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

To minimize intraoperative blood loss a watertight knitted Dacron aortoiliac prosthesis has been developed by impregnation with bovine collagen. A potential disadvantage is that collagen may be associated with an increase in thrombus formation. We conducted a prospective randomized trial to study the systemic effects of collagen-impregnated prostheses and of aortoiliac operation as such on the coagulation mechanism during the first 10 days after operation. Forty-one patients randomly received either a collagen-impregnated (n = 20) or a nonimpregnated prosthesis (n = 21). Twelve patients who underwent cholecystectomies served as controls. Three markers of the coagulation mechanism were monitored: beta-thromboglobulin, fibrinopeptide A, and fibrin/fibrinogen degradation products. We found no significant differences in median beta-thromboglobulin, fibrinopeptide A, and fibrin/fibrinogen degradation product levels between patients in the collagen-impregnated prosthesis group and patients in the nonimpregnated prosthesis group. This indicates that collagen does not stimulate the coagulation cascade any more than conventional Dacron protheses do. In a comparison of patients who underwent aortoiliac reconstruction and patients who underwent cholecystectomies, the results indicated a significant increased platelet activation and fibrin metabolism in aortoiliac reconstruction group compared with the control group. Finally, we observed a significantly higher preoperative fibrin metabolism in patients with vascular disease than in control subjects. This difference is attributable to the high preoperative fibrin/fibrinogen degradation product values in patients with aortic aneurysms.
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PMID:Systemic effects of collagen-impregnated aortoiliac Dacron vascular prostheses on platelet activation and fibrin formation. 182 89

Hemostatic disorders in coronary heart disease and cerebrovascular disease patients were examined by studying two groups of prothrombotic and prethrombotic markers. Sixty subjects (28 male, 32 female aged 64 +/- 6 years) were included in the study of which 30 suffered from coronary heart disease and 30 from cerebral vascular disease; the first group was subdivided into those subjects with quiescent preinfarction angina (21 cases) and those with acute myocardial infarction (9 cases), whereas the second group was subdivided into subjects with cerebral stroke (20 cases) and those with TIA (10 cases). Each subject underwent an assay to assess fasting blood levels of fibrinogen, factor VII, antithrombin III (using a chromogenic method), plasminogen tissue activator, beta-thromboglobulin and dimer-D (ELISA method) 24 hours after being admitted to hospital. From an analysis of results it was observed that of the four prothrombotic markers used, fibrinogen and factor VII showed a generic increase in comparison to coronary heart disease and cerebrovascular disease patients; this was paralleled by significant reduction of antithrombin III; differences were even more marked and significant in acute thrombo-occlusive (infarction, stroke) compared to functional forms (angina, TIA). In line with other studies, the Authors favour an irritative type endothelial response leading to a marked and surprising increase of tPA. The two prothrombotic markers (BTG, D-D) also showed a thrombotic development in the two groups of patients examined with more significant findings in the occlusive forms (infarction, stroke) in comparison to transitory forms. On the basis of these and other published results the Authors confirm the usefulness of monitoring prothrombotic markers (fibrinogen, factor VII, AT III) in apparently normal subjects with or without risk factors or with slight initial signs of arteriosclerotic disease; these call for longitudinal or cross-sectional studies of an epidemiology type, in addition to isolated assay for a generic assessment of the patient's biological status, even if it is not yet possible to elaborate a protocol for the certain and specific diagnosis of a thrombophilic condition. The value of prethrombotic markers is apparent in the acute occlusive stage of the disease as a form of prognostic and therapeutic monitoring, and in preinfarction and above all silent transitory forms where, together with the use of other techniques (Holter), it provides interesting openings for confirming the diagnosis of an in vivo microthrombotic genesis and the consequent introduction of antithrombotic drug therapy.
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PMID:[The thrombophilic status and ischemic cardiopathy]. 195 44

Picotamide (G 137), a new non prostanoid inhibitor of in vitro arachidonic acid induced platelet aggregation, has been further characterized in in vitro and ex vivo studies. When whole blood was activated with collagen in the presence of picotamide 5 x 10(-4) M, thromboxane B2 production was decreased, and 6-keto-PGF1 alpha generation was significantly increased, suggesting a reorientation of platelet endoperoxide metabolism following blockade of thromboxane synthetase. Picotamide also inhibited platelet aggregation and clot retraction induced by the endoperoxide analogue U46619 in human platelets, indicating thromboxane A2-receptor antagonism, possibly of competitive nature. A single oral dose of picotamide 1 g in 24 healthy volunteers produced a significant inhibition of collagen, arachidonic acid and U46619-induced platelet aggregation. Serum levels of thromboxane B2 were also reduced. Chronic administration of picotamide 1.2 g/d to patients with vascular disease resulted in a prompt and persistent fall in their increased plasma levels of beta-thromboglobulin. The results indicate that picotamide is a combined thromboxane B2-synthetase inhibitor and thromboxane A2-receptor antagonist in human platelets, and that it may prove useful as an antithrombotic agent.
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PMID:"In vitro" and "ex vivo" effects of picotamide, a combined thromboxane A2-synthase inhibitor and -receptor antagonist, on human platelets. 196 45

In 30 patients with varying degrees of claudication and 40 normal subjects, plasma levels of beta-thromboglobulin were determined. These were significantly higher (p less than 0.01) in the patients than in age-matched controls; in the control group the beta-thromboglobulin values resulted slightly higher in older subjects. No correlation was found between beta-thromboglobulin and the severity of the vascular disease, assessed on the basis of the pain-free interval on the treadmill.
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PMID:Plasma beta-thromboglobulin levels and claudication degrees in patients with peripheral vascular disease. 242 48

Individuals with diabetes mellitus may have increased in vivo platelet activity. Abnormal platelet function could contribute to the increased incidence of vascular disease in diabetes mellitus. The biochemical mechanism(s) for platelet hyperactivation is unknown. We examined the hypothesis that platelet phosphoinositide turnover, a key signal-transducing mechanism involved in platelet activation, was abnormal in diabetic subjects. Platelets were harvested from 16 subjects with insulin-dependent diabetes mellitus (IDDM) and 19 healthy, nondiabetic control subjects of comparable age. Plasma beta-thromboglobulin (beta-TBG), a specific marker of platelet activity in vivo, was increased in IDDM (67.1 +/- 7.3 ng/ml) compared with control (41.0 +/- 6.0 ng/ml) subjects (P less than .005). [32P]orthophosphate (32Pi) incorporation into the individual phosphoinositides and phosphatidic acid (PA) reached isotopic equilibrium by 120 min for IDDM and control subjects. Specific activity (dpm 32P/micrograms phosphorus) of phosphatidylinositol 4-phosphate (PIP) and phosphatidylinositol 4,5-bisphosphate (PIP2) was not different between IDDM and control subjects. Under these conditions, basal 32Pi incorporation into PIP2 and PIP but not phosphatidylinositol (PI) or PA was significantly lower in IDDM subjects. There was significantly decreased [32P]PIP2 and [32P]PIP hydrolysis and decreased [32P]PA formation in IDDM after platelet stimulation with 4 U/ml human thrombin. There were no differences in [32P]PI hydrolysis between the two groups. The mass of PIP2 was reduced (P less than .005) in the platelets from IDDM (0.71 +/- 0.23 nmol/10(9) platelets) compared with control (1.65 +/- 0.53 nmol/10(9) platelets) subjects. Similarly, PIP was lower (P less than .001) in IDDM (0.66 +/- 0.09 nmol/10(9) platelets) than in control (2.92 +/- 0.43 nmol/10(9) platelets) subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased platelet phosphoinositide turnover and enhanced platelet activation in IDDM. 254 8

We measured simultaneous plasma beta-thromboglobulin (BTG) and adhesion of 51Cr-labelled, washed platelets to confluent, bovine aortic endothelial monolayers in 50 insulin-dependent diabetic patients and 30 normal subjects (respective mean ages (+/- SD) = 45.1 +/- 16.4 and 45.8 +/- 17.2 years). Compared to normal subjects without arteriosclerotic complications, diabetic patients had higher plasma BTG (34.8 +/- 1.8 (SEM) vs. 21.3 +/- 1.8 ng/ml) and platelet adhesiveness to endothelium (PAE) (3240 +/- 170 vs. 2430 +/- 120 X 10(3) platelets per well) (p less than 0.0002, respectively). Results in diabetic patients did not correlate with plasma glucose, hemoglobin AIa-c, known duration of disease, or sex; plasma BTG correlated with age (r = +0.36), and PAE correlated with plasma creatinine (r = +0.39). Those with clinically evident vascular disease, who were also older (47.8 +/- 2.6 (SEM) vs. 37.3 +/- 4.5 years, p less than 0.05), showed trends to higher plasma BTG (36.7 +/- 2.2 (SEM) vs. 28.8 +/- 3.4 ng/ml, p = 0.06) and PAE (3400 +/- 200 vs. 2800 +/- 280 X 10(3) platelets per well, p = 0.09). A strong correlation was found between plasma BTG and PAE in diabetic patients (r = +0.62, p less than 0.0001) either with or without vascular disease, which remained strong after statistical correction (partial Pearson correlation) for age and plasma creatinine, but not in normal subjects (r = +0.08, p greater than 0.1). These studies demonstrate that platelets in some diabetic patients are excessively adhesive to vascular endothelium, and that plasma BTG and platelet adhesiveness are intercorrelated.
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PMID:Plasma beta-thromboglobulin is correlated with platelet adhesiveness to bovine endothelium in patients with diabetes mellitus. 257 51

Endothelial injury and platelet activation may be involved in the pathogenesis of hypertensive vascular disease. The aim of this study was to evaluate the change in endothelial cell and platelet activation plasma markers after an acute physiological increase in blood pressure. Plasma renin activity (PRA), serum angiotensin-converting enzyme (ACE), plasma factor VIIIR:Ag, and plasma beta-thromboglobulin (BTG) were determined before and after handgrip in subjects with borderline (n = 8) and established (n = 11) hypertension and in age-matched normal volunteers (n = 10). A significant mean increase in ACE, factor VIIIR:Ag, and BTG was observed after handgrip in all groups of subjects. A greater response in BTG changes was found in hypertensive subjects when compared with normal subjects. No correlations were found between the blood pressure response after handgrip and the handgrip-induced changes in plasma markers of endothelial cells and platelet activation. Changes in endothelial cells and platelet activity occurring after handgrip did not appear to depend on the associated blood pressure elevations.
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PMID:Plasma markers of endothelial cells and platelet activation following handgrip in normals and hypertensive patients. 283 26

There are conflicting reports of platelet function abnormalities in diabetic patients without vascular complications. We have studied in vitro platelet aggregation, using platelet rich plasma and whole blood techniques, in 18 patients with uncomplicated insulin-dependent diabetes and a matched group of 24 non-diabetic subjects. In addition we measured plasma beta-thromboglobulin levels in these groups, as an index of in vivo platelet activation, and compared the indices of in vitro and in vivo platelet function before and after maximal bicycle exercise. Before exercise plasma beta-thromboglobulin levels and platelet sensitivities to ADP, collagen or adrenaline, as assessed by both methods of platelet aggregation, were the same in diabetic and control subjects. Both groups showed similar increases in beta-thromboglobulin levels and in platelet sensitivity to all agonists in whole blood following exercise. Using platelet rich plasma there were no changes in platelet sensitivity in either group after exercise. In non-diabetic subjects, increases in noradrenaline levels after exercise correlated with increases in platelet sensitivity to adrenaline in whole blood. This was not observed in the diabetic group. Abnormalities of platelet function, using the techniques described here, are not present in diabetic patients who do not have clinical evidence of vascular disease.
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PMID:Platelet function in uncomplicated insulin-dependent diabetic patients at rest and following exercise. 297 Sep 23

Platelets are believed to play a role in the pathogenesis of atherosclerosis and of the vascular obstruction that causes the acute complications of coronary artery disease. Since specific behavioral patterns appear to be related to the development of coronary artery disease and since emotional stress may predispose an individual to acute cardiovascular ischemia, it was hypothesized that platelet activation by catecholamines might be involved in these events. To study emotional stress, plasma samples were obtained from 61 senior medical residents immediately before they were to speak in public. There were significant increases in the plasma concentrations of the platelet-secreted proteins platelet factor 4 and beta-thromboglobulin and epinephrine and norepinephrine immediately before speaking, which demonstrates that platelet activation and secretion occur in association with this type of emotional stress. Four trials were carried out to study the mechanism for this observed platelet secretion: (1) phenoxybenzamine, (2) propranolol, (3) 650 mg aspirin, and (4) 80 mg aspirin were given several hours before the public speaking engagement. Neither phenoxybenzamine nor propranolol in doses that blocked the hemodynamic effects of alpha 1- and beta 1-adrenergic stimulation modified platelet secretion. Aspirin also did not block platelet secretion, which suggests that platelets were not being stimulated through a cyclooxygenase-dependent pathway. This study provides direct evidence of platelet secretion in vivo in association with emotional stress, and underscores the potential importance of platelet activation and secretion in the acute events that occur in patients with vascular disease.
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PMID:Platelet activation and secretion associated with emotional stress. 298 76

Mean levels of beta-thromboglobulin and platelet factor 4 were highly significantly elevated in diabetes compared to controls (72.6 v. 36.3 ng/ml, P less than 0.0005; 48.5 v. 16.5 ng/ml, P less than 0.0005; respectively) as was malondialdehyde formation (12.4 v. 8.1 nmol/10(9) platelets, P less than 0.0005). Diabetes with retinopathy had significantly higher levels of beta-thromboglobulin than those without retinopathy (79 v. 70 ng/ml; P less than 0.042). However, those diabetics without clinical evidence of vascular disease had levels of beta-thromboglobulin and platelet factor 4 significantly higher than controls. beta-Thromboglobulin did not correlate with glycosylated haemoglobin but did correlate significantly with individual lipid and lipoprotein levels (beta-thromboglobulin v. total triglyceride, P less than 0.029; v. VLDL triglyceride, P less than 0.041; v. LDL cholesterol, P less than 0.042; v. HDL/total cholesterol ratio, P less than 0.02). Abnormal platelet function may contribute to the vascular complications of diabetes mellitus.
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PMID:Platelet function in diabetes mellitus in relationship to complications, glycosylated haemoglobin and serum lipoproteins. 617 May 15


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