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PubMed2005

Assessment of a platelet function analyser in horses: reference range and influence of a platelet aggregation inhibitor.

The objective of this study was to assess whether a new human platelet function analyser (the PFA-100) could be used to evaluate platelet function in horses and detect acetylsalicylic acid (ASA)-induced platelet dysfunctions. Citrated blood samples from 40 healthy horses were processed to obtain reference values for closure time (CT) using cartridges with collagen-ADP (CT-ADP) and collagen-epinephrine (CT-EPI) as platelet agonists. In addition, CT-ADP and CT-EPI were also measured before and 24 h after oral ASA administration in another 12 healthy horses. The sensitivity and specificity of the test were also determined. In normal horses, means+/-SD value for CT-ADP was 85.1+/-13.1 s (median, 82 s), and CT-EPI ranged from 158 to >300 s (median 291 s). Calculated reference ranges were 60.5-115.9 s and 158.5->300 s for CT-ADP and CT-EPI, respectively. Administration of ASA significantly (P<0.001) prolonged CT-ADP values from 91.0+/-13 to 113.5+/-14.4 s, and CT-EPI values were also significantly (P<0.008) prolonged after ASA administration. Sensitivity and specificity results for ADP cartridges showed that a prolonged CT value would be highly suggestive of a platelet aggregation inhibition. In conclusion, ADP cartridges can be used in horses to assess primary haemostasis and may be a valuable test for the detection of platelet aggregation inhibition.

Animals↗
PubMed2006

Biological efficacy of low against medium dose aspirin regimen after coronary surgery: analysis of platelet function.

The failure of aspirin to inhibit platelet function has been documented in patients undergoing coronary artery bypass graft (CABG) surgery, but the causes of "aspirin-resistance" remain uncertain. The aim of this study was to investigate the efficacy of aspirin in patients undergoing CABG surgery receiving either 100 mg or 325 mg of oral aspirin for 5-days. Platelet function was tested the day before surgery and on day +1 and day +5, and evaluated by changes in collagen-induced thromboxane-A2 (TxA2) release and platelet aggregation following stimulation with collagen, ADP and epinephrine. In all patients, baseline platelet aggregation was significantly inhibited by pre-incubation with in vitro aspirin (150 micromol/l), with a mean reduction in TxA2-release of >or=95.5% (82.3,99.1). After 5-days of oral aspirin, platelet aggregation was significantly inhibited, and was not further inhibited by in vitro aspirin. Oral aspirin was also associated with a >or=99.5% (97.8, 99.7) reduction in TxA2-release, and with the reversal of the second-phase of ADP-induced aggregation which is TxA2-dependent. In addition a single-dose of 325 mg aspirin on the first post-operative morning may have a greater inhibitory effect on collagen-induced aggregation than 100 mg aspirin. Western blot analysis provided no evidence for the presence of COX-2 in platelets, while the up-regulation of p38-MAPK following platelet-stimulation and surgery was seen. The inhibition of COX-2 (NS398) or p38-MAPK (SB203580) activity did not affect platelet aggregation and TxA2-release on day +5. In summary, there was no evidence for inherent or acquired aspirin-resistance in this surgical population, or for the involvement of either COX-2 or p38-MAPK.

Adenosine Diphosphate↗
PubMed2005

Effect of increasing doses of aspirin on platelet function as measured by PFA-100 in patients with diabetes.

INTRODUCTION: Platelets of diabetic patients have been reported to be less sensitive to aspirin. The aim of this study is to compare a medium (300 mg) and low (100 mg) dose of aspirin on platelet function in diabetic patients. METHODS: We have included one hundred and two patients with type 2 diabetes mellitus. Platelet function was measured as closure time (CT) with the Platelet Function Analyzer (PFA)-100 before the administration of aspirin. Initially the patients were given 100 mg aspirin once daily for seven days, and then the measurements were repeated. If the CT exceeded the upper limit of 300 s, the study was terminated. If not, the patients continued the aspirin therapy with a dose of 300 mg daily for another seven days, and the CTs were measured again. RESULTS: After taking 100 mg aspirin, the CT significantly increased from 126+/-29 s to 256+/-66 s (p<0.001). In 68 of 102 (67%) patients, the CT increased to 300 s. In the remaining 34 patients, the baseline CT was 113+/-29, and increased to 170+/-45 s after 100 mg aspirin (p<0.001). In these patients, there was a further increase in the CT from 170+/-45 to 229+/-75 s following 300 mg aspirin (p<0.001). On average, the CT was increased by 60% and 39% following ingestion of 100 and 300 mg aspirin, respectively. CT>300 s were obtained in 15 (44%) of 34 patients after 300 mg aspirin. CONCLUSIONS: Although, a daily dose of 100 mg aspirin effectively inhibited platelet function in a majority of diabetics, a considerable proportion of patients showed a greater platelet inhibition with the use of 300 mg aspirin. The PFA-100 closure time may be used to separate those patients who require a higher dose of aspirin to achieve desired antiplatelet effect.

Adult↗
PubMed1996

Platelet size: measurement, physiology and vascular disease.

Platelet volume is a marker of platelet function and activation. It is readily measured as mean platelet volume (MPV) by clinical haematology analysers using sodium citrate as the anticoagulant. Measurement in EDTA can be unreliable since MPV increases significantly in a time-dependent manner. MPV correlates with platelet function and activation, whether measured as aggregation, thromboxane synthesis, beta-thromboglobulin release, procoagulant function, or adhesion molecule expression. MPV is increased in certain vascular risk factor states, including hypercholesterolaemia and diabetes mellitus, but not essential hypertension. It is increased in acute myocardial infarction, acute ischaemic stroke, pre-eclampsia and renal artery stenosis. Importantly, an elevated MPV predicts a poor outcome following myocardial infarction, restenosis following coronary angioplasty, and the development of pre-eclampsia. Research into the epidemiology of MPV is now required to determine whether thrombomegaly is a risk factor for developing vascular disease. Similarly, the physiological mechanisms which regulate MPV within the megakaryocyte need to be elucidated. Whether MPV ever becomes a routinely requested test remains to be seen but changes in methodology will be required first.

Blood Platelets↗
PubMed1985

Alpha-adrenoceptor number and function in platelets from treated and untreated patients with essential hypertension and age- and sex-matched controls.

Alpha 2-receptor number was measured on platelets from 19 healthy normotensive volunteers and 19 patients with essential hypertension, using [3H]-yohimbine binding. Platelet function was assessed using the primary aggregation response to adrenaline. The mean alpha 2-receptor number (Bmax fmol/10(8) platelets) in platelets from normotensive controls was 31 (188 sites/cell) and was significantly higher than in age- and sex-matched hypertensive subjects, for whom Bmax = 24 (144 sites/cell) (P < 0.01 by paired t-test). There was no change in the affinity for [3H]-yohimbine binding. Platelet aggregation responses to adrenaline did not differ between hypertensive and normotensive subjects. Blood pressure reduction with prazosin in eight hypertensive subjects did not alter receptor number either acutely or following 1 month of treatment. These findings may be interpreted as evidence for enhanced receptor coupling to functional responses of a significantly smaller receptor population in patients with essential hypertension.

Adult↗
PubMed1976

Defective platelet function following the administration of penicillin compounds.

Platelet function and blood coagulation were studied in five human volunteers receiving penicillin-G in incremental doses of 1.2--48 million U/day, in six volunteers receiving ampicillin in incremental doses of 60--300 mg/kg/day (4--20 g/day), and in six volunteers receiving methicillin in incremental doses of 60--300 mg/kg/day. Coagulation tests remained normal in all 17 volunteers. However, ADP-induced platelet aggregation became abnormal in every subject except one receiving ampicillin and one receiving methicillin. Defective aggregation occurred with predictability with the following doses: penicillin-G, 24 million U/day; ampicillin, 300 mg/kg/day; methicillin, 300 mg/kg/day. All volunteers given penicillin-G and all given ampicillin experienced dose-related prolongation of bleeding time which did not occur with methicillin. Striking prolongation of bleeding time occurred only with penicillin-G in doses of 48 million U/day. Other tests of platelet function including clot retraction, platelet factor 3 availability, and collagen-induced or epinephrine-induced aggregation remained normal during the administration of these drugs. Measurement of intracellular adenine nucleotides revealed that the ADP and ATP content of platelets was unaffected. It appears that at least one mechanism by which the penicillin compounds alter platelet behavior is by interfering with activation of these cells by ADP.

Adenosine Diphosphate↗
PubMed1996

Inhibition of blood platelet functions by cationic amphiphilic drugs in relation to their physico-chemical properties.

The effects of bromadryl, dithiaden, chloroquine and propranolol on thrombin-stimulated rat platelet aggregation (measured turbidimetrically) and thromboxane B2 generation (detected by an RIA method) were compared with four selected physico-chemical parameters of these drugs. Platelet aggregation was inhibited in the rank order of potency: bromadryl > dithiaden > propranolol > chloroquine, which corresponded with the decrease in the net charge of the terminal methyl-(or ethyl-) groups in the side chain and with the increase of the dipole moment of drug molecules. On the other hand, the rank order of potency in which the drugs tested inhibited thromboxane B2 formation (chloroquine > dithiaden > bromadryl > propranolol) correlated well with the decline in molar refractivity of the drugs. No relationship was found between inhibitory effects of drugs and their partition coefficients. The results presented indicate that inhibition of platelet functions might consist of several types of drug-cell interactions, depend on the structure and physico-chemical properties of the drugs and cannot be estimated simply on the basis of partition coefficients.

Animals↗
PubMed1989

In vitro bleeding test--a simple method for the detection of aspirin effects on platelet function.

We investigated platelet function of 21 healthy blood donors before, 4 hrs and 1 to 7 days after a single oral dose of 0.02 (n = 3), 0.05 (n = 3), 0.1 (n = 3), 0.5 (n = 2) and 1.0 g (n = 10) aspirin. Three additional donors received 0.02 g aspirin/day for 5 days. A new and simple in vitro bleeding test (Thrombostat) using whole blood was far more sensitive than all other tests for platelet function (subaquatic bleeding time, thrombelastrogram, resonance-thrombogram, platelet adherence, spreading and aggregation). With this method using 2mM CaCl2 as additional agent all donors showed significantly increased in vitro bleeding volumes, for at least 2 days after ingestion of 0.1 to 1 g aspirin. In the majority of cases the aspirin effect could be detected even after 5-6 days. In 2 of 3 donors even 0.05 g aspirin was detectable. There was already a definite effect seen after 2 days in all 3 cases when 0.02 g was ingested daily. The new in vitro bleeding test should be suitable for the control of low dose aspirin prophylaxis of arterial thromboembolic disorders.

Aspirin↗
PubMed1983

Indexes of intravascular hemolysis, quantification of coagulation factors, and platelet survival in patients with porcine heterograft valves.

Ten patients with porcine heterograft valves who were not receiving anticoagulant agents were evaluated to determine the effect of the valve on red blood cell survival and on platelet activation and consumption as measured by (1) quantification of the coagulation mechanism, (2) platelet function studies, and (3) 51-chromium platelet survival time. There was no evidence of significant intravascular hemolysis as determined by the reticulocyte count, serum iron and iron binding capacity, serum bilirubin level, or lactic dehydrogenase activity. The coagulation profile and the platelet function studies were normal. No statistically significant difference was found in the platelet survival time in the 10 patients with porcine heterograft valves (half-life 3.2 +/- 0.8 days) and the 11 normal control subjects (half-life 3.6 +/- 0.6 days) (p greater than 0.2). The finding of a normal platelet survival time in patients with porcine heterograft valves is consistent with clinical experience indicating that this device is associated with a low incidence of systemic embolization, approximating 3% per year.

Adult↗
PubMed2006

Platelet function monitoring with the Sonoclot analyzer after in vitro tirofiban and heparin administration.

OBJECTIVE: Reliable platelet function monitoring is desirable in patients treated with glycoprotein IIb/IIIa receptor inhibitors. The aim of the present laboratory-based study was to assess platelet function after administration of clinically relevant doses of the glycoprotein IIb/IIIa antagonist tirofiban with or without heparin by using Sonoclot (Sienco Inc) and platelet aggregometry. METHODS: Tirofiban (0-100 ng x mL(-1)) and heparin (0 or 1 U x mL(-1)) were added to blood samples obtained from 20 healthy volunteers. Coagulation analysis was performed on citrated whole blood by using the Sonoclot analyzer. The glass bead-activated test and the new glass bead test with heparinase were used. The results were compared with adenosine-5'-diphosphate-activated platelet aggregometry. RESULTS: Administration of tirofiban showed a similar increase of platelet inhibition detected with the Sonoclot glass bead-activated test and glass bead test with heparinase, as well as by means of aggregometry. Bias between the different techniques was comparable; Spearman rank correlation was strong (glass bead-activated test vs aggregometry: rho = 0.823, P < .001; glass bead test with heparinase vs aggregometry: rho = 0.856, P < .001). After additional administration of heparin, platelet inhibition was only comparable for the glass bead test with heparinase and aggregometry, and the correlation coefficient remained unchanged for the glass bead test with heparinase versus aggregometry (rho = 0.878, P < .001). By contrast, the glass bead-activated test showed a nearly complete platelet inhibition with a significant bias compared with the glass bead test with heparinase and aggregometry. Correlation was weak for the glass bead-activated test versus aggregometry (rho = 0.407, P = .004). CONCLUSIONS: When compared with platelet aggregometry, the glass bead-activated test from Sonoclot reliably detects glycoprotein IIb/IIIa receptor inhibition with tirofiban in unheparinized whole blood. However, in heparinized blood the glass bead test with heparinase is essential to accurately assess platelet function.

Adult↗
PubMed2004

Enhanced anticoagulant activity of enoxaparin in patients with ESRD as measured by thrombin generation time.

BACKGROUND: Patients with renal dysfunction who undergo systemic anticoagulation with enoxaparin are at increased risk for bleeding. Although there is decreased renal clearance of enoxaparin in this population, the clinical utility of monitoring antifactor Xa activity is controversial because it is weakly correlated to bleeding. The goal of this study was to investigate the role of other novel anticoagulation markers, such as thrombin generation time, platelet contractile force, and clot elastic modulus, while controlling for antifactor Xa activity in patients with and without renal dysfunction. METHODS: Thirty anticoagulant- and antiplatelet-naive subjects completed this trial (10 controls, 10 patients with chronic kidney disease, and 10 patients with end-stage renal disease [ESRD]). Blood samples were obtained and spiked ex vivo with increasing concentrations of enoxaparin antifactor Xa activity (0.25, 0.5, 1.0, and 3.0 IU/mL). Thrombin generation time, platelet contractile force, and clot elastic modulus were measured in each group at each antifactor Xa activity concentration. RESULTS: Subjects with ESRD had an approximately 50% greater anticoagulant effect, determined by thrombin generation time prolongation, than controls at antifactor Xa activity concentrations of 0.5 to 3.0 IU/mL. This may explain why subjects with ESRD with seemingly therapeutic antifactor Xa levels still experience adverse bleeding. There were no intergroup differences in platelet function, determined by platelet contractile force and clot elastic modulus. CONCLUSION: Antifactor Xa poorly predicts the degree of anticoagulation in patients with ESRD administered low-molecular-weight heparin (LMWH). Thrombin generation time may be a clinically useful anticoagulation monitoring tool to monitor LMWH therapy, especially in patients with renal dysfunction. Additional randomized prospective studies are needed to corroborate these findings.

Adult↗
PubMed2006

Altered hemostasis in migraineurs studied with a dynamic flow system.

INTRODUCTION: Livedo reticularis (LR) refers to the violaceous netlike pattern of skin related to arteriopathy at the dermis-subcutis border. Livedo is associated with migraine, and among migraineurs, LR is more common in those with prior stroke. Other evidence of vascular perturbation in migraine comes from studies showing elevated von Willebrand factor (vWF). The purpose of this study is to evaluate global hemostasis in migraineurs, including the subset with LR, using a dynamic flow system simulating physiological conditions, and measuring vWF activity and antigen levels. MATERIALS AND METHODS: Patients with migraine were enrolled from the headache clinic and presence or absence of LR was noted. Age-matched healthy, non-migraine, LR-free individuals were recruited as controls. To evaluate hemostasis, we used the Clot Signature Analyzer (CSA) measuring platelet hemostasis time (PHT), collagen-induced thrombus formation (CITF), and clot time (CT). vWF activity and vWF antigen levels were also measured. RESULTS: The mean vWF activity level (142.7 vs. 103.4, p<0.01) and antigen level (132.1 vs. 104.5, p<0.05) were higher, and all three hemostasis parameters shorter in the episodic migraineurs than in the controls. The subset of migraineurs with LR had the highest vWF activity (155+/-59, p<0.05) and vWF antigen (141+/-43, p<0.05) levels, and the shortest PHT (3.7+/-1.6, p<0.05). In this subset there was a significant inverse correlation between vWF activity and PHT (r=-0.51, p=0.01). CONCLUSIONS: For migraineurs, the differences from controls in vWF and PHT are most robust in the LR subset, with the inverse correlation suggesting that endothelial perturbation may be causally related to the response of the platelets.

Adult↗
PubMed1997

Platelet morphology in patients with mechanical circulatory support.

OBJECTIVE: Mechanical circulatory support is a therapy for patients with end stage cardiac insufficiency. The thromboembolic events are feared complications during support, due to the surface thrombogenicity of the implanted device. Activated blood platelets play a major role in this context. Consequently the platelet morphology of patients was investigated. METHODS: Platelets of eight patients were observed by means of scanning electron microscopy during the period of support with the Novacor left ventricular assist system N100. Blood was collected preoperatively and daily during the first week as well as weekly during the first 3 months. Samples were fixed with cacodylic-acid buffered glutaraldehyde. Platelet alterations were classified as non-activated, activated and aggregated, based on the so-called 'shape change' morphology. In addition, blood coagulation parameters were evaluated (e.g. activated partial thromboplastin time, prothrombin time, antithrombin III). RESULTS: Preoperatively, 15.0 +/- 4.6% (overall mean values) of activated platelets were found. Within the first postoperative week, the mean level of activated platelets increased to 32.8 +/- 8.0% (P < 0.05). Comparing short- (< 30 days; n = 4) vs. long-period (> 30 days; n = 4) support, a significant difference of activated platelets was evaluated (24.3 +/- 3.3% vs. 34.8 +/- 3.4%, P = 0.004). A correlation was found between the values of activated clotting time and activated platelets. Specific platelet deformations and damages appeared during support, which could not be found preoperatively. CONCLUSIONS: The platelet morphology showed alterations in all patients probably most strongly induced by the surface activation of the implanted device. These observations should be taken into consideration in management of postoperative anticoagulation therapy.

Adult↗
PubMed1990

Global and molecular hemostatic markers in acute myeloid leukemia.

Patients with acute myeloid leukemia have multiple hemostatic and thrombotic complications, which may or may not result from disseminated intravascular coagulation. Previous studies incorporating routine coagulation analyses failed to detect any clinically useful information in most of these patients. In this study, the first comprehensive evaluation of the various aspects of the hemostatic system in a population of patients with acute myeloid leukemia was performed. Eighteen patients (23-71 years of age) were studied at either diagnosis or relapse. Hemostatic studies were performed at onset and on days 3, 7, and 30 after initiation of therapy. The bone marrow blast counts ranged from 8% to 98%; prothrombin time and activated partial thromboplastin time showed only minor prolongations in a few of these patients. However, in all patients measurement of platelet-associated markers revealed elevated platelet factor 4 and thromboxane B2 and normal 6-keto-prostaglandin F1 alpha levels. Fibrinolytic markers showed an increase in D-dimer and tissue plasminogen activator and a decrease in alpha 2-antiplasmin levels. Plasminogen, plasminogen activator inhibitor, and fibrinogen levels were normal. Coagulation markers demonstrated a decrease in protein C and antithrombin III levels and an elevation of the thrombin-antithrombin complex. The pretreatment values for all hemostatic markers studied were similar to the values obtained on days 3, 7, and 30 during treatment. This investigation demonstrated a subclinical activation of the components of the hemostatic system possibly leading to a hypercoagulable state. Although only six patients (33%) experienced hemorrhagic complications, the risk of bleeding and/or thrombosis was strongly evident in all patients. The significance of finding abnormal levels of specific molecular markers of hemostasis will be established in the future application of such markers in clinical evaluations of leukemic patients known to be at risk for coagulation disorders.

Acute Disease↗
PubMedDate not supplied

Preoperative test of bleeding time in ear surgery.

In 300 patients subjected to ear surgery the bleeding time according to Ivy was determined preoperatively. In 25 cases prolonged bleeding time was found. Further investigations revealed mild thromboasthenia in 4 cases and enhanced fibrinolytic activity in one instance. In 10 patients the cause was intake of drugs containing acetylsalicylic acid. During operation the patients were treated with AMCA and in two cases fresh blood also was given. Even slightly enhanced bleeding can affect the results in microsurgery of the ear. We therefore suggest that bleeding time should be determined as a preoperative routine in order to detect the patients in need of specific treatment. Patients also should be recommended to avoid drugs containing acetylsalicylic acid for a fortnight before surgery.

Adolescent↗
PubMed2005

Thrombelastograph (TEG) analysis of platelet gel formed with different thrombin concentrations.

Autologous blood transfusion is the safest and most successful way to decrease transfusion-related risks such as postoperative infections, allo-immunization, and short- and long-term immunosuppression. In addition, these fibrin sealants are known to provide coagulation support at the surgical site and act as an adjunct to the control of postoperative bleeding. The physical formation of autologous platelet fibrin gel clot is dependent on both the common pathway of the coagulation cascade and platelet activation. Platelet gel can help provide control of intraoperative and postoperative bleeding. The Thrombelastograph Hemostasis Analyzer (TEG) measures the viscoelastic properties of a clot as it forms. Based on the information that the TEG provides, it promises to be a good choice for point of care measurement of the integrity of thrombus formed by platelet gels. Bovine blood from a single donor was sequestered into platelet-rich plasma and was made into platelet gel using calcium and three different concentrations of thrombin. The platelet gel samples were then analyzed with the TEG analyzer. The results for MA, tMA, CI, and angle were recorded and statistical analysis was performed to accept or reject the null hypothesis, which is: There is no difference between TEG parameters when analyzing platelet gels formed with calcium chloride, platelet-rich plasma and three different concentrations of thrombin A one-way analysis of variance test was performed between thrombin concentrations for MA (p = 0.19), tMA (p = 0.443), CI (p = 0.257), and angle (p = 0.323). The results showed that thrombin concentration did not affect the MA, tMA, CI, or angle as measured by the TEG analyzer. The null hypothesis was accepted. Based on a one-way analysis of variance test for MA, tMA, CI, and angle there was no significant statistical difference for the TEG samples in this experiment as reported with a 95% confidence interval.

Animals↗