Longitudinal Effects of Serum Calcium and Phosphate Levels and Their Ratio on Incident Ischemic Heart Disease among Korean Adults

Abstract

Serum calcium and phosphate levels are controlled by a regulatory system, but their individual concentration tendencies and interactions may affect long-term vascular health. This study aimed to assess the effects of serum calcium and phosphate levels on incident ischemic heart disease (IHD) in a large-scale community-dwelling Korean cohort. We evaluated 15,259 non-diabetic individuals (median age, 45 years; range, 30–85) without previous IHD or ischemic stroke using the Korean National Health Insurance data. The study population was classified based on the calcium, phosphate, and calcium/phosphate ratios. Using Cox proportional hazards regression models, we estimated hazard ratios (HRs) with 95% confidence intervals (CIs) for IHD over 50 months after baseline enrolment. The age- and sex-adjusted incidence of IHD gradually increased with serum calcium and phosphate quartiles and decreased with calcium/phosphate ratio quartiles, with an overall crude rate of 2.1% (315/15,259). After setting the lowest calcium, phosphate, and calcium/phosphate ratio quartiles as a reference group, the HRs (95% CIs) of the highest calcium, phosphate, and calcium/phosphate ratio quartiles for IHD were 1.77 (1.15–2.72), 1.73 (1.18–2.55), and 0.58 (0.39–0.87), respectively, after adjusting for potential confounding variables. Serum calcium and phosphate levels were positively associated with IHD incidence, while the serum calcium/phosphate ratio exhibited an inverse relationship. Serum calcium and phosphate homeostasis may merit serious consideration to understand the pathogenesis of coronary atherosclerosis as a risk modifier for IHD.

Rifampicin efficacy against doxorubicin-induced cardiotoxicity in mice

“…Additionally, doxorubicin stimulates a reduction in the calcium storing amplitude of mitochondria and exacerbates calcium overload. In harmony with Jung et al [ 57 ], serum phosphorus levels showed elevation in our cardiotoxicity model. Hyperphosphatemia may result from doxorubicin's indirect toxic effects on the kidneys.…”

“…These calcium ions induce free radicals production that is responsible for oxidative stress and subsequent cardiac dysfunction. This is in consent with many former studies [ 55 – 57 ] who proved the doxorubicin-induced calcium ions imbalance and overload. According to Mitry and Edwards [ 58 ], doxorubicin causes loss of calcium homeostasis by affecting the calcium pump found in the membrane and interfering with calcium reservation by the sarcoplasmic reticulum.…”

Glycine protects against doxorubicin-induced heart toxicity in mice

“…Hyperkalemia is also markedly related to poor prognosis in those patients and may influence survival (Toledo et al 2021 ). Other studies, like Jung et al ( 2022 ), reported increased Ca and P levels in heart failure. In the current study, DOXO intoxication did not alter Ca and P serum levels but showed marked increases in serum Na and K levels that might be due to DOXO-induced renal complications or/and neurohormonal disturbances behind cardiotoxicity pathogenesis.…”

Predictive Value of Serum Uric Acid to HDL Cholesterol Ratio for Incident Ischemic Heart Disease in Non-Diabetic Koreans

“…After applying exclusion criteria, 16,455 individuals (8425 men and 8029 women) were included in the final analysis ( Figure 1 ). The materials and methodology of the HERAS-HIRA datasets were described in detail in previous studies [ 19 , 20 ]. UHR (%) was calculated as uric acid (mg/dL) divided by HDL cholesterol (mg/dL).…”