Differential and Predictive Value of Galectin-3 and Soluble Suppression of Tumorigenicity-2 (sST2) in Heart Failure with Preserved Ejection Fraction

Abstract

BackgroundGalectin-3 and soluble suppression of tumorigenicity-2 (sST2) are promising biomarkers of cardiac fibrosis and ventricular remodeling. The purpose of this study was to investigate the diagnostic and predictive value of galectin-3 and sST2 for use in patients who have heart failure with preserved ejection fraction (HFpEF).Material/MethodsA total of 217 hospitalized patients with HF and 30 controls from a physical examination center were included. Venous blood was collected for the detection of circulating expression of galectin-3 and sST2. All the included patients were followed up regularly for 1 year (12±1 months).ResultsThe concentrations of galectin-3 and NT-proBNP were substantially higher following decreased ejection fraction (both P=0.000), except for sST2 (P=0.068 vs. control). In ROC analyses, galectin-3 and NT-proBNP distinguished HFpEF from controls with an area under the curve (AUC) of 0.819 (95% CI: 0.75–0.89, P=0.000) and 0.806 (95% CI: 0.66–0.82, P=0.000). In contrast, sST2 obtained a lower AUC of 0.584 (95% CI: 0.49–0.68, P=0.17) compared to galectni-3 and NT-proBNP. After adjustment for clinical factors and NT-proBNP, galectin-3 was strongly correlated with an increased risk of the endpoint events in HFpEF patients, and the hazard ratio per 1 SD increase of the galectin-3 level was 2.33 (95%CI: 1.72–2.94, P=0.009).ConclusionsGalectin-3 is superior to sST2 in distinguishing HFpEF from controls and HFrEF.

Natriuretic peptides for the detection of diastolic dysfunction and heart failure with preserved ejection fraction—a systematic review and meta-analysis

“…Twenty-eight were performed in Europe [ 20 , 32 – 36 , 38 , 40 , 41 , 43 – 45 , 50 , 52 , 53 , 55 – 57 , 59 , 63 , 64 , 66 , 69 , 73 , 76 – 78 ], 11 in North America [ 22 , 37 , 39 , 46 , 49 , 54 , 65 , 70 , 72 , 74 , 75 ], 11 in Asia [ 31 , 42 , 47 , 51 , 58 , 60 – 62 , 67 , 68 , 71 ] and one was a multi-country study [ 48 ]. The control populations were either healthy controls ( N = 14) [ 31 , 35 , 59 , 60 , 62 , 65 , 67 – 69 , 71 , 72 , 75 – 77 ] or were recruited at the same department as the patient population, but without DD or HFpEF ( N = 37) [ 32 – 34 , 36 – 42 , 58 , 61 , 63 , 64 , 66 , 70 ]. The mean age of the DD and HFpEF populations ranged from 51 to 74 years and...…”

“…Five DD studies included patients with HFpEF [ 38 , 43 , 48 , 73 , 76 ], one DD study included patients with signs and symptoms [ 44 ], but did not exclude on LVEF, and eight DD studies only included patients with LVEF above 45 or 50% [ 18 , 20 , 45 , 47 , 50 , 52 , 53 , 77 ]. The reference diagnoses used in the included studies varied from use of maximal velocity of the E-wave (e’) ( N = 10) [ 43 – 45 , 49 , 50 , 52 , 54 , 56 , 57 , 74 ] versus no tissue Doppler (TDI) measures ( N = 14) [ 18 , 20 , 22 , 38 , 46 – 48 , 51 , 53 , 55 , 73 , 76 – 78 ] for DD studies and, use of extensive criteria ( N = 13) [ 31 , 32 , 34 , 35 , 38 , 41 , 59 , 61 , 63 , 64 , 66 , 69 , 72 ], signs and symptoms of HF in combination with LVEF ( N = 11) [ 36 , 40 , 42 , 58 , 60 , 62 , 65 , 67 , 68 , 70 , 71 ], expert opinion ( N = 1) [ 33 ] or catheterization ( N = 3) [ …”

Galectin-3 as a Next-Generation Biomarker for Detecting Early Stage of Various Diseases

“…Recently, Gal-3 has been indicated to be involved in the following broad pathological processes: Inflammation [9], fibrosis, cell-to-cell [10,11] or cell-to-matrix [12] contacts, cell proliferation [13,14], and protection from apoptosis [15,16]. Furthermore, many studies have revealed that Gal-3 expression is detected in many disease conditions, such as heart disease [17][18][19][20][21][22][23], kidney disease [24][25][26][27], diabetes mellitus [24,25,28], viral infection [29][30][31][32], autoimmune disease [33][34][35][36], neurodegenerative disorders [37][38][39][40][41][42], and tumor formation [43][44][45][46][47][48][49][50][51][52].…”

Circular RNA circCHFR Facilitates the Proliferation and Migration of Vascular Smooth Muscle via miR-370/FOXO1/Cyclin D1 Pathway

“…In the pathogenesis of AS, the proliferation of vascular smooth muscle cells (VSMCs) is the typical high-probability event accompanied by the generation of collagen fibers and the accumulation of lipids 5 . During the vasculopathy, the aberrant proliferation and migration of VSMCs from tunica media into the subendothelial layer triggers the vascular remodeling 6 . Besides, VSMCs are exposed to complex and diverse microenvironments, in return leading to the mutability of VSMCs.…”