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PubMed1993

[Platelet functions in atherosclerosis].

Recent advances on platelet functions involved in atherosclerosis and subsequent thromboembolic diseases are reviewed. Platelets show multiple roles in hemostasis/thrombosis, wound healing, allergy, inflammation, metastasis of malignant cells and vasospasms through aggregation/secretion reaction. In atheromatous plaque, migration and proliferation of vascular smooth muscle cells and macrophages are the most prominent findings. In this pathological state, platelet may play as an enhancer by the secretion of bioactive substances including platelet-derived growth factor, serotonin and platelet factor 4. Investigation on platelet dynamics must be carried out not only for monitoring but also for the assessment of progressive factors in atherosclerotic disease.

Arteriosclerosis↗
PubMed2001

A comparison of von Willebrand Factor antigen with platelet activity in vitro in normal and venous occlusion blood.

Von Willebrand Factor (vWF) is essential for normal haemostasis involving platelet aggregation induced by high shear forces. In vitro a functional test of platelet aggregation using the filterometer is abnormal in von Willebrand's disease. However in normal people there is no significant correlation between the antigenic assay of vWF and the filter results. To study this discrepancy normal blood before and during venous occlusion, and blood before and after infusion of 1 deamino-(8-D-arginine) vasopressin was studied. During venous occlusion (VO) the increase in vWF due to the release of large multimers correlated precisely with the increase in the filterometer results. That this was due to the plasma vWF and not to any change induced in the platelets was shown as follows: The methodology was altered so that a small amount of the donor's platelet-poor plasma (PPP) was added to homologous normal substrate blood. The effect of the added donor's PPP was then shown to be closely correlated to the increase in the antigenic assay. Analysis of vWF multimer size showed during VO an increase in large multimers. We conclude that the effect of vWF on normal blood may be obscured by variation in platelet aggregability. In the filterometer system as elsewhere the large active multimers probably play a major part in causing platelet adhesion, aggregation and filter blocking. The filterometer test is influenced by the amount of vWF antigen, by the molecular size and activity of the vWF and by platelet sensitivity. Clinically this is a useful global test.

Adult↗
PubMed1975

Portsmouth syndrome: review of the literature and clinicopathological correlation.

Hereditary and acquired abnormalities of platelet function are recognized more frequently. Recent advances in platelet physiology have led to new tests of platelet function. Assessment of platelet adhesiveness and aggregation have allowed more definitive classification of platelet dysfunction. Platelet abnormalities will not be diagnosed before surgery. It would be impractical to perform these tests for platelet function as screening procedures on all patients; however, they should be considered as an important part of the laboratory screening for abnormal postoperative bleeding.

Adult↗
PubMed2004

Use of a new platelet function analyzer to detect von Willebrand disease in women with menorrhagia.

OBJECTIVE: The purpose of this study was to assess the usefulness of a new platelet function analyzer in the detection of von Willebrand disease and platelet dysfunction in women with menorrhagia. STUDY DESIGN: Women with menorrhagia and control subjects were tested with a platelet function analyzer. If the results were abnormal, further testing was performed for possible von Willebrand disease or platelet dysfunction. Results were compared. RESULTS: Of the 108 women with menorrhagia, 28 had an abnormal platelet function analysis results: 7 results were suggestive of von Willebrand disease; 17 results were suggestive of platelet dysfunction, and 4 results were inconclusive. Of the 100 control subjects, 18 subjects had an abnormal platelet function analysis result: 2 results were suggestive of von Willebrand disease; 12 results were suggestive of platelet dysfunction, and 4 results were inconclusive. The prevalence of suspected von Willebrand disease was 6% among women with menorrhagia and 2% among control subjects. Among white women, the prevalence was 10% compared with 1% among control subjects. CONCLUSION: We demonstrated that the platelet function analyzer could be used to detect von Willebrand disease in women with menorrhagia.

Adolescent↗
PubMed2002

PFA-100 and flow cytometry: can they challenge aggregometry to assess antiplatelet agents, other than GPIIbIIIa blockers, in coronary angioplasty?

INTRODUCTION: Platelet response to inhibitors varies widely, leading to a higher risk of abrupt closure events in insufficiently treated-coronary heart disease patients. The aim of this study was to compare, in patients under various antiplatelet regimens, three platelet function assays: aggregometry, PFA-100 and flow cytometry. These assays stand for available tests, as "ready-to-use" device (PFA-100) and sophisticated assay (cytometry). We chose the setting of percutaneous coronary intervention as a standardized procedure to determine which test was appropriate to detect the effect of (1) an aspirin bolus in patients under long-term aspirin treatment, and (2) ticlopidin in case of stent implantation. METHODS: Fifty patients under oral aspirin treatment were randomized to receive a bolus of 500 mg aspirin before angioplasty (n=25). Ticlopidin was given at a 500 mg loading dose in the case of stent implantation (n=38). Platelet function was assessed before, at 2 and 24 h after angioplasty. RESULTS: Considering aspirin antiplatelet effect, the following was observed: (1) a lack of further inhibition after the bolus whatever assay was used and (2) a disagreement between aggregometry and PFA-100 to classify patients as being poor or good aspirin responders (kappa were 0.11 and 0.28 between ADP 4 or 6 microM aggregation, respectively, and PFA-100). Another finding was the good performance of flow cytometry, which evaluated GPIIbIIIa activation, and aggregometry, to detect ticlopidin the day after the loading dose. In contrast, PFA-100 was insensitive to ticlopidin. CONCLUSION: Current assays are not interchangeable to monitor antiplatelet treatment in daily practice.

Angioplasty, Balloon, Coronary↗
PubMed1990

The bleeding time response to aspirin. Identifying the hyperresponder.

The authors measured the template bleeding time in 11 normal people before and 2, 4, 12, 24, and 48 hours after the subjects ingested a single dose of 74 mg of aspirin (ASA). The entire experiment was repeated twice at two-week intervals, with the dose of ASA increased to 325 mg and finally 3,900 mg. The mean increase was maximal at 4 and 12 hours, regardless of the dose administered, with a return to baseline by 48 hours. The authors then performed bleeding times in a prospective randomized double-blinded fashion on an additional 39 subjects at baseline and seven hours after they ingested either placebo or ASA 325 mg. The mean baseline bleeding time was 5.2 minutes (SD +/- 1.4), with a mean prolongation after ASA of 2.1 minutes (SD +/- 1.9). The authors identified 5 of 37 (14%) subjects as hyper-responders (HRs) using the criterion of a bleeding time prolongation of greater than 5.9 minutes (greater than 2 SD beyond the mean prolongation). Neither baseline bleeding time, threshold sensitivity of collagen-induced platelet aggregation, nor other tests of hemostatic function discriminated HRs from normals. The authors conclude that in subjects with normal baseline bleeding times, a prolongation of greater than 5.9 minutes when measured seven hours after the administration of a single dose of 325 mg of ASA can discriminate HRs from normals.

Adult↗
PubMed1979

beta-Thromboglobulin, platelet production time and pletelet function in vascular disease.

Plasma beta-thromboglobulin (beta TG) levels were measured in 103 healthy controls and 112 patients suffering from either peripheral vascular disease (PVD), or cerebrovascular disease (CVD) or deep vein thrombosis (DVT). Plasma beta TG was significantly elevated in 46 PVD patients and 24 recent DVT patients compared to controls, but did not differ significantly in 18 chronic DVT and 24 old CVD patients. In addition, heparin neutralizing activity (HNA) and platelet aggregation induced by adenosine diphosphate, 1-epinephrine and thrombin were compared in 33 out of the 46 PVD patients to 33 controls. The mean HNA was significantly shorter in the PVD patients than in controls. The rate and extent of platelet aggregation were increased in PVD patients compared to controls, but the difference was not statistically significant. Platelet production time (PPT) was measured in 20 controls, 35 PVD patients, nine chronic DVT and 12 chronic CVD patients; significantly shorter PPT was only observed in 14 patients with advanced PVD compared to controls, suggesting increased platelet consumption in these patients. All four assays (plasma beta TG, HNA, platelet aggregation and PPT) were performed in 25 patients; no correlation between the four tests was found in these patients suggesting that the tests were measuring various aspects of platelet function. These results suggest that in vivo platelet consumption as well as platelet aggregation and 'release reaction' are presumably enhanced in PVD and recent DVT patients and that plasma beta TG and PPT assays may be better and more specific indicators of in vivo platelet activation than in vitro platelet aggregation test.

Adolescent↗
PubMed1999

Platelet function abnormalities in Gaucher disease patients.

Bleeding manifestations are common in Gaucher disease patients. Although usually attributed to thrombocytopenia, some patients with relatively high platelet counts and normal coagulation tests have hemorrhagic phenomena. To investigate whether perturbed platelet function could explain these bleeding manifestations we performed platelet aggregation tests on 32 type I adult Gaucher patients who were not severely thrombocytopenic (platelet counts >50 x 10(9)/L). Seven patients (22%) had abnormal platelet aggregation. In five, platelet aggregation was markedly reduced in response to collagen and ADP and virtually absent in response to epinephrine, whereas two patients had isolated severely impaired epinephrine-induced aggregation. In one patient platelet aggregation markedly improved following one year of enzyme replacement therapy. Incubating normal platelets with high concentrations of glucocerebroside did not impair their ability to aggregate, suggesting that plasma glucocerebroside does not directly interfere with platelet function. Platelet dysfunction is a hitherto unrecognised, relatively common cause of excessive bleeding in Gaucher patients.

Adolescent↗
PubMedDate not supplied

The PFA-100: analysis and interpretation of a platelet function measurement.

The PFA-100 is a laboratory test designed to measure platelet function. Adequate platelet function depends upon the platelet's ability to adhere to the site of endothelial injury, activate surface receptors to attract other platelets and aggregate or clump together to form a platelet plug. This process is necessary to stop bleeding but may be harmful if it causes occlusion of a vessel. Platelet altering medication therapy is widely used in the prevention and treatment of coronary artery disease, peripheral arterial occlusive disease, and cerebrovascular ischemia. The PFA-100 provides the clinician with valuable information about platelet function. This information is helpful in determining the therapeutic effectiveness of antiplatelet medications, assisting in evaluating risk of bleeding and identifying primary platelet dysfunction.

Blood Platelets↗
PubMedDate not supplied

[The in-vivo effect of dihydroergocristine on human platelet function].

An acute test was run on healthy volunteers to assess the effect of i.v. dihydroergocristine methansulphonate on platelet function. The number of platelets was virtually unaffected, whereas adhesion to glass was significantly reduced. A direct and specific effect was noted on the 1st, adrenaline aggregation wave, while the 2nd wave (expression of ADP) induced aggregation did not appear to have been significantly altered. It is felt that further examination of the alpha-adrenergic block induced by the drug should be under-taken in view of the recent literature data which explain the inability of commonly employed anti-aggreganting drugs, such as acetylsalicylic acid, to prevent and treat atherothrombosis, in spite of the encouraging experimental results.

Adenosine Diphosphate↗
PubMed1985

Platelet survival and function in rats with enhanced thrombotic tendency.

We have investigated the relevance of some laboratory tests of platelet function in predicting conditions of thrombotic tendency. For this purpose, we studied platelet survival, platelet aggregation in response to different stimuli, TxB2 and 6-keto-PGF1 alpha production in serum of rats bearing a nephrotic syndrome induced by adriamycin. These animals show a heavy predisposition to the development of both arterial and venous thrombosis. The mean survival time was normal in nephrotic rats in comparison to controls. As to aggregation tests, a lower aggregating response was found in ADR-treated rats using ADP or collagen as stimulating agents. With arachidonic acid (AA) we observed similar aggregating responses at lower AA concentrations, whereas at higher AA concentrations a significantly lower response was found in nephrotic rats, despite their higher TxB2 production. Also TxB2 and 6-keto-PGF1 alpha levels in serum of nephrotic rats were significantly higher than in controls. No consistent differences were found in PGI2-activity generated by vessels of control or nephrotic rats. These data show that platelet function may appear normal or even impaired in rats with a markedly increased thrombotic tendency. On the other hand, the significance of high TxB2 levels in connection with mechanisms leading to thrombus formation remains a controversial issue.

6-Ketoprostaglandin F1 alpha↗