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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

W examined the short-term effects of a high-complex carbohydrate, low fat diet on the plasmin-dependent fibrinolytic pathway. A population of 27 adult American Caucasians exposed to the diet for 3 weeks showed highly significant reductions in the levels of plasminogen (P = 0.0001), tissue plasminogen activator (tPA) (P = 0.0001) and plasminogen activator inhibitor (tPAI) (P = 0.0017). Fibrinogen levels also decreased, but the changes did not reach statistical significance (P = 0.07). In contrast, the levels of the Lpa(a) lipoprotein, a potential inhibitor of fibrinolysis, remained remarkably constant despite a marked decrease in the levels of apolipoprotein B, a major constituent of Lp(a). Correlations between the levels of tPA, tPAI and plasma triglyceride were observed among the individuals both before and after the dietary challenge. Although the mechanisms responsible for the effects are unknown, the dramatic responsiveness of the thrombolytic pathway to dietary challenge is likely to be of importance in understanding the etiology of coronary artery disease and other vascular disorders.
Atherosclerosis 1990 Sep
PMID:Dietary regulation of fibrinolytic factors. 214 72

The influence of invasive investigations on parameters of hemostasis and fibrinolysis is generally unknown, although this has consequences for the design of prospective studies on the association between those parameters and regression or progression of atherosclerosis. We therefore determined hemostatic and fibrinolytic factors in 12 patients who were admitted to the hospital for coronary angiography (CAG; n = 5) or percutaneous transluminal coronary angioplasty (PTCA; n = 7). Blood samples were drawn under basal circumstances on the day before, the day of and the day after CAG or PTCA. Significant changes occur in the concentrations of platelets and white blood cells, hematocrit (Ht), von Willebrand factor antigen (vWF:ag), antithrombin III-activity (AT III-ag), antithrombin III-antigen (AT III-ant), fibrinogen, plasminogen, alpha2-antiplasmin (alpha2-AP), histidine-rich glycoprotein (HRG), and plasminogen activator inhibitor (PAI)-activity. Mean values of beta-thromboglobulin, platelet factor 4, factor VIII:C, tissue-type plasminogen activator activity (t-PA act) and euglobulin clot lysis time (ECLT) do not differ significantly. After correction for Ht, no significant differences exist between the day before and the day of the procedure; but on the day after CAG and PTCA significant differences occur in white blood cells, factor VIII:C, AT III-ag, alpha2-AP and PAI-act. It is concluded that principally blood samples for investigations on fibrinolysis may be taken on the day before or the day of CAG or PTCA without a loss of quality, if the values are corrected for Ht. Samples taken on the day after the procedure are not useful for such purposes.
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PMID:The influence of coronary angiography and angioplasty on parameters of hemostasis and fibrinolysis. 214 44

The levels of plasminogen activator inhibitor (PAI), protein C (pC), total cholesterol (TC), high and low density lipoprotein cholesterols (HDLC and LDLC), apolipoproteins A1 (apoA1) and B (apoB) were measured in 45 patients with coronary heart disease angiographically documented and 10 healthy subjects without coronary heart disease and coronary atherosclerosis as evidenced by coronary angiography and provocative tests. Twenty three patients had primary angina (PA) with a duration of less than 3 months, twenty two patients presented with chronic coronary heart disease (CCHD) with a duration of more than 4 months. In general, a negative correlation between PAI and HDLC levels in the patients under study (r = -0.413; p = 0.02), it was higher in PA (r = -0.687; p = 0.02), but disappeared in CCHD (r = 0.027). The content of PAI correlated with the cholesterol index (r = 0.654; p less than 0.001 in the whole group), more greatly in PA (r = 0.865; p = 0.001) than in CCHD (r = 0.506, NS). There was a good correlation between the levels of pC and apoB in the whole group (r = 0.606; p less than 0.001) and in PA (r = 0.662; p = 0.001), but not in CCHD (r = 0.288, NS). The content of pC also correlated with a apoB/apoA1 ratio (r = 0.445; p = 0.002 in the whole group of patients). This correlation was significantly positive in PA (r = 0.455; p = 0.044), but not in CCHD (r = 0.022). Thus, higher levels of PAI coincided with atherogenic changes in those of HDLC, and an increase in the content of pC was in agreement with that of apoB. The interrelationships are particularly typical of early stages of CHD.
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PMID:[Plasminogen activator inhibitor and protein C: their relation to plasma lipids and lipo- and apoproteins in ischemic heart disease of different duration]. 239 63

Diabetes mellitus (DM) is associated with an increased incidence of vascular complications. Abnormalities in the hemostatic system contribute at least in part to the development of vascular disease or atherosclerosis. In order to assess the actual degree of activation of the coagulation and fibrinolytic systems in diabetics, plasma levels of thrombin-antithrombin III complex (TAT) and plasmin-alpha 2-plasmin inhibitor complex (PAP) were measured together with tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1) in 18 patients with DM (three patients with type I DM and 15 with type II DM). Mean plasma levels of TAT (2.5 +/- SD 1.2 ng/mL) and PAP (0.9 +/- 1.2 micrograms/mL) were significantly elevated in diabetics as compared with healthy subjects (1.7 +/- 0.3 ng TAT and 0.2 +/- 0.1 micrograms PAP per mL of plasma; p = 0.009 and 0.02, respectively). Plasma antigen concentration of t-PA but not of PAI-1 was also elevated. No difference was found in the levels of these variables between type I and type II diabetics or between patients with and without retinopathy or nephropathy. These findings indicate that continuous activation of coagulation and fibrinolysis actually occurs in the majority of the patients with DM.
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PMID:Activation of blood coagulation and fibrinolysis in diabetes mellitus: evaluation by plasma levels of thrombin-antithrombin III complex and plasmin-alpha 2-plasmin inhibitor complex. 238 33

Serum lipids, lipoprotein (a), plasminogen activator inhibitor and tissue plasminogen activator levels were measured in 260 subjects, constituting a cross-section sample of 30-60-year-old men and women. For Lp(a), there were positive correlations with age and cholesterol, but not with any of other measured parameters. Triglyceride, cholesterol, and HDL-cholesterol (inversely) levels were associated with waist-to-hip girth circumference ratio: this variable remained significant in a multiple regression model. PAI-1 activity and tPA antigen levels were positively associated with triglycerides and inversely associated with HDL-cholesterol. Moreover, tPA antigen was positively related to total cholesterol level. In multiple regression analysis, however, only triglycerides were found to contribute significantly to the variance of tPA antigen and PAI-1 activity levels, when BMI (in men) and abdominal skinfold thickness (in women) were entered into the model. Insulin or glucose postload responses to an OGTT were not independently related to any lipid or fibrinolytic variable. These data demonstrate the importance of anthropometric variables both for fibrinolytic variables and traditional lipid risk factors. Only Lp(a) was found to be largely unrelated to the endocrine-metabolic and anthropometric variables.
Atherosclerosis 1989 Nov
PMID:Interrelationships between plasma levels of plasminogen activator inhibitor, tissue plasminogen activator, lipoprotein (a), and established cardiovascular risk factors in a north Swedish population. 253 10

To clarify whether the inverse relation between habitual fish consumption and cardiovascular mortality in the Dutch town of Zutphen could be explained by changes in platelet function or fibrinolysis, 40 healthy elderly men were selected from the Zutphen study population on the basis of their fish consumption over the last 26 years. In the high-fish group (n = 25) fish consumption was on average 33 g per person per day; in the low-fish group (n = 15) it was on average 2 g per person per day. This difference was reflected by significant differences in the concentrations of timnodonic acid (20:5n - 3) and cervonic acid (22:6n - 3) in the serum phospholipids of the participants. Between both groups no significant differences were observed in cutaneous bleeding time, platelet number, and collagen-induced platelet aggregation and ATP-release in whole blood. The same holds for the actual as well as the potential thromboxane B2 formation of activated platelets and for the activity of the plasminogen activator inhibitor. For most of the platelet-related variables a trend was found for a lower activity in the high-fish group. Therefore changes in platelet function might not explain, but may have slightly contributed to the inverse relationship between coronary heart disease and fish consumption, as observed in Zutphen.
Atherosclerosis 1989 Feb
PMID:Habitual fish consumption, fatty acids of serum phospholipids and platelet function. 271 61

Type 1 plasminogen activator inhibitor (PAI-1) is the primary inhibitor plasminogen activator and has been found to be increased in a number of clinical conditions generally defined as prothrombotic. Since in aging and in atherosclerosis the changes observed in the endothelium resemble those of in vitro aged endothelial cells, we have examined the expression of PAI-1 in cells at different population doublings. In senescent endothelial cells, PAI-1 mRNA and protein are constitutively high, but uninducible by exogenous interleukin 1 alpha as well as by the phorbol ester TPA. Interestingly the increase of PAI-1 levels correlates with the upregulation of interleukin 1 alpha, which characterizes endothelial cell senescence. Since PAI-1 expression is not increased in young cells made nondividing by contact inhibition, we anticipate that PAI-1 expression can be used as an appropriate marker of endothelial senescence. Moreover, PAI-1 was not upregulated in senescent or in progeric human fibroblasts, which do not overexpress interleukin 1 alpha, thus suggesting that multiple pathways may exist to regulate aging of human fibroblasts and endothelial cells.
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PMID:Senescence-dependent regulation of type 1 plasminogen activator inhibitor in human vascular endothelial cells. 762 47

We investigated the vessel status of coronary and peripheral arteries and those arteries supplying the brain in 929 consecutive male patients admitted to a coronary rehabilitation unit. The severity of coronary atherosclerosis was scored using coronary angiography. Changes in extracranial brain vessels and manifest cerebrovascular disease (CVD) were determined by B-mode ultrasound and Doppler examination. Peripheral arterial disease (PAD) was diagnosed using base-line and stress oscillography. We assessed variables of coagulation, fibrinolysis, and the acute phase response. There was a significant increase in plasma fibrinogen, plasminogen, d-dimer and C-reactive protein (CRP) with increasing severity of coronary heart disease. Compared to men with unaffected arteries, men with 3 diseased coronary arteries had 58% greater d-dimer concentrations. Patients with CVD and PAD, respectively, also had significantly higher fibrinogen, d-dimer and CRP concentrations. We did not find an association between plasminogen activator inhibitor activity and the severity of coronary atherosclerosis. In conclusion, plasma fibrinogen, d-dimer and CRP concentrations were significantly related to atherosclerosis in the coronary, peripheral and extracranial brain arteries.
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PMID:Association of variables of coagulation, fibrinolysis and acute-phase with atherosclerosis in coronary and peripheral arteries and those arteries supplying the brain. 766 18

In this population-based case-control study, we examined the relationship between the fibrinolytic variables tissue-plasminogen activator (t-PA) antigen and plasminogen activator inhibitor (PAI) activity, cardiovascular risk factors and peripheral arterial disease. Cases and controls were selected from the Edinburgh Artery Study, a random sample survey of men and women, aged 55-74 years. Mean levels of t-PA antigen and PAI activity were significantly elevated in 121 cases compared to 126 controls. The increased risks of peripheral arterial disease with increasing PAI activity and t-PA antigen levels were partly mediated by interactions with serum triglycerides, high density lipoprotein (HDL) cholesterol and cigarette smoking. For example, adjustment for triglycerides significantly reduced the odds of disease for PAI activity from 1.41 (95% confidence intervals 1.08, 1.86) to 1.24 (0.93, 1.65) and from 1.47 (1.09, 1.98) to 1.34 (0.99, 1.82) for t-PA antigen. We conclude that impaired fibrinolytic potential (raised PAI activity and t-PA antigen) is associated with peripheral atherosclerosis and that this relationship is partly influenced by lipids and cigarette smoking.
Atherosclerosis 1995 May
PMID:Tissue-plasminogen activator, plasminogen activator inhibitor and risk of peripheral arterial disease. 766 86

Accumulation of plasminogen activator inhibitor type 1 (PAI-1) in the arterial wall may accelerate atherogenesis by inhibiting fibrinolysis, diminishing proteolysis of extracellular matrix proteins, or modifying migration of vascular smooth muscle cells. Increased intramural expression of the PAI-1 gene is induced by thrombosis. To determine whether it occurs also in response to a sustained mechanical insult to endothelium, hypercholesterolemia, or both, rabbits were subjected to sustained aortic injury induced by implantation of indwelling polyethylene tubing, to hyperlipidemia induced by cholesterol and peanut oil feeding over a period of 8 weeks, or both. Sustained vascular injury alone did not increase plasma PAI-1. However, hypercholesterolemia with or without mechanically induced vascular injury increased plasma PAI-1 twofold. The expression of PAI-1 mRNA in aorta (Northern blots) was significantly increased when vascular injury was combined with hyperlipidemia. In situ hybridization showed that the increase with mechanical injury alone occurred in endothelial cells covering the neointima (positive for factor VIII and thrombomodulin), in abnormally differentiated vascular smooth muscle cells (positive for embryonic myosin heavy chain), and in macrophages (positive for the RAM-11 anti-macrophage antibody). Qualitatively similar but much more marked increases in PAI-1 gene expression were seen when arterial injury was accompanied by hypercholesterolemia. Neither vitronectin, known to stabilize PAI-1, nor vitronectin mRNA increased in liver. However, immunocytochemistry and Western blots demonstrated marked aortic accumulation of vitronectin protein with hyperlipidemia, particularly in subendothelial fibrotic regions, accompanied by increased neointimal vitronectin mRNA as shown by in situ hybridization. These results suggest that increased synthesis and stabilization of vascular PAI-1 may potentiate accumulation of extracellular matrix, thereby accelerating atherosclerosis.
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PMID:Potentiation by hypercholesterolemia of the induction of aortic intramural synthesis of plasminogen activator inhibitor type 1 by endothelial injury. 769 Mar 10


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