“…Multiple potential mechanisms have been suggested including leucocyte aggregation and adhesion with vessel plugging, activation of the coagulation system, interaction with platelets to promote thrombin generation, increased expression of monocyte and neutrophil tissue factors, and release of soluble mediators such as proteases, reactive oxygen species, growth factors, interleukins, and myeloperoxidase [ 16 – 18 ]. Patients with CLL may also develop amyloid infiltration of the heart, either paraprotein-related AL amyloid [ 19 ] or, less commonly, non-AL; the latter group appears to have a better prognosis [ 20 ]. Amyloid can also deposit within vessels causing occlusion [ 21 ].…”