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Abstract
Aims
Abnormalities of mineral metabolism (MM) have been related to cardiovascular disorders. There are no reports on the prognostic role of MM after an acute coronary syndrome (ACS). We aim to assess the prognostic role of MM after an ACS.
Methods and results
Plasma levels of components of MM [fibroblast growth factor 23 (FGF23), calcidiol, parathormone, klotho, and phosphate], high‐sensitivity C‐reactive protein, and N‐terminal‐pro‐brain natriuretic peptide were measured in 1190 patients at discharge from an ACS. The primary outcome was a combination of acute ischaemic events, heart failure (HF) and death. Secondary outcomes were the separate components of the primary outcome. Age was 61.7 ± 12.2 years, and 77.1% were men. Median follow‐up was 5.44 (3.03–7.46) years. Two hundred and ninety‐four patients developed the primary outcome. At multivariable analysis FGF23 (hazard ratio, HR 1.18 [1.08–1.29], P < 0.001), calcidiol (HR 0.86 [0.74–1.00], P = 0.046), previous coronary or cerebrovascular disease, and hypertension were independent predictors of the primary outcome. The predictive power of FGF23 was homogeneous across different subgroups of population. FGF23 (HR 1.45 [1.28–1.65], P < 0.001) and parathormone (HR 1.06 1.01–1.12]; P = 0.032) resulted as independent predictors of HF. FGF23 (HR 1.21 [1.07–1.37], P = 0.002) and calcidiol (HR 0.72 [0.54–0.97), P = 0.028) were independent predictors of death. No biomarker predicted acute ischaemic events. FGF23 predicted independently the primary outcome in patients with estimated glomerular filtration rate > 60 mL/min/1.73 m2.
Conclusions
FGF23 and other components of MM are independent predictors of HF and death after an ACS. This effect is homogeneous across different subgroups of population, and it is not limited to patients with chronic kidney disease.
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Details
; Pello, Ana 1 ; Cánovas, Ester 2 ; Aceña, Álvaro 1 ; González‐Casaus, María Luisa 3 ; Tarín, Nieves 4 ; Cristóbal, Carmen 5 ; Gutiérrez‐Landaluce, Carlos 6 ; Huelmos, Ana 7 ; Rodríguez‐Valer, Aida 8 ; González‐Lorenzo, Óscar 1 ; Alonso, Joaquín 9 ; López‐Bescós, Lorenzo 10 ; Egido, Jesús 11 ; Mahillo, Ignacio 12 ; Lorenzo, Óscar 13 ; Tuñón, José 14 1 Department of Cardiology, IIS‐Fundación Jiménez Díaz, Madrid, Spain, Faculty of Medicine, Autónoma University, Madrid, Spain
2 Department of Cardiology, IIS‐Fundación Jiménez Díaz, Madrid, Spain
3 Department of Laboratory Medicine, Unit of Mineral Metabolism, Hospital La Paz, Madrid, Spain
4 Department of Cardiology, Hospital Universitario de Móstoles, Madrid, Spain, Faculty of Medicine, Rey Juan Carlos University, Madrid, Spain
5 Faculty of Medicine, Rey Juan Carlos University, Madrid, Spain, Department of Cardiology, Hospital Universitario de Fuenlabrada, Madrid, Spain
6 Department of Cardiology, Hospital Universitario de Fuenlabrada, Madrid, Spain
7 Department of Cardiology, Hospital Universitario Fundación Alcorcón, Madrid, Spain
8 Faculty of Medicine, Autónoma University, Madrid, Spain
9 Department of Cardiology, Hospital de Getafe, Madrid, Spain
10 Faculty of Medicine, Rey Juan Carlos University, Madrid, Spain
11 CIBERDEM, Madrid, Spain, Department of Nephrology, IIS‐Fundación Jiménez Díaz, Madrid, Spain, Laboratory of Vascular Pathology, IIS‐Fundación Jiménez Díaz, Madrid, Spain
12 Laboratory of Epidemiology, IIS‐Fundación Jiménez Díaz, Madrid, Spain
13 Faculty of Medicine, Autónoma University, Madrid, Spain, CIBERDEM, Madrid, Spain, Laboratory of Vascular Pathology, IIS‐Fundación Jiménez Díaz, Madrid, Spain
14 Department of Cardiology, IIS‐Fundación Jiménez Díaz, Madrid, Spain, Faculty of Medicine, Autónoma University, Madrid, Spain, Laboratory of Vascular Pathology, IIS‐Fundación Jiménez Díaz, Madrid, Spain, CIBERCV, ISCIII, Madrid, Spain





