Abstract
Aims: Immune activation and disturbances of vitamin D metabolism are frequently encountered in patients with heart failure. Elevated fibroblast growth factor 23 (FGF23) levels as well as immune activation have been associated with a worse outcome in patients with heart failure. We evaluated the relationship of vitamin D metabolism and FGF23 levels with immune activation and its association with cardiac function and outcome in patients with heart failure. Methods and Results: In 149 patients with heart failure caused by nonischaemic cardiomyopathy, parameters of vitamin D metabolism (vitamin D, parathormone, phosphate, C-terminal FGF23, calcium), inflammation (hsCRP, neopterin) and cardiac function were investigated. Patients with elevated inflammatory parameters had significantly higher Ct-FGF23 levels (37.33 RU/mL vs. 17.60 RU/mL, p < 0.001). The highest Ct-FGF23 and phosphate levels were found in patients with elevated neopterin and hsCRP levels as well as in in patients with progressive heart failure. Patients with high Ct-FGF23 and neopterin levels (Ct-FGF23 > 22.60 RU/mL, neopterin > 6.90 nmol/L) had a significantly higher risk for adverse events compared to patients with low Ct-FGF23 and neopterin levels (HR 7.386, [95%CI 2.543 – 21.447], p < 0.001). Conclusions: Our study indicates a strong relationship of vitamin D metabolism, especially FGF23, with Th1 immune activation in patients with heart failure. Elevated Ct-FGF23 and neopterin levels are additive predictors for adverse cardiovascular events in patients with heart failure.
Highlights
Disturbances of vitamin D metabolism, such as low vitamin D concentrations or elevated levels of fibroblast growth factor 23 (FGF23), are common in patients with heart failure (HF) and have been associated with adverse outcomes in patients with chronic heart failure (CHF) [1, 2]
Our study indicates a strong relationship of vitamin D metabolism, especially FGF23, with Th1 immune activation in patients with heart failure
Ct-FGF23 was the only parameter of vitamin D metabolism that was associated with HF severity
Summary
Disturbances of vitamin D metabolism, such as low vitamin D concentrations or elevated levels of fibroblast growth factor 23 (FGF23), are common in patients with heart failure (HF) and have been associated with adverse outcomes in patients with chronic heart failure (CHF) [1, 2]. FGF23 has been identified as central regulator of vitamin D and phosphate homeostasis [3]. It is mainly secreted by osteoblasts and osteocytes in the bone marrow in response to 1,25(OH) vitamin D3, parathormone (PTH) or elevated serum phosphate (Pi) levels. FGF23 is the key regulator of Pi homeostasis by inhibiting renal Pi reabsorption independent of PTH and 1,25(OH) vitamin D3. This mechanism seems to be a protective response to decreased kidney function with impaired. Proteolytic cleavage maintains normal circulating iFGF23 levels in case of FGF23 overproduction [7,8,9]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
