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Harmful calcification of structures in the cardiovascular system proceeds alongside the development of the fatty lesions of atherosclerosis. Both disease processes are accelerated by chronic inflammation, but derive from very different, distinct underlying mechanisms. There is presently little that can be done to reverse calcification effectively; EDTA chelation therapy is the best option on the table at present, but isn’t well regarded in the medical community. Other treatments are more focused on slowing the progression of calcification, and can achieve that goal to some degree.
The primary cause of worldwide mortality and morbidity stems from complications in the cardiovascular system resulting from accelerated atherosclerosis and arterial stiffening. Frequently, both pathologies are associated with the pathological calcification of cardiovascular structures, present in areas such as cardiac valves or blood vessels (vascular calcification). The accumulation of hydroxyapatite, the predominant form of calcium phosphate crystals, is a distinctive feature of vascular calcification. This phenomenon is commonly observed as a result of aging and is also linked to various diseases such as diabetes, chronic kidney disease, and several genetic disorders.
A substantial body of evidence indicates that vascular calcification involves two primary processes: a passive process and an active process. The physicochemical process of hydroxyapatite formation and deposition (a passive process) is influenced significantly by hyperphosphatemia. However, the active synthesis of calcification inhibitors, including proteins and low-molecular-weight inhibitors such as pyrophosphate, is crucial. Excessive calcification occurs when there is a loss of function in enzymes and transporters responsible for extracellular pyrophosphate metabolism.
In clinical practice, it is crucial to assess phosphate and pyrophosphate homeostasis by evaluating both plasma phosphate and pyrophosphate levels. When elevated phosphate levels are detected in the blood, the initial therapeutic strategies to prevent vascular calcification should include the administration of phosphate binders to reduce circulating phosphate levels and address any dysregulated phosphate homeostasis if present. Furthermore, in cases of low pyrophosphate levels, therapeutic strategies should involve the administration of exogenous pyrophosphate and interventions to enhance the availability of endogenous pyrophosphate.
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