The use of impedance aggregometry to evaluate platelet function after the administration of DDAVP in healthy dogs treated with aspirin or clopidogrel

2021 ◽  
Vol 82 (10) ◽  
pp. 823-828
Author(s):  
Igor Yankin ◽  
Andy M. Carver ◽  
Amy M. Koenigshof
2008 ◽  
Vol 100 (10) ◽  
pp. 634-641 ◽  
Author(s):  
Mark K. Larson ◽  
Joseph H. Ashmore ◽  
Kristina A. Harris ◽  
Jessica L. Vogelaar ◽  
James V. Pottala ◽  
...  

SummaryOmega-3 fatty acids (n-3 FA) from oily fish are clinically useful for lowering triglycerides and reducing risk of heart attacks. Accordingly, patients at risk are often advised to take both aspirin and n-3 FA. However, both of these agents can increase bleeding times, and the extent to which the combination inhibits platelet function is unknown. The purpose of this pilot study was to determine the effects of a prescription omega-3 FA product (P-OM3) and aspirin, alone and in combination, on platelet aggregation assessed by whole blood impedance aggregometry (WBA). Ten healthy volunteers provided blood samples on four separate occasions: Day 1, baseline; Day 2, one day after taking aspirin (2 x 325 mg tablets); Day 29, after 28 days of P-OM3 (4 capsules/day); and Day 30, after one day of combined P-OM3 and aspirin. WBA was tested with two concentrations of collagen, with ADP and with a thrombin receptor activating peptide (TRAP). Compared to baseline, aspirin alone inhibited aggregation only with low-dose collagen stimulation;P-OM3 alone did not inhibit aggregation with any agonist; and combined therapy inhibited aggregation with all agonists butTRAP. Significant interactions between interventions were not observed in response to any agonist. In conclusion, P-OM3 alone did not inhibit platelet aggregation, but did (with two agonists) when combined with aspirin. Since previous studies have not reported a clinically significant risk for bleeding in subjects on combined therapy, P-OM3 may safely enhance the anti-platelet effect of aspirin.


Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1150
Author(s):  
Alberto Zanetto ◽  
Marco Senzolo ◽  
Elena Campello ◽  
Cristiana Bulato ◽  
Sabrina Gavasso ◽  
...  

Hyper-functional platelets are being proposed as a potential therapeutic target in multiple cancers. Whether this can be considered in patients with cirrhosis and hepatocellular carcinoma (HCC) is unknown as their platelet function has not yet been investigated. We evaluated platelet function in cirrhosis patients with HCC. Patients with cirrhosis with and without HCC were prospectively recruited. Platelet aggregation, a marker of platelet function, was assessed by impedance aggregometry with adenosine diphosphate (ADP), arachidonic acid (ASPI), and thrombin (TRAP) stimulation. Plasmatic levels of Von Willebrand factor antigen (VWF) were also determined. One-hundred patients were recruited (50 cirrhotics with and 50 without HCC). Cirrhosis severity by Child class and platelet count were comparable between cirrhotics with and without HCC. Cirrhotics with HCC had higher ADP- (45 vs. 28; p < 0.001), ASPI- (47 vs. 28; p < 0.001), and TRAP- (85 vs. 75; p = 0.01) induced platelet aggregation than cirrhotics without HCC, all indicative of platelet hyper-function. The relatively increased platelet aggregation in patients with HCC was confirmed after adjusting the analysis for platelet count/severity of thrombocytopenia. Levels of VWF were higher in patients with vs. without HCC (348 vs. 267; p = 0.006), particularly in compensated cirrhosis. In patients with cirrhosis, HCC is associated with increased platelet aggregation and higher VWF. The clinical implications of these findings deserve further investigation.


2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Andrew D Meyer ◽  
Anjana Raghunath ◽  
Patricia Heard ◽  
Jannine Cody

Inappropriate platelet function is a significant risk factor for cardiovascular disease, the leading cause of death in the United States. Although abnormal platelet function has a strong genetic component, very few human genes have been linked to platelet function. Mice with a homozygous deletion of EMILIN2 (Elastin Microfibril Interface Located Protein2) gene, located on Chromosome 18p, have a significant decrease in platelet function and clot formation. However, deletion or inactivation of only one copy of a gene is most relevant to human disease modeling. Our hypothesis is that blood samples from people with single 18p deletions that include EMILIN2 will have decreased platelet function compared to healthy individuals. We conducted a case-control study of nine adult individuals with chromosome 18p deletions matched with healthy men and women (n=20). Routine coagulation measurements were performed on a STAGO STA-R instrument. Platelet aggregation was measured with whole blood impedance aggregometry and Thromboelastography with PlateletMapping using the manufacturers’ protocols. There was no significant difference in platelet count, prothrombin time, partial thromboplastin time, d-dimer, or fibrinogen between individuals with a single 18p gene copy number and normal controls. However, platelet aggregation was impaired in individuals with 18p deletions compared to normal controls in response to collagen and arachidonic acid (ASPI), respectively ( p <0.0001, Figure 1). Moreover, Thromboelastography with PlateletMapping was decreased in individuals with 18p deletions compared to normal controls for ADP and ASPI, ( p <0.001). Individuals with one copy of 18p have decrease platelet function compared to normal controls. These results identify a novel human genetic loci linked to a specific phenotype of platelet function. Future will studies will determine if this gene can be used for diagnostic or therapeutics for cardiovascular disease.


Perfusion ◽  
2019 ◽  
Vol 35 (2) ◽  
pp. 138-144
Author(s):  
Helena Argiriadou ◽  
Polychronis Antonitsis ◽  
Anna Gkiouliava ◽  
Evangelia Papapostolou ◽  
Apostolos Deliopoulos ◽  
...  

Introduction: Cardiac surgery on conventional cardiopulmonary bypass induces a combination of thrombocytopenia and platelet dysfunction which is strongly related to postoperative bleeding. Minimal invasive extracorporeal circulation has been shown to preserve coagulation integrity, though effect on platelet function remains unclear. We aimed to prospectively investigate perioperative platelet function in a series of patients undergoing cardiac surgery on minimal invasive extracorporeal circulation using point-of-care testing. Methods: A total of 57 patients undergoing elective cardiac surgery on minimal invasive extracorporeal circulation were prospectively recruited. Anticoagulation strategy was based on individualized heparin management and heparin level–guided protamine titration performed in all patients with a specialized point-of-care device (Hemostasis Management System – HMS Plus; Medtronic, Minneapolis, MN, USA). Platelet function was evaluated with impedance aggregometry using the ROTEM platelet (TEM International GmbH, Munich, Germany). ADPtest and TRAPtest values were assessed before surgery and after cardiopulmonary bypass. Results: ADPtest value was preserved during surgery on minimal invasive extracorporeal circulation (58.2 ± 20 U vs. 53.6 ± 21 U; p = 0.1), while TRAPtest was found significantly increased (90 ± 27 U vs. 103 ± 38 U; p = 0.03). Postoperative ADPtest and TRAPtest values were inversely related to postoperative bleeding (correlation coefficient: −0.29; p = 0.03 for ADPtest and correlation coefficient: −0.28; p = 0.04 for TRAPtest). The preoperative use of P2Y12 inhibitors was identified as the only independent predictor of a low postoperative ADPtest value (OR = 15.3; p = 0.02). Conclusion: Cardiac surgery on minimal invasive extracorporeal circulation is a platelet preservation strategy, which contributes to the beneficial effect of minimal invasive extracorporeal circulation in coagulation integrity.


2020 ◽  
pp. 1098612X2097206
Author(s):  
Kellyi K Benson ◽  
Jessica M Quimby ◽  
Sarah B Shropshire ◽  
Stacie C Summers ◽  
Kristy L Dowers

Objectives The aims of this study were to determine if stable chronic kidney disease (CKD) cats and uremic crisis cats have altered platelet function, and to determine the prevalence of positive fecal occult blood in CKD cats. Methods Platelet function in normal cats, clinically stable International Renal Interest Society (IRIS) stage 2–4 CKD cats and CKD cats experiencing a uremic crisis were evaluated using impedance aggregometry. Area under the curve (AUC) at 6 mins was calculated for saline, adenosine diphosphate (AUCADP) and arachidonic acid (AUCASPI). The AUC in addition to hematocrit, platelet count and mean platelet volume (MPV) were compared between groups using the Kruskal–Wallis test followed by Dunn’s post-hoc analysis. Guaiac fecal occult blood tests were performed on fecal samples and results were compared between groups using a χ2 for trend test. Results AUCADP ( P = 0.04) and AUCASPI ( P = 0.05) were significantly higher in uremic crisis cats compared with normal cats at 6 mins. Hematocrit was significantly higher in normal cats when compared with IRIS stage 3 and 4 ( P = 0.002) and uremic crisis ( P = 0.0008) cats, with no difference among groups for platelet count or MPV. The proportion of cats with positive fecal occult blood samples was significantly different between groups ( P = 0.0017); 50% uremic crisis cats, 33% IRIS stage 3 and 4 cats, and 10% IRIS stage 2 cats were positive, while no normal cats were positive. The proportion of cats with platelet clumping was significantly different between groups ( P = 0.03). Conclusions and relevance Platelet hyper-reactivity may be occurring in CKD cats experiencing a uremic crisis. The etiology of positive fecal occult blood samples in CKD cats is unclear and did not appear to be related to decreased platelet function as measured in this study and requires further investigation.


2012 ◽  
Vol 73 (5) ◽  
pp. 595-601 ◽  
Author(s):  
Bobbi J. Conner ◽  
Rita M. Hanel ◽  
Bernard D. Hansen ◽  
Alison A. Motsinger-Reif ◽  
Makoto Asakawa ◽  
...  

2010 ◽  
Vol 71 (3) ◽  
pp. 349-358 ◽  
Author(s):  
Shauna L. Blois ◽  
Dana G. Allen ◽  
R. Darren Wood ◽  
Peter D. Conlon

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