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)

It is unknown whether the pathogenetic mechanisms underlying acute myocardial infarction (AMI) differ according to the clinical presentation of preinfarction angina, so the present study measured plasma levels of C-reactive protein (CRP) in 280 patients with AMI in whom serum creatine kinase levels were normal on admission and increased subsequently. Patients were classified into 3 groups according to the type of preinfarction angina: no angina (n=95), stable angina (n=48), and unstable angina (n= 137). Patients with unstable angina were subdivided according to the Braunwald classification: class IB (n=39), class IIB (n=22), and class RIB (n=76). There were no differences among the 5 groups in baseline characteristics. CRP on admission was significantly higher and the level of physical activity at symptom onset was significantly lower in the Braunwald class RIB group than in the other groups, but no differences were observed among the other groups. Patients with preinfarction Braunwald class IIB unstable angina had higher CRP levels on admission and symptom onset at a lower level of physical activity. In such patients, the pathogenetic mechanisms may differ from those in other subsets of patients with AMI and active inflammation may play a more important role in AMI onset.
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PMID:Differences in inflammatory activity at the onset of acute myocardial infarction according to the clinical presentation of preinfarction angina. 1150 46

Risk stratification of patients with acute coronary syndromes (ACS) is pivotal for correct allocation of health resources and for maximizing the benefit of available treatment modalities. However, clinical and electrocardiographic indicators of high risk lack sufficient sensitivity for the detection of major cardiac events. The complementary information provided by the measurement of different biomarkers is believed to be very useful. Specifically, elevations of cardiac troponin I (cTnI) and T (cTnT) are strongly associated with a high-risk profile both at short- and long-term. This has been definitely demonstrated in many studies as well as in cumulative meta-analysis. The role of different biomarkers, such as those reflecting activation of hemostasis and the presence of inflammation, is however less defined. At the moment, no study has prospectively evaluated these biomarkers in the whole spectrum of unselected patients with ACS. It is also unclear whether these biomarkers add independent prognostic value to the clinical and electrocardiographic indicators of adverse outcome and whether they offer additional information when compared to each other. The Early Prognostic Value of Biochemical Markers of Myocardial Damage, Activation of Hemostatic Mechanism and Inflammation in Acute Ischemic Syndromes (EMAI) study has been prospectively designed to solve these issues. In this study, we have evaluated the prognostic value of cTnI and cTnT, D-dimer, prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT) and C-reactive protein (CRP) in patients with ACS at the time of admission. We have enrolled in 31 Italian Coronary Care Units 1971 patients with rest anginal pain within 12 h from admission and electrocardiographic evidence of myocardial ischemia. Of these, 730 patients resulted to have ST-segment elevation myocardial infarction eligible for a reperfusion strategy and 1241, an acute coronary syndrome without persisting ST-segment elevation. Primary outcome measure of the study is the composite of death and non-fatal MI within 30 days from admission, which has occurred in 8.9% of the study population.
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PMID:Cardiac markers and risk stratification: an integrated approach. 1155 47

The aim of the study was to evaluate the effects of the presence, extent, and clinical stability of coronary artery disease on endothelial function parameters, C-reactive protein and homocysteine levels. Fifty-eight patients with angiographically documented coronary artery disease and 25 patients with normal coronary arteries were evaluated for risk factors, plasma homocysteine, C-reactive protein, and soluble adhesion molecule levels. Vascular cell adhesion molecule-1 and sE-selectin were significantly higher in the group with coronary artery disease than in healthy subjects (p = 0.005 and p = 0.031, respectively). Patients with unstable angina had significantly higher C-reactive protein (p < 0.001), troponin I (p < 0.01), and leukocyte counts (p < 0.05) than those with stable angina. sE-selectin levels were correlated with the extent of coronary atherosclerosis (r = 0.444, p < 0.05), and plasma homocysteine levels were associated with vascular cell adhesion molecule-1 (r = 0.479, p < 0.05) in unstable cases. These results suggest that vascular cell adhesion molecule-1 and sE-selectin are useful for determining the presence of coronary atherosclerosis, whereas C-reactive protein, troponin 1, and leukocyte count are predictors of clinical stability.
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PMID:Extent of coronary atherosclerosis and homocysteine affect endothelial markers. 1157 Jun 57

The designation of atherosclerosis as a chronic inflammatory process represents an exciting and logical paradigm shift for cardiologists. Plasma concentrations of interleukin-6 (IL-6) and its hepatic by-product C-reactive protein (CRP) appear to reflect the intensity of occult plaque inflammation and by inference may determine vulnerability to rupture. Indeed, circulating IL-6 levels are elevated in patients with acute myocardial infarction (AMI), and also in patients with unstable, but not with stable angina. Coronary sinus IL-6 concentrations are also increased after percutaneous coronary intervention (PCI), and late restenosis correlates with an increase in IL-6 concentration after the procedure, indicating that IL-6 expression may be not only related to instability of atheromatous plaques, but also to the formation of restenotic lesions after PCI. These observations suggest the advantage of screening for circulating IL-6 concentration and the use of anti-inflammatory treatment for those thought be at high risk to reduce the risk of future AMI.
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PMID:Interleukin-6 and acute coronary syndrome. 1171 26

High-sensitivity C-reactive protein (CRP), proposed as a new coronary risk marker, may reflect either an acute phase reaction or the level of chronic inflammation. Thus, CRP may be less predictive of long-term outcomes when measured after acute myocardial infarction (AMI) than after unstable angina pectoris (UAP) or stable angina pectoris (SAP). A total of 1,360 patients with severe coronary artery disease (>/=1 stenosis >/=70%) had CRP levels obtained at angiography. Presenting diagnoses were SAP (n = 599), UAP (n = 442), or AMI (n = 319). During follow-up (mean 2.8 years), death or nonfatal AMI (D/AMI) occurred in 19.5%, 16.1%, and 17.2% (p = NS) with SAP, UAP, and AMI, respectively. Corresponding median CRP levels were 1.31, 1.27, and 2.50 mg/dl (p <0.001). For the overall cohort, increasing age, low ejection fraction, revascularization, and elevated CRP were the strongest of 6 independent predictors for D/AMI. Among those presenting with SAP, CRP levels above the first tertile were associated with an adjusted hazard ratio of 1.8 (95% confidence interval [CI] 1.2 to 2.8, p <0.009) for D/AMI. After UAP, the hazard ratio was 2.7 (95% CI 1.4 to 5.0, p <0.002). However, when measured during hospitalization for AMI, CRP was not predictive of long-term outcome (hazard ratio 1.0 [95 % CI 0.5 to 1.7] p = 0.86). In conclusion, predischarge CRP levels are higher after AMI than after UAP or SAP. However, whereas CRP is strongly predictive of long-term D/AMI for patients presenting with SAP or UAP, it is not predictive shortly after AMI, suggesting that measurements should be delayed until the acute phase reaction is over and levels have returned to baseline.
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PMID:Usefulness of high-sensitivity C-reactive protein in predicting long-term risk of death or acute myocardial infarction in patients with unstable or stable angina pectoris or acute myocardial infarction. 1179 32

Elevated C-reactive protein (CRP) can identify patients with coronary artery disease who are prone to future acute events. We investigated whether elevated CRP is related to the activation of the terminal complement cascade in 66 patients with unstable angina pectoris (UAP), in 45 patients with stable angina pectoris, and in 42 controls. CRP, additional acute phase reactants, the terminal complement complex (sC5b-9), leukocytes, and troponin T were measured. In 47 patients with UAP the CRP values were regarded as elevated (>0.3 mg/dl). In patients with UAP and elevated CRP, the plasma levels of sC5b-9 were markedly higher than in patients with UAP and lower CRP (245 +/- 14 vs 188 +/- 19 ng/ml, p <0.02) and in patients with stable angina pectoris with slightly (0.4 +/- 0.1 mg/dl) increased CRP (sC5b-9 173 +/- 21 vs 130 +/- 7 ng/ml [controls; p <0.05]). A further acute phase reaction was present only in patients with UAP and elevated CRP already on admission (p <0.01). sC5b-9 was not related to troponin release. Thus, elevated CRP levels are associated with activation of the plaque destabilizating terminal complement system in patients with UAP during the acute phase reaction. This may explain the prognostic value of CRP in acute coronary syndromes (ACS).
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PMID:Comparison of C-reactive protein and terminal complement complex in patients with unstable angina pectoris versus stable angina pectoris. 1195 Apr 26

Epidemiologic studies have suggested a relation between white blood cell (WBC) counts and the incidence of coronary heart disease. However, the relation between vasospastic angina pectoris (VAP) and WBC counts remains to be elucidated. To clarify the relation between differential and WBC counts in VAP, we compared the hematologic values, blood chemical values, plasma fibrinogen levels, C-reactive protein levels, and coronary risk factors in patients with spontaneous attacks of VAP (n = 39) with those in patients with stable effort angina pectoris (EAP, n = 35) and in control subjects (n = 19). Patients with VAP were further divided into mild VAP (n = 22) and severe VAP groups (n = 17). There were no differences in the coronary risk factors, body temperature, total WBC counts, and C-reactive protein levels among the control, EAP, mild VAP, and severe VAP groups, except that the high-density lipoprotein cholesterol in the EAP group was significantly lower than that in the control group (p <0.01). In contrast, the eosinophil counts were significantly higher in the severe VAP group than in the other 3 groups (p <0.01). Plasma fibrinogen levels were also significantly higher in the severe VAP group than in the other 3 groups (p <0.05). The follow-up study for differential and WBC counts in patients with VAP (n = 23) demonstrated that, after medical therapy, the eosinophil counts were significantly decreased to the some level as those in the control group (p <0.0001). Thus, the eosinophil counts and plasma fibrinogen levels could predict the severity of VAP. Furthermore, a follow-up study in patients with VAP suggests that coronary vasospasm could result in an increase in eosinophil counts.
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PMID:Eosinophil counts and plasma fibrinogen in patients with vasospastic angina pectoris. 1200 45

C-reactive protein (CRP) is a sensitive marker of inflammation, and elevated levels have been associated with future risk of cardiovascular events. To explore the role and relationship of CRP and coronary stenosis in the development of unstable angina (UA), plasma levels of CRP were determined on admission in 45 patients with UA, and in 42 patients with stable angina (SA) using high-sensitivity ELISA. Coronary angiography was performed in all patients with coronary heart disease (CHD), and severity of coronary stenosis was evaluated by a quantitative analysis. Lipid measurement was performed using automatic biochemical analyzer. Data available from patients with CHD were compared with those of 41 control subjects. The results showed that plasma levels of CRP are significantly higher in patients with UA than those in patients with SA and control subjects (5.1 +/- 1.4 mg/L vs 1.7 +/- 0.4 mg/L and 1.3 +/- 0.2 mg/L, p<0.01, respectively) with no difference between the latter two groups (p>0.05); the total incidence of clinical events during in-hospital follow-up was higher in the group A (p<0.01); the scores of coronary stenosis are significantly higher in patients with SA than those in patients with UA (4.9 +/- 2.1 vs 3.4 +/- 1.4, p<0.05); there is no correlation between plasma levels of CRP and serum total cholesterol (TC) as well as high-density lipoprotein cholesterol (HDL-C) in both groups (p>0.05 respectively); there was no correlation between plasma levels of CRP and severity of coronary stenosis was found in patients with UA (p>0.05) but a significant positive association in patients with SA (p<0.001); and the patients with persistent, severe, treatment-unresponsive UA had significantly higher CRP levels as well as incidence of clinical events than patients with treatment-responsive UA (7.4 +/- 1.8 mg/L vs 2.6 +/- 1.3 mg/L, p<0.01; 0 vs 22.2%, p<0.05). The present data suggested that inflammation may play an important role in the pathogenesis of UA, and the plasma levels of CRP might have a higher prognostic value than the severity of coronary stenosis correlated with the clinical outcome of instability despite of lipid profile status.
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PMID:Elevated level of plasma C-reactive protein in patients with unstable angina: its relations with coronary stenosis and lipid profile. 1202 13

Periprocedural levels of various inflammatory markers have been correlated with prognosis in patients undergoing percutaneous coronary interventions. However, long-term variations of interleukin-1 receptor antagonist (IL-1Ra) or C-reactive protein (CRP) during follow-up after coronary interventions were not previously investigated. The aim of our study was to perform serial evaluations of these markers before and after coronary stenting and to correlate them with clinical status. Plasma levels of IL-1Ra and CRP were measured at baseline and 3 and 6 months after the procedure in 31 patients with symptomatic coronary artery disease undergoing stent implantation, who had no evidence of myocardial ischemia at 6-month follow-up. While at 3 months there were no significant variations of baseline values, 6 months after the procedure a significant decrease from baseline was observed both in IL-1Ra and CRP levels (median -24 pg/ml, P = 0.048, and -0.13 mg/dl, P = 0.017, respectively). Six-month reduction in both IL-1Ra and CRP levels was significant in patients with unstable angina (n = 18; IL-1Ra: from 175 to 119 pg/ml, P = 0.001; CRP: from 0.52 to 0.18 mg/dl, P = 0.002) and nonsignificant in those with stable angina (n = 13) on admission (IL-1Ra: from 123 to 158 pg/ml, P = 0.22; CRP: from 0.19 to 0.10 mg/dl, P = 0.44). In conclusion, a significant reduction of IL-1Ra and CRP levels is observed 6 months after stent implantation in patients with preprocedural unstable angina who remain free of ischemia. This decrease suggests a stabilization of the inflammatory process and may be associated with a favorable prognosis after coronary interventions.
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PMID:Inflammatory markers and coronary interventions: a potentially useful follow-up modality after stenting. 1211 86

The aim of the study was the assessment of selected inflammatory markers in patients with stable and unstable angina pectoris, in comparison to patients with dyslipidemia without coronary artery disease. The study group included 61 patients (37-79 years old), divided into three subgroups: group I. 26 (43%) with unstable angina, group 2. 19 (26%) with stable angina, group III. 16 (26%) dyslipidemia without coronary artery disease. We measured serum levels of cytokines (IL-1B, IL-1Ra, IL-2, IL-6, TNF-alpha), immunoglobulins (IgG, IgE, IgM), fibrinogen. C-reactive protein and subclass of lymphocytes T CD4 and T CD8. In stable and unstable angina pectoris group we found lower percentage of T CD4, T CD8 and higher level of TNF-alpha. In unstable angina group the level of IL-1 beta was lower and the concentration of C-reactive protein, IgE was higher in comparison to group without coronary artery disease. Observed immunoregulatory disorders confirm immune mechanism in the origin of unstable angina pectoris.
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PMID:[Selected inflammatory markers in patients with acute coronary syndrome]. 1236 2


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