Figure 6.
Effects of the BTKi’s ibrutinib and acalabrutinib on platelet aggregation in blood stimulated by HIT serum and heparin. Blood samples were incubated for 30 minutes with solvent (DMSO, 0.1%) or BTKi’s (ibrutinib, 0.2 µM and acalabrutinib, 1 µM) and subsequently for 30 minutes with HIT-positive serum (100 µL) before addition of heparin (0.5 U/mL) for 3 minutes and start of stirring. Aggregation was measured for 10 minutes. (A) Representative MEA tracings of 2 healthy blood donors showing the effect of BTKi's on low (donor X) and high (donor Y) platelet aggregation upon stimulation by HIT serum. The numbers above the tracings indicate cumulative aggregation values (AU/min) measured for 10 minutes. (B) Bar diagram showing the effects of BTKi's on platelet aggregation stimulated by HIT-serum and heparin. Values are mean ± SD (n = 5 different blood donors). **P < .01.

Effects of the BTKi’s ibrutinib and acalabrutinib on platelet aggregation in blood stimulated by HIT serum and heparin. Blood samples were incubated for 30 minutes with solvent (DMSO, 0.1%) or BTKi’s (ibrutinib, 0.2 µM and acalabrutinib, 1 µM) and subsequently for 30 minutes with HIT-positive serum (100 µL) before addition of heparin (0.5 U/mL) for 3 minutes and start of stirring. Aggregation was measured for 10 minutes. (A) Representative MEA tracings of 2 healthy blood donors showing the effect of BTKi's on low (donor X) and high (donor Y) platelet aggregation upon stimulation by HIT serum. The numbers above the tracings indicate cumulative aggregation values (AU/min) measured for 10 minutes. (B) Bar diagram showing the effects of BTKi's on platelet aggregation stimulated by HIT-serum and heparin. Values are mean ± SD (n = 5 different blood donors). **P < .01.

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