Triadic capabilities of sales personnel in power generation enterprises under China's electricity market reform: Generation and evolution mechanisms.

Cardiovascular disease (CVD), including coronary heart disease, cerebrovascular disease, and peripheral vascular disease, accounts for one‐third of deaths worldwide (Betai et al., ; Campbell, ). Both modifiable risk factors, such as cholesterol levels, insulin resistance, and psychological stress, and nonmodifiable risk factors, such as sex and age, contribute to CVD onset and progression (Mosca et al., ). Importantly, despite sex differences in cardiovascular outcomes being well established, the mechanisms underlying these differences remain poorly understood. Although males and females share most classic CVD risk factors that increase susceptibility to adverse cardiovascular events, their risk profiles differ across the lifespan. Young females appear relatively protected compared to age‐matched males, reflected in lower rates of adverse cardiovascular events, which has been attributed to biological protection in females due to both hormonal and nonhormonal factors (Mosca et al., ). Despite this, a rising incidence of hospitalized myocardial infarction (MI) among females aged 35–54, even as rates decline among age‐matched males, has been reported recently (Vaccarino, ). Furthermore, females who do experience cardiovascular events face higher mortality and worse prognosis, highlighting sex‐specific variations in vascular physiology that may exacerbate disease severity (Gao et al., ). One prevailing theory attributes sex difference in cardiovascular events to hormonal mechanisms, including alterations in sex hormones estrogen and progesterone. This theory is strongly supported by evidence that the female‐specific advantage against males diminishes with age, likely due to the sharp decline in sex hormones during menopause (Campbell, ; El Khoudary et al., ; Pardhe et al., ; Ryczkowska et al., ). Menopause is associated with a worsening coronary heart disease profile, driven by shifts in body fat distribution, increased systolic blood pressure, and hypercholesterolemia, factors that are partially due to declining estrogen levels (Maas & Appelman, ). Further supporting this hypothesis, females experiencing premature menopause are at a significantly higher risk of a nonfatal cardiovascular event (Ryczkowska et al., ), while oophorectomy has been shown to worsen the overall cardiovascular risk profile (Allison et al., ). Overall, the incidence of CVD converges between sexes in older populations, underscoring the importance of hormonal transitions in shaping risk trajectories (Mosca et al., ). Evidence also supports nonhormonal mechanisms behind these sex differences, including intrinsic protection and social factors. Notably, some measures of cardiovascular risk including glycemic indices, inflammatory markers, and vascular reactivity appear independent of hormonal fluctuations, suggesting intrinsic mechanisms of protection in females (Saxena et al., ). Hypertension, considered the strongest causal risk factor for CVD by some researchers, differs between the sexes (Fuchs & Whelton, ). Although more prevalent in males (Connelly et al., ), females develop CVD at lower blood pressure thresholds, increasing their disease burden. In addition, hypertensive females clinically present atypically, which can reduce detection and heighten susceptibility to CVD (Betai et al., ; Ryczkowska et al., ). Furthermore, female hypertension and CVD are not only under‐diagnosed but also under‐treated. A two‐fold gap in care amplifies female vulnerability to accelerated remodeling and other CVD complications, undermining the cardiovascular protection observed in younger females and highlighting the need for sex‐specific investigation into early, detectable risk factors. Finally, psychosocial stressors, which exacerbate CVD and its risk factors, disproportionately impact females (Dar et al., ; Vaccarino et al., ). Collectively, these findings illustrate how both biological and psychosocial factors converge to drive sex‐specific differences in CVD outcomes. However, the pathways linking sex, hormonal status, and other risk factors to cardiovascular dysfunction and adverse outcomes remain poorly understood.