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. (Anatol J Cardiol 2016; 16: 344-8)