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)

Coagulation factor levels predict arterial thrombosis in epidemiological studies, but studies of older persons are needed. We studied 3 plasma antigenic markers of fibrinolysis, viz, plasminogen activator inhibitor-1 (PAI-1), fibrin fragment D-dimer, and plasmin-antiplasmin complex (PAP) for the prediction of arterial thrombosis in healthy elderly persons over age 65. The study was a nested case-control study in the Cardiovascular Health Study cohort of 5201 men and women >/=65 years of age who were enrolled from 1989 to 1990. Cases were 146 participants without baseline clinical vascular disease who developed myocardial infarction, angina, or coronary death during a follow-up of 2.4 years. Controls remained free of cardiovascular events and were matched 1:1 to cases with respect to sex, duration of follow-up, and baseline subclinical vascular disease status. With increasing quartile of D-dimer and PAP levels but not of PAI-1, there was an independent increased risk of myocardial infarction or coronary death, but not of angina. The relative risk for D-dimer above versus below the median value (>/=120 microg/L) was 2.5 (95% confidence interval, 1.1 to 5.9) and for PAP above the median (>/=5.25 nmol/L), 3.1 (1.3 to 7.7). Risks were independent of C-reactive protein and fibrinogen concentrations. There were no differences in risk by sex or presence of baseline subclinical disease. D-dimer and PAP, but not PAI-1, predicted future myocardial infarction in men and women over age 65. Relationships were independent of other risk factors, including inflammation markers. Results indicate a major role for these markers in identifying a high risk of arterial disease in this age group.
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PMID:Fibrinolytic activation markers predict myocardial infarction in the elderly. The Cardiovascular Health Study. 1007 48

The prognostic role of C-reactive protein levels in patients with a first acute myocardial infarction, an uncomplicated in-hospital course, and the absence of residual ischemia on a predischarge ergometer test and with an echocardiographic ejection fraction > or = 50% has not been described. C-reactive protein was determined during hospitalization in 64 patients (55 men, mean age 64.6 +/- 10.4 years). The patients were followed up for 13 +/- 4 months and the following cardiac events were recorded: cardiac death, new-onset angina pectoris, and recurrent myocardial infarction. Patients who developed cardiac events during the follow-up period had significantly higher C-reactive protein values than patients without events (3.61 +/- 2.83 vs 1.48 +/- 2.07 mg/dl, p <0.001). The probability of cumulative end points was: 6%, 12%, 31%, and 56% (p = 0.006; RR 3.55; confidence interval 1.56 to 8.04), respectively, in patients stratified by quartiles of C-reactive protein (< 0.45, 0.45 to 0.93, 0.93 to 2.55 and > 2.55 mg/dl). In the Cox regression model, only increased C-reactive protein levels were independently related to the incidence of subsequent cardiac events (chi-square 9.8, p = 0.001). Thus, increased C-reactive protein levels are associated with a worse outcome among patients with a first acute myocardial infarction, an uncomplicated in-hospital course without residual ischemia on the ergometer test, and with normal left ventricular function.
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PMID:C-reactive protein as a marker for cardiac ischemic events in the year after a first, uncomplicated myocardial infarction. 1039 60

Serum or plasma sialic acid and C-reactive protein have recently been shown to be cardiovascular risk factors. Our aim was to determine whether plasma sialic acid or C-reactive protein concentration correlate with atheromatous load on coronary angiography. Plasma sialic acid concentration and plasma C-reactive protein concentration were determined in 128 consecutive patients attending day case coronary angiography. Patients were excluded for previous coronary angioplasty, coronary artery bypass grafting, recent myocardial infarction, acute or chronic inflammatory disease and proximal occlusions precluding analysis of distal coronary anatomy. Total cholesterol, triglyceride, HDL cholesterol and glucose concentrations were assayed on fasting samples of venous blood. Angiograms were graded according to a semisubjective scoring system. There was no significant correlation between plasma sialic acid (r = 0.19, P = 0.07), or C-reactive protein concentration (r = 0.17, P = 0.13) and atheromatous load. There was no significant correlation between sialic acid (P = 0.13), or C-reactive protein concentration (P = 0.32) and the number of diseased coronary vessels. The difference in plasma sialic acid concentration between those with normal coronary angiograms and those with coronary artery disease did not reach significance (P = 0.08). Plasma sialic acid concentration correlated with C-reactive protein (r = 0.58, P = 0.0001), serum triglyceride (r = 0.32, P = 0.002), and blood cholesterol concentration (r = 0.22, P = 0.04). Plasma sialic acid concentration does not correlate with atheromatous load on coronary angiography in patients with stable angina.
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PMID:Plasma sialic acid and coronary artery atheromatous load in patients with stable chest pain. 1048 51

Inflammation and activation of immune cells have important roles in the pathogenesis of atherosclerosis. We analyzed the plasma levels of inflammatory markers and the degree of activation of peripheral blood monocytes and T-lymphocytes isolated from 12 unstable angina, 12 stable angina, and 12 normal subjects. In 20%-33% of patients, monocytes expressed high basal levels of IL-8, tissue factor, IL-1beta, and monocyte chemoattractant protein-1 mRNA. Furthermore, basal mRNA levels of these cytokines showed strong correlation with each other (p < 0.01 in all combination) but not with tumor necrosis factor-alpha or transforming growth factor-beta1. Plasma level of C-reactive protein was highest in the unstable angina patients (1.63+/-0.70 mg/l) and lowest in the control subjects (0.22+/-0.08 mg/l) (P = 0.03). We also observed a high correlation between C-reactive protein level and the occurrence of minor and major coronary events during 6 months of follow-up. Activation status of T-cells, assessed by the percentage of HLA-DR positive cells, was highest in the unstable angina patients (26.8+/-1.4%) compared with that in the control (14.7+/-1.2%) (P = 0.0053). Our data represent the first case showing that the circulating monocytes in angina patients are activated to a state express numerous proatherogenic cytokines. These results may help to diagnose angina patients according to the inflammatory markers and evaluate the prognosis of the disease.
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PMID:Activation of monocytes, T-lymphocytes and plasma inflammatory markers in angina patients. 1055 Dec 65

Several studies have shown that inflammation plays an important role in the pathogenesis of coronary heart disease (CHD). Serum amyloid A (SAA) and C-reactive protein (CRP) reactants of the acute phase of inflammation, have been shown to be increased in patients with CHD. Recently ex vivo studies demonstrated that some types of atherosclerotic plaques show substantially warmer regions. A catheter-based technique has been developed to measure the temperature of human arteries in vivo. Therefore, the aim of the present study was to measure the luminal surface temperature in patients with CHD and to correlate it with the acute phase proteins in order to discriminate the role of inflammation in heat production in acute coronary syndromes. Sixty patients were studied with CHD (20 with stable angina, 20 with unstable angina and 20 with acute myocardial infarction) and 20 sex- and age-matched controls without coronary artery disease, by measuring plasma levels of SAA, CRP, plasma lipids and intracoronary arterial luminal wall temperature. Intracoronary temperature was measured with a thermography catheter developed in our Institution: a thermistor probe with a temperature accuracy of 0.05 degrees C, was attached at the distal end of a long 3F polyurethane shaft. It was found that the median temperature differences at the site of the lesion from the core temperature was increased in patients with unstable angina (1.025 degrees C) and acute myocardial infarction (2.150 degrees C) compared with stable angina (0.300 degrees C), P<0.001 for each comparison. Furthermore, stable angina has increased temperature differences compared with controls (0.200 degrees C, P<0.001). There were very good correlations between CRP and SAA with the temperature (r=0.796, P=0.01 and r=0.848, P=0.01, respectively). Local heat at the site of lesion is increased in patients with acute coronary syndromes and may arise from an aggressive inflammatory response occurring in these situations. The sensitive measurement of plaque temperature as a prognostic marker may be useful in the management of coronary heart disease.
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PMID:Heat production of atherosclerotic plaques and inflammation assessed by the acute phase proteins in acute coronary syndromes. 1065 89

C-reactive protein may predict the risk of cardiovascular disease, but its association with angina pectoris in the general population has not been clearly established, however. We used data from National Health and Nutrition Examination Survey III conducted from 1988-1994 to examine the associations between serum C-reactive protein and plasma fibrinogen concentrations and self-reported angina pectoris and myocardial infarction among 7,948 U.S. men and women aged 40 years and older. C-reactive protein and fibrinogen concentrations were moderately correlated (r = 0.43). After adjustment for age, sex, race or ethnicity, education, smoking status, systolic blood pressure, serum cholesterol, high-density lipoprotein cholesterol, history of diabetes mellitus, body mass index, and physical activity, fibrinogen (but not C-reactive protein) concentration was significantly associated with self-reported angina pectoris. Neither fibrinogen or C-reactive protein concentrations were significantly associated with angina pectoris when entered in the model simultaneously. C-reactive protein and fibrinogen concentrations were positively associated with myocardial infarction when entered separately into models, but only C-reactive protein concentration was significantly associated with myocardial infarction when both variables were entered simultaneously. These cross-sectional data showed a significant positive association between C-reactive protein concentration and myocardial infarction but not self-reported angina pectoris in the U.S. population.
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PMID:Serum C-reactive protein and fibrinogen concentrations and self-reported angina pectoris and myocardial infarction: findings from National Health and Nutrition Examination Survey III. 1069 9

Acute coronary syndromes not associated with ST-segment elevation, i.e. unstable angina and non-Q wave myocardial infarction, represent a heterogeneous group of clinical disorders sharing similar pathogenic mechanisms, clinical presentation and medical management. Current guidelines recommended an early anti-thrombotic and anti-ischemic treatment in these patients, as well as their prompt risk evaluation based on easily available clinical and instrumental data, to identify those subjects at greater risk in whom a more aggressive management is warranted. Despite the association of aspirin, heparin and anti-ischemic drugs, the 30-day rate of death or myocardial infarction remains high (9-15%) in patients with markers of greater risk (i.e. Braunwald class III, ST-segment depression, abnormal creatine kinase or troponin values). Moreover, in patients with acute coronary syndromes undergoing percutaneous coronary interventions (PCI), complex coronary lesions increase the peri-procedural risk of thrombotic complications. Regardless of the agonist responsible for platelet activation and aggregation, platelet glycoprotein (GP) IIb/IIIa receptor activation is the key factor in thrombosis formation. Several clinical trials in the past few years have documented the beneficial value of GP IIb/IIIa inhibitors in patients treated with aspirin and heparin, with a significant reduction in the cumulative end-point of death and/or myocardial infarction at 48-96 hours (odds ratio--OR 0.81, 95% confidence interval--CI 0.71-0.92, p < 0.01). Such therapeutical benefit is still present at 30 days (OR 0.88, 95% CI 0.81-0.97, p < 0.001) and 6 months (OR 0.88, 95% CI 0.79-0.97, p < 0.001). In patients treated with abciximab, eptifibatide or tirofiban, undergoing early PCI, a remarkable relative reduction in the risk of death and non-fatal acute myocardial infarction was shown before PCI (-34%, p < 0.001). The pre-PCI administration of GP IIb/IIIa inhibitors is associated with a significant reduction in peri-procedural complications (-41% relative reduction of death or acute myocardial infarction in the 48 hours after PCI, p < 0.001). In this subset of patients the benefit correlates with abnormal pre-PCI values of troponin, a reliable surrogate marker of active thrombosis. The greatest clinical benefit from GP IIb/IIIa inhibitors is expected in patients presenting high-risk features (early post-infarction angina; older age with a history of left ventricular dysfunction or diabetes; heart failure symptoms, ST-segment depression, abnormal troponin, creatine kinase, and C-reactive protein values at admission) as well as in patients with recurrent ischemic attacks and those undergoing early PCI. Although the combination of GP IIb/IIIa inhibition and standard doses of unfractionated heparin is associated with an increased risk of major bleeding, such risk can be remarkably reduced adopting simple technical suggestions.
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PMID:[The clinical use of the GPIIb/IIIa inhibitors eptifibatide and tirofiban in the treatment of acute coronary syndromes of the "non-ST elevation" type]. 1093 49

In the acute phase of unstable angina, activation of the hemostatic mechanism is demonstrated by an increase in the plasma levels of markers of thrombin generation (prothrombin fragment 1+2) and thrombin activity (fibrinopeptide A). Increased concentrations of plasma C-reactive protein, an acute-phase reactant, have also been reported in patients with unstable angina. However, whether there is a correlation between the activation of the hemostatic mechanism and the acute-phase reaction of inflammation remains unclear. We measured the plasma levels of prothrombin fragment 1+2, fibrinopeptide A, and C-reactive protein in 91 patients consecutively hospitalized with recent-onset rest angina (Class IIIB Braunwald's classification), finding that they were above the normal limits in 48 (53%), 45 (49%), and 30 (33%) patients, respectively. There was no correlation between prothrombin fragment 1+2 and fibrinopeptide A (P = 0.34), prothrombin fragment 1+2 and C-reactive protein (P = 0.10), or fibrinopeptide A and C-reactive protein (P = 0.75). Plasma levels of prothrombin fragment 1+2 and fibrinopeptide A were both above normal levels in 32% of patients; 19% had both prothrombin fragment 1+2 and C-reactive protein, and 18% both fibrinopeptide A and C-reactive protein levels above the upper normal limits. All three markers were abnormally high in 11% of patients. According to the kappa cofficient test, the agreement between the elevation of the plasma concentrations of the markers was "random." In approximately half of the patients with acute unstable angina, there was an increase in the markers of the activation of the hemostatic mechanism and, in a smaller proportion, an increase in plasma C-reactive protein levels. The activation of the coagulation cascade and the acute-phase reaction of inflammation were infrequently associated in individual patients.
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PMID:Lack of Correlation Between Activation of Hemostatic Mechanism and Inflammation in Unstable Angina Pectoris. 1076 13

The aim of this study was to identify the risk factors affecting the immediate 30-day postoperative outcome of infrapopliteal bypass grafts. A series of 511 revascularization procedures to the infrapopliteal arteries have been performed in 439 patients with critical leg ischemia. There were 306 crural bypasses and 205 pedal bypasses. The 30-day postoperative primary and secondary patency rates were 77.5% and 83.4%, respectively; the leg salvage rate was 89.8%; the survival rate was 94.7%; and 85.1% of patients were alive with a salvaged leg. A history of myocardial infarction, angina pectoris, or stroke had a great impact on the postoperative cardiac and cerebrovascular fatal and nonfatal complications. C-reactive protein arose as an important predictor of the length of hospital stay (p = 0.03), postoperative cardiac complications (p = 0.02), leg salvage (p = 0.009), amputation with patent graft (p = 0.009), and patients who survived with a salvaged leg (p = 0.006). Poor results were achieved in patients on long-term dialysis. Surgical experience had an influence on leg salvage (p = 0.02) and on patients alive with salvaged leg rates (p = 0.009). Infrapopliteal bypass surgery is a demanding procedure requiring high surgical skill and experience. Revascularization may be contraindicated when severe coronary disease, previous stroke, renal failure requiring long-term dialysis, diabetes, or high serum concentration of C-reactive protein coexist with critical leg ischemia, as these patients are at high risk for early postoperative leg or life loss.
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PMID:Limits of infrapopliteal bypass surgery for critical leg ischemia: when not to reconstruct. 1077 27

The aim of this study was to ascertain the relationship of raised serum levels of fibrinogen and C-reactive protein at admission with in-hospital major adverse cardiac events in patients with unstable angina and to delineate their angiographic morphology. This single centre, prospective study consisted of 192 patients admitted in an intensive coronary care unit of a large municipal hospital with final diagnosis of unstable angina. The clinical endpoints were: in-hospital recurrent angina, new myocardial infarction or cardiac death. Patients with elevated levels of serum fibrinogen and C-reactive protein at admission showed a significantly higher incidence of an in-hospital recurrent major adverse cardiac event (p = 0.001). The mean levels of these markers were also significantly higher in patients with an in-hospital cardiac event as compared to patients with an uneventful hospital stay (p = 0.001). At angiographic evaluation, patients with type B and type C lesions and intracoronary thrombus had significantly higher levels of these markers as compared to patients with type A lesions (p = 0.001). It is concluded that in patients with unstable angina, elevated levels of serum fibrinogen and C-reactive protein at admission indicate an adverse in-hospital outcome and a more complex coronary morphology. The elevated levels of these easily measurable serum markers can therefore be useful in risk stratification of patients with unstable angina.
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PMID:Serum fibrinogen and C-reactive protein levels predict major adverse cardiac events in unstable angina. 1082 Sep 31


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