Thank you very much, Naveed Saleh.

Key Points
• Source: Thrombus Research
• Conclusions. “Treatment of patients with haematological disorders with the Btk inhibitor ibrutinib reduces in vitro platelet deposition, thrombus size and contraction on human atherosclerotic plaque around a stenosis when compared to patients not receiving ibrutinib.”
• Investigators assessed the effects of ibrutinib on in vitro thrombus formation using blood drawn from CLL and mantle-cell lymphoma patients, as well as those with Waldenström macroglobulinemia.
• The decreased adhesion and thrombus formation could be due to an inability of plaque collagen to support platelet adhesion at increasing shear rates along with an insufficient ability of plasma derived VWF to compensate. Of note, endothelial-derived VWF is important in thrombus formation at pathological shear rates
• “Despite the reduced thrombus formation on plaque by increasing shear rate, ibrutinib treatment still inhibited platelet adhesion, thrombus size and contraction around the stenosis,” the authors wrote. “Knowing that Btk is also involved in signaling downstream of GPIb and the dominant role of VWF via GPIb and αIIbβ3 to platelet aggregation at supraphysiological shear stress, it is relevant to study the inhibition of Btk under these conditions.”
• Limitations of the current study include the small sample size, with only 6 patients receiving ibrutinib and 5 not receiving the agent. Furthermore, the investigators only looked at in vitro thromhus formation and did not do other platelet function tests.