Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The handgrip test has been proposed for the evaluation of the hemodynamic reserve in patients with coronary artery disease and to quantitate the impairment of left ventricular (LV) function. The present study was designed to evaluate the effect of thrombolytic therapy in patients with refractory unstable angina in order to test the hypothesis that a reduction in intracoronary thrombosis could ameliorate their hemodynamic response to the handgrip test. During left heart catheterization, 20 patients with refractory unstable angina of recent onset performed a handgrip test before (HG1) and 24-72 hours after (HG2) being randomized to receive recombinant tissue-type plasminogen activator or placebo, according to a double-blind parallel group design. HG1 induced an increase in heart rate (p < 0.001), in systolic pressure (p < 0.001), and a reduction in ejection fraction (p < 0.05). Changes in LV end-diastolic pressure during baseline handgrip were highly different in individual patients, resulting in a trend toward an increase. Similarly, a different individual response was observed in the behavior of the isovolumetric and relaxation indices. In comparison with HG1, no difference was detected during HG2 in the 2 treatment groups with respect to changes in LV volumes, ejection fraction, LV systolic and diastolic pressures, +dP/dt, (dP/dt)/P, -dP/dt, and tau index. In patients with refractory unstable angina of recent onset, the handgrip test performed before and after thrombolysis did not prove to be useful in assessing directional changes of LV performance, mainly because of the different individual response to the baseline handgrip test.
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PMID:Assessment of left ventricular function by isometric handgrip exercise after thrombolysis in patients with refractory unstable angina. 827 51

Thrombomodulin (TM) is a very efficient natural anti-thrombin glycoprotein expressed on the endothelial cell surface. Circulating soluble thrombomodulin is also detected by enzyme immunoassay in plasma and represents some fragments of membrane TM with various molecular weight. Plasma TM (TMp) levels are elevated in diseases associated with endothelium damage. We have explored TMp in patients with atheromatous disease and compared its level with others endothelial cell markers, particularly those who indicate cell activation, as tissue-type plasminogen activator (t-PA), inhibitor of plasminogen activator (PAI-1) and prostacyclin (PG12). Thirty seven patients with documented atheromatous artery disease were included in this study. They were not diabetics and their hepatic and renal functions were normal. Mean age was 71 +/- years. Routine serum parameters were checked out as well as others more specific for endothelium activation (TMp, PG12, PAI-1, t-PA) measured by enzyme immunoassay. Patients were classified according to three localizations of atheromatous involvement: - 15 patients with peripheral occlusive arteriopathy disease (POAD) - 6 with coronary artery disease (CAD); and 16 with polyvascular involvement (POLY). They were compared with 21 controls without any vascular lesions (mean age: 43 +/- 13 years). In controls TMp was 36 +/- 8 ng/ml without significant change according with age and sex. In patients whatever the localization of atheroma, TMp was found significantly higher: POAD = 51.3 +/- 19.7 ng/ml (p = 0.003); CAD = 49.2 +/- 15.4 ng/ml (p = 0.008); POLY = 49.6 +/- 17.2 ng/ml (p = 0.003). A positive correlation was pointed out in all patients between TMp and t-PA (p = 0.047), TMp and PG12 (p = 0.008). A positive correlation between TMp and t-PA (p = 0.034) was found only in the subgroup with POAD. In this study, there was no correlation between TMp and the following parameters: leucocytes, haemoglobin, cholesterol, HDL, LDL-cholesterol, Lp(a), fibrinogen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Evidence of elevated soluble plasma thrombomodulin in atherosclerosis]. 839 2

Several observations have suggested that lipoprotein (a) (Lp(a)) is a risk factor for coronary artery disease because of potential interference with fibrinolysis secondary to its activation of plasminogen. However, there are few data on the possible role of Lp(a) in liver cirrhosis. The present study was carried out, to better elucidate its relationship to the fibrinolytic system in liver cirrhosis. We studied the plasma levels of Lp(a) and the fibrinolytic parameters of 95 patients with liver cirrhosis (57 men, 38 women, aged 26-81). Patients in Child-Pugh class C (n = 32) had significantly lower levels of Lp(a) than those in class B (n = 45), and the class B had lower Lp(a) values than class A (n = 18) (1.4 (0.0-3.7) vs 2.9 (0.0-6.1) vs 3.4 (1.8-5.5); the data are log-transformed). Alpha-2-antiplasmin and plasminogen, had patterns similar to those of Lp(a), tissue plasminogen activator (t-PA) was significantly increased only in class C (class A: 7.5 +/- 5.8 ng/ml; class B: 10.8 +/- 7.7 ng/ml; class C: 19.1 +/- 11.3 ng/ml). Patients with systemic hyperfibrinolysis (cross-linked fibrin degradation products, XDP > 200 ng/ml) also had lower levels of Lp(a) than those without 1.6 (0.0-4.4) vs (0.0-6.1); p = 0.0002. There was a significant correlation between Lp(a) and plasminogen (r = 0.43; p = 0.001). Lipoprotein (a) progressively decreases as liver cirrhosis worsens but it appears unlikely to be involved in causing the hyperfibrinolytic state often observed in advanced liver cirrhosis, in which there are marked abnormalities of several other fibrinolytic parameters, also including increased t-PA and decreased inhibitors.
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PMID:Lipoprotein (a) and fibrinolytic system in liver cirrhosis. Coagulation Abnormalities in Liver Cirrhosis (CALC) Study Group. 856 64

Five cases of spontaneous coronary artery dissection (SCAD) are reported, three in women and two in men (mean age 44 years; range 28-65), all of whom suffered a myocardial infarction. Common risk factors for coronary artery disease were present in the two men; in the female group one patient was taking an oral contraceptive, one was in the postpartum period, and the third was a smoker. Only the three women received intravenous alteplase and their ejection fraction was normal; both men had impaired left ventricular function. Two patients had SCAD of the left anterior descending coronary artery and three of the right coronary artery. Only the two men had angiographic features of coronary atherosclerotic involvement. No patients required surgical revascularisation or percutaneous transluminal coronary angioplasty. At a mean follow up of 27 months (range 6 to 40) all patients were alive and all but one were asymptomatic.
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PMID:Follow up after spontaneous coronary artery dissection: a report of five cases. 867 63

To assess whether plasminogen activator inhibitor 1 (PAI-1) activity is elevated in the progeny of young coronary men, 193 young subjects were recruited and divided into two groups. Group A consisted of 104 children whose fathers had suffered a myocardial infarction before the age of 55 ("cases"). Eighty-nine young subjects matched for age, sex, body mass index (BMI) and smoking habits without familial history of coronary artery disease (CAD) served as controls (group B). Children with a family history of diabetes mellitus or hypertension were excluded from both groups. We measured PAI-1 activity, tissue-type plasminogen activator (t-PA) antigen, a2-antiplasmin, fibrinogen, lipids and apolipoproteins in both groups. PAI-1 activity levels were also determined in the men who suffered a premature myocardial infarction 4 months after their discharge. PAI-1 activity levels were higher in cases compared to controls (3.13 +/- 1.9 vs 2.17 +/- 1.9 U/ml, p = 0.0014). t-PA antigen and a2-antiplasmin did not differ significantly between the two groups, while fibrinogen, total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B and lipoprotein(a) were significantly higher in group A. PAI-1 was positively correlated with triglycerides (r = 0.22, p = 0.024), apolipoprotein B (r = 0.21, p = 0.039) and fibrinogen (r = 0.22, p = 0.029) in cases and with BMI in both cases (r = 0.37, p = 0.0003) and controls (r = 0.23, p = 0.044). In stepwise multiple regression analysis, only apolipoprotein B (p = 0.008) and BMI (p = 0.0014) were significant determinants of PAI-1 activity in cases. There was also a positive correlation between PAI-1 activity levels of the affected fathers and their children (r = 0.30, p = 0.01). The present data support the hypothesis that elevated PAI-1 levels in the offspring of men with premature myocardial infarction impair their fibrinolytic capacity contributing to their familial predisposition to CAD.
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PMID:Plasminogen activator inhibitor 1 is elevated in the children of men with premature myocardial infarction. 888 80

Utilization of angiography after acute myocardial infarction (AMI) treated with thrombolytics has been shown in large clinical trials to be related primarily to the availability of the procedure and not individual clinical circumstances. This study evaluated the regional influence of overall population cardiovascular mortality on utilization of angiography in the United States participants of the Global Utilization of Streptokinase and t-PA for Occluded Arteries (GUSTO-1) trial. Published summary statistics from GUSTO-1 and U.S. Census Bureau 1991 data were evaluated using simple and multiple linear regression with analysis for outliers. Region predictor variables (age adjusted) included mean total cardiovascular deaths/100,000/year (ICD/9 codes 390 to 459), mean coronary artery disease deaths/ 100,000/year (ICD/9 codes 410 to 414), and mean stroke deaths/100,000/year (ICD/9 codes 430 to 438), with the major outcome being regional proportion of GUSTO-1 patients undergoing angiography during the hospital stay after treatment with thrombolysis. All 3 cardiovascular death rates varied significantly by region (p < 0.00002) with no significant difference in GUSTO-1 mortality by region (p = 0.25). Simple linear regression analysis revealed associations between regional death rates and angiography use (r = 0.60, p = 0.12; r = 0.39, p = 0.33; r = 0.81, and p = 0.015). Multiple stepwise linear regression analysis found regional death rate due to stroke as the strongest predictor of angiography use with 65.86% of the variation explained by the model. New England was found to be a consistent outlier with reduced angiography use because of its background regional disease burden. This study confirms regional bias in the use of angiography in GUSTO-1. This form of operator bias appears to be due to more aggressive practice patterns in regions, except New England, where the overall cardiovascular disease burden is greater in terms of lives lost per 100,000 per year.
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PMID:Influence of regional cardiovascular mortality on the use of angiography after acute myocardial infarction. 906 11

In recent years, a prodigious amount of information has been gathered regarding the relationship between vascular biology and the mechanisms underlying cardiovascular disease. Activation of elements of the reninangiotensin system (RAS) appear to play an important role in the development and progression of conditions such as hypertension, coronary artery disease, and heart failure. Indeed, converging lines of evidence indicate that angiotensin-converting enzyme (ACE) regulates a delicate balance among a multitude of factors responsible for vascular tone, cellular growth promotion and inhibition, and pro- and anti-inflammatory effects. Because angiotensin II inhibits fibronectin, stimulates expression of plasminogen activator inhibitors, and degrades bradykinin, thereby impairing production of nitric oxide, ACE and the RAS are also involved in thrombosis and fibrinolysis. The favorable effects of ACE inhibition on endothelial function and, potentially, on cardiovascular morbidity and mortality are believed to result not only from angiotensin II suppression but also its consequent bradykinin preservation and nitric oxide production.
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PMID:The integrated effects of angiotensin II. 912 15

Elevated fibrinogen levels as well as an impaired activity of the fibrinolytic system are regarded as important cardiovascular risk factors. To elucidate a potential interrelation between fibrinogen as an indicator of a hypercoagulable state and the endogenous fibrinolytic function hemostatic and rheological as well as lipid parameters were determined in 224 consecutive patients, who underwent elective coronary angiography. In the selected study population of 81 men and 19 women with fibrinogen concentration either > or = 3.5 g/l (n = 70) or < or = 2.5 g/l (n = 30) hyperfibrinogenemia was found to be significantly associated with increased concentrations of plasmin-alpha 2-antiplasmin complex [PAP [median (25.-75. percentile)], 534 (361-680) micrograms/l vs. 289 (243-440) micrograms/l; p < 0.001] and tissue plasminogen activator (t-PA) antigen [9 (6-11) micrograms/l vs 8 (5-9) micrograms/l; p < 0.05] while this association was lost in the subgroup of patients with angiographically normal coronary arteries (n = 26). In addition to these findings fibrinogen was significantly correlated with PAP (r = 0.40, p < 0.001; n = 224) and t-PA antigen (r = 0.2, p < 0.01; n = 224) after adjustment for age, diabetes mellitus, lipid parameters and leucocyte counts. It can be argued that elevated fibrinogen levels in patients with coronary artery disease are concomitant with an activation of the fibrinolytic system.
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PMID:Activation of the fibrinolytic system in patients with coronary artery disease and hyperfibrinogenemia. 918 12

The purpose of this study was to evaluate fibrinolytic potential at rest and after a fibrinolytic stressor in men with a history of myocardial infarction (MI) compared with an age- and activity-matched group of men without coronary artery disease (CAD). All men were currently enrolled in exercise programs. Tissue-type plasminogen activator (TPA) and plasminogen activator inhibitor 1 (PAI-1) activity and antigen levels were measured at rest and after a maximal exercise test. A 2 x 2 (group x time) ANOVA with repeated measures was used to evaluate fibrinolytic potential. Bivariate regressions were conducted to evaluate relations between fibrinolytic potential and maximal oxygen uptake (VO2max). Age was similar between groups (CAD, 57.5 +/- 6.6; non-CAD, 58.1 +/- 7.3 years); however, VO2max was higher in non-CAD subjects (36.2 +/- 6.2 vs 27.5 +/- 5.9 mL.kg-1.min-1). Mean +/- SEM resting TPA and PAI-1 activities were similar between CAD and non-CAD subjects (TPA, 2.8 +/- 0.2 vs 2.8 +/- 0.2 IU/mL; PAI-1, 15.9 +/- 3.1 vs 13.1 +/- 4.1 AU/mL). Both groups showed similar significant increases in TPA activity with exercise (P < .05), and postexercise TPA activity was also similar (CAD, 9.1 +/- 2.0 IU/mL; non-CAD, 11.7 +/- 2.6 IU/mL). Both groups also showed similar significant decreases in PAI-1 activity with exercise (P < .05) and no differences in postexercise PAI-1 activity (CAD, 13.2 +/- 2.5 AU/mL; non-CAD, 10.4 +/- 3.6 AU/mL). Significantly higher resting TPA antigen levels were seen in CAD (14.8 ng/mL) than non-CAD (10.2 ng/mL) subjects (P < .05), but neither group showed significant changes with exercise (CAD, 12.9 ng/mL; non-CAD, 11.8 ng/mL). Resting PAI-1 antigen was similar in the two groups (CAD, 71.4 ng/mL; non-CAD, 74.2 ng/mL) and did not significantly change with exercise (CAD, 77.9 ng/mL; non-CAD, 72.3 ng/mL). VO2max was positively correlated with postexercise TPA activity (r = .52, P < .05) and negatively correlated with resting TPA antigen (r = -.43, P < .05). Resting TPA antigen was also directly correlated with body mass index (r = .63, P < .05). The finding that functional fibrinolytic activity was not different in physically active men with and without CAD contrasts with previous reports. This suggests that matching subjects on the bases of age and habitual physical activity status and controlling exercise intensity are important factors to consider when evaluating fibrinolytic potential.
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PMID:Fibrinolytic activity is similar in physically active men with and without a history of myocardial infarction. 919 61

Hemostatic factors are involved in the pathogenesis of native coronary artery disease. However, their role in transplant coronary artery disease is less established. To assess the role of hemostatic factors in transplant coronary artery disease we studied 52 consecutive cardiac transplant patients. The presence of transplant coronary artery disease was determined by angiography. Plasma levels of tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), von Willebrand Factor (vWF), and fibrin D-dimer were determined by enzyme-linked immunosorbent assays. Serum lipids were measured by enzymatic methods. Patients with transplant coronary artery disease had higher circulating t-PA (8.6 +/- 0.8 vs. 5.4 +/- 0.6 ng/ml, p = 0.021) and PAI-1 antigen concentrations (38.0 +/- 3.4 vs 25.8 +/- 2.2 ng/ml, p = 0.037). t-PA and PAI-1 antigen concentrations correlated with the severity of angiographic disease (R = 0.34; p = 0.014 for t-PA, and R = 0.45; p = 0.001 for PAI-1). Serum cholesterol levels were higher in patients with transplant coronary artery disease (221 +/- 7.6 vs 191 +/- 9.2 mg/dl, p = 0.039). Serum triglycerides were also higher in patients with transplant coronary artery disease by angiography (246 +/- 38.3 vs 139 +/- 20.8 mg/dl, p = 0.050). Multivariate analysis identified t-PA antigen (p = 0.003) and triglyceride levels (p = 0.038) as independent predictors for the presence of transplant coronary artery disease. We conclude that cardiac transplant patients with evidence of transplant coronary artery disease on coronary angiography have altered hemostatic function which is reflected by elevated levels of circulating t-PA and PAI-1 antigens. The interaction of the hemostatic system and serum lipids in the development of transplant coronary artery disease warrants further study.
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PMID:Plasma levels of tissue plasminogen activator and plasminogen activator inhibitor-1 are correlated with the presence of transplant coronary artery disease in cardiac transplant recipients. 923 Jan 49


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