatory cytokines and cardiovascular disease. 1456 Nov 60

To investigate whether marked and sustained lipid-lowering in subjects with stable angina pectoris and dyslipidemia reduces exercise-induced myocardial ischemia, 17 subjects were treated with dose-adjusted atorvastatin over 1 year and underwent serial evaluation of exercise electrocardiographic ischemic parameters, serum biomarkers, and brachial artery endothelial function. Endothelial function improved progressively and C-reactive protein, P-selectin, and tissue plasminogen activator inhibitor levels decreased, but there was no decrease in exercise electrocardiographic ischemia.
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PMID:Effect of atorvastatin on exercise-induced myocardial ischemia in patients with stable angina pectoris. 1460 94

To assess the in-hospital prognostic value of cellular adhesion molecules (CAMs), the levels of soluble CAMs were measured at admission in 114 patients with severe unstable angina. Patients with an eventful in-hospital course (death, nonfatal acute myocardial infarction, and recurrence of angina) had higher levels of soluble vascular cell adhesion molecule-1 than those without events (p = 0.01); this association was independent of classic risk factors and C-reactive protein.
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PMID:Usefulness of elevated levels of soluble vascular cell adhesion molecule-1 in predicting in-hospital prognosis in patients with unstable angina pectoris. 1460 95

Increased oxidative stress is associated with rapid progression of atherosclerosis. In this study we sought to determine whether premature onset of clinical coronary atherosclerosis is associated with increased levels of lipid peroxidation. We measured plasma levels of malondialdehyde (MDA), using high-pressure liquid chromatography, in 42 male patients with early- (<56 years) or late-onset (>64 years) unstable angina and in 2 age-matched control groups (n=20). Plasma MDA levels were higher in the patients with unstable angina than in the control groups (1.57 +/- 0.07 vs 1.14 +/- 0.03 nmol/mL; P<.001). Patients with early-onset angina showed higher MDA levels than those in late-onset patients (1.75 +/- 0.11 vs 1.44 +/- 0.097 nmol/mL; P<.05), despite a similar prevalence of risk factors for atherothrombosis. The inflammatory component, measured with the use of a high-sensitivity enzyme-linked immunosorbent assay for C-reactive protein, and platelet activity, measured as prothrombin fragment 1+2, failed to predict MDA level. Fasting glucose (P<.05) was the best predictor of MDA level in patients with early-onset unstable angina; uric acid (P=.09) and body-mass index (P=.15) showed trends toward significant correlation with MDA level in the same group of patients. Metabolic abnormalities related to insulin resistance in patients with premature coronary atherosclerosis appear to be important mediators of major plasma oxidative damage.
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PMID:Intense lipid peroxidation in premature clinical coronary atherosclerosis is associated with metabolic abnormalities. 1496 65

In recent years, it has been reported that the acute-phase proteins C-reactive protein(CRP) and serum amyloid A(SAA), the sera levels of which are elevated in inflammation, are also elevated in coronary artery disease such as acute myocardial infarction. Also, high-sensitivity CRP assay is thought to be useful in predicting the prognosis of coronary heart disease. While investigating complexes of acute-phase proteins and low-density lipoprotein(LDL), we found a complex of LDL and SAA(SAA/LDL complex). The SAA/LDL complex in blood are formed from LDL and HDL by an oxidation reaction. Therefore, we developed an ELISA using anti-human SAA antibody and anti-human apoB, and determined a new method for measuring SAA/LDL complex in sera. We evaluated SAA/LDL complex as a new marker for prediction of prognosis in addition to the ordinary markers in consecutive 140 patients with stable coronary heart disease who had at least 1 coronary artery stenosis more than 50% in diameter at the diagnostic coronary angiography. Of these 140 patients, 2 developed fatal myocardial infarction, 2 cerebral infarction, and 17 angina pectoris requiring coronary revascularization therapy during 1 year and 6 months after blood examinations. The SAA/LDL complex value in this EVENT group of 21 patients was significantly higher than that in the control group of 119 individuals. High-sensitivity CRP (hs-CRP) assay and SAA measurement showed no significant difference between the 2 groups. The SAA/LDL complex reflects intravascular inflammation directly and can be a new marker more sensitive than hs-CRP or SAA for prediction of prognosis in patients with stable coronary artery disease.
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PMID:[Development of blood examination method of serum amyloid A and LDL complex, and clinical application to prediction of cardiovascular event]. 1496 63

C-reactive protein (CRP) mRNA was detected in coronary plaque. Plasma CRP levels across the coronary circulation were increased much more in patients with unstable angina pectoris and somewhat more in those with stable angina pectoris compared with controls whose coronary arteries were angiographically normal. Thus, CRP within coronary plaque might contribute to increased plasma CRP levels across coronary circulation, particularly among patients with unstable angina pectoris.
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PMID:Possible contribution of C-reactive protein within coronary plaque to increasing its own plasma levels across coronary circulation. 1499 90


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