Academic literature on the topic 'Multiplate aggregometry'

Impedance aggregometry (Multiplate®) detects the effects of platelet aggregation inhibitors and can predict thrombotic complications after coronary and cerebrovascular stent interventions. The bedside method uses whole blood samples not corrected for platelet count. It is claimed but not proved that the findings are unrelated to platelet count in the physiological range. We therefore investigated in the experimental study: (1) whether impedance aggregometry findings and platelet count are correlated and (2) whether the aggregation/platelet count ratio expresses platelet function independent of platelet count. Following ethics committee approval, platelet-rich plasma from healthy probands was diluted with platelet-poor plasma to obtain different platelet counts. Thereafter, platelet count was measured and samples were subjected to impedance aggregometry using thrombin receptor activating peptide (TRAP) for platelet activation. In all probands, impedance aggregometry findings and platelet count were highly correlated (r = 0.88 to 0.94; p < 0.05). The combination of all experiments revealed the proportionality between impedance aggregometry findings and platelet count (n = 31, r = 0.78, p = 0.0001). In contrast, the ratio of impedance aggregometry findings and platelet count was not significantly correlated with platelet count (r = 0.017; p = 0.3) and thus constitutes a specific measure for platelet function. In conclusion, impedance aggregometry findings subsequent to the activation with TRAP are dependent on both platelet function and platelet count. Normalization of impedance aggregometry findings for platelet count can be achieved by a ratio resulting in more specific results.

Abstract BACKGROUND Anticoagulation protocols used during mechanical circulatory support call for titration of antiplatelet agents. We compared the precision and reliability of 5 platelet function tests in healthy volunteers and donors on daily antiplatelet therapy to distinguish their efficacy for titrating antiplatelet therapy. METHODS We assessed arachidonic acid–induced platelet function by light transmission aggregometry (LTA), Multiplate impedance aggregometry, VerifyNow, and platelet mapping by thromboelastography (TEG PM). We assessed ADP-induced platelet function by the same methods and flow cytometry. Forty healthy volunteers and 10–13 volunteers on daily aspirin and/or clopidogrel therapy were evaluated. We compared tests for intraassay precision, interassay precision (samples from 2 separate blood draws), and reliability coefficient. RESULTS For arachidonic acid–induced platelet aggregation in healthy volunteers, intra- and interassay CVs were ≤10% for all methods. Intra- and interassay precision among donors on daily aspirin was ≤30% for all methods except LTA (38% interassay CV) and TEG PM (95% intraassay and 104% interassay CV). For ADP-induced platelet function, intra- and interassay precision was ≤10% and ≤30% for all methods. Only Multiplate demonstrated moderate or greater (R > 0.40) reliability coefficients for arachidonic acid–induced platelet function among all subjects. All methods of ADP-induced platelet function, except TEG PM, demonstrated substantial or greater (R > 0.60) reliability among all subjects. CONCLUSIONS TEG PM is least suited to monitor effects of antiplatelet agents. Multiplate impedance aggregometry was the only method to demonstrate an acceptable reliability coefficient among healthy volunteers and donors on both aspirin and clopidogrel therapy.

Introduction Reduced antiplatelet activity of aspirin (ALR) or clopidogrel (CLR) is associated with an increased risk of thromboembolic events. The reported prevalence data for low-responders vary widely and there have been few investigations in vascular surgery patients even though they are at high risk for thromb-embolic complications. The aim of this prospective observational monocentric study was to elucidate possible changes in ALR or CLR after common vascular procedures. Methods Activity of aspirin and clopidogrel was measured by impedance aggregometry using a multiple electrode aggregometer (Multiplate®). Possible risk factors for ALR or CLR were identified by demographical, clinical data and laboratory parameters. In addition, a follow-up aggregometry was performed after completion of the vascular procedure to identify changes in antiplatelet response. Results A total of 176 patients taking antiplatelet medications aspirin and/or clopidogrel with peripheral artery disease (PAD) and/or carotid stenosis (CS) were included in the study. The prevalence of ALR was 13.1% and the prevalence of CLR was 32% in the aggregometry before vascular treatment. Potential risk factors identified in the aspirin group were concomitant insulin medication (p = 0.0006) and elevated C-reactive protein (CRP) (p = 0.0021). The overall ALR increased significantly postoperatively to 27.5% (p = 0.0006); however, there was no significant change in CLR that was detected. In a subgroup analysis elevation of the platelet count was associated with a post-procedure increase of ALR incidence. Conclusion The incidence of ALR in vascular surgery patients increases after vascular procedures. An elevated platelet count was detected as a risk factor. Further studies are necessary to analyse this potential influence on patency rates of vascular reconstructions.

The complement system is a long and complicated event of reactions where activation leads to cleavage of different factors and ends with either inflammation or cell lysis.     Recent studies have shown that the complement system and coagulation have some elements in common. Therefore in this study it was relevant to look at the inhibition of the complement system in two different whole blood analyses of coagulation activation, thromboelastography and impedance aggregometry. Thromboelastography, or TEG®, measures the clot forming properties of whole blood and the impedance aggregometry, or Multiplate®, measures platelets’ ability to adhere and aggregate to an electrode. Four different inhibitors where used: Eculizumab, C1 inhibitor, Compstatin and OMS721, which all inhibits different parts of the complement system.     The curves from Multiplate® was presented in standard deviation and the number of reduction, while the results from TEG® was presented in before and after added inhibitor in graphs.     In conclusion, impedance aggregometry show a more specific and secure results of the inhibitors effect, which was seen by that both C1 inihibitor and Compstatin had a major influence on the area under the curve (AUC). In TEG® there were no detectable difference, which could mean TEG® is not specific enough for platelets efficiency, which is affected by the complement inhibition.

Background: the link between venous thromboembolism (VTE) and arterial thromboembolic events (ATE) is still uncertain. In 2003 Prandoni et al published the first study that reported a connection, in term of etiopathogenesis between VTE and atherosclerosis. During the last few years several other study confirm this association, that could be attributed to common risk factors for the two conditions. The contribution of thrombophilic defects to the link between VTE and ATE has yet to be defined. Thrombophilic conditions (hereditary deficiencies of protein S, protein C and antithrombin) have been recognized as most potent thrombophilic conditions for VTE. Whether hereditary protein S, Protein C or antithrombin deficiency also are involved in the development of ATE need to be confirmed and the evidence of a possible association has been showed mainly from case reports. Blood haemostasis is a complex mechanism influenced from coagulation factors, aggregation proteins, blood cells (platelets, leucocytes) and vascular endothelium. Most of biochemical tests focused on coagulation system asses only a part of this complex mechanism and, in particular, the laboratory tests analyze only the coagulations cascade. But the role of platelets and vascular endothelium is not clear. The contribution of thrombophilic defects as common risk factor between VTE and ATE has yet to be defined compared with nondeficient family members. Moreover in this study the endothelial dysfunction could be the real cause for both conditions VTE and ATE. There are no data concerning the role of platelets function or vascular endothelium function in this thrombophilic patients population. The aim of the study is to define, in thrombophilic patients (Prot C, Prot S and antithrombin defects) compared with non-deficient family members. the role of platelets function using a new analyzer named Multiplate® whole blood aggregometry that evaluated platelets aggregations in whole blood and to define also the possible implication of endothelial function, by the non-invasive assessment of flow mediated dilatation (FMD) of the brachial artery, by B-mode ultrasonography, using a standardized procedure Material and Methods: after signing an informed consent, we enrolled patients with thrombophilic defects (cases) and create three subgroups (cases with deficit of protein C, protein S and antithrombin) with and without a history of thromboembolic disease, and subjects without thrombophilic defects (controls). We collected baseline data of all (cases and controls) on previous episodes of VTE and ATE, risk factors for atherosclerosis (i.e. hypertension, diabetes mellitus, cigarette smoking; hyperlipidemia) All patients were tested for thrombophilic defects in addition to their index deficiencies (FV Leiden, G20210 A prothrombin, lupus anticoagulant; PC and PS, AT). Moreover, we study platelets aggregations with a new analyzer named Multiplate® whole blood aggregometry that evaluated platelets aggregations in whole blood with thrombin inibitor (irudin); this instrument identify the electrical impedance (as area under curve, AUC) caused from platelets aggregation. The platelets aggregation was triggered by different activators: adenosine-5 diphosphate (ADP test), arachidonic acid (ASPI test) and thrombin receptor activatin peptide (TRAP -6) All cases and controls underwent evaluation of endothelial function by the non-invasive assessment of flow mediated dilatation (FMD) of the brachial artery, by B-mode ultrasonography, using a standardized procedure. Results: patients with thromphilic defects versus controls have similar demographical charatistics. The valutation of the platelets aggregation by Multiplate® with different tests (ASPI, ADP and TRAP) show a different in the two groups but it is no statistically significant; we observed the same results if analyze the three subgroups (Protein C defects, Protein S and antithrombin deficiency) protein separately. The ultrasonography evaluation of endothelial function show that there is a reduction of the flow mediated dilatation (FMD) in patients with thrombophilic defects versus controls. The FMD calculated in thrombophilic patients is statistically significant (3.7±0.5% vs 5.2±0.6% ,p value = 0.015) compared the controls. Discussion: Our preliminary data show that in patients with thrombophilic deficiency there is increased of platelets aggregation but it’s no statically significant. This results is confirm also in all different subgroups of thromphilic deficiency (Prot C, S, and AT deficiency ). However an endothelial dysfunction is showed in thrombophilic patients compared the controls. Although we speculated with this data, as other study have reported, that endothelial dysfunction rather than coagulation disorders is the main actor in the link between VTE and ATE in thrombophilic subjects. It is yet unclear the role of the different actors (endothelium dysfunction, platelet aggregation and coagulation factors) in the development on VTE and ATE, but this study can show that endothelium dysfunction can be one of the most important trigger factor in the thrombophilic patients<br>Introduzione: La correlazione tra malattia trombo embolica venosa e patologia arteriosa è un dato che ormai affascina e riscuote l’interesse di molti studiosi. Già nel 2003 Prandoni et al misero in evidenza tale possibile correlazione; molti altri studi hanno successivamente consolidato tale dato dimostrando anche la condivisione di numerosi fattori di rischio (diabete, ipertensione arteriosa, dislipidemia, fumo di sigaretta). Il complesso meccanismo coagulativo è influenzato da molteplici attori: fattori della coagulazione, cellule ematiche (leucociti, piastrine) e dall’endotelio vascolare. Molte delle indagini tuttora utilizzate per la coagulazione valutano solo una parte di questa complessa cascata coagulativa, ma il ruolo svolto dalle piastrine e dall’endotelio non è ancora chiarito. In particolare, in uno specifico sottogruppo della popolazione, i soggetti trombofilici, i quali presentano un deficit degli inibitori naturali della coagulazione (proteina C, proteina S e antitrombina) e che manifestano una maggiore incidenza della malattia tromboembolica venosa e, anche se in misura differente, dell’aterotrombosi. Lo scopo del nostro studio è stato quello di valutare la funzione endoteliale, attraverso l’utilizzo di tecnica ecografica dell’arteria brachiale della dilatazione flusso mediata (FMD) e l’aggregazione piastrinica, attraverso l’uso di aggregometro basato sull’impedenziometria con elettrodi multipli (Multiplate®), in un gruppo di soggetti con difetto degli inibitori naturali della coagulazione rispetto ad un gruppo di volontari sani. Materiali e metodi: nel gruppo dei casi sono stati arruolati, dopo consenso informato, 68 soggetti con difetto noto degli inibitori della coagulazione (deficit di Prot C, Prot S o antitrombina) e nel gruppo dei controlli 59 soggetti volontari sani confrontabili per sesso ed età ( 3 anni). Sono stati esclusi dallo studio soggetti con età inferiore ai 18 aa, che si sono rifiutati di firmare il consenso informato, che assumevano terapia anticoagulante o antiaggregante piastrinica o con piastrinopenia (conta piastrinica <150 x109/L) o piastrinosi (conta piastrinica >450 x109/L). Tutti i soggetti arruolati allo studio sono stati sottoposti a raccolta anamnestica dettagliata relativa a fattori di rischio e precedenti cardiovascolari o tromboembolici venosi; ciascuno di essi inoltre è stato sottoposto a prelievo di 18 ml di sangue venoso per esecuzione di test della coagulazione classica e studio ipercoagulabile (proteina C, proteina S, antitrombina, variante protrombinica, fattore V Leiden anticorpi antifosfolipidi). Su ogni campione di sangue veniva effettuato studio dell’ aggregazione piastrinica con aggregometro ad impedenza ad elettrodi multipli (Multiplate®), che eseguiva contemporaneamente più test (ASPItest, ADPtest e TRAPtest). Infine su ogni soggetto è stato eseguita valutazione ecografica della disfunzione endoteliale mediante valutazione della dilatazione flusso mediata (FMD) con misurazione dell’arteria brachiale prima e dopo iperemia. Risultati: i soggetti con difetto trombofilico presentavano caratteristiche demografiche sovrapponibili a quelle dei controlli sani. L’incidenza di eventi trombo embolici venosi e risultata ovviamente più elevata nel gruppo dei casi; mentre i soggetti trombofilici hanno mostrato di aver sviluppato in età più giovane eventi cardiovascolari. Nella valutazione dell’aggregazione piastrinica studiata con il Multiplate® , con differenti test di stimolazione (ASPI, ADP e TRAP) sono emerse differenze della AUC (area sotto la curva) che esprime in modo quantitativo l’aggregazione piastrinica che tuttavia non sono risultate statisticamente significative; il dato si è confermato anche nella valutazione dei casi, prendendo in considerazione singolarmente ogni difetto trombofilico. In relazione alla valutazione della disfunzione endoteliale mediante ecografia dell’arteria brachiale si è evidenziato un decremento statisticamente significativo della dilatazione flusso mediata (FMD) nei casi rispetto ai controlli (3.7±0.5% vs 5.2±0.6% , p value = 0.015), mentre sono risultati di dimensioni sovrapponibili il diametro e il flusso basale del vaso. Discussione: Per quanto riguarda la valutazione aggregometrica su sangue intero, i dati raccolti, non hanno evidenziato una differenza significativa dell’aggregazione piastrinica valutata con i test di induzione (TRAP, ADP, ASPI) nei soggetti trombofilici rispetto ai controlli. Tale dato potrebbe quindi essere interpretato come l’assenza di una “intrinseca” iperaggregabilità delle piastrine di questi soggetti che possa essere l’innesco della cascata trombotica a cui essi vanno più spesso incontro. In relazione allo studio della funzione endoteliale i dati hanno mostrato che esiste una riduzione della dilatazione dell’arteria brachiale post fase iperemica che in valore percentuale è significativamente piu bassa nei soggetti trombofilici rispetto ai controlli. Il dato quindi sembra confermare che nei soggetti con deficit degli inibitori della coagulazione, con noto incremento dell’incidenza di eventi tromboembolici, sia la disfunzione endoteliale a rappresentare il determinante capace di innescare tale processo

Transfusion of platelet concentrates (PC) can be necessary for patients to maintain coagulability. It is vital that the platelets maintain viability and function during processing and storage to obtain enhanced coagulability in the transfused patient. Today, no test is used to verify platelet function in either donors or in PC’s. Observing swirling effect is the only test applied to control platelets before transfusion but the method is based on platelet morphology and does not directly evaluate platelet function.Impedance aggregometry (IA) (Multiplate analyzer, Roche Diagnostic) is a promising method for measuring platelet function, measuring changes in impedance over time when platelets adhere to electrodes. IA has been well evaluated for the purpose of analyzing whole blood but analyzing PC’s is a relatively new application of the method.Samples from platelet donors and PC’s were analyzed with IA to evaluate correlation in function between donors and PC’s, in the hope of being able to predict function in PC. Different platelet concentrations were also analyzed to evaluate the impact of varying concentration on impedance. Adenosine diphosphate (ADP), collagen and thrombin receptor activating peptide 6 (TRAP-6) were used to induce aggregation. Platelet function was measured in PC’s on day 1 and 4 after donation.A significant correlation was observed between platelet function in donors and in PCs on day 1, measured with ADP. An important finding was also that platelet concentration does affect impedance, in collagen-induced aggregation more than ADP-induced. It is therefore possible that a correlation would also have been found between donors and PC’s analyzed with collagen if the platelet concentration would have been standardized.