Formation of calcium phosphate bions in patients with carotid and coronary atherosclerosis

Aim. To study the formation of calcium phosphate bions (CPB), a trigger of endothelial dysfunction in the patients with coronary and carotid atherosclerosis as compared to healthy blood donors.

Material and methods. The study included 264 individuals: 88 patients with cerebrovascular disease who underwent carotid endarterectomy due to ischemic stroke (n=44) or chronic cerebral ischemia (n=44)); 88 patients with coronary artery disease (44 patients with stable angina requiring coronary artery bypass graft surgery and 44 patients with myocardial infarction); 88 healthy volunteers enrolled into Prospective Urban Rural Epidemiology (PURE) study who did not have symptomatic coronary or hemodynamically relevant carotid atherosclerosis as measured by ultrasound. We further measured serum parameters defining mineral homeostasis: total and ionized calcium, phosphate, total protein, albumin, and fetuin-A. We also determined serum calcification propensity by means of supersaturation (+2 mmol/L) with CaCl₂ and Na₂HPO₄ followed by incubation at 37° С for 24 hours.

Results. Patients with carotid atherosclerosis (either with ischemic stroke or chronic cerebral ischemia) or myocardial infarction were characterized by an increased calcification propensity in combination with reduced total protein and albumin and elevated ionized calcium. Correlation analysis revealed that serum calcification was associated with a decrease in serum total protein and albumin. Therefore, depletion of serum protein mineral depot leads to the elevation of ionized calcium which is further aggregated into calcium phosphate bions, a secondary mineral depot.

Conclusion. Formation of CPB in the serum is induced by an elevation of ionized calcium caused by a reduction of total protein and albumin and is associated with increased risk and progression of atherosclerosis.

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