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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

PARD is a prospective study sponsored by the German research council with the aim to establish whether spontaneously enhanced platelet aggregation or changes of other hemostatic parameters are risk factors for new vascular occlusion in diabetic patients. Hemostatic parameters have been measured in diabetic patients at 3 month-intervals (363 patients aged 45-65 at recruitment). Of the 232 men, 53 were on diet, 104 on oral antidiabetic drugs and 75 on insulin. Of 131 women 16 were on diet, 46 on oral antidiabetic drugs and 69 on insulin. Baseline data and preliminary results obtained between May 1977 and December 31, 1983 are presented. 22 patients have died. 17 diet from cardiovascular disease, 3 from pancreatic cancer and 2 from other causes. 51 patients suffered a myocardial infarction, stroke or peripheral arterial occlusions. The mean levels of spontaneous aggregation (angle alpha-PAT III), F VIIIC, F VIII R:AG, fibrinogen, antithrombin III and plasminogen were higher in men who died or suffered cardiovascular occlusions than in those without these events. In women this difference is less pronounced or absent. In women the mean values of several hemostatic parameters at baseline were higher than in men and the incidence of cardiovascular occlusions was lower. The interim results lead to the hypothesis that spontaneous aggregation, high levels of F VIIIC, F VIII R:AG and to some extent also high levels of fibrinogen, antithrombin III and plasminogen may be indicators of progressive vascular disease and could be useful as predictors of vascular occlusions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:PARD: platelet aggregation as a risk factor in diabetics: results of a prospective study. 293 12

Estrogen-progestogen oral contraceptives (OCs) have been shown in numerous studies to increase the risk of venous thromboembolic disease, myocardial infarction, and thrombotic stroke. Until recently, it has been assumed that the increased risk of vascular disease was attributable to the estrogen component of the OC. However, available evidence suggests that venous thromboembolic complications are determined by the estrogen component, whereas arterial complications may be due to both the estrogenic and progestogenic components. The authors investigated the comparative effect of different low-dose combined OCs on the hemostatic system. The effects of ethinyl estradiol on coagulation fibrinolysis and platelet function were found to be dose-related: 50 mcg of ethinyl estradiol produced significantly greater changes than 30 mcg, and the effects of 30 mcg ethinyl estradiol were modified by the progestogen used. Further studies compared 50 mcg and 30 mcg estrogen contraceptives and a triphasic formulation containing levonorgestrel. Again, changes in coagulation activity and fibrinolysis were related to the dose of estrogen and progestogen. The absence of significant changes in antithrombin III with monophasic and triphasic levonorgestrel suggests that levonorgestrel counteracts the action of estrogen in depressing this coagulation inhibitor. The fewest changes in coagulation factors and inhibitors occurred among women taking low-dose estrogen combined with levonorgestrel, indicating that progestogen used in combination modifies the estrogenic effects on the coagulation system. Current research is aimed at finding estrogen-progestogen combinations that produce fewer changes in the hemostatic system and in other metabolic processes. The combination of low-dose ethinyl estradiol with levonorgestrel in a triphasic preparation should reduce the risk of vascular complications and contribute to the safety of OCs.
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PMID:Oral contraceptives and blood coagulation. 294 71

To determine the effect of improved, short-term glycemic control on various functions of hemostasis in insulin-dependent diabetes, we measured changes in plasma fibrinogen, fibrinopeptide A (FPA), functional antithrombin III (AT-III), factor VIII:ristocetin cofactor ( VIIIRCoF ), beta-thromboglobulin (BTG), platelet factor 4 (PF4), and platelet aggregation responses to ADP and collagen in 12 patients with low or undetectable stimulated (postprandial) serum C-peptide levels during 4-8 wk (median, 6 wk) of treatment with constant subcutaneous insulin infusion. Mean plasma fibrinogen, FPA, AT-III, VIIIRCoF , and BTG at baseline were elevated compared with normal. Three patients had heightened platelet responses to ADP that did not correlate to other indicators of a hypercoagulable state; the affected patients, in fact, had significantly lower plasma BTG (25.5 +/- 5.3 [SEM] versus 44.6 +/- 4.6 ng/ml, P less than 0.05) and FPA (1.1 +/- 0.1 versus 2.5 +/- 0.5 ng/ml, P less than 0.05) than the remaining patients. Patients with clinically evident vascular disease had higher baseline plasma BTG and FPA than those without vascular disease (44.6 +/- 5.4 versus 30.2 +/- 4.6, and 2.6 +/- 0.6 versus 1.3 +/- 0.2 ng/ml, P less than 0.05, respectively). During treatment, all patients had declining blood glucose (200 +/- 18 to 102 +/- 5 mg/dl, P less than 0.001) and HbA1 (11.8 +/- 0.6 to 10.2 +/- 0.4%, P less than 0.005). No statistically significant changes in hemostatic functions were noted. During treatment, one patient had an acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma beta-thromboglobulin, platelet factor 4, fibrinopeptide A, and other hemostatic functions during improved, short-term glycemic control in diabetes mellitus. 620 89

Both micro and macro-angiopathy involve interaction of blood vessel and plasma factors which may be altered in diabetes. Little is known concerning changes in contact and fibrinolysis factors as prekallikrein, plasminogen and fast antiplasmin in diabetes. We tested also the plasminogen/antiplasmin ratio in 151 diabetics and 64 normal subjects (18 to 74 years old). Our conclusion is:--the absence of correlation between the clinical characteristic of diabetes and prekallikrein level,--the decrease of plasminogen/antiplasmin ratio in complicated diabetes,--in complicated diabetes, correlation between antithrombin III, VIII factor and fibrinogen levels, perhaps, in relation with inflammation signs.
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PMID:[Contact (prekallikrein) and fibrinolytic (plasminogen/antiplasmin value) system in the physiopathology of vascular complications of diabetes]. 681 91

The possibility of occurrence of daily variations in blood fibrinogen levels, platelets aggregation. Howell's time values and values for PTT, TT and antithrombin III was explored in 10 healthy subjects and in 10 patients with vascular disease. In normal subjects blood fibrinogen, platelets aggregation in ADP, PTT, Howell's time and TT values showed statistically significant daily variations, while the AT III values showed no significant variations over the 24-h cycle. In patients with vascular disease, on the other hand, the daily variations of the fibrinogen blood levels, of the maximum amplitude of platelets aggregation and of the Howell's values were not detected. In fact, the first two parameters remained consistently high and the third parameter remained consistently low throughout the 24-h cycle. In contrast, the PTT as well as the TT values in these patients showed statistically significant daily variations but with time patterns different than those found in normal subjects. Also, unlike to what obtained in healthy subjects, the AT III values in patients with vascular disease showed highly significant variations over the period of 24-h.
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PMID:Daily modifications of plasma fibrinogen platelets aggregation, Howell's time, PTT, TT, and antithrombin II in normal subjects and in patients with vascular disease. 711 42

Forty patients with atherosclerotic peripheral vascular disease, as compared to 29 healthy controls, showed a significant increase in platelet number and activity, a neutrophil leucocytosis, and a raised level of several acute-phase reactant proteins (fibrinogen, antithrombin III, factor VIII, and serum globulin). The hyperproteinaemia was associated with increases in plasma-, serum-, and blood-viscosity and is the likely cause of the hyperviscosity of vascular disease. These multiple haemostatic abnormalities closely resemble the non-specific, haematological stress-syndrome response to acute and chronic inflammatory disorders. In atherosclerosis also they may represent a non-specific, secondary response and neither be of aetiological significance nor reflect continuing low-grade intravascular coagulation.
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PMID:Haematological stress syndrome in atherosclerosis. 725 88

The correlation between elevated serum lipids, shortened coagulation time, and the accelerated thrombosis measured in vivo was found in experimental animals. Elevated levels of some coagulation factors were found in samples of human hyperlipoproteinemic plasma. Experimental hypertension induced significant rise of serum cholesterol and some coagulation factors also. If thrombosis is important in the genesis of atheroclerosis, these findings could indicate that elevation of plasma lipids may play a role, via the coagulation pathway, in the production of human vascular disease. These findings encouraged us to test the group of patients with rised blood pressure and to correlate their lipid and coagulation status. Statistically significant difference between hyperlipemia and normolipemic hypertonics was seen in level of factors V and VII reduced fibrinolytic activity, decreased antithrombin III, and in higher rate of hypercoagulabilic thromboelastograms.
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PMID:[Signs of hypercoagulability in hyperlipemic hypertensives]. 733 84

The authors investigated the behaviour of some markers of the haemostatic balance in a group of patients with acute focal cerebral vasculopathy. The series consists of 70 female patients (mean age: 61 +/- 5), 25 of whom suffering from TIA and 45 from thrombotic stroke; 40 normal controls (mean age 43 +/- 5) were also considered. For each patient after an overnight fasting a withdrawal of venous blood was done within 24-36 hours after the admission. For each sample the determination of seven prothrombotic markers [(fibrinogen (F), factor VII (F VII), antithrombin III (AT III), protein C (PC), protein S (PS) (coagulometric method IL), tissue plasminogen activator (t-PA), plasminogen activator inhibitor (PAI-1) (ELISA method Boehringer)] and of three prethrombotic markers [(fibrinopeptide A (FPA), beta-thromboglobulin (BTG) and D-dimer (D-D) (ELISA method, Boehringer)] was performed. The results obtained in the group of the cerebrovasculopathic patients compared to the controls showed a significant increase of F (p < 0.001), F VII (p < 0.005), BTG (p < 0.05) and D-D (p < 0.01), whereas significant differences regarding AT III, PC, PS, t-PA, PAI and FPA were not observed. The authors hypothesized that the increased levels of fibrinogen and factor VII in the cerebrovascular subjects, globally considered, may depend on a marked prothrombotic state, linked in a pathogenetic sense to the vascular disease; the existence of a prethrombotic state is also documented by the increase of betathromboglobulin and D-dimer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Haemostatic balance in patients with acute focal cerebral vasculopathy. 760 35

Microalbuminuria, i.e., slightly elevated urinary albumin excretion rate (UAER), notifies increased risk for atherosclerotic disease and may reflect an early generalized vascular abnormality in healthy subjects. This study was designed in order to examine whether such abnormality is associated with a shift of the haemostatic balance in prothrombotic direction. The following haemostatic factors were measured in two representative groups of clinically healthy subjects, 28 with microalbuminuria (UAER of 6.6-150 micrograms/min) and 60 age- and sex-matched controls with normoalbuminuria (UAER < 6.6 micrograms/min): Coagulation factors: blood platelet count and mean volume, plasma Factor VII antigen concentration and coagulant activity, and plasma concentrations of prothrombin fragment 1 + 2, thrombin-antithrombin III complexes, fibrinogen, and fibrinopeptide A; fibrinolytic and endothelial factors: plasma concentrations of tissue plasminogen activator antigen and plasminogen activator inhibitor type 1 antigen; and endothelial factor: plasma von Willebrand factor antigen concentration. The fibrinolytic and endothelial factors were measured both before and after 10 minutes of venous occlusion of the arm. None of the haemostatic factors were significantly altered in the microalbuminuric group. Plasma fibrinogen concentration tended to be elevated but not statistically significant ((mean (95% C.I.) 7.8 (7.2-8.3) vs. 7.2 (6.9-7.5) mumol/l; p < 0.1). Neither did any of the haemostatic factors correlate with UAER in regression analyses. It is concluded that the haemostatic balance is unaltered in healthy subjects with microalbuminuria. It is unlikely that a prothrombotic state is present as an intermedial factor early in a causal chain between microalbuminuria and atherosclerotic vascular disease.
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PMID:Aspects of haemostatic function in healthy subjects with microalbuminuria--a potential atherosclerotic risk factor. 777 57

Diabetes mellitus is associated with disturbances of the hemostatic system, which might contribute to the development of diabetic vascular disease. We investigated the effect of metabolic improvement by insulin therapy on the haemostatic system in 61 patients with type 2 diabetes mellitus and secondary sulfonylurea failure compared with 45 healthy control subjects matched for age, sex and BMI. Median age was 65, median diabetes duration 10 years. Median HbA1c (10%) and fructosamine (4.0 mM) levels were elevated before induction of therapy and decreased significantly within 6 months of insulin treatment to 7.5% and 3.0 mM, respectively (p < 0.0001). Compared with control subjects, median plasma levels of fibrinogen (317 vs 286 mg/dl), coagulation factor VII activity (1.1 vs 0.89 U/l), von Willebrand factor (1.6 vs 1.3 U/l), D-dimer (105 vs 86 micrograms/l), protein C:Ag (1.24 vs 0.95 U/l), total protein S:Ag (1.15 vs 0.91 U/l), and antithrombin III activity (1.17 vs 1.08 U/l) were significantly elevated. Levels of free protein S were not different from control values. No significant decline of coagulation parameters could be recorded during insulin therapy. Patients with diabetic vasculopathy had higher levels of D-dimer than those without (133 vs 76 micrograms/l before, 109 vs 88 micrograms/l during therapy), whereas the other haemostatic parameters were not different. Our data indicate a significant activation of the coagulation system in diabetic patients with secondary failure to sulfonylurea drugs, with signs of a prethrombotic state and endothelial cell disturbance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Haemostatic abnormalities persist despite glycaemic improvement by insulin therapy in lean type 2 diabetic patients. 858 33


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