Substantial evidence from previous clinical studies, randomized trials, and patient registries confirms the existence of significant differences in cardiac morphology, pathophysiology, prevalence of specific coronary artery disease (CAD), and clinical course of myocardial infarction (MI) between men and women. The aim of this review is to investigate the impact of sex or gender on the development and clinical course of MI, the mechanisms and features of left ventricular (LV) remodeling, and heart failure (HF). The main sex-related difference in post-MI LV remodeling is adverse LV dilatation in males versus concentric LV remodeling or concentric LV hypertrophy in females. In addition, women have a higher incidence of microvascular dysfunction, which manifests as impaired coronary flow reserve, distal embolism, and a higher prevalence of the no-reflow phenomenon. Consequently, impaired myocardial perfusion after MI is more common in women than in men. Regardless of age or other comorbidities, the incidence of reinfarction, hospitalization for HF, and mortality is significantly higher in females. There is therefore a “sex paradox”: despite the lower prevalence of obstructive CAD and HF with reduced ejection fraction (HFrEF), women have a higher mortality rate after MI. Different characteristics of the coronary network, such as plaque formation, microvascular dysfunction, and endothelial inflammation, as well as the prolonged time to optimal coronary flow restoration, secondary mitral regurgitation, and pulmonary vascular dysfunction, lead to a worse outcome in females. A better understanding of the mechanisms responsible for MI occurrence, LV remodeling, and HF in men and women would contribute to optimized patient therapy that would benefit both sexes.

Backgrounds: Galectin-3 (gal-3) is upregulated in remodeling, and failing myocardium and gal-3 levels are increased in hypertrophy, fibrosis and inflammation. The aim of this study was to investigate the potential role of sex-related differences in the following: risk factors, left ventricular (LV) structural and functional changes, coronary angiography, expression of the gal-3 encoding gene LGALS-3 and plasma gal-3 levels in heart failure (HF). Materials and Methods: This prospective study included 137 men and 44 women with first MI who underwent Doppler echocardiography within 2–4 days of MI and after 6 months. Relative LGALS-3 mRNA expression in peripheral blood mononuclear cells (PBMCs) was detected using TaqMan^® technology. Plasma gal-3 concentration was determined by ELISA method. Results: In the acute phase of MI, LV end-diastolic and end-systolic volume indexes (LVEDVI and LVESVI) were significantly lower in women compared to men (58.2 ± 13.1 vs. 46.3 ± 11.1, p < 0.001; 33.7 ± 9.5 vs. 27.0 ± 9.2, p < 0.001, respectively). The incidence of LV hypertrophy (LVH) and HF was significantly higher in women compared to men (70.0% vs. 44.6%, p = 0.03; 37.5% vs.19.5%, p = 0.02, respectively). There was a significant correlation between the grade of LV diastolic dysfunction (LVDD) and plasma gal-3 levels (p < 0.001). The relative expression of LGALS-3 mRNA in PBMCs was higher in females (fold induction = 1.326, S.E. range = 0.748–2.587, p = 0.007). Plasma gal-3 levels were higher in women compared to men (44.66 ± 28.04 vs. 16.30 ± 12.68, p < 0.001) and higher in patients with HF than in patients without HF (31.14 ± 27.09 vs.21.39 ± 18.17, p = 0.025). Conclusions: Gender-specific factors such as LVH, LVDD, LGALS-3 mRNA expression and plasma gal-3 levels may explain the increased incidence of HF in women. The differences in the model and determinants of HF between men and women may be relevant for further therapeutic strategies including the inhibition of gal-3.