“…Since VEGF is a multifunctional cytokine that stimulates vasodilation, vascular hyperpermeability, and angiogenesis, and was reported to stimulate endothelial nitric oxide production (7), we suspect that VEGFmay have decreased systemic vascular resistance in our patient resulting in the development of a high cardiac output state, which was followed by high-output heart failure. Onthe other hand, multiple myelomawas also reported to cause a high cardiac output state (8,9). Since both multiple myelomaand Crow-Fukase syndrome exhibit plasma cell dyscrasia, and since cytokines are suspected in the pathogenesis of both of these diseases (10, 1 1), we suspect that there may be a commonmechanism for the high cardiac output state in both multiple myelomaand Crow-Fukase syndrome, which might be mediated by VEGF.Further studies are necessary to clarify these points.…”