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PubMed1986

Storage of platelets for tests of platelet function: effects of temperature on platelet aggregation, platelet morphology and liberation of beta-thromboglobulin.

We have studied the effect of temperature on platelets during storage for tests of platelet function. Aliquots of PRP were stored at constant pH at 37 degrees C, room temperature and 4 degrees C. At intervals up to five hours, samples were taken for estimation of platelet shape, plasma levels of beta-thromboglobulin and 14C-serotonin, and assessment of platelet aggregation in response to a range of concentrations of ADP and collagen. When PRP was stored at 37 degrees C there was a gradual decrease in the aggregation response during the period of storage. At room temperature the decrease was slower but the response to ADP often increased dramatically before decreasing; at this temperature there was pronounced liberation of beta TG while there was none at 37 degrees C. Platelets stored at 37 degrees C were smooth and elliptical when examined by electron microscopy, but those stored at room temperature showed partial loss of discoid shape and formation of some pseudopodia. Storage at 4 degrees C was associated with total loss of discoid shape and formation of many large pseudopodia. Light transmission studies also showed loss of discoid shape at room temperature and 4 degrees C. We conclude that storage at 4 degrees C or at room temperature causes platelet activation. To avoid this PRP should be stored at 37 degrees C prior to tests of platelet function.

Blood Platelets↗
PubMed1989

Qualitative platelet defects in chronic myeloproliferative disorders: evidence for reduced ATP secretion.

19 consecutive untreated patients with chronic myeloproliferative disorders and thrombocytosis were subjected to comprehensive platelet function tests including platelet aggregometry. 12 patients had essential thrombocythaemia (ET) and 7 patients had polycythaemia vera (PV). Bleeding time was normal. Arachidonic acid, collagen and ristocetin aggregation were abnormal only in a minority of patients, whereas ADP aggregation was impaired in 16 out of 19 patients. The most conspicuous findings were abolished second-wave adrenalin aggregation, increased ADP aggregation threshold, and markedly reduced ATP secretion during collagen-induced aggregation. This triad of qualitative platelet defects seems to be a good diagnostic marker of chronic myeloproliferative disease with thrombocytosis.

Adenosine Diphosphate↗
PubMed1988

Platelet dysfunction in malaria.

Platelet function tests including platelet aggregation, PF3, bleeding time and clot retraction were studied in 48 malarial patients. The suppression of platelet aggregation was demonstrated in both P. vivax and P. falciparum infection. However, this abnormality was more prominent in malarial patients who had systemic complications and bleeding. The recovery of the impaired platelet aggregation was observed at period of 7 and 14 days after parasitemia in malarial patients without and with systemic complications. The correlation between the suppression of platelet aggregation and thrombocytopenia was observed. From this study, bleeding in malaria are operated by two mechanisms: thrombocytopenia and severely depressed platelet aggregation.

Adult↗
PubMed1987

Low-dose aspirin protects against lipid accumulation in primate vein bypass grafts.

Platelet inhibition with high-dose aspirin combined with dipyridamole reduces lipid accumulation and improves early patency of coronary artery bypass grafts. However, recent evidence suggests that platelet inhibition can be achieved with substantially lower aspirin doses than have been conventionally prescribed. To evaluate whether low-dose aspirin protects against lipid accumulation in bypass grafts, we studied 15 stump-tailed macaque monkeys in which autologous cephalic veins were grafted into the femoral arteries. A control group received no treatment, a second group was treated with a low, single daily dose of aspirin (12 mg), and a third group was given a higher dosage of aspirin (80 mg/day) combined with dipyridamole (50 mg/day) divided into two daily doses. A special diet was fed that resulted in plasma cholesterol levels (224 +/- 50 mg/dl, mean +/- standard deviation) and plasma lipoprotein distributions that mimic the profile in humans. Cholesterol concentration in grafts removed 3 months after insertion was 0.47 +/- 0.12 mg/100 mg tissue in the control group; it was reduced to 0.23 +/- 0.04 mg/100 mg (p less than 0.001) by low-dose aspirin and to 0.17 +/- 0.05 mg/100 mg (p less than 0.001) by combined aspirin and dipyridamole therapy. Graft apolipoprotein B concentration was 66 +/- 19 micrograms/100 mg in control group; it was reduced to 40 +/- 8 micrograms/100 mg (p less than 0.05) by low-dose aspirin and to 23 +/- 7 micrograms/100 mg (p less than 0.001) with the combination treatment. There were no differences between groups in either cholesterol concentration (0.09 +/- 0.02 mg/100 mg) or apolipoprotein B concentration (10 +/- 3 micrograms/100 mg) in normal ungrafted vein. Platelet function tests demonstrated platelet aggregation in all control monkeys, in none of the combined therapy group, and in two of five monkeys receiving low-dose aspirin. This study indicates that low-dose aspirin is protective against graft lipid accumulation in monkeys. The mechanism of this antilipid effect and its relation to any antithrombotic effect remain to be elucidated.

Animals↗
PubMed1996

[Antiplatelet agents (inhibitors of platelet function) orally administered. Bases for their practical use in coronary artery disease].

Long-term antithrombotic therapy, administered orally, is necessary in all patients with symptomatic coronary artery disease; the most commonly used drugs are those which inhibit platelet aggregation. Aspirin and ticlopidine do not act on the same point of platelet function. They have the common property of inhibiting platelet function irreversibly and of partially inhibiting platelet aggregation. Flurbiprofenee acts like aspirin on thromboxane synthesis but the effect is reversible in 24 hours. The full effect of ticlopidine is only observed after several days' administration. The association of aspirin and ticlopidine is used over short periods after implantation of a stent. The dosage of ticlopidine is 2 tablets per day; that of aspirin is not well established (100 to 330 mg per day in a single dose). Special galenic forms are marketed for this indication in France. Biological monitoring (white cell count) is required with ticlopidine. It has not been shown to be of value to investigate the parameters of primary haemostasis (bleeding time, platelet function--tests of platelet aggregation). However, under certain circumstances, the advice of a haematologist may be useful, especially before an invasive procedure.

Administration, Oral↗
PubMed2002

The laboratory evaluation of platelet dysfunction.

An algorithm for platelet function testing is presented in Fig. 2. The proposed algorithm takes into account the importance of a thorough clinical bleeding history and provides an integration of screening tests with more specific diagnostic assays. As our understanding of the biochemical and molecular aspects of platelet function becomes increasingly refined, it is becoming clear that current clinical testing strategies may not be adequate to identify all significant platelet function defects. The repertoire of distinct platelet agonists is increasing to allow a more discrete look at the function of isolated platelet membrane agonist receptors, especially those involved in platelet activation by ADP, thrombin, and collagen. In addition, FACS analysis of platelets, with emphasis on surface membrane glycoprotein expression, may offer a more specific and quantitative view of platelet membrane constituents and their function. Furthermore, screening tests evaluating platelet function under physiologic and pathologic flow conditions are becoming important adjuncts to in vitro analyses, and may accentuate platelet function abnormalities, not easily discerned by platelet aggregation studies. It remains to be seen whether such screening tests will better predict clinical bleeding or thrombotic risk.

Algorithms↗
PubMed1986

Platelet function and coagulation studies in patients with mitral valve prolapse.

Twenty-eight consecutive patients with mitral valve prolapse (MVP), seven of whom had previous cerebrovascular disorders (CVD), were studied for platelet function and coagulation tests. While platelet function tests were found to be normal with the exception of platelet aggregation rate (PAR), there was a significant rise of factors VIII vWF:Ag (Von Willebrand) and (FPA) fibrinopeptide A. Six cases had high levels of both these factors, suggesting the existence of a particular subset of patients with MVP, with a higher risk of thromboembolic episodes, although only three out of seven patients with previous CVD had either FPA or VIII vWF:Ag levels. The broad spectrum of subjects with MVP probably explains the different results obtained when studying platelet function and coagulation factors. Therefore, larger population studies and prolonged follow-up of cases with either coagulation abnormalities similar to the ones found in the present report and/or altered platelet function tests are suggested to discover if it is possible to detect patients with a potential for thromboembolism.

Adolescent↗
PubMed1986

Thrombocytopenia and pseudothrombocytopenia: a clinical and laboratory problem.

During a 4-month period, the patients with thrombocytopenia (N = 14) at a haematological outpatient clinic were subjected to a special laboratory investigation. Evidence of pseudothrombocytopenia was found in 5 of the patients. 1 patient with a giant platelet syndrome associated with deficient platelet function was also found. It is concluded that pseudothrombocytopenia and various thrombocytopathies provide a significant confounding factor in the management of patients with alleged thrombocytopenia. It is therefore suggested that the initial diagnostic work-up of alleged thrombocytopenia patients should include an assessment of platelet morphology in addition to an overall haemostatic test (bleeding time) and platelet function tests.

Bleeding Time↗
PubMed1996

Intravenous ketorolac tromethamine worsens platelet function during knee arthroscopy under spinal anesthesia.

Ketorolac prolongs bleeding time and inhibits platelet aggregation and platelet thromboxane production in healthy, awake volunteers. However, platelet function was recently shown not to worsen after ketorolac was given during general anesthesia. The purpose of this study was to investigate platelet function changes during a standardized spinal anesthetic and surgery, as well as after a single intraoperative dose of intravenous (IV) ketorolac. The study comprised 30 ASA physical status I patients undergoing spinal anesthesia for knee arthroscopy. Subjects were randomized to receive either ketorolac 60 mg IV 15 min after skin incision or placebo IV. Platelet function testing consisted of an Ivy bleeding time, platelet aggregometry with adenosine diphosphate (ADP) and collagen, thromboelastography (TEG), and serum thromboxane B2 (TxB2) assays. Platelet function testing was performed: 1) 15 min prior to the performance of spinal anesthesia; 2) 10 min after surgical skin incision; and 3) 45 min after administration of study drug. The placebo group demonstrated no changes in any platelet function variable during spinal anesthesia and surgery relative to preoperative values. The ketorolac group, however, demonstrated a significant increase in bleeding time from postincision to poststudy drug data points (213 +/- 60s to 275 +/- 85s, mean +/- SD; P < 0.01). Further, platelet aggregometry to collagen was diminished in the ketorolac group from preoperative to poststudy drug data points (90.8% +/- 7.6% to 60.5% +/- 32.5%; P < 0.01). Platelet aggregometry with ADP, however, was unchanged in the ketorolac group. Platelet TxB2 production decreased dramatically in the ketorolac group from preoperative to poststudy drug data points (157.2 +/- 129.4 to 0.3 +/- 0.3 ng/mL; P < 0.01). Platelet function does not appear to be accentuated during spinal anesthesia as it is during general anesthesia. Unlike during general anesthesia, platelet function during spinal anesthesia is impaired, with respect to bleeding time and platelet aggregometry to collagen, by a single intraoperative dose of IV ketorolac.

Adolescent↗
PubMed2002

Platelet functions in patients with meningococcal meningitis at the Kenyatta National Hospital, Nairobi.

OBJECTIVE: To determine platelet abnormalities in patients with menigococcal meningitis. DESIGN: Case control study. SUBJECTS: Fifty seven cases of mennigococcal meningitis based on a cerebrospinal fluid gram stain for gram negative diplococcus or positive culture were recruited. Fifty-seven controls matched for age and sex were also recruited. The following platelet functions tests were performed; platelet counts, platelet adhesiveness, platelet aggregation and clot retraction. RESULTS: Fifty seven patients (41 males and 16 females) with meningococcal meningitis were studied. Their mean age was 25.5 +/- 8.32 years with a range of 15 to 45 years. Five patients had purpura, four peripheral gangrene, eight conjunctival haemorrhages and one was in shock. There was a statistical significant difference in the platelet aggregation and clot retraction between the patients and controls at p-values of 0.0001 and 0.0002 respectively. There was no significant difference in the platelet count and adhesiveness between the patients and the controls at a p-value of 0.203 and 0.22 respectively. No association was found between the platelet functions and the clinical presentations. CONCLUSION: Patients with meningococcal meningitis have abnormalities in the platelet functions mainly in aggregation and adhesiveness.

Adolescent↗
PubMed2006

The antiplatelet drug target in atherosclerotic diseases.

The aim of this review is (1) to give a rationale for anti-platelet therapy based on mechanisms of platelet rich arterial thrombosis, (2) to point out the pitfalls involved in monitoring therapy with platelet function tests and (3) to outline the potential clinical applications of such therapy based on the various modes of action of anti-platelet drugs. The primary event in arterial thrombosis is platelet-mediated, either due to increased shear or exposed collagen, followed by fibrin-rich thrombosis. Anti-platelet therapy needs to be monitored but most platelet function tests, now in use, do not reflect in vivo function; the anticoagulant used for blood samples removes extra-cellular calcium ions, platelets are often separated before the test, or very high doses of agonist are used: all of these can give misleading results. We review means whereby platelet function can be monitored in whole blood samples anticoagulated with the pure thrombin inhibitor, hirudin. We review the available methods of modifying platelet activity and are particularly interested in agents that do not cause bleeding. Present therapy causes bleeding by interference with COX1, the P2Y(12) receptor or the platelet fibrinogen receptor complex, all of which can be associated with bleeding complications. In contrast, serotonin does not influence formation of haemostatic layers although it is implicated in shear-induced aggregation and thrombus propagation by positive feedback from the large amount of intraplatelet serotonin. We suggest that further investigation of selective serotonin 5HT(2) antagonism would allow effective management of intravascular thrombosis without bleeding complications. This would be safer both as prophylaxis and would also allow cardioprotection of vascular patients undergoing surgical operations.

Atherosclerosis↗
PubMed1996

Bleeding time and platelet function in essential thrombocythemia and other myeloproliferative syndromes.

Bleeding time (BT) and platelet function tests have been widely used in patients with essential thrombocythemia (ET), with the aim to support diagnosis and to identify laboratory predictors of haemorrhagic and thrombotic complications. BT is significantly prolonged in 7-19% of ET patients and several functional abnormalities have been observed in platelet structure, biochemistry and survival. However, the attempt to relate these in vivo and in vitro platelet dysfunctions with diagnosis or clinical sequelae has been generally disappointing. Therefore, BT and platelet function tests are currently not recommended in the initial evaluation or during the follow-up of patients with ET, unless in the setting of a clinical or biological study. A noteworthy exception is represented by a subset of patients characterized by very high platelet count (> 1500 x 10(9)/L) and bleeding symptoms, who can have an acquired von Willebrand disease. In these cases, prolonged BT and abnormal multimeric pattern of von Willebrand factor are useful for diagnosing and monitoring this acquired hemorrhagic disease. BT and platelet function tests should be included in the baseline evaluation of ET patients enrolled in prospective clinical trials aiming assess their predictive role on clinical end-points.

Arachidonic Acid↗
PubMed2006

The paradox of platelet activation and impaired function: platelet-von Willebrand factor interactions, and the etiology of thrombotic and hemorrhagic manifestations in essential thrombocythemia and polycythemia vera.

Patients with essential thrombocythemia (ET) and polycythemia vera (PV), complicated by microvascular ischemic or thrombotic events, have shortened platelet survival, increased beta-thromboglobulin, platelet factor 4, and thrombomodulin levels, and increased urinary thromboxane B2 excretion. These are all reversible by inhibition of platelet cyclooxygenase 1 with aspirin, and are therefore indicative of platelet activation and platelet-mediated thrombotic processes. The thrombotic tendency persists as long as platelet counts are above the upper limit of normal (400 x 10 (9)/L). Despite strong evidence of in vivo platelet activation, the ex vivo platelet function tests are impaired. Platelet dysfunction in ET and PV typically is characterized by a missing second-wave adrenaline aggregation, an increased adenosine diphosphate aggregation threshold, and reduced secretion products, but a normal arachidonic acid or collagen-induced aggregation. The proposed concept is that platelets in thrombocythemia (ET and PV) are hypersensitive. Due to the existing high shear stress in the microvasculature (end-arterial circulation), platelets spontaneously activate, secrete their products, form aggregates mediated by von Willebrand factor (vWF) that transiently plug the microcirculation, deaggregate, and then recirculate as exhausted defective platelets with secondary storage pool disease on ex vivo analysis. At increasing platelet counts from below to above 1000 x 10 (9)/L, the thrombotic condition changes into an overt spontaneous bleeding tendency as a result of a functional vWF deficiency that is caused by proteolysis of large vWF multimers. This is consistent with acquired type 2 von Willebrand syndrome (AvWS). AvWS is reversible by reduction of the platelet count to normal. The acquired JAK2 V617F gain of function mutation is the cause of trilinear myeloproliferative disease with the sequential occurrence of ET and PV. Heterozygous JAK2 V617F mutation with slightly increased kinase activity is enough for the induction of spontaneous megakaryopoiesis and erythropoiesis, and an increase of hypersensitive platelets is the cause of aspirin-sensitive, platelet-mediated microvascular ischemic and thrombotic complications in ET and early PV mimicking ET. Homozygous JAK2 mutation with pronounced increase of kinase activity is associated with pronounced trilinear megakaryocyte, erythroid, and granulocytic myeloproliferation, with the most frequent clinical picture of classical PV complicated by major thrombosis, in addition to the platelet-mediated microvascular thrombotic syndrome of thrombocythemia.

Aspirin↗
PubMed1983

Aldolase release rate and platelet function.

We have developed a new platelet function test which is a method to estimate the rate of release of aldolase from platelets into a low osmotic pressured artificial medium and into PRP, which we called the platelet aldolase release rate. As this aldolase release rate have a good reproducibility and correlate well with other platelet function test, this test can be utilized for clinical examination.

Blood Platelets↗
PubMed2006

Evaluation of platelet function, a method comparison.

Platelet function can be studied using many different methods why it is of interest to understand how data from different assays relate to each other. In the present study we compare two methods suitable for screening purposes with two established although laborious methods, impedance aggregometry and platelet-rich plasma (PRP) aggregation. The alternative assays tested were: (i) exposure of active alphaIIbbeta3, in diluted whole blood and (ii) whole blood aggregation assessed by residual platelet counting. The fibrinogen receptor activation assay was found to have the lower variability, higher sensitivity to ADP, and higher signal to noise ratio compared with residual platelet counting. The sensitivity and response profile of the fibrinogen receptor activation assay and residual platelet counting were more similar to PRP aggregation than to impedance aggregometry, whereas impedance aggregometry displayed lower sensitivity to ADP. The two alternative assays correlated well with PRP aggregation as well as with each other. The fibrinogen receptor activation assay displayed the highest potency for AR-C69931MX, possibly due to a lower protein content compared with residual platelet counting. The two studied assays compare well with the more established assays, and are thus both good alternatives for platelet function testing and evaluation of new potential platelet antagonists.

Adenosine Diphosphate↗
PubMed2006

A prospective, randomized platelet-function study of heparinized oxygenators and cardiotomy suction.

OBJECTIVE: The purpose of this study was to determine if substitution of a heparin-coated oxygenator and salvaged autologous blood for cardiotomy suction would improve platelet function. DESIGN: A prospective, randomized trial. SETTING: A large academic medical center. PARTICIPANTS: Sixty adult patients undergoing coronary artery bypass graft surgery with cardiopulmonary bypass (CPB). INTERVENTIONS: Patients were randomized into 1 of 4 groups in a 2 x 2 factorial design by oxygenator (heparinized v nonheparinized) and blood salvage during CPB (cardiotomy suction v salvaged autologous blood). MEASUREMENTS AND MAIN RESULTS: Primary outcome measures were platelet function, glass-bead retention, platelet dense-body adenosine triphosphate secretion, platelet-rich plasma (PRP) aggregometry, Plateletworks platelet-function analyzer (Helena Laboratories Corp, Allen Park, MI), and platelet count. Secondary outcome measures were chest-tube drainage and allogeneic blood transfusion requirements. All platelet-function tests except thrombin-receptor activator peptide-induced PRP aggregometry showed a reduction in platelet function during and immediately after CPB (all p < 0.05). The only statistically significant difference in platelet-function tests between the groups was the glass-bead assay at 5 minutes before discontinuation of CPB (p < 0.05). This difference resolved 10 minutes after protamine administration. There were no differences between the groups in the amount of blood transfused, chest-tube drainage, and routine laboratory test results. CONCLUSIONS: The authors concluded that the effects of these changes to the CPB circuit were small and inconsequential in this cohort of patients.

Adult↗
PubMed1978

Platelets, thromboembolism and the clinical utility of antiplatelet drugs.

Experience has established a major role for platelets in the pathogenesis of a variety of thromboembolic disorders. Despite advances in several areas, many problems remain. The relevance of platelet function testing to thromboembolic disorders needs clarification. Whether the association of enhanced platelet function and the aforementioned disorders represents cause, effect or nonspecific accompaniment is unknown. The concept of identifying individuals at risk by platelet function testing is attractive but unproved. Whether such individuals would benefit from prophylactic antiplatelet therapy is also unknown. For treatment of most established thromboembolic disorders as well as prophylaxis, the place of antiplatelet drugs is not established. Whether this form of therapy is superior to conventional treatment, adjunctive or of no benefit is not resolved in most instances. Also, the most appropriate antiplatelet drug or combination of drugs, and in which dosages for specific disorders, remains unclear. Well designed, prospective clinical investigation, although cumbersome and time-consuming, will be necessary to answer most of these questions. A final problem area concerns research into the pharmacology of platelet inhibition. It is probable that the ideal antiplatelet agent remains undiscovered. Currently, several investigators are looking into the possibility of manipulating prostaglandin metabolic pathways in hopes of specifically blocking thromboxane generation while allowing production of metabolites inhibitory to aggregation. This exciting approach and other investigations into the biochemical basis of platelet function should lead to the discovery of new antiplatelet agents.

Animals↗