Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aetiology of non-arteritic ischaemic optic neuropathy (ION) is multifactorial with local anatomical and systemic haemodynamic abnormalities both playing a role. A careful search for treatable vascular disease risk factors is required to allow rational therapy, to optimise the visual prognosis and to allow new insights into pathogenesis. We describe 7 cases in which there was an associated thrombophilic (prothrombotic) state; 4 had deficiencies of the physiological anticoagulants proteins C and S and antithrombin III and 2 had anti-phospholipid antibody (lupus anticoagulant) syndromes. A further patient had reduced levels of the physiological fibrinolytic agent tissue plasminogen activator (t-PA). In 5 patients other risk factors for small vessel occlusive disease were also present, and 4 had recurrent episodes of ION in the same eye. The visual prognosis in these patients may be improved by anticoagulation with warfarin.
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PMID:Coagulation abnormalities in ischaemic optic neuropathy. 801 26

The effects of acute smoking on hemostatic functions were investigated in healthy young volunteers. Immediately after the volunteers smoked, a significant increase in blood pressure and heart rate was accompanied by a rise in plasma epinephrine. Fibrinopeptide A and thrombin-antithrombin III complex as markers of thrombin generation in vivo were significantly increased after smoking. The increase in thrombin-antithrombin III complex was significantly correlated with that of plasma epinephrine. Both antigen and activity of tissue plasminogen activator and plasmin-inhibitor complex as markers of fibrinolytic activity in vivo were markedly increased after smoking, whereas D-dimer, plasminogen activator inhibitor antigen, fibrinogen, and both beta-thromboglobulin and platelet factor 4 as markers of platelet activation in vivo were not changed. No effects were observed after sham smoking under exactly identical conditions in the same subjects. Thus thrombin generation was observed as acute hemostatic effects of smoking. Enhanced fibrinolytic response may counteract an increased procoagulant activity. Patients with vascular disease might be more susceptible to a state of disequilibrium in favor of coagulation, which may partly explain a mechanism by which cigarette smoking leads to cardiovascular morbidity and mortality.
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PMID:Thrombin generation as an acute effect of cigarette smoking. 801 87

Immunohistochemical studies of human atherosclerotic lesions have demonstrated the occurrence of fibrin deposition and its degradation in the arterial wall. We studied fibrinogen, the generation of thrombin, and the degradation of fibrin in 40 patients with stable peripheral arterial occlusive disease of varying severity, as assessed by the ankle/brachial pressure index and duplex ultrasonography and/or angiography. Circulating fibrinogen (functional and immunological), fibrinopeptide A, thrombin-antithrombin III complex, and D-dimer were measured. The severity of atherosclerosis was associated with both fibrinogen (both functional and immunological) and D-dimer (r = .57, P < .0002, and r = .57, P < .0001, respectively). Fibrinogen and D-dimer showed a significant positive correlation (r = .50, P < .001). Generation of thrombin was detected in 24 patients (60%) by fibrinopeptide A and levels of thrombin-antithrombin III complex. As a sign of coagulation activation and fibrinolysis, we found that thrombin-antithrombin III complex and the degradation of cross-linked fibrin were progressively associated with the extent of vascular disease. The plasmin-mediated fibrin breakdown contributed to increased levels of circulating fibrinogen, an established risk factor for thrombotic complications. The significant correlations between fibrinogen/D-dimer and the severity of atherosclerosis support previous pathological studies and imply that local degradation of cross-linked fibrin is involved in the progression of atherosclerosis.
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PMID:Severity of peripheral atherosclerosis is associated with fibrinogen and degradation of cross-linked fibrin. 824 Oct 93

Homocystinuria is a rare inherited metabolic disease. Arterial and venous thromboembolic events represent frequent and life-threatening complications in homocystinuric patients. It has been suggested that mild homocysteinemia could be a risk factor for vascular disease. We have therefore measured total plasma homocysteine (HCy) concentrations by radioisotopic assay in 50 subjects with venous or arterial thrombosis and studied the relationship between HCy, coagulation and fibrinolytic parameters. Values were considered abnormal if they were higher than 2.7 standard deviations (SD) above the mean, i.e., 14.1 mmol/l. Thus, eighteen of the 50 patients with thrombosis were classified in the hyperhomocysteinemia group. Nine of these subjects had only this isolated risk factor. No correlations were found between HCy and antithrombin III, protein C, protein S and plasminogen levels, or plasma plasminogen activator inhibitor activity. Nevertheless, the correlation between tissue-plasminogen activator antigen and total plasma HCy was significant (r = 0.61, p < 0.001). Increased homocysteinemia seems to be a risk factor for thrombotic events especially knowing that HCy presents a direct cytotoxic effect. Vitamin therapy, already used in homozygote homocystinuric patients, might be beneficial in the prevention of thromboembolic disease in heterozygous patients.
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PMID:Elevated total plasma homocysteine, a risk factor for thrombosis. Relation to coagulation and fibrinolytic parameters. 832 83

The effect of exercise on plasma coagulant activity was studied in 16 subjects with newly-diagnosed type II diabetes without vascular complications and 9 healthy volunteers. Generation of thrombin was determined by a computer-assisted chromogenic method and results expressed as time to generate 50% maximal thrombin activity (T50/s). In addition, APTT, factor VIII and thrombin-antithrombin III (TAT) complex levels were measured. Pre-exercise FVIII:C [mean (+/- SD)] was increased in diabetic compared to control subjects [1.5 (0.4); 0.9 (0.2) IU ml-1; (p < 0.001) respectively]. No significant differences in APTT, TAT or T50 were detected between the groups. Exercise induced a rise in FVIII complex, reduction of APTT [33 (2) s to 31 (2) s; (p = 0.004)] and T50 [58 (6) s to 53 (6) s; (p = 0.01)] in controls and an increase in FVIII complex but no significant changes in APTT or T50 in diabetic patients, with no change in TAT in either group. A greater increase in FVIII:C than vWF levels occurred in controls [0.2 (0.1); 0.1 (0.1) IU ml-1; (p = 0.005)] and patients [0.3 (0.4); 0.2 (0.1) IU ml-1; (p = 0.032)]. In patients, FVIII:C correlated inversely with APTT (r = -0.522, p = 0.038) and T50 (r = -0.592, p = 0.016). The results show that FVIII:C levels are increased at diagnosis in patients with type II diabetes without vascular disease but there is no enhancement of plasma procoagulant activity. In healthy individuals, exercise induced activation of coagulation which was not seen in patients, suggesting that it does not precipitate a state of accelerated thrombogenesis in subjects with uncomplicated type II diabetes.
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PMID:The effect of short-term exercise on plasma procoagulant activity in patients with type II (non-insulin-dependent) diabetes and healthy volunteers. 836 78

Increased urinary albumin loss in patients with Type 1 diabetes is associated with accelerated atherosclerosis. Prothrombotic factors known to be associated with cerebrovascular and coronary artery disease in the general population, antithrombotic factors, were studied in 52 patients with Type 1 diabetes and varying urinary albumin loss and 24 non-diabetic control subjects. Fibrinogen increased from 2.5 g l-1 (95% confidence interval 2.3-2.8) in control subjects and 2.8 g l-1 (2.6-3.0) in diabetic patients without microalbuminuria to 3.1 g l-1 (2.7-3.5) with microalbuminuria (p < 0.005 vs control; p < 0.001 vs without microalbuminuria). Factor VIIc increased from 81% (75-86% in non-diabetic control subjects and 84% (78-90%) in diabetic patients without microalbuminuria to 103% (89-117%) with microalbuminuria (p < 0.005 vs control; p < 0.05 vs without microalbuminuria) and 118% (86-150%) with albuminuria (p < 0.005 vs control and p < 0.001 vs without microalbuminuria). Levels of the antithrombotic factors protein C, protein S, and antithrombin III also rose in the diabetic patients with evidence of renal damage. Elevation of prothrombotic factors has been associated with increased risk of microvascular disease, whereas elevation of antithrombotic factors has no known protective effect. Therefore, this pattern of alteration of haemostatic factors in diabetic renal disease may contribute to the increased risk of vascular disease associated with both microalbuminuria and albuminuria.
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PMID:Prothrombotic and antithrombotic factors are elevated in patients with type 1 diabetes complicated by microalbuminuria. 845 88

Diabetes mellitus is associated with disturbances in hemostasis that could contribute to the development of diabetic vascular disease. We investigated the changes in parameters of blood coagulation and the fibrinolytic system and in plasma levels of lipoprotein(a)(Lp(a)) in 124 patients with type II diabetes mellitus and 44 healthy control subjects matched for age and body mass index (BMI) to determine whether hemostatic disturbances may lead to increased cardiovascular mortality. Median levels of fibrinogen (P < 0.0001), thrombin-antithrombin III complex (TAT) (P < 0.005), and plasminogen activator inhibitor-1 (PAI-1) activity (P < 0.05) in plasma were significantly elevated in diabetic patients compared with controls. The median concentration of Lp(a) was significantly higher in diabetic patients than in normal controls (18.2 vs. 12.6 mg/dl. P < 0.0005). Lp(a) levels tended to be elevated in patients with a prolonged history of diabetes. There was no evidence that Lp(a) levels were affected by metabolic control or by type of treatment. Twenty-two diabetics with coronary heart disease (CHD) had significantly higher levels of fibrinogen (P < 0.05), TAT (P < 0.05), and Lp(a) (24.7 vs. 13.7 mg/dl, P < 0.01) than the 51 patients without diabetic angiopathy. Our data indicate that impaired hemostatic balance in diabetes may cause hypercoagulability and may thus contribute to the increased cardiovascular mortality in diabetes.
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PMID:Hypercoagulability and high lipoprotein(a) levels in patients with type II diabetes mellitus. 864 73

The aim of the present study was to evaluate some metabolic, coagulation and fibrinolytic parameters in 35 patients (24 males and 11 females, mean age 57 +/- 4 years) suffering from myocardial infarction more than 6 months before with or without carotid atherosclerotic lesions. After evaluation by B-mode duplex scanning system of extracranial carotid arteries, the patients were subdivided into two groups: Group 1 (n = 16, with carotid plaques or intima-media thickening) and Group 2 (n = 19, without carotid plaques or intima-media thickening). Eighteen age- and sex-matched subjects were recruited as controls (Group 3). Groups 1 and 2 displayed significantly higher levels of total cholesterol and apolipoprotein B and significantly lower levels of HDL-cholesterol and apolipoprotein A1 than Group 3, while serum triglyceride and lipoprotein (a)-Lp (a) levels were significantly higher in Group 1 as compared to the control group. Moreover, Group 1 and 2 displayed significantly higher levels of factor VII, fibrinogen, F1+2, thrombin-antithrombin complex and plasminogen activator inhibitor (PAI) post venous occlusion and significantly lower levels of tissue plasminogen activator (t-PA) post venous occlusion than Group 3. Significantly higher levels of t-PA and PAI pre venous occlusion and significantly lower levels of antithrombin III, C-protein and S-protein were observed in Group 1 as compared to controls. In patients with highest Lp(a) level, the lowest t-PA level post venous occlusion and the highest PAI level post venous occlusion were observed. Our data show an activation of coagulation and a deficient fibrinolysis in survivors of myocardial infarction, particularly in those with associated carotid atherosclerotic lesions. We speculate that this thrombophilic state may play a key role in the pathogenesis of atherosclerotic vascular disease and thromboembolic complications.
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PMID:[Thrombophilic state inpatients suffering from myocardial infarction with or without carotid atherosclerotic lesions]. 870 61

We identified a group of 24 young (less than 50 years of age) women with isolated, premature atherosclerotic aortoiliac occlusive disease and attempted to identify distinguishing hemostatic characteristics. Most of these patients (62%) presented with acute thromboembolic events (blue toe syndrome, n = 6; macroemboli, n = 6; or aortoiliac thrombosis, n = 3). Aortoiliac reconstruction (aortoiliac endarterectomy, n = 10, aortobifurcation bypass grafts, n = 6; and percutaneous angioplasty, n = 4) was complicated by early thrombosis in 6 of 20 cases (30%), (1 of 10 endarterectomies, 4 of 6 bypass grafts, and 1 of 4 angioplasties). Fresh thrombus overlying an atherosclerotic plaque was a common finding at surgery. This observation and the relatively high incidence of thromboembolic events led us to hypothesize that a characteristic hemostatic profile might underlie the remarkably similar clinical presentations of these women. Levels of antiphospholipid antibodies (anticardiolipin antibodies and lupus anticoagulant), plasminogen activator inhibitor-1, fibrinogen, antithrombin III, protein C, protein S, plasminogen, prothrombin fragment F1 + 2, and D-dimer were determined for these young women and for 21 age-matched white female control subjects without vascular disease and nine white male patients with aortoiliac occlusive disease (mean 61 years, range 43 to 74 years). The incidence of anticardiolipin antibodies was 42% (8 of 19) in the female patients, which was significantly elevated (p = 0.028). The female (62.5%) and male (100%) patients had significantly elevated D-dimer levels (p < 0.001). Deficiencies of antithrombin III, protein C, and protein S were rare. A unique pattern of premature aortoiliac atherosclerosis exists in some young women. Intra-arterial thromboembolic events are common at presentation and complicate surgical management. The role of antiphospholipid antibodies remains uncertain.
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PMID:Young women with advanced aortoiliac occlusive disease: new insights. 898 71

The advent of improved diagnostic tests for primary hypercoagulability has led to increased recognition of this entity as a problem in surgical patients. We treated 20 patients with documented evidence of increased coagulability from 1975 to 1995. Clinical presentations included venous (16) and arterial (4) thrombosis. Symptoms usually occurred early in life (mean age, 38 years) and developed spontaneously without a secondary inciting event or factor. Deficiencies in naturally occurring anticoagulant proteins including antithrombin III (n = 7), protein C (n = 3), and protein S (n = 1) were seen, as were problems with lupus anticoagulant (n = 2) and anticardiolipin antibody (n = 4) deficiencies. Treatment of these patients is difficult, and results are often suboptimal. A total of 12 vascular reconstructions were required in 5 of the 20 patients; 11 eventually failed. Patients with primary venous thrombosis were often successfully treated with anticoagulant therapy in the short term but fared less well in the long term. There were three deaths directly related to thrombotic complications. Surgeons may encounter patients with primary hypercoagulable syndromes. The diagnosis should be expected in patients with unusual patterns of vascular disease or arterial or venous thrombosis without cause or at an early age, or in patients with recurrent or migratory clotting. Evaluation of this population, although expensive, is indicated. Treatment with chronic anticoagulation is also generally indicated. Arterial reconstruction in this subset of patients usually leads to a poor outcome.
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PMID:Surgical implications of hypercoagulable syndromes. 901 31


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