UMLS:C0002962 - FACTA Search

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 complement system is part of the host defence response. However, considerable evidence suggests that complement plays an important role in the pathophysiology of ischemic heart disease. The aim of this study was to evaluate complement activation in patients with all forms of acute coronary syndromes (ACS) and to examine the relationship between the degree of complement activation and myocardial injury. The study population included 152 subjects (26 females): 82 with ACS (35 acute myocardial infarction (AMI), 22 non-Q wave MI (NQMI), 25 unstable angina (UAP)) (Group A), 35 stable angina (SA) (Group B), and 35 healty control subjects (Group C). Complement 3 (C3), Complement 4 (C4), C-reactive protein (CRP), troponin I (TnI) as well as creatine kinase MB (CK-MB) were evaluated. Patients' blood samples were taken on admission (day 1) and after 2, 3 and 7 days in group A. However, only one measurement was performed in the groups B and C. Plasma C3 and C4 peak levels were significantly higher in patients with AMI (141+/-29 and 35+/-11 mg/dl) and NQMI (136+/-13 and 35+/-7 mg/dl) than in patients with SA (128+/-14 and 27+/-10 mg/dl) and the control subjects (114+/-22 and 22+/-7 mg/dl) (p<0.03). Also, C3 and C4 serum levels in patients with SA and UAP (126+/-16 and 31+/-7 mg/dl) were significantly higher than those in control subjects (p<0.01, p<0.03, respectively). At 1-week follow-up, there were no significant differences between the plasma levels of C3 and C4 in patients with UAP (p>0.05). However, plasma levels of C3 and C4 were significantly different between days in patients with AMI and NQMI (p<0.0001). Plasma C3 and C4 levels in ACS showed a relationship with peak CK-MB and Tn I levels (p<0.01). Plasma CRP level in ACS showed positive correlation with C3 (p<0.01) and C4 (p<0.001). In this study, we determined that plasma C3 and C4 levels were elevated in ACS and SA. Although C3 and C4 were higher in ACS and SA, the systemic levels of inflammatory markers in patients with SA and UAP were lower than those found in the AMI and NQMI groups. The relationship between C3, C4 levels and ACS further suggests that the complement activation is related to necrosis within the myocardium.
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PMID:Complement activation in acute coronary syndromes. 1579 59

The purpose of the study was to determine clinical importance of high serum levels of ferritin, fibrinogen and C-reactive protein (CRP) in patients with various forms of coronary heart disease (CHD) such as stable angina, painless myocardial ischemia (PMI) and instable angina (IA). The subjects of the study were 60 patients with CHD, whose clinical variant (stable angina, PMI or IA) had been determined by stress echocardiography. The control group consisted of 20 patients, not suffering from CHD, but having cardiovascular risk factors (arterial hypertension, dyslipoproteinemia, male gender, obesity, elderly age). All patients underwent routine clinical examination and biochemical blood tests. Serum levels of CRP, fibrinogen and ferritin were highest in the patients with IA and significantly differed from those in the control group. The difference in serum iron levels and total iron-binding capacity in serum (TIBC) between the groups were insignificant. Correlations between serum level of iron, TIBC and ferritin level were found neither in CHD patients (r = 0.1) nor in the control group (r = 0.15). No correlation between serum level of ferritin and CRP level was observed in the control group, but in all CHD groups this correlation was significant. The strongest correlation between these values was observed in the patients with IA. Besides, correlations between serum levels of ferritin and CRP (r = 0.46, p < 0.02) and between ferritin and fibrinogen levels (r = 0.39, p < 0.05) were found in the patients with IA. In patients with CHD, especially those who have IA, serum ferritin should be considered among acute phase proteins, reflecting destabilization of atherosclerotic plaque.
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PMID:[Ferritin and other acute phase proteins in various forms of coronary heart disease]. 1580 27

The aim of this study was to show clinical benefit of simultaneous determinations of troponin I (cTnI) and high sensitivity C-reactive protein (hsCRP) at early diagnosis in the group of patients with stenocardia admitted to the Emergency Unit of 5-th Military Hospital in Krakow. The study group consisted of 38 (51.3%) patients with acute myocardial infarction (AMI) and 36 (48.6%) with unstable angina pectoris. ROC function analysis for cTnI (cutoff value 0.69 ng/mL) and hsCRP (3.33 mg/L) indicated significant amelioration of diagnostic sensitivity into 84.9% at early diagnostics of AMI in group of patients with acute coronary syndrome (ACS). Moreover, studies of mutual relationship between elevated levels of hsCRP and cTnI concentrations have shown a remarkably positive correlation (r = 0.90; p < or = 0.01) in the group of patients with AMI.
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PMID:[The role of serum troponin I and high sensitivity C-reactive protein concentrations in early diagnosis of acute coronary syndrome in patients admitted to Emergency Unit]. 1580 96

Low-grade inflammation as detected by increased C-reactive protein (CRP) levels predicts the risk of cardiovascular events. However, there is still controversy over the mid-term predictive value of CRP in patients referred for elective percutaneous coronary revascularization (PCI) for stable angina pectoris. The aim of this study was to assess the relationship between baseline CRP level and mid-term outcome of patients undergoing PCI. Two groups of patients with stable angina pectoris were prospectively studied. Group A consisted of 150 consecutive patients with a CRP level < or = 3 mg/L, and group B consisted of 150 consecutive patients with a CRP level > 3 mg/L undergoing PCI at our institution. Comparing both groups of patients, the analysis confirmed a significant difference between medians of the CRP levels (0.5 versus 8 mg/mL; P < 0.001). A higher level of CRP in group B was associated with a lower presence of male gender (P < 0.05) and history of myocardial infarction (P < 0.05). On the other hand, in group B there was higher occurrence of smoking (P < 0.001), hypertension (P < 0.05), hypertriglyceridemia (P < 0.001), and diabetes mellitus (P < 0.01). The incidence of myocardial infarction based on post-interventional release of TnI > 1.5 ng/mL reached 12% in group A and 14% in group B (P = 0.73). Analyses were repeated with adjustment for significant baseline variables, which did not change our findings. The incidence of adverse cardiovascular events during a six month follow-up was 13% in both groups (NS). Increased CRP serum prior to PCI was not associated with the risk and extent of procedure-related myocardial injury measured by TnI release and does not portend heightened cardiovascular risk at six months after percutaneous revascularization. On the other hand, a CRP level > 3 mg/L was associated with a higher occurrence of cardiovascular risk factors (smoking, hypertension, hypertriglyceridemia, and diabetes mellitus).
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PMID:Relationship of C-reactive protein to adverse cardiovascular events in patients treated by percutaneous coronary intervention for stable angina pectoris. 1587 3

The effects of nifedipine on inflammation and endothelial function in the coronary circulation were studied in patients who had angina pectoris (n = 17). Long-term treatment with nifedipine (nifedipine CR, 20 mg/day for 4 months) decreased levels of C-reactive protein in the coronary sinus (from 0.35 +/- 0.09 mg/dl to 0.07 +/- 0.01 mg/dl, mean +/- SEM, p <0.05) and enhanced acetylcholine-induced increases in coronary blood flow. Thus, nifedipine is effective in decreasing inflammation and incresing endothelial function in the coronary circulation.
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PMID:Effect of nifedipine on C-reactive protein levels in the coronary sinus and on coronary blood flow in response to acetylcholine in patients with stable angina pectoris having percutaneous coronary intervention. 1587 99

Interleukin 6 (IL-6) may represent an early marker of inflammatory activation and may be useful to ameliorate risk stratification in patients with ischemic heart disease. The aim of this study was to verify the performance characteristics of an ultrasensitive immunoassay (Biosource International, Camarillo, CA) for high-sensitivity (hs)-IL-6 measurement in comparison with hs-R&D Systems (Abingdon, United Kingdom) and Immulite System (Diagnostic Products Corporation [DPC], Los Angeles, CA) methods in patients with ischemic heart disease. In addition, hs-C-reactive protein (hs-CRP) concentrations were measured, to evaluate the correlation with hs-IL-6 levels. We measured IL-6 and CRP serum levels in 39 patients with ischemic heart disease and in 12 controls. Out of the 39 patients studied, 13 were affected by unstable angina, 13 by post-acute myocardial infarction (AMI) unstable angina, and 13 by stable angina. The imprecision profile and functional sensitivity were performed measuring 9 different serum pools in 10 runs. The Biosource method had the best performance characteristics as compared to the others. Mean IL-6 level was higher in patients with unstable and post-AMI unstable angina with respect to controls. CRP levels were elevated in patients with post-AMI. In the whole population a high significant linear regression was observed between Biosource hs-IL-6 and hs-CRP serum levels. The Biosource method for IL-6 measurement is characterized by a high functional sensitivity that allows a better stratification of patients with ischemic heart disease.
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PMID:Usefulness of high-sensitivity IL-6 measurement for clinical characterization of patients with coronary artery disease. 1590 May 66

The material composition and morphology of the atherosclerotic plaque components are considered to be more important determinants of acute coronary ischemic syndromes than the degree of stenosis. When a vulnerable plaque ruptures it causes an acute thrombotic reaction. Rupture prone plaques contain a large lipid pool covered by a thin fibrous cap. The stress in these caps increases with decreasing thickness. Additionally, the cap may be weakened by macrophage infiltration. IntraVascular UltraSound (IVUS) elastography might be an ideal technique to assess the presence of lipid pools and to identify high stress regions. Elastography is a technique that assesses the local elasticity (strain and modulus) of tissue. It is based on the principle that the deformation of tissue by a mechanical excitation is a function of its material properties. The deformation of the tissue is determined using ultrasound. For intravascular purposes, the intraluminal pressure is used as the excitation force. The radial strain in the tissue is obtained by cross-correlation techniques on the radio frequency signals. The strain is color-coded and plotted as a complimentary image to the IVUS echogram. IVUS elastography, and IVUS palpography (which uses the same principle but is faster and more robust), have been extensively validated using simulations and by performing experiments in vitro and in vivo with diseased arteries from animals and humans. Strain was shown to be significantly different in various plaque types (absent, fatty, fibrous or calcified). A high strain region with adjacent low strain at the lumen vessel-wall boundary has 88% sensitivity and 89% specificity for detecting vulnerable plaques. High strain regions at the lumen plaque-surface have 92% sensitivity and 92% specificity for identifying macrophages. Furthermore, the incidence of vulnerable-plaque-specific strain patterns in humans has been related to clinical presentation (stable angina, unstable angina or acute myocardial infarction) and the level of C-reactive protein. In conclusion, the results obtained with IVUS (strain and modulus) elastography/palpography, show the potential of the technique to become a unique tool for clinicians to assess the vulnerability and material composition of plaques.
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PMID:Intravascular Ultrasound Elastography: A Clinician's Tool for Assessing Vulnerability and Material Composition of Plaques. 1592 38

To assess the value of serial C-reactive protein (CRP), serum amyloid A (SAA), tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) evaluation in the risk stratification in patients undergoing percutaneous coronary intervention. The study was designed as a prospective cohort trial with a 1-year follow-up. Eighty patients (70 with stable angina, 10 with unstable angina) were enrolled. Blood samples were collected before the procedure and after 6 and 24 h, and 1 month. Clinical follow-up visits were performed (*with exercise test) 7 days* and 1*, 3, 6* and 12 months after the procedure. Any symptoms of restenosis were verified angiographically. Multivariate logistic regression analysis identified increased preprocedural TNF-alpha and CRP levels and elevated CRP concentrations evaluated 24 h after the procedure as significant predictors of both clinical restenosis and major adverse cardiac events (MACE), while high SAA values at 24 h accurately predicted clinical restenosis. Patients, who were in the highest tertile of, either, baseline TNF-alpha and/or baseline CRP/CRP at 24 h, were more prone to develop restenosis and MACE than stratified only on the basis of a single marker. Our data indicate that combined analysis of CRP and TNF-alpha might be an effective approach to the clinical restenosis and MACE prediction. Additionally, long-term outcome is markedly influenced by the periprocedural activation of inflammation.
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PMID:Combined periprocedural evaluation of CRP and TNF-alpha enhances the prediction of clinical restenosis and major adverse cardiac events in patients undergoing percutaneous coronary interventions. 1594 95

Atherosclerosis is a diffuse, systemic process. In addition, acute coronary syndromes (ACS) are associated with inflammatory marker elevations that are hypothesized to affect the function of nonculprit coronary as well as peripheral vessels. We investigated whether femoral vascular reactivity and/or fibrinolytic capacity are impaired in ACS patients over and above any dysfunction associated with stable coronary artery disease. Patients undergoing diagnostic coronary angiography (n = 42 total, 14 patients/group) were recruited into three groups as follows: 1) stable coronary syndromes (SAP group), 2) ACS as defined by rest angina with ECG changes and troponin rise (ACS group), and 3) angiographically normal coronary arteries (control group). After diagnostic coronary angiography, femoral artery endothelial and smooth muscle function were assessed by infusing acetylcholine (ACh) and nitroglycerin (GTN), and tissue-type plasminogen activator (t-PA) release across the femoral circulation was measured as the difference between arterial and venous concentrations before and after ACh and GTN stimulation. There were no significant differences between groups in relevant baseline characteristics apart from significantly higher C-reactive protein levels and reduced net t-PA release in the ACS group at baseline (P < 0.05). The ACS and SAP groups had equivalent angiographic severity of coronary artery disease. Endothelium-dependent dilatation was significantly higher in control individuals (14.9 +/- 9.1%; P < 0.001) compared with either stable patients (2.3 +/- 8.1%) or those with unstable syndromes (2.6 +/- 8.9%, who were similar to each other; P = not significant). Although baseline t-PA release was impaired in the ACS patients (0.09 +/- 0.06 compared with 0.39 +/- 0.33 and 0.49 +/- 0.56 ng/ml; P = 0.03), stimulation of t-PA release by ACh and GTN occurred only in the control subjects and not in the ACS or SAP patients. Coronary artery disease is associated with impaired endothelium-dependent dilatation and impaired stimulation of t-PA release in the systemic circulation. These aspects of endothelial dysfunction, however, were equally severe in acute and chronic coronary syndrome patients.
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PMID:Endothelial dysfunction occurs in peripheral circulation patients with acute and stable coronary artery disease. 1601 11

The pathogenesis of ischemic coronary events involves degradation of the extracellular matrix in atherosclerotic lesions. The cysteine protease inhibitor cystatin-C may be involved in this phenomenon. The association of plasma cystatin-C with the incidence of myocardial infarction-coronary death and angina, was examined in a nested case-control (two controls per case) design within the prospective cohort study (Prospective Epidemiological Study of Myocardial Infarction (PRIME Study)) which included 9,758 men aged 50-59 years who were free of coronary heart disease (CHD) on entry and followed for a 5-year period. Three hundred and thirteen participants suffered myocardial infarction or coronary death (n = 159) or angina pectoris (n = 154) during follow-up. Cystatin-C was positively correlated with body mass index (BMI), low-density lipoprotein (LDL)-cholesterol, triglycerides and several inflammatory markers such as fibrinogen (r = 0.18), C-reactive protein (CRP) (r = 0.24), interleukin-6 (= 0.20), tumor necrosis factor-alpha (TNFalpha) (r = 0.27) and two TNFalpha receptors: TNFR1A (r = 0.43) and TNFR1B (r = 0.41); and negatively with high-density lipoprotein (HDL)-cholesterol (r = -0.25). After adjustment for traditional risk factors (age, diabetes, smoking, hypertension, BMI, triglycerides, LDL- and HDL-cholesterol), cystatin-C was significantly associated with the occurrence of the first ischemic coronary event. However, this association was no longer significant when CRP was included in the analysis. A decrease in glomerular filtration rate did not explain higher cystatin-C in cases than in controls. Cystatin-C appears to participate in the inflammatory phenomenon observed in the atherosclerotic process. Cystatin-C is not a more predictive risk marker of CHD than CRP or interleukin-6, but could be useful in detecting moderate chronic renal disease.
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PMID:Plasma cystatin-C and development of coronary heart disease: The PRIME Study. 1604 22

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