Sexual dimorphism of some parameters in healthy control and patients with ischemic heart disease, arterial hypertension and their comorbidity

Abstract

Background: Cardiovascular diseases (CVD) represent the leading cause of mortality worldwide, with documented sex differences in disease incidence, presentation, and outcomes. However, the extent of sexual dimorphism in underlying pathophysiological mechanisms remains incompletely characterized.

Objective: To conduct a comprehensive mathematical-statistical analysis of sex differences in cardiovascular, metabolic, endothelial, hematological, and renal parameters in patients with established cardiovascular disease.

Methods: This cross-sectional study included 162 patients with documented cardiovascular disease (91 women, 71 men) comprising patients with isolated ischemic heart disease (IHD), isolated arterial hypertension (AH), comorbidity IHD&AH, and comorbidity Alcoholism&AH, as well as 21 healthy controls (14 women, 7 men). Twenty-eight parameters were assessed including circulating desquamated endothelial cells (CEC), lipid profile, blood pressure, glucose, renal function, and hematological indices. Statistical analyses included independent samples t-tests, Mann-Whitney U tests, discriminant analysis, and entropy calculations.

Results: Among 28 examined parameters, only 6 demonstrated statistically significant sex differences and were included in the discriminant model: body mass index (women: 28.65 ± 0.32 kg/m²; men: 27.47 ± 0.33 kg/m²; F-to-enter = 6.412, p = 0.012), leukocyte count (women: 7.06 ± 0.14 × 10⁹/L; men: 6.56 ± 0.17 × 10⁹/L; F-to-enter = 5.202, p = 0.024), metabolic syndrome index (women: 0.91 ± 0.10; men: 0.61 ± 0.09; F-to-remove = 8.50, p = 0.004), Klimov atherogenic index (women: 2.88 ± 0.11; men: 3.11 ± 0.14; F-to-remove = 3.87, p = 0.051), ankle-brachial index (women: 0.823 ± 0.011; men: 0.792 ± 0.018; F-to-remove = 2.96, p = 0.088), and endotheliocytogram entropy (women: 0.694 ± 0.012 bits; men: 0.668 ± 0.016 bits; F-to-remove = 1.492, p = 0.224). Discriminant analysis achieved 60.5% classification accuracy with canonical correlation r* = 0.374 (explaining 14.0% of variance; Wilks' Λ = 0.860; χ²(6) = 23.7; p = 0.0006). Circulating endothelial cells showed no sex differences in total count (women: 1934 ± 88 cells/mL; men: 1982 ± 113 cells/mL) or in distribution patterns across alteration categories.

Conclusions: Despite epidemiological evidence of sex disparities in cardiovascular disease, the underlying pathophysiology as reflected in biomarker profiles demonstrates remarkable similarity between women and men with established disease. Modest sex differences exist primarily in body composition, inflammatory activation, and integrated metabolic indices, but substantial overlap between sexes (39.5% misclassification rate) emphasizes the importance of individualized rather than sex-stratified approaches to cardiovascular risk assessment and management. The finding that 22 of 28 parameters showed no significant sex differences, including all endothelial dysfunction markers, lipid components, blood pressure parameters, and renal function indices, suggests that once cardiovascular disease is established, pathophysiological mechanisms converge between sexes.