The influence of atrial fibrillation on the levels of NT-proBNP versus GDF-15 in patients with heart failure

Abstract

Background In heart failure (HF), levels of NT-proBNP are influenced by the presence of concomitant atrial fibrillation (AF), making it difficult to distinguish between HF versus AF in patients with raised NT-proBNP. It is unknown whether levels of GDF-15 are also influenced by AF in patients with HF. In this study we compared the plasma levels of NT-proBNP versus GDF-15 in patients with HF in AF versus sinus rhythm (SR). Methods In a post hoc analysis of the index cohort of BIOSTAT-CHF (n = 2516), we studied patients with HF categorized into three groups: (1) AF at baseline (n = 733), (2) SR at baseline with a history of AF (n = 183), and (3) SR at baseline and no history of AF (n = 1025). The findings were validated in the validation cohort of BIOSTAT-CHF (n = 1738). Results Plasma NT-proBNP levels of patients who had AF at baseline were higher than those of patients in SR (both with and without a history of AF), even after multivariable adjustment (3417 [25th-75th percentile 1897-6486] versus 1788 [682-3870], adjusted p < 0.001, versus 2231 pg/mL [902-5270], adjusted p < 0.001). In contrast, after adjusting for clinical confounders, the levels of GDF-15 were comparable between the three groups (3179 [2062-5253] versus 2545 [1686-4337], adjusted p = 0.36, versus 2294 [1471-3855] pg/mL, adjusted p = 0.08). Similar patterns of both NT-proBNP and GDF-15 were found in the validation cohort.

The impact of growth differentiation factor 15 on the risk of cardiovascular diseases: two-sample Mendelian randomization study

“…Similar results were observed in patient with acute coronary syndrome (ACS) [6], stable coronary artery disease (CAD) [7], and high risk population [8]. Inconsistently, BIOSTAT-CHF trial has reported that GDF-15 levels were not in uenced by the presence of atrial brillation (AF) in patients with heart failure (HF) [9]. Since those observational studies inevitably blend with some confounding factors (where some factors associated with GDF-15 actually result in the disease) and reverse causality bias (where some patients with CVD may be more likely to higher GDF-15), it remains controversial whether GDF-15 is causally associated with the incidence of CVD.…”

“…Furthermore, serum GDF-15 level was associated with incident AF with the hazards ratios of 1.31 after adjusted for age and gender [30]. However, some inconsistent studies showed that serum GDF-15 level was not in uenced by the presence of AF in patient with HF from the BIOSTAT-CHF trial [9] and patients with chronic kidney disease (CKD) from the CRIC study [34]. Potential pathologic mechanisms of AF include atrial remodeling, reentry, pulmonary vein trigger, abnormal autonomic nerve modulation and in ammation.…”

The impact of growth differentiation factor 15 on the risk of cardiovascular disease: evidence from Mendelian randomization study

“…Similarly, GDF-15 was reckoned independently associated with paroxysmal AF after multivariable analyses in a study where a signi cantly higher serum level of GDF-15 was found in patients with paroxysmal AF than controls (1473.14 ± 628.52 vs. 1233.592 ± 262.76 pg/ml, P < 0.05) [28]. In contrast, Santema BT, et al and Lamprea-Montealegre JA, et al suggested that serum GDF-15 level was undifferentiated with AF or not in folks with HF from BIOSTAT-CHF trial [29] and people with chronic kidney disease(CKD) from CRIC study [30] respectively. Dissimilitude could have been explained for speci c reasons.…”

Düşük ejeksiyon fraksiyonlu kalp yetersizliği, atriyal fibrilasyon ve natriüretik peptidler: retrospektif kapalı kohort verileri

“…NT-proBNP düzeylerinin AF'da yüksek olduğu bilinmekle beraber, bu yükselmenin ne kadarından AF'un, ne kadarından KY'nin [11,19]. Bizim çalışmamızın literatüre en önemli katkısı, NP üst sınırı için bir konsensus olmayan DEF-KY ve AF bulunan hastalarda (eşlik eden ılımlı böbrek yetmezliği ile beraber), stabil kronik fazdaki ortalama NT-proBNP düzeyleri ile ilgili bir fikir vermesi, bu hastalarda dekompansasyon tanısı için standart üst sınırların yeterli olmadığını düşündürmesidir.…”