Galectin-3 levels in patients with hypertrophic cardiomyopathy and its relationship with left ventricular mass index and function

Abstract

Objective:Cardiac fibrosis is an important contributor to adverse left ventricular (LV) remodeling and arrhythmias in patients with hypertrophic cardiomyopathy (HCM). Galectin-3 (Gal-3) is a novel marker of cardiac fibrosis and inflammation. In this study, we investigated Gal-3 levels in patients with HCM and controls and assessed the relationship between Gal-3 level and echocardiographic indices using strain echocardiography in patients with HCM.Methods:Forty patients with HCM in sinus rhythm and 35 healthy controls were prospectively enrolled in this case-control study. The HCM diagnosis was based on two-dimensional echocardiographic demonstration of a hypertrophied and non-dilated left ventricle (LV) with a wall thickness ≥15 mm in one or more LV myocardial segments in the absence of any cardiac or systemic disease capable of inducing LV hypertrophy. Patients with one of the followings were excluded: coronary artery disease, atrial fibrillation episodes on 24-h Holter electrocardiogram (ECG) monitoring, history of an invasive intervention to alleviate an LV outflow (LVOT) obstruction, inadequate image quality, renal disease, diabetes mellitus, hyperlipidemia, liver cirrhosis, and pulmonary fibrosis. Global LV longitudinal, circumferential strain and strain rates, peak torsion, and LV mass index (LVMI) of all subjects were assessed by echocardiography. Gal-3 levels were measured in all subjects.Results:Left ventricular global longitudinal strain (-13.37±4.6% vs. -18.93±2.5%, p<0.001) and strain rate (0.66±0.22 s-1 vs. 1.08±0.14 s-1, respectively; p<0.001) values were lower in patients with HCM than in controls. Gal-3 levels were significantly higher in patients with HCM than in controls (16.9±6.64 ng/mL vs. 13.21±3.42 ng/mL, p=0.005). Gal-3 levels were associated with the thickness of the interventricular septum (r=0.444, p=0.004) and LVMI (r=0.365, p=0.021); however, they were not associated with LV global longitudinal strain (p=0.42) or strain rate (p=0.28).Conclusion:Gal-3 levels increased and were correlated with the degree of LV hypertrophy in patients with HCM. Gal-3 is not a good marker of decreased myocardial LV diastolic and systolic functions in these patients.

The usefulness of sST2 and galectin-3 as novel biomarkers for better risk stratification in hypertrophic cardiomyopathy

“…Considering Gal-3, there is a report that plasma Gal-3 levels positively correlate with the thickness of the interventricular septum and with LV mass index evaluated by transthoracic echocardiography in patients with HCM [17]. However, our findings differ from those of Yakar Tülüce et al [17].…”

“…Stężenia sST2 i Gal-3 różniły się między grupami pacjentów w różnych klasach niewydolności serca wg New York Heart Association (NYHA) (p = 0,008; p = 0,009, odpowiednio) i wzrastały wraz z nasileniem objawów niewydolności serca. Pacjenci, u których zarejestrowano nsVT w 48-godzinnym badaniu Holter EKG, charakteryzowali się istotnie wyższym stężeniem sST2 (19,1 ng/ml [12,2] vs. 13,2 ng/ml [10,[0][1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17]1]; p = 0,02). Nie zaobserwowano związku między stężeniami badanych biomarkerów a ryzykiem SCD obliczonym wg kalkulatora HCM SCD-risk, omdleniami, wywiadem SCD w rodzinie oraz parametrami echokardiograficznymi.…”

Biomarkers of cardiovascular stress and fibrosis in preclinical hypertrophic cardiomyopathy

“…These findings contrast with a prior case–control study showing that galectin-3 was higher in 40 patients with HCM compared with 35 unrelated healthy controls. 36 This discrepancy may be due to differences in age, as our sample was over 20 years younger on average, compared with the prior case–control study. It is also important to note that galectin-3 levels are in part genetically determined, 37 which may blunt potential differences among related individuals such as in our study.…”

Galectin-3- Mediated Transdifferentiation of Pulmonary Artery Endothelial Cells Contributes to Hypoxic Pulmonary Vascular Remodeling

“…Inhibition of Gal-3 reduced atherosclerosis in apolipoprotein E-deficient mice [18]. In addition, Gal-3 has been used as a novel biomarker for better risk stratification in hypertrophic cardiomyopathy and the prognosis of heart failure [1,19]. Furthermore, it has been demonstrated that elevated Gal-3 can be used as a method to predict mortality in PAH [20].…”