Atherosclerosis is a pathological process underpinning many
cardiovascular diseases; it is the main cause of global mortality.
Atherosclerosis is characterized by an invasion of inflammatory cells, accumulation of
lipids and the formation of fatty streaks (plaques) which subsequently allow accumulation of
calcium and other minerals leading to a disturbance in the vascular endothelium and its regulatory role in arterial function.
Vascular calcification is a different process, stringently regulated mainly by local factors, in which osteoblast-like cells accumulate in the muscular layer of arteries ultimately taking on the physiological appearance of bone. The elevated stiffness of the arteries leads to severe vascular complications in brain, heart and kidneys. Recently, evidence from animal experiments as well as clinical and epidemiological results suggests that long-term treatment with
warfarin, but not with the novel direct
anticoagulants, can increase the risk or even induce
vascular calcification in some individuals. Gamma-carboxylation is an enzymatic process not only needed for activation of
vitamin K but also other
proteins which participate in bone formation and
vascular calcification. Thus, reduced expression of the
vitamin K-dependent
proteins which physiologically inhibit calcification of cellular matrix could be postulated to lead to
vascular calcification. Published clinical data, describing at present a few thousand patients, need to be supplemented with controlled studies to confirm this interesting hypothesis.