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Sex-Related Differences in Heart Failure Development in Patients After First Myocardial Infarction: The Role of
Milica Dekleva1, Tamara Djuric2, Ana Djordjevic2
1Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia.
This study reveals that women experience higher rates of heart failure (HF) after myocardial infarction (MI) due to sex-specific factors like left ventricular hypertrophy (LVH) and elevated galectin-3 (gal-3) levels. Understanding these gender differences in HF development is crucial for targeted therapeutic strategies.
Area of Science:
- Cardiology
- Biochemistry
- Genetics
Background:
- Galectin-3 (gal-3) is implicated in myocardial remodeling, hypertrophy, fibrosis, and inflammation.
- Upregulation of gal-3 is observed in failing myocardium.
Purpose of the Study:
- To investigate sex-related differences in risk factors, left ventricular (LV) structural and functional changes, and galectin-3 (gal-3) expression in heart failure (HF) post-myocardial infarction (MI).
- To explore the role of LGALS-3 gene expression and plasma gal-3 levels in sex-specific HF development.
Main Methods:
- Prospective study of 137 men and 44 women post-first MI, with Doppler echocardiography at 2-4 days and 6 months.
- Analysis of relative LGALS-3 mRNA expression in peripheral blood mononuclear cells (PBMCs) using TaqMan technology.
- Quantification of plasma gal-3 concentration via ELISA.
Main Results:
- Women exhibited lower LV end-diastolic and end-systolic volume indexes but higher incidence of LV hypertrophy (LVH) and HF compared to men.
- A significant correlation was found between LV diastolic dysfunction (LVDD) grade and plasma gal-3 levels.
- Females showed higher relative LGALS-3 mRNA expression in PBMCs and significantly higher plasma gal-3 levels than males.
Conclusions:
- Gender-specific factors, including LVH, LVDD, LGALS-3 mRNA expression, and plasma gal-3 levels, contribute to the increased HF incidence in women.
- Differences in HF determinants between sexes may inform future therapeutic strategies, potentially involving gal-3 inhibition.
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