Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.1.1.194 (CAD)
 4,384 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased plasma levels of plasminogen activator inhibitor-1 (PAI-1) have been shown to exist in 40 to 60% of patients with stable coronary artery disease and have been suggested to be responsible for the development of coronary thrombotic complications. However, it is also discussed whether PAI-1 elevation might mainly be due to variables like increased age or to reactive mechanisms caused e.g. by the chest pain itself. To exclude age dependent or pain related influences, age-matched patients with stable angina pectoris (NHYA II) and angiographically proven coronary artery disease (CAD, n = 16) or without evidence for coronary sclerosis (variant angina, n = 10; angina-like syndrome with normal coronary angiogram, n = 5; non-CAD, n = 15) have been investigated for their plasma PAI-1 activity and t-PA antigen levels. The mean PAI activity in CAD patients (17.5 U/ml) was significantly higher than in non-CAD patients (9.6 U/ml) (p less than 0.0001). In the CAD patients no significant variation in plasma PAI-1 values could be demonstrated when related to the extent of the disease or to a history of previous myocardial infarction. t-PA antigen was also elevated in CAD patients as compared to the non-CAD group (p less than 0.02). The results suggest therefore a strong correlation between coronary artery disease itself and elevated levels of components of the plasma fibrinolytic system.
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PMID:Plasminogen activator inhibitor-1 levels in patients with chronic angina pectoris with or without angiographic evidence of coronary sclerosis. 211 22

We studied the relationship between thrombolysis and late potentials (LP) in 137 patients with acute myocardial infarction (AMI). Among 37 patients treated with tissue-type plasminogen activator(t-PA treated group), LP were recorded in 2 patients (5%). In contrast, among 100 conventionally treated patients (control group), LP were seen in 26 (26%, P less than 0.01). When the two groups were matched with respect to age, sex, absence of prior infarction, LVEF, number of abnormal Q waves, ECG score and CAD score, the same incidence of LP was seen, i.e. 6% of the 34 t-PA treated patients had LP as compared with 24% of the 42 conventionally treated patients (P less than 0.05). Angiographic examination following t-PA infusion revealed that the incidence of LP was 0% and 40% in patients with patent and closed infarct-related coronary artery respectively. 1 year follow-up data showed that no deaths occurred in the t-PA treated group, while in the control group. 18 deaths were recorded and 8 of them were classified as sudden death. These observations suggest that patients with AMI treated early with thrombolysis have electrically more stable ventricles due to improvement of ischemia.
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PMID:[The relationship between tissue type plasminogen activator therapy and ventricular late potentials in acute myocardial infarction]. 212 51

The aim of this study was to determine the association of tPA antigen levels with CAD and ischaemic stroke and whether associations are independent of levels of PAI-1 antigen. In subjects with CAD (n = 247) tPA was associated with the number of coronary arteries with > or = 50% stenosis, but this association was lost after adjustment for PAI-1, which was found to be the largest determinant of tPA levels in linear regression models and accounted for as much as 38% of the variation in levels. Levels of tPA were significantly higher in patients with a history of MI compared with those without, even after adjustment for covariates and PAI-1 (MI: 10.0 [9.4-10.6] ng/ml; no MI: 8.9 [8.5-9.4] ng/ml, p = 0.004). In a logistic regression model comparing patients with MI to patients without MI, the odds ratio for tPA levels in the upper quartile compared with the lowest quartile was 2.03 (1.33-3.10). Levels of tPA in subjects with ischaemic stroke (n = 338) were significantly higher than age matched healthy control subjects (n = 366) and again this difference remained after adjustment (patients: 10.4 [9.9-10.9] ng/ml; controls: 9.0 [8.7-9.3] ng/ml, p <0.0001). In a logistic regression model comparing patients with ischaemic stroke to healthy control subjects the odds ratio for tPA in the upper quartile compared with the lowest quartile was 4.23 (3.02-5.92). These data suggest that the associations of tPA with acute thrombosis are independent of levels of PAI-1 but the mechanisms whereby enhanced fibrinolysis may predispose to thrombosis remain unclear.
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PMID:Determinants of tPA antigen and associations with coronary artery disease and acute cerebrovascular disease. 979 83

It is generally accepted that atherosclerosis is a dynamic process in which many factors of lipid, hemostatic or other nature play their negative and positive roles. The purpose of the study was to determine the relationship between the atheromatous changes in coronary arteries being assessed angiographically and the lipid and hemostatic risk factors, as well as to select biochemical parameters, which would be helpful for prognosing the degree of intensity with regard to atheromatous changes in coronary arteries. Studies of lipid parameters and hemostasis system were performed in 31 men with atherosclerosis of coronary vessels being angiographically estimated. The degree of intensity concerning the atheromatous changes was defined in a point scale according to Gensini based on the magnitude of coronary artery stenosis and its localization in respect of significance for myocardial function. The studied patients were divided into two groups, which differed by the degree of the intensity of atheromatous changes in coronary arteries: group I--men with mild (M-CAD, score < 32) n = 15, group II--men with severe atherosclerotic changes (S-CAD, score > or = 32) n = 16. The characteristics of both groups are given in table 1. All patients were on nitrates, salicylates, beta-blockers and calcium channel blockers. No antilipemics or anticoagulants were administered. The following biochemical parameters were determined in all men: cholesterol-Ch; triglycerides-TG; phospholipids-PL; apolipoproteins: Apo A, Apo A-I, Apo B; lipoproteins: VLDL, LDL, HDL and their lipids and proteins components; lipoprotein (a)-Lp(a); fibrinogen-Fb; euglobulin lysis time-ELT; inhibitor tissue plasminogen activator PAI-1; antithrombin III--AT III; spontaneous platelet aggregation-SPA, platelet factor 4-PF 4 and glucose. Table 2 lists the lipid parameters in serum and lipoprotein fractions. The levels for apolipoproteins A, A-I, B, lipoprotein (a), hemostatic parameters and glucose are given in table 3. Tables 4 and 5 present the results of multiple regression analysis for severity of atherosclerotic changes (score--dependent variable y) lipid and hemostatic parameters and glucose (independent variables x) in both groups. Prognostic variables necessary for the best fit in the model of relationship studied have been selected. Independent variables x are listed in descending order according to the absolute value of b*x. On the basis of the performed statistical analysis of the results of studies it has been ascertained that the biochemical parameters differentiating the patients with regard to the intensity of atheromatous changes are the coefficients: LDL-Ch/HDL-Ch and Apo B/Apo A ratio, LDL-PL, Fb and ELT whose values were higher as well as HDL-Apo A-I whose value was lower in the group of men with more severe atherosclerotic changes in coronary arteries (S-CAD). The stepwise multivariate analysis indicates that the most profound prognostic significance in risk of coronary atherosclerosis is claimed successively by: glucose, LDL-PL, HDL-Apo A-I, AT III, Fb, ELT, PAI-1, SPA, Lp(a), Apo B and PF 4. The results of the accomplished studies point out that the above-mentioned lipid, hemostatic parameters and glucose may be helpful in prognosing the severity of coronary atherosclerosis.
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PMID:[Determination of the usefulness of selected biochemical parameters for assessing the advanced atheromatous changes in human coronary arteries]. 985 30

The effects of 12 months hormone replacement therapy (HRT) on biochemical markers associated with endothelial function were studied in 98 postmenopausal women with CAD, who were randomized to transdermal HRT or a control group. A significant reduction in the levels of von Willebrand factor in the HRT-group compared to controls was seen after 3 months, maintained after 12 months (p <0.001). Significant reduction in the HRT-group compared to controls was also seen in VCAM-1 after 3 months, sustained after 12 months (p = 0.013 and p = 0.045, respectively), and E-selectin was reduced by about 20% after 3 months on HRT, the reduction being statistically significant after 12 months (p <0.001). Significantly reduced levels of ICAM-1 were also seen after 12 months (p = 0.048). No effects could be observed on tPA-antigen or thrombomodulin. The reduction in procoagulant and proinflammatory markers of endothelial function after long-term transdermal HRT could indicate a beneficial effect on the endothelium and thus a potentially modulating effect on the progression of atherosclerosis in women with CAD.
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PMID:Reduced expression of endothelial cell markers after long-term transdermal hormone replacement therapy in women with coronary artery disease. 1089 53