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 aim of this study was to investigate the effects of stent carbon coating on inflammatory response. The authors serially measured plasma concentrations of C-reactive protein (CRP), fibrinogen, and several cytokines (tumor necrosis factor, interleukin [IL]-1-beta, IL-6, and IL-8) in patients with single-vessel coronary stenosis who underwent primary stent implantation. None of the subjects had inflammatory or infectious disease at the time of the procedure. Forty-six patients (38 males; mean age 55 +/-9 years) were studied. Blood samples were collected before and at 2, 4, 6, 24, and 48 hours after stent implantation. Patients were randomly assigned 1 of 2 different stent types, an uncoated MAC (AMG Raesfeld-Erle, Germany) (UC-MAC) or a carbon-coated MAC (CC-MAC) stent. Implantations were performed without predilatation, and stents were deployed at a maximum pressure of 6 atmospheres for 90 seconds. Of the 46 patients, 14 had stable, 27 had unstable, and 5 had atypical angina. According to ACC/AHA classification, 35 lesions (76.1%) were type A, 10 (21.7%) were type B, and 1 (2.2%) was type C. Single stenosis of 28 left anterior descending, 12 circumflex, and 6 right coronary arteries were treated. Serum IL-6 increased in both the UC-MAC and CC-MAC groups, with concentrations significantly elevated above baseline at 6 hours, and then decreasing after 24 hours (baseline, 6-hour, and 24-hour values = 3.1 +/-2.3, 5.7 +/-3.8, and 6.3 +/-4.6 pg/mL, respectively, in UC-MAC; 3.7 +/-2.6, 6.2 +/-6.0, and 4.6 +/-3.7 pg/mL, respectively, in CC-MAC [p=0.002]). Plasma fibrinogen, CRP, and leukocyte concentrations also increased in both groups over the 24 hours (p < 0.05). The elevations of IL-6, CRP, and fibrinogen were similar in the 2 groups. The percent increases in IL-6, fibrinogen, and CRP were not associated with stent length, size, or clinical presentation (all p > 0.05). The results showed that stent implantation increases plasma IL-6, fibrinogen, and CRP concentrations, but carbon coating of the stent does not seem to affect this inflammatory response.
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PMID:Carbon coating of stents has no effect on inflammatory response to primary stent deployment. 1236 64

Patients with sleep disordered breathing (SDB) are at increased risk for cardiovascular disease including hypertension, angina, myocardial infarction, and stroke. Neurohumoral and hemodynamic responses to untreated sleep apnea are likely mechanisms that produce functional and structural changes within the cardiovascular system. Obesity, higher blood pressure, and advancing age, which are common characteristics of patients with SDB, contribute to the overall risk for cardiovascular disease. Recent studies indicate that OSA is associated with or aggravates other risk markers for cardiovascular disease. These factors include leptin, C-reactive protein, homocysteine, and insulin resistance syndrome. Elevations in C-reactive protein and glucose intolerance may be correlated with the severity of SDB. The impact of alleviating SDB on these cardiovascular risk factors has not been fully elucidated. Regardless, assessment of overall cardiovascular risk in patients with sleep apnea is warranted to identify those individuals that are high-risk who require immediate attention and intervention or in those that should be treated more aggressively.
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PMID:Sleep disordered breathing and risk factors for cardiovascular disease. 1239 60

Inflammatory mechanisms are central in human atherosclerosis. Although C-reactive protein (CRP) as a serum marker is highly predictive for cardiovascular events, the intimal expression of CRP in clinically relevant coronary lesions is unknown, in particular in acute coronary syndromes (ACS). Shown by reduced CRP serum values, statins have antiinflammatory and plaque-stabilizing effects. In the present study, the presence of CRP in coronary atheromas with ACS versus stable angina (SA) as well as its possible modification by chronic statin medication was assessed. Coronary atherectomy probes from 90 primary stenoses were immunohistochemically analyzed with regard to the presence and the localization of CRP. Intimal results of patients with ACS (n=36), categorized according to the Braunwald classification, were compared with those of patients with SA (n=54). In 40 of 90 lesions (44%), immunoreaction specific for CRP was observed demonstrating a mean CRP expression of 1.7%. CRP was focally localized in a maximum of 69% of all plaque cells, the most in macrophages/foam cells, infrequently in smooth muscle cells. CRP-positive plaques showed more thrombus than plaques without CRP (63% vs 41%). Intact non-atherosclerotic control tissue revealed no signaling. As a central finding, intimal presence and expression were higher (each p<0.001) with ACS (69% and 3.1%, respectively) compared to SA (28% and 0.8%, respective). Subgroup analysis of target lesions associated with ACS according to the clinical Braunwald classification showed an increase of intimal CRP with classes I-III. In the presence of statin medication, intimal CRP was significantly lower than that without statin therapy (29 and 1.3%, vs 61 and 2.6%, respectively; p<0.01), in particular in the subgroup of ACS patients. Intimal CRP is frequently found in coronary primary stenoses, very often with macrophages/foam cells, and shows a highly significant prevalence with ACS. In this subgroup of patients, statin therapy is associated with significantly reduced intimal CRP. Our in situ findings as shown might explain the well-known serum constellations with statin therapy.
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PMID:[C-reactive protein in coronary plaques -- prevalence with acute coronary syndrome]. 1244 94

We analyzed the concentrations of interleukins (IL)-6, IL-10, IL-12, and IL-18, interferon (IFN)-gamma, and high-sensitivity C-reactive protein (hsCRP) in 40 patients with unstable angina (UAP), 39 patients with stable angina (SAP), and 52 age- and gender-matched controls. Compared with the control group, IL-12 concentrations were significantly higher in both the SAP and UAP groups, especially in the UAP group, and the IL-18 concentrations tended to be higher in the UAP group. Conversely, IL-10 concentrations were significantly lower in the SAP and UAP groups. Both IL-6 and hsCRP concentrations were significantly higher in the UAP group. The levels of hsCRP were positively correlated with inflammatory or proinflammatory cytokines (IL-6, IL-12, and IL-18), and negatively correlated with anti-inflammatory cytokine (IL-10). Moreover, the levels of IL-12 were positively correlated with IL-18, and negatively correlated with IL-10, and the results revealed the T-helper 1 dominant state. These results suggested that the inflammatory response was strongly associated with coronary atherosclerosis and angina pectoris, and that the T-helper 1 dominance may play an important role in these diseases.
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PMID:Concentrations of interleukins, interferon, and C-reactive protein in stable and unstable angina pectoris. 1508 94

The aim of this study was to assess the relations between inflammation, immune response, and coronary angiographic findings in patients with unstable angina pectoris (UAP). Recent studies suggest a role for inflammation in the pathophysiology of UAP. Although activation of neutrophils, monocytes and lymphocytes has been shown in UAP, no studies have correlated the activation findings with clinical and angiographic features of patients with UAP. Seventy-three patients undergoing coronary angiography were classified according to their ischaemic syndrome, stable angina pectoris (SAP) (n = 25) and UAP (n = 48). Patients with UAP were classified using the Braunwald classification; UAP class I (n = 15), UAP class II (n = 15), and UAP class III (n = 18). Patients with UAP were also classified into a progression to myocardial infarction (MI (+)) group (n = 15) and a non-progression to myocardial infarction (MI(-)) group (n = 33). Venous blood samples were taken from all patients. Cell surface receptors (CD4, CD8, CD3, CD14, CD45, CD56+16, and HLA-DR) were detected by flow cytometry using monoclonal antibodies tagged with fluorescent markers and serum levels of C-reactive protein (CRP) were measured. The serum levels of CRP and the percentages of HLA-DR, CD14, and CD16+56 were higher in UAP than SAP. The serum levels of CRP and percentages of HLA-DR, CD14, and CD16+56 were higher in UAP class II than UAP class I. The serum levels of CRP and percentages of HLA-DR, CD14, and CD16+56 were higher in UAP class III than UAP class II and UAP class I. The serum levels of CRP and percentages of CD16+56 were higher in the MI(+) group than the MI(-) group. The CRP levels in serum and the percentages of cell surface antigens had no correlation with extent of coronary artery disease (no differences among one, two or three vessels) but Type C lesion had significantly higher percentages of HLA-DR, CD14, CD16+56 and the serum levels of CRP than Type A and Type B lesions. This investigation shows that inflammatory and immunologial components may be detectable in UAP and were correlated with the clinical severity, progression to myocardial infarction, and lesion morphology, but were not correlated with the extent of coronary artery disease.
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PMID:Inflammation and immune system response against unstable angina and its relationship with coronary angiographic findings. 1255 24

We investigated whether positive immunohistochemical staining of C-reactive protein (CRP) in initial culprit lesions is related to coronary plaque instability and whether it could affect the outcome of directional coronary atherectomy (DCA). The plasma level of CRP is a reliable marker of the risk of coronary events and restenosis after percutaneous coronary intervention. However, the influence of tissue CRP in atheromatous plaque on plaque vulnerability and restenosis remains unknown. Samples of DCA obtained from 12 patients with stable angina pectoris and 15 patients with unstable angina pectoris were immunohistochemically stained with a monoclonal antibody against CRP. We performed follow-up coronary angiography on 22 of 27 patients to evaluate the presence of restenosis after DCA. Immunoreactivity to CRP was localized to macrophages, smooth muscle cells, and necrotic areas. The ratio of CRP positive cells to total cells was significantly higher in DCA samples from patients with unstable (17.9 +/- 2.0%) than with stable angina (11.0 +/- 2.5%) (p <0.05). Follow-up coronary angiography showed that 12 of 22 patients developed restenosis after DCA. The ratio was also significantly higher in DCA specimens from patients with restenosis (19.3 +/- 2.8%) compared with those without restenosis (11.0 +/- 2.0%) (p <0.05). In addition, the ratio significantly correlated with late luminal loss (r = 0.428, p <0.05) and loss index (r = 0.636, p = 0.0011) after DCA. Immunoreactivity to CRP in coronary atheromatous plaque increases in culprit lesions of unstable angina, and it affects restenosis after DCA. These findings suggest that CRP in atheromatous plaque plays an important role in the pathogenesis of unstable angina and restenosis after coronary intervention.
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PMID:Involvement of C-reactive protein obtained by directional coronary atherectomy in plaque instability and developing restenosis in patients with stable or unstable angina pectoris. 1256 84

It is known that local and systemic inflammatory processes play an important role in the genesis and development of atheroclerotic lesions and in the pathophysiology of acute coronary syndromes. This hypothesis is supported by findings of elevated parameters of the "inflammatory" reaction in the affected blood vessels but also in the blood of atherosclerotic patients. Known risk factors do not explain quite satisfactorily epidemiological cardiovascular phenomena and different manifestations of coronary heart disease. It is very probable that also Chlamydia pneumoniae is a risk factor. This assumption is based on evaluation of seroepidemiological data, examination of atherosclerotic plaques not only in humans but also in animal models with chlamydial infection. Based on retrospective and prospective evaluation of case-records the authors analyzed the incidence of cardiovascular complications in 83 patients with acute myocardial infarction (AIM), incl. 51 patients (31 men and 20 women, mean age 64.4 +/- 3.4 years who had a non-specific inflammation and chlamydial infection, and 32 patients (24 men and 8 women, mean age 64.7 +/- 3.6 years) who had chlamydial infections but no non-specific inflammation (in the blood). These patients were selected from all patients hospitalized during 1998-2001. When diagnosing acute myocardial infarction we applied WHO criteria, and the presence of at least two of three criteria was necessary: a history of prolonged (more than 20 min). stenocardia, electrocardiographic changes typical for ischaemia and/or necrosis and elevation of myocardial enzymes in serum, Non-specific inflammatory activity was present in patients (i.e. positive) if the following laboratory parameters were recorded: C-reactive protein > 5 mg/l assessed by the radial immunodiffusion method; fibrinogen > 4 mg/l assessed by the coagulation method according to Claus; leukocytes > 9.6 x 10(3)/microliter, leukocytes were counted automatically in a Coulter chamber; lymphocytes > 3.4 x 10(3)/microliter. Red cell sedimentation rate > 20 mm/hour. The activity was evaluated as positive when all parameters were elevated. The presence of chronic infection with Chlamydia pneumoniae was assessed qualitatively by antibody positivity (IgG) in serum using the microimmunoflurescent method (using a set from Labsystems Co.). The incidence of associated risk factors (obesity, smoking, diabetes, hyperlipidaemia and hypertension) is higher in the sub-group of patients with Chlamydia infections without inflammation, however, the difference is not statistically significant. The incidence of cardiovascular attacks was higher in the sub-group of patients with chlamydial infection and concurrent inflammation as compared with the sub-group of patients with chlamydial infection without inflammation. In case of re-infarction of the myocardium, a sudden cerebrovascular attack, death and arrhythmia the difference was statistically significant, while in case of cardiac failure and cardiogenic shock the difference was not significant. Patients with acute myocardial infarction with chlamydial infection and a concurrent non-specific inflammation had to be treated more often by combined (i.e. more intense) treatment, thrombolytic treatment, PTCA and surgery (bypass) of the coronary vessels as compared with patients with Chlamydia infections but without inflammation. The authors assume therefore that not only different risk factors but also the effect of non-specific inflammation and Chlamydia infection contribute towards the increased number of cardiovascular postinfarction complications. Therefore a therapeutic approach involving eradication of infection and suppression of the inflammatory reaction should be considered.
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PMID:[Effect of chronic Chlamydia infection with non-specific inflammation on cardiovascular complications in acute myocardial infarct]. 1272 71

Coronary lesion instability at the onset of acute myocardial infarction (AMI) was evaluated. The mechanism of AMI has been considered to be coronary lesion instability with occlusive thrombus, although more than one half of AMI occurs in clinically stable patients. A total of 313 AMI patients treated by primary percutaneous transluminal coronary angioplasty with provisional stenting (rate, 41%) were studied. They were divided into 2 groups: group 1A (n = 211), without unstable angina before AMI onset, and group 1B (n = 102), with unstable angina before onset. Moreover, angina patients treated similarly were studied: group 2A (n = 180), with stable angina, and group 2B (n = 204), with unstable angina. Coronary lesion instability at AMI onset was also predicted by C-reactive protein (CRP) levels within 6 hours after onset, before they were affected by myocardial damage. The incidence of repeated AMI and/or target vessel revascularization was 1.9% in group 1A, 7.8% in 1B (p=0.035), 1.7% in 2A, and 5.9% in 2B (p=0.043). Event-free survival curves were consistent with each other in groups 1A and 2A and in groups 1B and 2B. CRP levels on admission were 2.0 +/- 1.7 mg/L in group 1A, 3.3 +/- 4.8 mg/L in group 1B (p<0.001), 2.1 +/- 1.7 mg/L in group 2A, and 3.4 +/- 4.7 mg/L in group 2B (p<0.001). Thus coronary lesion characteristics at AMI onset appeared to be similar in groups 1A and 2A and in groups 1B and 2B. A substantial number of patients have stable culprit lesions at the onset of AMI.
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PMID:Clinical evaluation of coronary lesion characteristics in acute myocardial infarction. 1278 20

Certain markers of systemic inflammation are powerful predictors of cardiovascular events. Fibrinogen, C-reactive protein (CRP), and cytokines are among the inflammatory markers associated with various cardiovascular end points. Fibrinogen and CRP both have been associated with coronary artery disease (CAD) mortality in patients with stable angina. High-sensitivity CRP (hs-CRP) and fibrinogen also have prognostic value in patients with unstable angina. In addition to prognostic implications, several cardiovascular risk factors (eg, smoking, obesity, diabetes) are associated with high levels of fibrinogen and hs-CRP. Benefits from aspirin are more likely in patients whose hs-CRP levels are very high. Some fibrates decrease fibrinogen levels and hs-CRP. Statin therapy either reduces the CAD risk associated with system inflammation or lowers circulating levels of hs-CRP.
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PMID:Utility of inflammatory markers in the management of coronary artery disease. 1286 50

This study investigates the association of several inflammatory markers with subclinical and clinical cardiovascular disease in older men and women. Data are from the baseline assessment of 3,045 well-functioning persons aged 70 to 79 years, participating in the Health, Aging and Body Composition study. The study sample was divided into 3 groups: "cardiovascular disease" (diagnosis of congestive heart failure, coronary artery disease, peripheral artery disease, or stroke), "subclinical cardiovascular disease" (positive findings on the Rose questionnaire for angina or claudication, ankle-brachial index <0.9, or electrocardiographic abnormalities), and "no cardiovascular disease." Serum levels of interleukin (IL)-6, C-reactive protein (CRP), tumor necrosis factor (TNF)-alpha, and the soluble receptors IL-6 soluble receptor, IL-2 soluble receptor, TNF soluble receptor I, and TNF soluble receptor II were assessed. Of those with IL-6 levels in the highest compared with the lowest tertile, the odds ratio (OR) for subclinical cardiovascular disease was 1.58 (95% confidence interval [CI] 1.26 to 1.97) and for clinical cardiovascular disease was 2.35 (95% CI 1.79 to 3.09). A similar association was found for TNF-alpha (OR 1.48, 95% CI 1.16 to 1.88 and OR 2.05, 95% CI 1.55 to 2.72, respectively). In adjusted analyses, CRP was not significantly associated with overall subclinical or clinical cardiovascular disease, although additional analyses did find a strong specific association between CRP and congestive heart failure (OR 1.64, 95% CI 1.11 to 2.41). Of the soluble cytokine receptors, only TNF soluble receptor I showed a significant association with clinical cardiovascular disease. Thus, our findings suggest an important role for IL-6 and TNF-alpha in clinical as well as subclinical cardiovascular disease. In this study, CRP had a weaker association with cardiovascular disease than the cytokines.
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PMID:Inflammatory markers and cardiovascular disease (The Health, Aging and Body Composition [Health ABC] Study). 1294 70


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