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)

To assess hemostatic risk factors for sudden death in patients with stable angina, 323 consecutive patients were recruited prospectively. Patients with clinical heart failure or recent myocardial infarction were excluded. The following clinical variables were recorded: age, gender, smoking habits, hypertension, previous myocardial infarction, left ventricular hypertrophy, and severe ventricular arrhythmia. Angiographic variables included coronary extent, assessed from Jenkins' and mean atherosclerotic scores, and left ventricular ejection fraction. Lipid variables included total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and apolipoproteins A-I and B. Hemostatic factors included fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2 antiplasmin, euglobulin clot lysis time, tissue plasminogen activator before and after venous occlusion, and plasminogen activator inhibitor. There were 34 deaths, 19 of which were sudden during the follow-up period (60 +/- 17 months). The association between each variable and the risk of sudden death was assessed by calculating the relative risk with the Cox univariate model. All significant predictors from the univariate analysis were then incorporated in a Cox multivariate model to select the independent predictors of sudden death. The independent predictors of sudden death were left ventricular hypertrophy (p < 0.04), lower left ventricular ejection fraction (p < 0.04), and shorter euglobulin clot lysis time after venous occlusion (p < 0.02), whereas fibrinogen (p < 0.07) and Jenkins' score (p < 0.08) were borderline. Determination of hemostatic variables, especially those pertaining to dynamic fibrinolysis, may thus be of value in assessing risk of sudden death.
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PMID:Predictive value of hemostatic factors for sudden death in patients with stable angina pectoris. 761 16

The diet of 17 patients with coronary heart disease whose angina duration was no more than 5 months was daily supplemented by 6.15 g of omega 3-polyunsaturated fatty acids (PUFA) in 125 g of canned Far-Eastern sardine for 4 weeks. This resulted in increases of eucosapentaenic and docosahexaenic acids (from 1.28 +/- 0.72 to 9.02 +/- 2.83 and from 2.48 +/- 0.91 to 6.54 +/- 2.01%, respectively; p = 0.0003) in the total lipid fraction of serum. The proportion of omega 6-PUFA decreased at the expense of a decline in the levels of linoleic acid from 24.9 +/- 3.9 to 19.7 +/- 5.2% (p = 0.0014). Triglycerides fell from 162.3 +/- 55.2 to 103.9 +/- 42.4 mg/dl (p < 0.0005). The mean activity values of the tissue activator inhibitor plasminogen and C-protein, the levels of plasminogen, antithrombin III, and fibrinogen remained unchanged. The changes found in the tissue activator inhibitor plasminogen were associated with the baselines of lauric and myristic acids. Thus, a short-term fish diet which leads to profound changes in the fatty acid spectrum in blood and to favourable lipid shifts fails to cause profibrinolytic changes in parameters of the fibrinolytic system.
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PMID:[The effect of a diet enriched with omega-3 polyunsaturated fatty acids on the indices of the blood fibrinolytic system in patients in the initial stages of ischemic heart disease]. 837 58

The ECAT Angina Pectoris Study is a European multicentre study investigating the pathogenetic and possibly predictive role of the haemostatic system in the progress of coronary heart disease. In this paper we report the cross-sectional analysis of haemostatic factors in 3043 patients, who underwent coronary angiography due to angina pectoris. Fibrinogen levels were higher in patients with one or more coronary stenoses of at least 50% than in patients without, by an average of 0.16 g.l-1 (P < 0.0001). Depressed fibrinolytic activity due to higher levels of PAI was also associated with the presence of coronary stenoses. There was no association with the extent of coronary arteriosclerosis, as assessed by the number of involved arteries, except that patients who had more vessels with total occlusions had higher fibrinogen levels. Depressed fibrinolytic activity was also clearly associated with diabetes, obesity, higher triglyceride levels, smoking and impaired cardiac pump function as assessed by ejection fraction. Cholesterol levels were particularly correlated with protein C and plasminogen.
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PMID:ECAT angina pectoris study: baseline associations of haemostatic factors with extent of coronary arteriosclerosis and other coronary risk factors in 3000 patients with angina pectoris undergoing coronary angiography. 843 97

In an attempt to discern biological (such as thrombotic or fibrinolytic) risk factors in patients developing restenosis after percutaneous transluminal coronary angioplasty, the following factors were measured prior to angiography in a population of 23 patients (20 men, 3 women, mean age 57 +/- 5 yr) treated by a successful angioplasty (gain > 20% and residual stenosis < 50%) for stable angina pectoris and who had a routine angiographic restudy. The following factors were thus assessed: lipid factors: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoprotein AI, apolipoprotein B; coagulation factors: fibrinogen, antithrombin III, fibrinopeptide A, factor VIII coagulant, factor VIII antigen, protein C; factors of physiological fibrinolysis: plasminogen, alpha 2-antiplasmin, tissue plasminogen activator and euglobulin clot lysis time before and after venous occlusion, plasminogen activator inhibitor before venous occlusion; and factors of platelet release: beta-thromboglobulin, platelet factor 4. Also studied were clinical characteristics: age, gender, diabetes, hypertension, smoking habits, previous myocardial infarction; angiographic data: global extent of coronary artery disease, location of the stenosis in a bend or branch point, complexity of the lesion, initial and residual stenosis and treatment during follow-up. The coronary angiograms were analyzed by a computer-assisted method with automatic edge detection. On angiographic criteria, 6 patients (restenosis group) were judged to have developed a restenosis (30% decrease in diameter and/or return to a 50% stenosis). The other 17 patients (those without restenosis) were considered to have a persistent success. Apart from age (group without restenosis: 55 +/- 6; restenosis group 61 +/- 5, p < 0.04), there were no differences in clinical, angiographic or treatment variables. There were no differences in lipid factors, but significant differences were observed in hemostatic variables: fibrinogen (without restenosis: 3.18 +/- 0.83; restenosis: 3.83 +/- 0.51 milligrams, p = 0.05), tissue plasminogen activator before venous occlusion (without restenosis: 10.9 +/- 26.8; restenosis: 232.5 +/- 371.2 IU, p < 0.04), euglobulin clot lysis time after venous occlusion (without restenosis: 176.5 +/- 100.5; restenosis: 78.6 +/- 40.2 min, p < 0.05) and for marker of the platelet release: platelet factor 4 (without restenosis: 10.8 +/- 7.9; restenosis: 20.5 +/- 7.5 ng/l, p < 0.04). These findings indicate that patients developing restenosis after coronary angioplasty tend to have an imbalance in the prothrombotic-antithrombotic equilibrium prior to the procedure.
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PMID:Biological risk factors for restenosis after percutaneous transluminal coronary angioplasty. 844 4

The aim of this study was to evaluate plasma levels of lipoprotein (a) [LP(a)] and plasminogen in patients affected with atherosclerotic disease and to understand the mutual relationships. Eighty-four patients affected with atherosclerosis were examined and divided as follows: group I, 24 patients with peripheral arteriopathy; group II, 40 patients with ischemic heart disease (myocardial infarction and/or angina pectoris); group III, 20 patients with multi-infarct dementia; group IV (control group) with 20 healthy young subjects. The results show that Lp(a) plasma levels, in atherosclerotic patients, are higher than 30 mg/dl, while the plasminogen levels are lower than 80 mg/dl. There is an inverse correlation between these two data. Moreover, a different behaviour of Lp(a) and plasminogen rate related to age of patients, to number of atherosclerotic lesions or to acuteness of ischemic heart disease, was observed.
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PMID:[Lipoprotein (a) and plasminogen in atherosclerosis]. 901 33

Prinzmetal's variant angina, primarily a vasospastic disease, is a glaring example of the gaps in our knowledge regarding the etiology of coronary heart disease. Half of all patients with coronary heart disease do not have any of the established coronary risk factors. Prinzmetal's variant angina, syndrome X, coronary embolization, and congenital coronary anomalies, are a few examples of conditions that may not be associated with established risk factors. New risk factors that are emerging in an attempt to establish an etiology in this group of patients are homocysteine plasma fibrinogen, estrogen-deficiency lipoprotein (a), C-reactive protein, Chlamydia pneumoniae, factor VII endogenous tissue plasminogen, and endogenous plasminogen activator/inhibitor type I. The battle against cardiovascular disease continues!
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PMID:Fifty percent of patients with coronary artery disease do not have any of the conventional risk factors. 957 51

Vascular disease is a multifactorial disease that involves atherosclerotic and thrombotic factors. Genetic polymorphisms have been associated with myocardial infarction and angina pectoris. The aim of the present study was to assess the relationship between some genetic polymorphisms and myocardial infarction (MI) or vasospastic angina pectoris in a population from southern France. Genetic polymorphisms of the renin angiotensin system (the D/I polymorphism of the ACE gene and the A1166C polymorphism of the angiotensin II type 1 receptor [AT1R]) and of haemostatic factors (the -675 4G/5G polymorphism of the plasminogen-activator inhibitor 1[PAI-1] gene, and the G to T common point mutation in exon 2, codon 34 of the Factor XIII A-subunit gene) were examined. We assessed the genotype distribution in consecutive coronary artery disease (CAD) patients with MI (n = 201) and vasospastic angina pectoris (n = 43) and in 244 healthy controls comparable in age, sex, body mass index and total cholesterol level. The genotype distribution of AT1R polymorphism was significantly different between controls and patients, the prevalence of the C allele carriers being higher in patients with MI after the age of 45 than in control individuals (61 vs 45%, p <0.01), leading to an odds ratio (OR) of 2 (CI: 1.2-3.4). When looking at the group of patients with vasospastic angina the difference was even higher (76 vs 45%, p <0.01) yielding an OR of 4.3 (CI: 1.4-17.4). Genotype distributions of ACE, PAI-1 and Factor XIII polymorphisms were similar in patients and in controls. This study is in favor of a role of ATIR gene polymorphism in myocardial infarction and vasospastic angina.
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PMID:Genetic polymorphisms and coronary artery disease in the south of France. 1073 75

Procarboxypeptidase U (proCPU) is the plasma precursor of carboxypeptidase U (CPU, carboxypeptidase R. plasma carboxypeptidase B or activated thrombin-activatable fibrinolysis inhibitor, TAFIa). CPU removes C-terminal lysine residues that act as plasminogen binding sites from partially degraded fibrin, thereby down-regulating plasminogen activation and fibrinolysis. The present study was carried out as a pilot study to examine whether the plasma proCPU concentration is related to the presence of coronary artery disease (CAD) and/or to levels of established risk indicators for CAD, in a case-control study of 110 men requiring coronary artery bypass grafting (CABG) because of stable angina pectoris. The preoperative plasma proCPU level in the CABG patients was significantly higher than in population-based controls (1029 +/- 154 vs. 974 +/- 140 U/L, p <0.05). In addition, in a subset of the patients (n = 31 ) the proCPU concentration, which was significantly lower on the third postoperative day (-17 +/- 10%), had increased significantly on the sixth day (+14 +/- 12%) after surgery, compared with the preoperative level. In both patients and controls, proCPU concentration was strongly and positively associated with factor VII amidolytic activity and protein C activity, suggesting a common mechanism modulating the plasma levels of these proteins. Otherwise, statistically significant correlations with proCPU were group-specific. In the patients, proCPU correlated significantly with plasma fibrinogen and protein S. In the controls, proCPU correlated significantly with concentrations of cholesterol in plasma. VLDL and LDL. In addition, proCPU correlated significantly with C-reactive protein and haptoglobin levels in the controls only, indicating that also inflammatory mechanisms are involved in the regulation of plasma proCPU. These results suggest that a mechanism exists by which fibrinolytic function is impaired in a manner that is likely to result in more stable fibrin deposits and increase the risk of precocious CAD as well as early occlusion of venous bypass grafts.
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PMID:Plasma procarboxypeptidase U in men with symptomatic coronary artery disease. 1101 56

Despite major advancements in the technology used for the percutaneous treatment of coronary artery disease, chronic total occlusions (CTOs) persist as a major challenge to the interventional cardiologist with relatively low success rates. CTOs are evident in 20% of patients undergoing cardiac catheterization and are responsible for the majority of cases that are referred to bypass surgery. There is growing evidence that patients may benefit from recanalization of a CTO by alleviation of angina, improving left ventricular function, and potentially long-term survival. The major obstacle to percutaneous recanalization of CTOs is the inability to cross the occlusion with coronary guidewires. Even when crossed, the operator has to deal with the exact location of the distal wire (e.g., dissection or true lumen) and the existence of relatively long lesion requiring multiple stents with high restenosis rates. New technologies for CTO revascularization have been focused mainly on a mechanical approach including specialized guidewires and more recently, specific devices using highly sophisticated technology such as laser guidewire, optical coherence reflectometry, and a blunt microdissection catheter. An alternate biological approach involves the local administration of enzymes such as plasminogen activators (urokinase) or collagenase, which can act locally to specifically degrade the collagen content of the CTO, thereby "softening" the occlusion and allowing easier guidewire crossing. In conclusion, CTOs emerge as a great technical challenge and are the focus of novel series of mechanical and biological approaches.
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PMID:Novel approaches for the treatment of chronic total coronary occlusions. 1554 94

A teaching hospital is working with the Victorian State Government and universities, integrating cost-effectiveness evidence into clinical practice guidelines (CPGs), protocols and pathways for respiratory and cardiology interventions. Acute myocardial infarction (AMI) findings are reported. Results will stimulate cost-effective practice and inform medical associations, federal and state governments and international organisations developing CPGs. Published CPGs by the American College of Cardiology/American Heart Foundation for AMI in 1999 are reviewed by a large interdisciplinary hospital-based committee given cost-effectiveness evidence. Levels of evidence criteria rating on methodological rigor for effectiveness and costs are applied. National Health and Medical Research Council (NHMRC) grades of recommendation criteria for combinations of relative effectiveness versus relative costs and cut-off points are used. Extrapolating results between countries was addressed by applying the OECD's health purchasing power parity series. Recommendations for revisions to United States guidelines and for local application are formulated. United States Guidelines require updating: Regarding angioplasty, percutaneous transluminal coronary angioplasty (PTCA) is cost-effective for men aged 60 years relative to recombinant tissue plasminogen activator (tPA), with additional cost per life year saved of 274 ecu. PTCA with discharge after 3 days is cost-effective in low-risk AMI. Regarding GP IIb/IIIa drugs, Abciximab during intervention incurred equal mean hospital costs for placebo, abciximab bolus, and abciximab bolus+infusion with incremental 6-month cost for the latter treatment costing 293 US dollars per patient. Agent recouped almost all initial therapy costs with significant benefits. Incremental cost of abciximab per event prevented is 3,258 US dollars. Tirofiban was compared to placebo after high-risk angioplasty for AMI or unstable angina. Tirofiban decreased the rate of hospital deaths, myocardial infarction, revascularisation at 2 days by 36% relative to placebo (8% vs. 12%) without increased cost. Clinical benefits were similar at 30 days. Tirofiban+heparin+aspirin was compared to heparin+aspirin. Tirofiban arm resulted in net savings of 33,418 ecu per 100 patients for the first 7 days of treatment. Regarding thrombolytics, tPA is more cost-effective than streptokinase. Incremental costs for each life saved when streptokinase is substituted by recombinant tissue plasminogen are 31%, 45%, 97% higher in Germany, Italy and the United States than in the United Kingdom. Regarding anticoagulants, enoxaparin is a promising alternative to unfractionated heparin for hospitalised patients with non-Q-wave myocardial infarction or unstable angina, saving 1,485 Canadian dollars per patient over 12 months with 10% reduction in 1 year risk of death, myocardial infarction or recurrent angina. Regarding antiarrhymics, the cost-effectiveness of no amiodarone, amiodarone for patients with depressed heart rate variability (DHRV), and amiodarone for patients with DHRV plus positive programmed ventricular stimulation (PPVS) for high-risk post-AMI was investigated. Amiodarone for DHRV+PPVS patients was dominated by a blend of the two alternatives. Compared to no amiodarone, the incremental cost-effectiveness of amiodarone for DHRV patients was 39,422 US dollars per quality adjusted life year gained. Amiodarone for DHRV is the most appropriate. Other CPG updates concern serum markers, for example, cardiac troponin I assay (c-Tnl), cost advantages of ad hoc angioplasty and secondary prevention through antioxidants and pravastatin. Australian costs are reported later in the paper.
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PMID:Integrating cost-effectiveness evidence into clinical practice guidelines in Australia for acute myocardial infarction. 1560 15


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