In the light of the above, our observation that, in the poststroke HF subjects, higher phosphate levels (without hyperphosphatemia) are associated with BSI, bone resorption markers, and osteocalcin, which also exerts a profound effect on energy metabolism [159, 160], can be interpreted as an additional factor contributing to the link between vascular dysfunction/calcification, subsequent stroke, and HF. Here, BGLAP is linked to hyperphosphatemia.