In Vitro Characterization of Platelet Dysfunction In Common Hematological Disorders Using the Verify Now® Assay

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1436-1436
Author(s):  
Nina D’Abreo ◽  
Vatsala Kirtani ◽  
Jennifer L. Kujawa Eisenstein ◽  
Yelda Nouri ◽  
Matt Geller ◽  
...  
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Conflicts Of Interest ◽  
Reference Ranges ◽  
Platelet Dysfunction ◽  
Platelet Defects ◽  
Verify Now ◽  
Instructions For Use

Abstract Abstract 1436 Objectives: Myelodysplastic syndrome (MDS), immune thrombocytopenia purpura (ITP) and myeloproliferative disorders (MPD) are frequent diagnoses in a community hematology practice. Qualitative platelet defects are common features of these disorders but are difficult to characterize in daily practice as specialized technology is not readily available. The Verify Now® (VN) is a rapid, point-of service assay to measure platelet aggregation. VN assesses the degree of inhibition of GPIIb/IIIa mediated aggregation and uses minimal sample preparation. Its main application currently, is to determine the adequacy of anti-platelet therapy with aspirin (ASA), thienopyridines, such as clopidogrel (CPL), and GPIIb/IIIa inhibitors in patients with cardiovascular disease. (Verify Now for IIb/IIIa, aspirin, and P2Y12, Instructions for Use, Accumetrics) We used VN to detect platelet aggregation defects in patients with ITP, MDS and MPD and compared the to a platelet function analyzer PFA -100. (Francis JL; In Michelson AD, ed. Platelets, 2nded. San Diego: Elsevier/Academic Press, 2007:535-544) Methods: Subjects with MDS, ITP, and MPD were identified from our Hematology practice. Informed consent was obtained from all patients. Patients taking aspirin and /or clopidogrel were not excluded. Platelet function was determined concurrently using VN and PFA-100 using standard reference ranges. (Verify Now for IIb/IIIa, aspirin, and P2Y12, Instructions for Use, Accumetrics), (Mammen EF et al; Semin Throm Hemost. 1998; 24 (2):195-205). Results: Thirty three patients are enrolled in the study, 21 with ITP, 6 with MDS and 6 with MPD. Assay results are available for 30 patients. Platelet counts for all patients ranged from 2 to 1206 ×103/cmm, mean platelet count being 184 ×103/cmm (SD ± 215) and median count was 120 ×103/cmm. ITP: In 15 patients with ITP and platelet count ≥ 100 ×103/cmm, 11 were not on ASA/CPL. PFA-100 and VN each detected abnormalities in 4 patients but results were non-concordant in 2 patients. In 4 patients on ASA, VN detected ASA effect in all 4 whereas the PFA-100 detected 2. In 2 patients with platelet count < 100 ×103/cmm not on ASA/CPL, VN detected abnormalities in both, whereas PFA detected only 1. (Table 1) MDS: Two patients had counts ≥ 100 ×103/cmm. One was on ASA and both assays detected ASA effect. Neither assay detected an abnormality in the patient not on ASA. In 4 patients with counts <100 ×103/cmm, 3 were not on ASA/ CPL. Both assays detected abnormalities in all 3 and ASA effect in 1 patient on ASA. (Table 2) MPD: In 4 patients with counts < 400 ×103/cmm, not on ASA/CPL, both assays detected non-concordant abnormalities in 1 patient. Both assays detected CPL and ASA effect in 1 patient taking both drugs. 2 patients had count ≥400,000. In 1 patient taking CPL, VN detected CPL effect but PFA did not. In 1 patient on ASA, PFA detected abnormality but VN did not. (Table 3) Conclusion: In patients with MDS, ITP, and MPD, abnormal platelet function is common. These results show that VN may be as sensitive for detecting platelet dysfunction as PFA-100. Results were especially concordant in MDS patients. We plan to include 150 patients to confirm these results. We hope to define qualitative platelet defects in this population so that appropriate intervention can be recommended prior to invasive procedures. Disclosures: No relevant conflicts of interest to declare.

The Effect of Dimethyl Sulfoxide on In Vitro Platelet Function

1976 ◽  
Vol 36 (01) ◽  
pp. 221-229 ◽  
Author(s):  
Charles A. Schiffer ◽  
Caroline L. Whitaker ◽  
Morton Schmukler ◽  
Joseph Aisner ◽  
Steven L. Hilbert
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Dimethyl Sulfoxide ◽  
Platelet Function ◽  
Platelet Volume ◽  
Short Term ◽  
Platelet Factor ◽  
Short Term Exposure ◽  
Structural Abnormalities

SummaryAlthough dimethyl sulfoxide (DMSO) has been used extensively as a cryopreservative for platelets there are few studies dealing with the effect of DMSO on platelet function. Using techniques similar to those employed in platelet cryopreservation platelets were incubated with final concentrations of 2-10% DMSO at 25° C. After exposure to 5 and 10% DMSO platelets remained discoid and electron micrographs revealed no structural abnormalities. There was no significant change in platelet count. In terms of injury to platelet membranes, there was no increased availability of platelet factor-3 or leakage of nucleotides, 5 hydroxytryptamine (5HT) or glycosidases with final DMSO concentrations of 2.5, 5 and 10% DMSO. Thrombin stimulated nucleotide and 5HT release was reduced by 10% DMSO. Impairment of thrombin induced glycosidase release was noted at lower DMSO concentrations and was dose related. Similarly, aggregation to ADP was progressively impaired at DMSO concentrations from 1-5% and was dose related. After the platelets exposed to DMSO were washed, however, aggregation and release returned to control values. Platelet aggregation by epinephrine was also inhibited by DMSO and this could not be corrected by washing the platelets. DMSO-plasma solutions are hypertonic but only minimal increases in platelet volume (at 10% DMSO) could be detected. Shrinkage of platelets was seen with hypertonic solutions of sodium chloride or sucrose suggesting that the rapid transmembrane passage of DMSO prevented significant shifts of water. These studies demonstrate that there are minimal irreversible alterations in in vitro platelet function after short-term exposure to DMSO.

IL-1β Plays An Important Role On Thrombocytosis In An Immune Vasculitis Model Via Promoting Megakaryopoiesis

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 2325-2325
Author(s):  
Mo Yang ◽  
Min Zhou ◽  
Su yi Li ◽  
Beng Chong ◽  
Xiao jing Li
Keyword(s):  
Bone Marrow ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Conflicts Of Interest ◽  
Serum Levels ◽  
Control Group ◽  
Type I ◽  
Anti Inflammation ◽  
Immune Vasculitis

Abstract Thrombocytosis and inflammation cytokines may be involved in the pathogenesis of vasculitis. Our previous study have showed that major inflammation cytokine IL-1β play an important role on in-vitro megakaryopoiesis (Yang M et al, Br J Haematol 2000). In this study, we investigated the changes of IL-1β and megakaryopoiesis and the effect of aspirin in an immune vasculitis model. Rabbit immune vasculitis model was established by intravenous injection of bovine serum albumin. In this model, platelet number and function of periphery blood, megakaryocyte number and the CFU-MK formation of the bone marrow, and serum levels of inflammatory cytokines were investigated. After treatment with BSA for 7 days, the platelet count, platelet aggregation and the expression of AnnexinⅤ were significantly increased in this vasculitis model group compared with normal control group (n=6). The serum levels of inflammatory cytokine IL-1β was also significantly higher in vasculitis model. There were positive correlations between platelet count and IL-1β levels (R=0.55), platelet aggregation and IL-1β levels (R=0.603). Treatment with aspirin (100 mg/kg/d) significantly decreased all these parameters, showing aspirin had anti-platelets and anti-inflammation effects. Our results also demonstrated that megakaryocyte number and the formation of CFU-MK were significantly increased in vasculitis group as compared to those in normal group. Treatment with aspirin significantly reduced the number of megakaryocytes and the formations of CFU-MK in bone marrow in this immune vasculitis model. Our study further demonstrated that IL-1β alone or in combination with TPO induced in-vitro CFU-MK formation. Using RT-PCR techniques, the mRNA of of IL-1 type I and type II receptors (IL-1 RI and RII) were detected in cultured CD61+ CD41+ cells and four megakaryocytic cell lines. The expression of IL-1 RI and RII was also confirmed by flow cytometry and immunofluorescence staining in bone marrow megakaryocytes. Moreover, the IL-1R bloker can reduced IL-1β induced megakaryopoiesis. This sudy showed that IL-1β may play an important role in the pathogenesis of immune vasculitis. Aspirin has anti-inflammation effects in this model which may be mediated via inhibiting megakaryopoiesis and platelet formation. Disclosures: No relevant conflicts of interest to declare.

Platelet Aggregation and Platelet Factor 3 Activity in Myeloproliferative Disorders

1971 ◽  
Vol 25 (02) ◽  
pp. 241-251 ◽  
Author(s):  
Y Tangün
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Myeloproliferative Disorders ◽  
Myeloproliferative Disorder ◽  
Platelet Factor ◽  
High Platelet Count ◽  
Platelet Defects

Summary33 patients with myeloproliferative disorder were studied and in 28 (84%) various anomalies of platelet function were observed. Single, or more commonly, multiple platelet aggregation defects and impaired release of platelet ADP and platelet factor 3 activity were the chief anomalies noted, whether thrombocytosis was present or not. The effect of myelosuppressive therapy upon the defects demonstrated varied from patient to patient, and from one anomaly to another. Reducing the high platelet count to normal levels does not seem to be sufficient to eradicate qualitative platelet defects.

scholarly journals The Intercept Blood System Affects Platelet Function and Survival By Inducing Apoptosis

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4283-4283 ◽  
Author(s):  
Simona Stivala ◽  
Sara Gobbato ◽  
Martin F Reiner ◽  
Sara C Meyer ◽  
Thomas F Lüscher ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Conflicts Of Interest ◽  
Blood System ◽  
Scid Mice ◽  
Post Injection ◽  
Immunodeficient Mice ◽  
Platelet Survival ◽  
Storage Area

Abstract Introduction The Intercept Blood System (IBS) is currently approved in 40 countries to prevent transfusion-transmitted diseases. It is mandatory in Switzerland since 2012. Our aim was to study the effects of this treatment on platelet function and survival and to investigate the underlying mechanisms. Methods 10 platelet apheresis units (AU) from healthy volunteers were left untreated (non-IBS) or treated with the IBS following standard blood center procedure and storage at 22°C under agitation. Samples were analyzed for aggregation, P-selectin exposure, integrin activation, PS/PE exposure, platelet aggregation over collagen and adhesion to vWF at day (d) 1, 5, 7 and 10. Platelet survival was analyzed in NOD-SCID mice after 1 day storage by injection of fluorescently-labeled non-IBS or IBS platelets and analysis of blood at 0.5/2/5 hours post-injection. Bak expression was analyzed in platelet lysates by Western blotting. Results IBS treatment substantially reduced platelet aggregation already after 1 day storage (area under the curve -AUC- for thrombin 45.3 non-IBS vs 26.7 IBS, p=0.02, fig. A; AUC for collagen 19.1 non-IBS vs 4.9 IBS, p=0.07). P-selectin exposure and activation of a2bb3 were not different between non-IBS and IBS samples, as well as phosphatidylserine exposure as measured by Annexin V binding. Adhesion to vWF under high shear flow was reduced after 1 day storage, albeit not significantly due to some variability (platelet-covered area 4950 um2 non-IBS vs 1481 um2 IBS, p=0.2). Aggregation on collagen under flow was again markedly reduced upon IBS treatment at day 1 and 10 of storage (area d1: 67974 um2 non-IBS vs 35490 um2 IBS, p=0.15; d10: 37761 um2 non-IBS vs 14033 um2 IBS, p=0.13. AUC: 511426 non-IBS vs 247750 IBS, p=0.08). Platelet survival was reduced in NOD-SCID mice injected with IBS platelets compared to non-IBS platelets (% platelets in blood 2h post-injection: 45.5% non-IBS vs 25.1% IBS; 5h: 30.35% non-IBS vs 8.87% IBS; n=3, fig. B). Fluorescent platelets were quantified in spleen sections and found to be significantly higher in mice injected with IBS platelets (average platelet area: 19083 um2 non-IBS vs. 79395 um2 non-IBS, n=3, p=0.03). Analysis of Bak expression in platelet lysates revealed an increased amount of this pro-apoptotic mediator in IBS samples (Bak/tubulin integrated intensities: 0.08 non-IBS vs 0.12 IBS, p=0.007, fig. C), while there was no difference in the anti-apoptotic Bcl-XL. Conclusions The IBS reduces platelet aggregation and responsiveness to physiological agonists in vitro, and platelet survival in the circulation of immunodeficient mice in vivo. This effect might be clinically relevant for patients receiving platelet transfusion and is possibly due to the induction of pro-apoptotic signaling in platelets by the method, which warrants further investigation. Figure 1 Figure 1. Figure 2 Figure 2. Figure 3 Figure 3. Disclosures No relevant conflicts of interest to declare.

The Effect of Tanshinone-IIa on IL-1β Induced-Thrombocytosis in an Immune Vasculitis Model

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 5082-5082
Author(s):  
Min Zhou ◽  
Li-xia Zhou ◽  
Hui-ying Shu ◽  
Xiao-jing Li ◽  
Qi-zhou Lian ◽  
...  
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Caspase 3 ◽  
Conflicts Of Interest ◽  
Tanshinone Iia ◽  
Control Group ◽  
Type I ◽  
Dependent Manner ◽  
Immune Vasculitis

Abstract Inflammation cytokines may be involved in the pathogenesis of thrombocytosis with vasculitis. Our previous study showed that inflammation cytokine IL-1β plays an important role on in-vitro megakaryopoiesis (Yang M et al, Br J Haematol 2000). The role of IL-1β and Tanshinone IIA (TIIA) (Isolated from Danshen, Radix Salviae Miltiorrhiza Bge) on platelets and megakaryocytes (MKs) in immune vasculitis model was investigated in this study. Rabbit model with immune vasculitis was established by injection (iv) of BSA. After treatment with BSA for 7 days, the platelet count, platelet aggregation and the expression of AnnexinⅤ were significantly increased in this vasculitis model group compared with normal control group (n=7). IL-1β levels was also significantly higher in vasculitis model. There were positive correlations between platelet count and IL-1β levels (R=0.65), platelet aggregation and IL-1β levels (R=0.60). Treatment with TIIA (5 mg/kg/day, iv) and aspirin significantly decreased all these parameters. MKs and CFU-MK number were also significantly increased in vasculitis group as compared to normal group. Treatment with TIIA and aspirin significantly reduced the number of MKs and CFU-MK in this model. Study further demonstrated that IL-1β alone or in combination with TPO induced in-vitro CFU-MK formation. The mRNA of of IL-1 type I and type II receptors (IL-1 RI and RII) were detected in cultured MK (CD61+ CD41+) cells. The expression of IL-1 RI and RII was also confirmed by immunofluorescence staining in bone marrow MKs. Moreover, the IL-1R bloker can reduced IL-1β induced megakaryopoiesis. TIIA on in-vitro megakaryopoiesis was also investigated. TIIA at 10-30 ug/ml significantly inhibited CFU-MK formation. TIIA also induced the apoptosis of MKs in a dose dependent manner by Anexin V assay. Caspase 3 assay showed the activation of Caspase 3 increased from 5% to 16%. Using JC-1 assay found that the depolarized cells increased from 9% to 17% suggesting the involvement of intrinsic apoptotic pathway. IL-1β may play an important role in the thrombocytosis of immune vasculitis by inducing megakaryopoiesis. TIIA has anti-platelet effect in this model which may be mediated via inhibiting IL-1β induced-megakaryopoiesis. Disclosures No relevant conflicts of interest to declare.

Clinical Experience with the Thrombostat 4000

1995 ◽  
Vol 21 (S 02) ◽  
pp. 1-10 ◽  
Author(s):  
Rasheed Alshameeri ◽  
Eberhard Mammen
Keyword(s):  
Platelet Aggregation ◽  
Clinical Experience ◽  
Test Performance ◽  
Room Temperature ◽  
Reference Ranges ◽  
Platelet Dysfunction ◽  
Major Drawback ◽  
Normal Volunteers ◽  
Primary Hemostasis ◽  
Platelet Defects

Bleeding times are presently widely used to screen patients with primary hemostasis defects although their accuracy and reliability has been questioned by many investigators. Platelet aggregation studies are not suited for routine use. We investigated the performance characteristics of the Thrombostat 4000, a device that assesses primary hemostasis. Tests can be performed by adding ADP, epinephrine, CaCl2 or NaCl to the collagen onto which platelets adhere. It was found, using normal volunteers and patients, that ADP and epinephrine had acceptable reference ranges with coefficients of variance between 9–12% for within run and between runs. However, major differences were seen when different filter badges were used–a reflection of differences in collagen. Regular citrated blood, routinely drawn for coagulation studies, can be used; test performance can be delayed for up to five hours when the blood is kept at room temperature. The effects of aspirin on volunteers could be detected when epinephrine was used, but not with ADP. ADP addition allowed the detection of more patients with primary hemostasis defects than bleeding times, and epinephrine was as useful as ADP in detecting these abnormalities. The data suggest that the broadest spectrum of platelet defects (ASA use and platelet dysfunction) can be detected with epinephrine. Inconsistencies in collagen used for coating of the filters is a major drawback for the routine use of this device in screening primary hemostasis defects.

Enhancement of ADP-induced Platelet Aggregation by Adrenaline in Vivo and Its Prevention

1973 ◽  
Vol 29 (02) ◽  
pp. 490-498 ◽  
Author(s):  
Hiroh Yamazaki ◽  
Itsuro Kobayashi ◽  
Tadahiro Sano ◽  
Takio Shimamoto
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
The Other ◽  
Endothelial Surface ◽  
Important Interaction ◽  
Blood Coagulability ◽  
The Difference

SummaryThe authors previously reported a transient decrease in adhesive platelet count and an enhancement of blood coagulability after administration of a small amount of adrenaline (0.1-1 µg per Kg, i. v.) in man and rabbit. In such circumstances, the sensitivity of platelets to aggregation induced by ADP was studied by an optical density method. Five minutes after i. v. injection of 1 µg per Kg of adrenaline in 10 rabbits, intensity of platelet aggregation increased to 115.1 ± 4.9% (mean ± S. E.) by 10∼5 molar, 121.8 ± 7.8% by 3 × 10-6 molar and 129.4 ± 12.8% of the value before the injection by 10”6 molar ADP. The difference was statistically significant (P<0.01-0.05). The above change was not observed in each group of rabbits injected with saline, 1 µg per Kg of 1-noradrenaline or 0.1 and 10 µg per Kg of adrenaline. Also, it was prevented by oral administration of 10 mg per Kg of phenoxybenzamine or propranolol or aspirin or pyridinolcarbamate 3 hours before the challenge. On the other hand, the enhancement of ADP-induced platelet aggregation was not observed in vitro, when 10-5 or 3 × 10-6 molar and 129.4 ± 12.8% of the value before 10∼6 molar ADP was added to citrated platelet rich plasma (CPRP) of rabbit after incubation at 37°C for 30 second with 0.01, 0.1, 1, 10 or 100 µg per ml of adrenaline or noradrenaline. These results suggest an important interaction between endothelial surface and platelets in connection with the enhancement of ADP-induced platelet aggregation by adrenaline in vivo.

A Comparison of the Effect of Decorsin and Two Disintegrins, Albolabrin and Eristostatin, on Platelet Function

1995 ◽  
Vol 74 (05) ◽  
pp. 1316-1322 ◽  
Author(s):  
Mary Ann McLane ◽  
Jagadeesh Gabbeta ◽  
A Koneti Rao ◽  
Lucia Beviglia ◽  
Robert A Lazarus ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Sequence Similarity ◽  
Platelet Aggregation Inhibitors ◽  
Antiplatelet Drug ◽  
Rgd Sequence ◽  
Fibrinogen Receptor ◽  
Activated Platelets

SummaryNaturally-occurring fibrinogen receptor antagonists and platelet aggregation inhibitors that are found in snake venom (disintegrins) and leeches share many common features, including an RGD sequence, high cysteine content, and low molecular weight. There are, however, significant selectivity and potency differences. We compared the effect of three proteins on platelet function: albolabrin, a 7.5 kDa disintegrin, eristostatin, a 5.4 kDa disintegrin in which part of the disintegrin domain is deleted, and decorsin, a 4.5 kDa non-disintegrin derived from the leech Macrobdella decora, which has very little sequence similarity with either disintegrin. Decorsin was about two times less potent than albolabrin and six times less potent than eristostatin in inhibiting ADP- induced human platelet aggregation. It had a different pattern of interaction with glycoprotein IIb/IIIa as compared to the two disintegrins. Decorsin bound with a low affinity to resting platelets (409 nM) and to ADP-activated platelets (270 nM), and with high affinity to thrombin- activated platelets (74 nM). At concentrations up to 685 nM, it did not cause expression of a ligand-induced binding site epitope on the (β3 subunit of the GPIIb/IIIa complex. It did not significantly inhibit isolated GPIIb/IIIa binding to immobilized von Willebrand Factor. At low doses (1.5-3.0 μg/mouse), decorsin protected mice against death from pulmonary thromboembolism, showing an effect similar to eristostatin. This suggested that decorsin is a much more potent inhibitor of platelet aggregation in vivo than in vitro, and it may have potential as an antiplatelet drug.

The Effect of Barbituric Acid Derivatives on Platelet Function in Vitro and in Vivo

1973 ◽  
Vol 30 (02) ◽  
pp. 315-326
Author(s):  
J. Heinz Joist ◽  
Jean-Pierre Cazenave ◽  
J. Fraser Mustard
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Barbituric Acid ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Primary Response ◽  
Sodium Pentobarbital ◽  
Barbituric Acid Derivatives

SummarySodium pentobarbital (SPB) and three other barbituric acid derivatives were found to inhibit platelet function in vitro. SPB had no effect on the primary response to ADP of platelets in platelet-rich plasma (PRP) or washed platelets but inhibited secondary aggregation induced by ADP in human PRP. The drug inhibited both phases of aggregation induced by epinephrine. SPB suppressed aggregation and the release reaction induced by collagen or low concentrations of thrombin, and platelet adherence to collagen-coated glass tubes. The inhibition by SPB of platelet aggregation was readily reversible and isotopically labeled SPB did not become firmly bound to platelets. No inhibitory effect on platelet aggregation induced by ADP, collagen, or thrombin could be detected in PRP obtained from rabbits after induction of SPB-anesthesia.

The Effect of Warfarin Sodium on the Duration of Platelet Aggregation

1967 ◽  
Vol 18 (03/04) ◽  
pp. 766-778 ◽  
Author(s):  
H. J Knieriem ◽  
A. B Chandler
Keyword(s):  
Platelet Count ◽  
Placebo Group ◽  
Platelet Aggregation ◽  
Prothrombin Time ◽  
Platelet Rich Plasma ◽  
Healthy Adults ◽  
Double Blind Study ◽  
Double Blind ◽  
Warfarin Sodium

SummaryThe effect of the administration of warfarin sodium (Coumadin®) on the duration of platelet aggregation in vitro was studied. Coumadin was given for 4 consecutive days to 10 healthy adults who were followed over a period of 9 days. The duration of adenosine diphosphate-induced platelet aggregation in platelet-rich plasma, the prothrombin time, and the platelet count of platelet-rich plasma were measured. Four other healthy adults received placebos and participated in a double-blind study with those receiving Coumadin.Although administration of Coumadin caused a prolongation of the prothrombin time to 2 or 21/2 times the normal value, a decrease in the duration of platelet aggregation was not observed. In most individuals who received Coumadin an increase in the duration of platelet aggregation occurred. The effect of Coumadin on platelet aggregation was not consistently related to the prothrombin time or to the platelet count. In the placebo group there was a distinct relation between the duration of platelet aggregation and the platelet count in platelet-rich plasma.The mean increase in the duration of platelet aggregation when compared to the control value before medication with Coumadin was 37.7%. In the placebo group there was a mean increase of 8.4%. The difference between the two groups is significant (p <0.001). Increased duration of platelet aggregation also occurred in two individuals who received Coumadin over a period of 10 and 16 days respectively.

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