Abstract
Heart failure is the most frequent cardiac complication of chronic kidney disease (CKD). Biomarkers help identify high-risk patients. Natriuretic peptides (BNP and NT-proBNP) are largely used for monitoring patients with cardiac failure but are highly dependent on glomerular filtration rate (GFR). Soluble suppression of tumorigenicity 2 (sST2) biomarker is well identified in risk stratification of cardiovascular (CV) events in heart failure. Furthermore, sST2 is included in a bioclinical score to stratify mortality risk. The aims of this study were to evaluate (i) the interest of circulating sST2 level in heart dysfunction and (ii) the bioclinical score (Barcelona Bio-Heart Failure risk calculator) to predict the risk of composite outcome (major adverse coronary events) and mortality in the CKD population. A retrospective study was carried out on 218 CKD patients enrolled from 2004 to 2015 at Montpellier University Hospital. sST2 was measured by ELISA (Presage ST2® kit). GFR was estimated by the CKD-EPI equation (eGFR). Indices of cardiac parameters were performed by cardiac echography. No patient had reduced ejection fraction. 112 patients had left ventricular hypertrophy, and 184 presented cardiac dysfunction, with structural, functional abnormalities or both. sST2 was independent of age and eGFR (ρ = 0.05, p = 0.44, and ρ = −0.07, p = 0.3, respectively). Regarding echocardiogram data, sST2 was correlated with left ventricular mass index (ρ = 0.16, p = 0.02), left atrial diameter (ρ = 0.14, p = 0.04), and volume index (ρ = 0.13, p = 0.05). sST2 alone did not change risk prediction of death and/or CV events compared to natriuretic peptides. Included in the Barcelona Bio-Heart Failure (BCN Bio-HF) score, sST2 added value and better stratified the risk of CV events and/or death in CKD patients (p < 0.0001). To conclude, sST2 was associated with cardiac remodeling independently of eGFR, unlike other cardiac biomarkers. Added to the BCN Bio-HF score, the risk stratification of death and/or CV events in nondialyzed CKD patients was highly improved.
Highlights
CV events and death are associated with reduced eGFR [1]
The prevalence of Left ventricular hypertrophy (LVH) is estimated between 16% and 31% in chronic kidney disease (CKD) patients with eGFR > 30 mL/min to reach 60 to 75% before dialysis and 90% after dialysis [6]
Compared to patients free of major adverse coronary events (MACE), eGFR and left ventricular ejection fraction (LVEF) were lower in patients with MACE, whereas age, LAVI, left atrial diameter (LAD), LVMI, levels of C-reactive protein (CRP), NT-proBNP, and high-sensitivity cardiac troponin T (hs-cTnT) were higher
Summary
The prevalence of most comorbid conditions, including heart failure (HF), increases with decreasing eGFR [2]. Heart failure with preserved ejection fraction (HFpEF) constitutes the main feature of uremic cardiopathy and is often referred to as type 4 cardiorenal syndrome [3, 4]. In May 2016, the European Society of Cardiology developed guidelines to help diagnosis of chronic HFpEF, including cardiac structural or functional alterations underlying HF [5]. Left ventricular hypertrophy (LVH) represents the major event in type 4 cardiorenal syndrome (chronic renocardiac damage). The prevalence of LVH is estimated between 16% and 31% in CKD patients with eGFR > 30 mL/min to reach 60 to 75% before dialysis and 90% after dialysis [6]. Diastolic dysfunction, defined by pseudonormal or restrictive pattern through tissue Doppler imaging (E/e’ ≥ 10) which appears in the early
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