scholarly journals Safety and Efficacy of 14-Day Cold Stored Platelets in Reversing Effects of Aspirin

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 353-353
Author(s):  
Valery J Li ◽  
Shawn Lawrence Bailey ◽  
Morgan Bawcom-Randall ◽  
Daire Byrne ◽  
Jeffrey Miles ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Function ◽  
Primary Endpoint ◽  
The Other ◽  
Autologous Transfusion ◽  
Safety And Efficacy ◽  
Time Points ◽  
Storage Product ◽  
Function Testing ◽  
Corrected Count Increment

Abstract Background: Aspirin is an antiplatelet therapy used to reduce the risk of vascular occlusive events. However, this therapy is associated with an increased risk of bleeding for which there is no antidote currently. Transfusion of 5-day room stored platelets (RSP) at 22°C can reverse the effect of aspirin but surprisingly, the recent randomized PATCH trial showed increased morbidity and mortality for patients who received RSP transfusion for intracranial hemorrhage while on aspirin. Prior studies have shown that cold stored platelets (CSP) at 4°C are mildly activated and may participate in clot formation immediately, thus may have the potential to reduce blood loss more rapidly than RSP in acutely bleeding patients. CSP also have the added advantages of decreased risk of bacterial contamination and longer shelf-life up to 14 days per current FDA variance. However, the function of 14-day CSP in plasma after transfusion is unclear and lacks high quality data. We aimed to evaluate the post-transfusion safety and efficacy of 14-day CSP in reversing the effects of aspirin therapy compared to that of 7-day RSP. Methods: Seven healthy human subjects were included in the analysis of this randomized, controlled, crossover study comparing transfusion of autologous 14-day CSP to 7-day RSP. Each subject participated in two study periods, which crossed over from one storage product to the other (CSP vs. RSP) according to randomization. For each study period, subjects underwent an apheresis platelet collection for autologous transfusion. Platelets were stored for either 14 days for CSP or 7 days for RSP. Subjects received a loading dose of aspirin 24 hours prior to transfusion. Blood was drawn at baseline, immediately pre-transfusion, at 1-hr, 4-hr, and 24-hr post-transfusion for an array of platelet function testing. After a washout period of 10-28 days, second study period commenced with similar sequence of events as the first study period using the other platelet storage product. The primary endpoint is the VerifyNOW Aspirin Reaction Units (ARU) at 1-hr after autologous transfusion. Secondary endpoints include ARU at 4-hr and 24-hr post transfusion, light transmission aggregometry in response to arachidonic acid and collagen, and the corrected count increment. Paired t-tests were used for statistical analysis between the two groups and, where appropriate, the change from pre-transfusion values were analyzed. Results: Transfusion of 14-day CSP and 7-day RSP units were well-tolerated by all subjects. Storage of platelets in the cold led to a non-significant trend for decreased platelet count, and the total platelet yield at the end of storage was significantly less in 14-day CSP compared to 7-day RSP (p=0.02). However, the corrected count increment did not differ significantly at 1-hr after transfusion. Platelet aggregation using the agonists, arachidonic acid 0.5mM and collagen 2.5ug/mL, did not reveal any significant difference between the two groups at any time points. The primary endpoint, platelet function testing by VerifyNOW, showed a larger change in platelet responsiveness at 1-hr post-transfusion in RSP than in CSP (p=0.03). Surprisingly, only RSP transfusion resulted in a significant change from the pre-transfusion VerifyNow measurements. Later time points showed a slight trend for improved platelet function as measured by VerifyNow with transfusion of both platelet products, but none were statistically significant. Conclusion: We report the first safety and efficacy data for 14-day cold stored platelets in in healthy humans. While prior in-vitro studies have demonstrated possible hemostatic superiority of cold stored over room temperature stored platelets, we observed inferior reversal of aspirin at early time points with CSP. This was in contrast to the results from our previous study, where 5 day-stored CSP were equivalent to RSP at early post transfusion time points. Further studies are needed to evaluate the maximal storage that provides functional equivalency between CSP and RSP. In addition, studies in actively bleeding patients are needed. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

Platelet Suruival and Function in Rats with Enhanced Thrombotic Tendency

1985 ◽  
Vol 54 (04) ◽  
pp. 739-743 ◽  
Author(s):  
Federica Delaini ◽  
Elisabetta Dejana ◽  
Ine Reyers ◽  
Elisa Vicenzi ◽  
Germana De Bellis Vitti ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Nephrotic Syndrome ◽  
Platelet Function ◽  
Laboratory Tests ◽  
Thrombus Formation ◽  
The Other ◽  
Mean Survival Time ◽  
The Mean ◽  
And Function ◽  
Thrombotic Tendency

SummaryWe 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-PGFlα 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 A A 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-PGFlα 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.

Abstract 4023: Aspirin “Resistance”: Role of Pre-existent Platelet Reactivity and Correlation Between Tests

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Andrew L Frelinger ◽  
Youfu Li ◽  
Matthew D Linden ◽  
Inge Tarnow ◽  
Marc R Barnard ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Normal Subjects ◽  
Aspirin Resistance ◽  
The Other ◽  
List Type ◽  
Platelet Function Test ◽  
Function Test

Background: Aspirin “resistance” (i.e. hyporesponsiveness to aspirin in a platelet function test) has been widely reported, but the underlying mechanism is unclear. We examined the role of pre-existent platelet hyperreactivity in aspirin “resistance”. We also determined the correlation between aspirin resistance defined by serum thromboxane (TX) B 2 (the most specific test of aspirin’s effect) and other assays of platelet function. Methods: Platelet function measured before and after aspirin 81 mg daily for 7 days was analyzed by Spearman’s rank correlation. Normal subjects (n=165) were studied because virtually all clinically relevant patients are already taking aspirin. An additional advantage of the use of normal subjects is that the platelet response to stimuli is not influenced (with resultant increased scatter of the data) by an underlying disease, e.g. coronary artery disease, which causes platelet hyperreactivity. Results: The proportion of the post-aspirin platelet function predicted by the pre-aspirin platelet function was 28.3 ± 7.5% (mean ± asymptotic standard error) for serum TXB 2 , 39.3 ± 6.8% for urinary 11-dehydro TXB 2 , 4.4 ± 7.7% for arachidonic acid-induced platelet aggregation, 40.4 ± 7.1% for ADP-induced platelet aggregation, 26.3 ± 9.2% for the VerifyNow Aspirin Assay®, and 45.0 ± 10.9% for the TEG® PlateletMapping ™ System with arachidonic acid. Spearman rank order correlations were highly significant for comparisons between assays when both pre-aspirin and post-aspirin results were included in the analysis. However, residual serum TXB 2 levels post-aspirin treatment were not significantly associated with post-treatment results of any of the other assays. Platelet count correlated with pre-aspirin serum TXB 2 and VerifyNow Aspirin Assay, but not with any post-aspirin platelet function test. Conclusions: Aspirin “resistance” (i.e. hyporesponsiveness to aspirin in a laboratory test) is in part unrelated to aspirin but is the result of underlying platelet hyperreactivity prior to the institution of aspirin therapy. Individuals identified as aspirin “resistant” defined by serum TXB 2 are not the same individuals identified by the other tests.

scholarly journals Remote Assessment of Platelet Function in Patients with Acute Stroke or Transient Ischaemic Attack

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Philip M. Bath ◽  
Jane May ◽  
Katie Flaherty ◽  
Lisa J. Woodhouse ◽  
Natalia Dovlatova ◽  
...  
Keyword(s):  
Acute Stroke ◽  
Platelet Function ◽  
Multicentre Trial ◽  
Platelet Reactivity ◽  
Antiplatelet Agents ◽  
Surface Expression ◽  
Safety And Efficacy ◽  
Remote Assessment ◽  
Ischaemic Attack ◽  
Function Testing

Background. The TARDIS trial assessed the safety and efficacy of intensive versus guideline antiplatelet agents given for one month in patients with acute stroke or TIA. The aim of this substudy was to assess the effect of antiplatelet agents taken at baseline on platelet function reactivity and activation.Methods. Platelet function, assessed by remotely measured surface expression of P-selectin, was assessed in patients at their time of randomisation. Data are median fluorescence values.Results. The aspirin P-selectin test demonstrated that platelet expression was lower in 494 patients taking aspirin than in 162 patients not: mean 210 (SD 188) versus 570 (435), difference 360.3 (95% CI 312.2–408.4) (2p<0.001). Aspirin did not suppress P-selectin levels below 500 units in 23 (4.7%) patients. The clopidogrel test showed that platelet reactivity was lower in 97 patients taking clopidogrel than in 585 patients not: 655 (296) versus 969 (315), difference 314.5 (95% CI 247.3–381.7) (2p<0.001). Clopidogrel did not suppress P-selectin level below 860 units in 24 (24.7%) patients.Conclusions. Aspirin and clopidogrel suppress stimulated platelet P-selectin, although one-quarter of patients on clopidogrel have high on-treatment platelet reactivity. Platelet function testing may be performed remotely in the context of a large multicentre trial. Trial registrationISRCTN47823388.

Influence of Antioxidants on Arachidonic Acid Metabolism and Platelet Function

1994 ◽  
Vol 51 (1) ◽  
pp. 74-79 ◽  
Author(s):  
G.H.R. Rao ◽  
M.R. Tate ◽  
M. Murthy ◽  
R.P. Hebbel ◽  
J.G. White
Keyword(s):  
Arachidonic Acid ◽  
Platelet Function ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism

scholarly journals Platelet count and platelet function testing in acute coronary syndromes

2014 ◽  
Vol 23 ◽  
pp. e26
Author(s):  
K. Hally ◽  
L. Johnston ◽  
A. Holley ◽  
P. Larsen ◽  
S. Harding
Keyword(s):  
Platelet Count ◽  
Platelet Function ◽  
Acute Coronary Syndromes ◽  
Platelet Function Testing ◽  
Coronary Syndromes ◽  
Function Testing

MO739EX VIVO THROMBOCYTE FUNCTION IN HEMODIALYSIS PATIENTS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Vera Bonell ◽  
Georg Lorenz ◽  
Thorsten Kessler ◽  
Uwe Heemann ◽  
Christoph Schmaderer ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Clinical Outcome ◽  
Platelet Function ◽  
Primary Endpoint ◽  
Hemodialysis Patients ◽  
Healthy Controls ◽  
Induce Platelet Aggregation ◽  
Platelet Counts ◽  
Hospitalization Rates ◽  
Multiplate Analyzer

Abstract Background and Aims Coagulation disorders with both risk for bleeding and thrombotic events are common in hemodialysis (HD) patients. Altered thrombocyte counts and function may account for that. Here, we sought to better characterize thrombocyte function in hemodialysis patients. Method Platelet function was investigated using the Multiplate analyzer (Roche) based on impedance aggregometry. Adenosine diphosphate (ADP) was used to induce platelet aggregation and area under the curve (AUC) was used as primary endpoint. Platelet counts and C-reactive protein (CRP) levels were measured. Hospitalization was the primary clinical outcome. Pearson regression was used to test for associations of thrombocyte function and the primary endpoint. Results In total 60 chronic HD patients undergoing dialysis 3 times per week, and 67 healthy controls were included. In general, HD patients presented with significantly lower thrombocyte numbers compared to healthy controls (Median: 221 vs. 245 G/l, p=0.029). Further, thrombocyte function as determined by AUC was significantly altered in HD patients versus healthy controls (Median: 455 vs. 677 AU*min, p&lt;0.001; figure 1) with a significant correlation for platelet count and platelet function (r=0.42, p=0.001). Platelet function also correlated with the inflammatory state as seen by systemic CRP levels (r=0.28, p=0.033). Regarding the clinical outcome, platelet function correlated with hospitalization rates for infectious disease (r=0.27; p=0.040) and cardiovascular events (r=0.30; p=0.022). In case of hospitalization rates for infectious disease this correlation remained stable irrespective of adjustment for thrombocyte counts (r=0.27, p=0.036). Conclusion Lower platelet counts and altered function in HD patients was associated with risk of hospitalization and markers of inflammation in this cohort. The Multiplate analyzer appeared to be a valid and easily accessible method to assess thrombocyte function. Further studies are needed to determine whether assessment of thrombocyte function in clinical routine should be used to stratify risk in the vulnerable population of HD patients.

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