Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unlike classical microvascular complications, large-vessel atherosclerosis can precede the development of diabetes, suggesting that rather than atherosclerosis being a complication of diabetes, both conditions have common genetic and environmental antecedents, i.e., they spring from a "common soil." It is now known that adverse environmental conditions, perhaps related to less-than-optimal nutrition, in fetal and early life are associated with an enhanced risk of both diabetes and cardiovascular disease many decades later. These same adverse environmental conditions are also associated with the development in adult life of abdominal obesity and the insulin-resistance syndrome (IRS). The IRS consists of glucose intolerance, hyperinsulinemia, dyslipidemia (high triglyceride and low high-density lipoprotein [HDL] cholesterol levels), and hypertension. Although the mechanism underlying this cluster is controversial, the statistical association is well established. All of the elements of the IRS have been documented as risk factors for type II diabetes. Some, but not all, of these elements are also cardiovascular disease risk factors, in particular, hypertension and low HDL cholesterol. Other factors associated with the IRS that may enhance cardiovascular disease risk are plasminogen activator inhibitor 1 and small, dense low-density lipoprotein particles. Whether insulin itself is a risk factor remains controversial, but recent epidemiological evidence has been mostly negative. This question has marked clinical relevance because if the IRS enhances cardiovascular disease risk by virtue of its concomitant factors and not the hyperinsulinemia per se, this would tend to alleviate concerns that intensive insulin management of type II diabetic subjects could enhance the risk of large-vessel atherosclerosis. Clinical trials are urgently needed to settle this point.
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PMID:Diabetes and cardiovascular disease. The "common soil" hypothesis. 769 2

D-dimer, plasminogen activator inhibitor (PAI-1) activity at rest and after exercise, and tissue plasminogen activator (t-PA) activity after exercise were measured in venous blood in 88 patients with atherosclerotic lesions of various degrees. According to clinical symptoms, coronary angiography (CAG), ultrasound Doppler signal and duplex and colour Doppler scanning of carotid arteries and their branches, subclavian, vertebral and peripheral arteries of the lower limbs, patients were divided into four groups. Group 1, 16 men without CAG and ultrasound signs of atherosclerotic lesions; group 2, 27 patients with CAG-confirmed coronary artery disease; group 3, 18 patients with peripheral artery occlusive disease; group 4, 27 patients with coexistence of two or more regions of atherosclerotic lesions. D-dimer was the highest in patients with the most extensive atherosclerosis: 432 +/- 164 ng.ml-1 in group 3, 429 +/- 98 ng.ml-1 in group 4 vs 163 +/- 25 ng.ml-1 in group 1, P < 0.05. There were correlations (P < 0.05) between: age and D-dimer (r = 0.29); D-dimer and t-PA (r = 0.34); D-dimer and PAI-1, r = -0.29. Patients were also analysed according to D-dimer level. In patients with the highest level of D-dimer, the lowest level of PAI-1 activity and the highest level of t-PA activity after exercise were observed. The low PAI-1 activity is probably the result of an increased release of t-PA in these patients.
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PMID:D-dimer and fibrinolysis in patients with various degrees of atherosclerosis. 773 19

The influence of cigarette smoking and use of smokeless tobacco on plasma fibrinogen level, fibrinolytic variables, glucose tolerance and serum insulin was studied in a randomly selected population sample consisting of 604 men and 662 females between 25 and 64 years. Subjects were grouped according to tobacco habits as follows: regular smokers (> 1 cig/day), ex-smokers, snuff dippers, and non-tobacco users. An oral glucose tolerance test was performed on 54% of the participants. Tissue plasminogen activator (tPA) activity and plasminogen activator inhibitor type 1 (PAI-1) activity were used to study fibrinolysis. Men who smoked had 0.34 g/l (95% CI 0.17 to 0.49) higher fibrinogen level than non-tobacco users and numbers of cigarettes smoked correlated with plasma fibrinogen levels (r = 0.21, P = 0.006). Female smokers had significantly higher fibrinogen levels than ex-smokers but the difference compared with non-smokers was not significant. Snuff dipping did not affect fibrinogen levels. We found no relationship between tPA activity, PAI-1 activity and tobacco use. Post-load plasma glucose was lower in women who smoked, otherwise no influence of tobacco use on glucose levels was seen. Lower post-load insulin levels (-8.8 mU/ml, 95% CI -2.4 to -16.3) than in non-smokers were also found in women who smoked. This was only partially explained by a lower body mass index in smokers. We conclude that cigarette smoking is associated with increased fibrinogen levels, unaltered fibrinolysis, normal glucose tolerance and insulin levels. The use of smokeless tobacco, as moist oral snuff, does not appear to affect these potential cardiovascular risk factors.
Atherosclerosis 1995 Feb
PMID:Relationship of cigarette smoking and snuff dipping to plasma fibrinogen, fibrinolytic variables and serum insulin. The Northern Sweden MONICA Study. 775 54

Morbidity and mortality through coronary atherosclerosis are higher in Type 2 diabetic patients than in nondiabetic subjects, roughly by a factor of 2 in males and 3 in females. Methodological problems in attempting to weigh the relative effects of each factor make it difficult to accurately interpret the numerous epidemiological data already available. Three issues are discussed here:--Do diabetics have more "classic" risk factors than nondiabetics? The incidence of hypertension, lipid disorders, and even smoking is practically consistently higher in diabetics, with "diabetic" lipid disorders (decreased HDL cholesterol and hypertriglyceridemia) topping the list.--Do diabetics have specific risk factors which could explain the observed increase in coronary morbidity and mortality? The answer would appear to be yes, as patent microalbuminuria--between 30 and 300 mg/24 hours--is found, as well as retinopathy and an increase in fibrinogen and PAI1 plasminogen activator inhibitor. Recent genetic studies have highlighted the role of Lp (a), and particularly that of angiotensin converting-enzyme gene polymorphism (DD allele).--What are the respective roles of hyperglycalmia and elevated levels of circulating insulin? In contrast to the importance of insulin in nondiabetics as demonstrated in longitudinal studies, insulin appears to play a marginal or even nil role in diabetics once the disease is established. It is probably glycaemia itself which remains the fundamental factor, even though the mechanisms leading from hyperglycemia to macrovascular complications remain unknown.
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PMID:[Cardiovascular risk factors in type 2 diabetes]. 782 79

The aim of this study was to examine whether there was a relationship between haemostatic factors and ultrasound-assessed morphology of the common carotid artery and cardiovascular disease in 57- to 77-year-old men at high risk for atherosclerotic disease (hypertension and at least one of the following risk factors: hypercholesterolaemia, smoking, diabetes mellitus). They were divided into one group with (n = 59) and one group without (n = 70) manifest cardiovascular disease. An age-matched reference group with no cardiovascular risk factors was used as a comparison (n = 51). Significant associations, independent of smoking, were found between plasma fibrinogen and both the maximal intima-media thickness and the occurrence of plaque in the high-risk group. High-risk patients with clinical signs of cardiovascular disease had higher levels of plasma fibrinogen and prothrombin 1 + 2 fragment compared with both high-risk patients without concomitant cardiovascular disease and low-risk subjects. Plasminogen activator inhibitor, von Willebrand factor and thrombin/antithrombin complex were increased in the high-risk group with signs of cardiovascular disease in comparison with the low-risk group. In conclusion the results indicate that plasma fibrinogen may be operative in the development of atherosclerosis. Clinical signs of cardiovascular disease were associated with increased plasma levels of fibrinogen, von Willebrand factor, plasminogen activator inhibitor, thrombin/antithrombin complex and prothrombin 1 + 2 fragment.
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PMID:Carotid artery wall morphology, haemostatic factors and cardiovascular disease. An ultrasound study in men at high and low risk for atherosclerotic disease. 789 27

In 87 patients (studied on average 1 year after their strokes) and 26 of their first-degree relatives, our specific aim was to assess the prevalence of the following stroke risk factors: hypofibrinolysis, familial hypofibrinolysis, high lipoprotein (a) level, and dyslipidemia. At least 2 months after their strokes (primarily ischemic), 87 patients had measures of lipids and lipoprotein (a); 69 and 67 patients had measures of basal and stimulated fibrinolytic activity, respectively, four new findings were as follows. (1) Hypofibrinolysis was common, with bottom decile-stimulated tissue plasminogen activator activity (the major stimulator of fibrinolysis) in 21% of stroke probands and in 30% of their first-degree relatives, versus 7% of 29 nomolipidemic control subjects (p = 0.09 and 0.026, respectively). (2) The hypofibrinolysis was mediated by top-decile levels of basal plasminogen activator inhibitor activity (the major inhibitor of fibrinolysis), which were observed in 20% of stroke probands and in 21% of their first-degree relatives, versus 8% of 175 nomolipidemic control subjects (p = 0.007 and 0.04, respectively). Mean (SD) basal plasminogen activator inhibitor activity and antigen level were higher in stroke probands (18 +/- 18 U/ml and 35 +/- 31 ng/ml, respectively) than in the 175 normolipemic control subjects (14 +/- 10 [p = 0.002], 28 +/- 34 [p = 0.016]). (3) Levels of basal tissue plasminogen activator antigen, a probable marker for atherosclerosis, were much higher in stroke probands than in the 175 normolipemic control subjects (15 +/- 7.3 ng/ml vs 7 +/- 3.8, p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypofibrinolytic and atherogenic risk factors for stroke. 789 94

To assess the hypothesis that beta blocker use and hypertension are associated with high lipoprotein(a) [Lp(a)] or with reduced basal fibrinolytic activity, the authors studied relationships of hypertension and beta blockers to Lp(a), lipids, lipoproteins, apolipoproteins, and basal fibrinolytic activity in 385 patients consecutively referred for diagnosis and therapy of hyperlipidemia. A second aim was to determine possible gender differences in fibrinolytic activity among patients with hypertension. Ninety-nine patients (58 women [88% post-menopausal] and 41 men) had drug-treated hypertension. In women, hypertension was a positive, independent predictor of the major inhibitors of fibrinolysis, plasminogen activator inhibitor antigen (p = 0.017), and plasminogen activator inhibitor activity (p = 0.004). In men and women, major risk factors for atherosclerosis were significant, independent predictors of reduced basal fibrinolysis. Median Lp(a) in the 99 patients with hypertension (16 mg/dL) did not differ from Lp(a) (18 mg/dL) in normotensive patients (p > 0.1). Of the 385 patients, the 39 beta blocker users had higher plasminogen activator inhibitor activity (p = 0.01), higher triglyceride (p = 0.02) levels, and higher Quetelet Indices (p = 0.01) than non-users (n = 346). After covariance adjusting for age, Quetelet Indices, sex, and triglycerides, plasminogen activator inhibitor activity was not higher in beta blocker users than in non-users (p > 0.1). Median Lp(a) did not differ in beta blocker users (16 mg/dL) and in non-users (17 mg/dL), p greater than 0.1. Hypertensive, predominantly post-menopausal women are likely to have high plasminogen activator inhibitor activity and plasminogen activator inhibitor antigen with concurrent reduced fibrinolytic activity, as well as high fibrinogen levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta blockers, Lp(a), hypertension, and reduced basal fibrinolytic activity. 790 48

Increased plasma activity of plasminogen activator inhibitor 1 (PAI-1) is considered as a risk factor for thrombosis associated with atherosclerosis by reduction of fibrinolysis. Since nephropathic patients with non-insulin-dependent diabetes mellitus (NIDDM) are a cardiovascular high-risk group, which has yielded only controversial results as to the regulation of PAI-1, we compared 19 overt nephropathic NIDDM patients (mean age 63 years, serum creatinine 1.9 mg/dl, proteinuria 4.2 g/day) to 17 nondiabetic nephropathic patients with various causes of renal insufficiency (mean age 63 years, serum creatinine 2.8 mg/dl, proteinuria 3.9 g/day). We found normal PAI-1 levels for patients with diabetic nephropathy and significantly elevated PAI-1 levels within the upper normal range for nondiabetic nephropathic patients. Common risk factors in both groups were very high levels of fibrinogen, lipoprotein(a), serum cholesterol, and LDL cholesterol.
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PMID:Plasminogen activator inhibitor 1 activity and lipoprotein(a) in nephropathic patients with non-insulin-dependent diabetes mellitus versus patients with nondiabetic nephropathy. 795 56

Individuals with elevated levels of plasminogen activator inhibitor type 1 are at risk of developing atherosclerosis. The mechanisms leading to increased plasma PAI-1 concentrations are not well understood. The link observed between increased PAI-1 levels and insulin resistance has lead workers to investigate the effects of insulin or triglyceride rich lipoproteins on PAI-1 production by cultured hepatocytes or endothelial cells. However, little is known about the contribution of these cells to PAI-1 production in vivo. We have studied the expression of PAI-1 in human liver sections as well as in vessel walls from different territories, by immunocytochemistry and in situ hybridization. We have observed that normal liver endothelial cells expressed PAI-1 while parenchymal cells did not. However, this fact does not refute the role of parenchymal liver cells in pathological states. In healthy vessels, PAI-1 mRNA and protein were detected primarily at the endothelium from the lumen as well as from the vasa vasorum. In normal arteries, smooth muscle cells were able to produce PAI-1 depending on the territory tested. In deeply altered vessels, PAI-1 expression was observed in neovessels scattering the lesions, in some intimal cells and in smooth muscle cells. Local increase PAI-1 mRNA described in atherosclerotic lesions could be due to the abundant neovascularization present in the lesion as well as a raised expression in smooth muscle cells. The increased PAI-1 in atherosclerosis could lead to fibrin deposit during plaque rupture contributing further to the development and progression of the lesion.
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PMID:Plasminogen activator inhibitor-1 expression in human liver and healthy or atherosclerotic vessel walls. 797 74

Due to the incidence of symptomatic atherosclerosis in uremic patients, hemostasis-derived cardiovascular risk factors, basal plasma concentrations of some endothelial-derived glycoproteins and desmopressin-induced variations of endothelial-derived proteins were studied in 22 uremic patients on prolonged maintenance hemodialysis with no cardiovascular antecedent. Compared to control subjects, patients had increased predialysis hemostasis-related cardiovascular risk factors: high fibrinogen, proconvertin, and type 1 plasminogen activator inhibitor plasma concentrations; low albumin values; generally low antithrombin III values but sometimes high. They had high predialysis plasma concentrations of endothelium-derived glycoproteins: von Willebrand factor, tissue-type plasminogen activator and urokinase-type plasminogen activator, which are secreted by endothelial cells, but also soluble thrombomodulin, a marker of endothelial cell injury. The desmopressin-induced release of tissue-type plasminogen activator and of von Willebrand factor were lower than in controls. High fibrinogen, type 1 plasminogen activator inhibitor and low albumin plasma concentrations may be linked to repeated acute phase reactions associated with hemodialysis. Data concerning endothelium-related proteins are concordant with the co-existence of a chronic in vivo endothelial activation and endothelial injury in uremia. This could be linked to the initiation and progression of atherosclerosis.
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PMID:Increased cardiovascular risk factors and features of endothelial activation and dysfunction in dialyzed uremic patients. 799 2


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