Coronary artery disease, specifically ST elevation myocardial infarction (STEMI), is a leading global cause of mortality in both sexes (1, 2). Variations in the etiology, clinical manifestations, treatments, outcomes, and epidemiology of myocardial infarction (MI) arise from biological and socioenvironmental differences between women and men. Notably, the average age at first MI in women was 71.8 years, whereas it was 65 years for men. Additionally, women exhibit a higher death rate within the first year post-MI. Atypical chest pain and angina-equivalent symptoms, such as dyspnea, weakness, fatigue, and indigestion, are more prevalent in women. In the pathophysiology of MI, plaque erosion is more common in women, while plaque rupture is more likely in men. Women also experience certain MI complications at a higher rate, such as heart failure and susceptibility to cardiogenic shock after MI (3).
These sex-specific variations may stem from distinct risk factors. Psychosocial factors such as smoking, depression, anxiety, and stress, as well as variations in the prevalence of diabetes, hyperlipidemia, hypertension, metabolic syndrome, and chronic kidney disease, contribute to these differences (4).
Sex hormones, notably estrogen, play a significant role in explaining these sex disparities. Numerous studies have explored how estrogen impacts MI incidence, and the results support the preventive role of endogenous estrogen in cardiovascular events (5). The effects of estrogen on the vascular endothelium lead to increased prostacyclin and nitric oxide levels, which induce vasodilation. Estrogen further promotes vasodilation by inhibiting mechanisms such as protein kinase C, calcium ions, and Rho kinase involved in smooth muscle contraction. Additionally, research indicates that estrogen influences lipid profiles and vascular inflammatory responses (6).
The effects of reproductive factors, which are influenced by sex hormones, on cardiovascular diseases have been extensively studied. A 2017 UK cohort study revealed associations between early menarche, early menopause, young age at first childbirth, abortion, stillbirth, and hysterectomy and an increased risk of cardiovascular diseases (7). A case‒control study in Italy linked parity and an irregular menstrual cycle to an increased risk of MI (8).
Patients who have experienced MI are at risk of recurrence and other cardiovascular events (9). Studies suggest that women with early-onset MI have a lower likelihood of early and late outcomes, such as cardiovascular death, MI recurrence, and stroke, than men (10, 11). However, in older age groups, women face a greater risk of early and late outcomes after MI than men (12, 13).
Age-related differences in outcomes provide insight into the potential protective effect of estrogen on cardiovascular outcomes after MI and the role of reproductive factors. However, validated data on the association between reproductive factors and the risk of major adverse cardiovascular events after MI are scarce.
Limited studies suggest that women experiencing menopause later may have better outcomes following acute coronary syndrome (ACS), while both early and late menarche are associated with an increased risk of serious adverse cardiovascular events (14, 15).
The present study aimed to investigate the associations between reproductive factors (age at menarche, age at menopause, reproductive years, number of gravidities and parities, first parity age, and duration of breastfeeding) and major cardiovascular events following ST-Elevation MI. This research is crucial given the importance of preventing cardiovascular events post-MI and the insufficient studies on this relationship. Recognizing reproductive risk factors in women with ST-Elevation MI may lead to more effective preventive treatments, follow-ups, and improved clinical outcomes.