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Galectin-3 levels in patients with hypertrophic cardiomyopathy and its relationship with left ventricular mass index
Selcen Yakar Tülüce1, Kamil Tülüce, Zafer Çil
1Department of Cardiology, İzmir Katip Çelebi University Atatürk Training and Research Hospital; İzmir-Turkey. selcenyakar@gmail.com.
Insights
In patients with hypertrophic cardiomyopathy (HCM), Galectin-3 (Gal-3) levels were higher and correlated with left ventricular (LV) hypertrophy. However, Gal-3 did not correlate with impaired LV systolic or diastolic function.
Area of Science:
- Cardiology
- Biomarkers
- Medical Imaging
Background:
- Cardiac fibrosis contributes to adverse left ventricular (LV) remodeling and arrhythmias in hypertrophic cardiomyopathy (HCM).
- Galectin-3 (Gal-3) is recognized as a marker for cardiac fibrosis and inflammation.
Purpose of the Study:
- To investigate Galectin-3 (Gal-3) levels in patients with HCM compared to healthy controls.
- To assess the relationship between Gal-3 levels and echocardiographic indices, including strain echocardiography, in HCM patients.
Main Methods:
- A case-control study involving 40 HCM patients and 35 healthy controls.
- Echocardiography was used to assess global LV longitudinal/circumferential strain, strain rates, peak torsion, and LV mass index (LVMI).
- Gal-3 levels were measured in all participants.
Main Results:
- HCM patients exhibited lower LV global longitudinal strain and strain rate compared to controls.
- Gal-3 levels were significantly elevated in HCM patients (16.9±6.64 ng/mL) versus controls (13.21±3.42 ng/mL).
- Gal-3 levels correlated with interventricular septum thickness and LVMI but not with LV global longitudinal strain or strain rate.
Conclusions:
- Galectin-3 levels are elevated and correlate with the degree of left ventricular hypertrophy in patients with HCM.
- Galectin-3 is not a reliable marker for assessing decreased LV diastolic and systolic functions in HCM patients.
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.
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