Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality worldwide, accounting for nearly one-third of all global deaths and imposing a substantial health and economic burden across populations [1,2]. Although traditionally perceived as a predominantly male condition, a growing body of evidence highlights that CVD is equally, if not more, fatal in women, particularly in older age groups [3,4]. Sex- and gender-based differences significantly influence the epidemiology, pathophysiology, clinical presentation, diagnostic accuracy, and treatment outcomes of cardiovascular conditions [5]. Understanding these disparities is crucial for improving diagnostic precision, therapeutic interventions, and public health strategies targeted at both sexes.

Biological sex determines fundamental differences in cardiovascular structure, hormonal milieu, and vascular reactivity. Estrogen exerts protective vascular effects through modulation of endothelial function, lipid metabolism, and nitric oxide bioavailability, which partly explains the lower incidence of atherosclerotic events among premenopausal women [6]. However, this advantage declines sharply after menopause, resulting in accelerated arterial stiffness, dyslipidemia, and increased susceptibility to ischemic heart disease [7]. In contrast, men tend to develop CVD approximately 7–10 years earlier than women due to higher exposure to traditional risk factors such as smoking, hypertension, and central obesity [8,9]. Recent studies suggest that women are more prone to non-obstructive coronary artery disease, microvascular dysfunction, and heart failure with preserved ejection fraction (HFpEF), whereas men more commonly experience obstructive coronary artery disease and systolic heart failure [10,11].

Despite these pathophysiological distinctions, a persistent gender gap in diagnosis and management remains. Women are less likely to receive timely diagnosis, undergo invasive procedures, or be prescribed evidence-based therapies such as antiplatelets, beta-blockers, or ACE inhibitors compared with men [12,13]. Multiple registries have demonstrated that women with acute coronary syndrome (ACS) often present atypically, with symptoms such as fatigue, nausea, or dyspnea rather than classical chest pain, leading to diagnostic delays and undertreatment [14,15]. Consequently, in-hospital mortality and long-term adverse cardiovascular outcomes are frequently higher in women [16,17]. Studies from both developed and developing nations consistently reveal that gender-based disparities extend across all levels of cardiovascular care — from primary prevention and diagnostic evaluation to interventional cardiology and rehabilitation [18,19].

Socio-behavioral and cultural determinants further aggravate these differences. Women often experience barriers to healthcare access due to socioeconomic dependence, family responsibilities, and gender bias within health systems [20]. Psychosocial stress, depression, and caregiving burden — disproportionately affecting women — have been independently associated with adverse cardiovascular events [21]. In addition, the underrepresentation of women in cardiovascular clinical trials limits the generalizability of evidence-based guidelines to female populations, perpetuating treatment inequalities [22]. Consequently, despite growing awareness, gender-specific cardiovascular research remains inadequately integrated into routine clinical practice, particularly in low- and middle-income countries [7,23].

Sex-related disparities are also evident in pharmacological responses and adverse drug reactions. Pharmacokinetic and pharmacodynamic variations, including differences in body composition, cytochrome P450 enzyme activity, and hormonal regulation, contribute to distinct efficacy and safety profiles of cardiovascular drugs between men and women [22]. For instance, digoxin therapy has been shown to increase mortality in women but not in men, highlighting the importance of sex-specific therapeutic considerations [21]. Similarly, emerging evidence suggests that hormonal and molecular factors modulate myocardial remodeling and neurohormonal activation differently across sexes, influencing the natural course and treatment response in heart failure [19].

The burden of CVD among women is often underestimated, especially in South Asian countries, where epidemiological transitions have increased exposure to metabolic risk factors such as diabetes, hypertension, and dyslipidemia at younger ages [7]. Indian studies indicate that women are less likely to receive reperfusion therapy or coronary angiography following myocardial infarction and experience higher 30-day mortality rates than men [8]. Furthermore, awareness of cardiovascular risk among women remains alarmingly low, with many perceiving cancer as their leading health threat despite higher CVD-related mortality [10]. These findings underscore the urgent need for sex-disaggregated data and gender-sensitive public health interventions.

The interplay between biological sex and sociocultural gender roles forms a multidimensional framework influencing cardiovascular health. While sex determines biological predispositions, gender shapes lifestyle behaviors, healthcare-seeking patterns, and treatment adherence [4,5]. Addressing gender differences, therefore, requires a holistic approach encompassing both biomedical and psychosocial determinants. International organizations such as the World Health Organization and American Heart Association have emphasized the inclusion of sex-specific analyses in cardiovascular research and clinical guidelines [3,4]. However, in practice, sex-based data remain underreported, and gender equity in CVD care is far from realized [12,18].

Given this background, it becomes imperative to systematically examine gender differences in the presentation, management, and outcomes of cardiovascular diseases within local clinical contexts. A comprehensive comparative study not only elucidates biological and behavioral factors underlying these disparities but also informs more equitable health policy and clinical decision-making. Therefore, the present study aims to evaluate the gender-based variations in clinical presentation, diagnostic patterns, management strategies, and treatment outcomes among patients with cardiovascular disease. By identifying the gaps and determinants that perpetuate these inequalities, this research seeks to contribute to the advancement of gender-responsive cardiovascular care and evidence-based policymaking [1–23].

1. Study Design:
   The present research employed a hospital-based comparative cross-sectional study design to analyze gender differences in cardiovascular disease (CVD) in terms of clinical presentation, management, and treatment outcomes. This design was chosen to allow concurrent comparison of male and female patients within a defined period.
2. Study Setting:
   The study was conducted in the Department of Cardiology, [Insert Institution Name], a tertiary care teaching hospital catering to both urban and rural populations. The institution provides advanced diagnostic and interventional cardiac services, making it suitable for comprehensive cardiovascular research.
3. Study Duration:
   The study was carried out over a period of 12 months (April 2024 – March 2025), including patient recruitment, follow-up, and data analysis.
4. Study Population:
   The study population included adult patients aged ≥18 years of both sexes, diagnosed with cardiovascular disease (coronary artery disease, heart failure, valvular disease, or arrhythmia) based on clinical assessment and supporting investigations.
5. Sample Size Determination:
   A minimum sample size of n = 300 patients (150 males and 150 females) was calculated using Cochran’s formula for proportions, assuming a 50% expected difference in treatment outcomes between genders, 95% confidence interval, and 10% allowable error. The sample size was increased to account for possible dropouts or incomplete data.
6. Sampling Technique:
   Consecutive sampling was applied, enrolling all eligible male and female CVD patients attending inpatient and outpatient cardiology units during the study period until the required sample size was achieved.
7. Inclusion Criteria:
   • Patients aged ≥18 years with confirmed diagnosis of CVD (acute coronary syndrome, chronic ischemic heart disease, heart failure, valvular disease, or arrhythmia).
   • Both male and female patients consenting to participate.
   • Patients with complete clinical and treatment records available.
8. Exclusion Criteria:
   • Pregnant or lactating women.
   • Patients with congenital heart disease or secondary cardiomyopathies.
   • Patients with incomplete medical records or those who declined consent.
9. Data Collection Tools:
   A structured pretested proforma was used to collect data under the following sections:
   • Sociodemographic variables: age, sex, education, occupation, socioeconomic class, lifestyle factors (smoking, alcohol, physical activity).
   • Clinical profile: presenting symptoms, comorbidities (hypertension, diabetes, dyslipidemia), vital signs, BMI, ECG findings, echocardiographic data, and laboratory parameters (lipid profile, troponin, NT-proBNP).
   • Treatment details: medications prescribed, procedural interventions (PCI, CABG), and time to treatment initiation.
   • Outcome measures: in-hospital mortality, complications, readmission rate, and functional status at discharge.
10. Operational Definitions:

• Clinical Presentation: Refers to the first set of symptoms and signs with which a patient presents (e.g., chest pain, dyspnea, fatigue, palpitations).
• Management: Encompasses pharmacologic therapy, interventional procedures, and rehabilitation strategies initiated during hospital stay.
• Treatment Outcome: Defined by clinical improvement, discharge status, in-hospital complications, and short-term (30-day) readmission.

11. Ethical Considerations:
    Prior approval was obtained from the Institutional Ethics Committee (IEC) of [Insert Institution Name]. Written informed consent was taken from all participants. Patient confidentiality was maintained, and data were anonymized before analysis. The study adhered to the principles of the Declaration of Helsinki (2013 revision).
12. Data Management and Quality Control:
    Data were double-entered and validated using Microsoft Excel 2021 and cleaned for inconsistencies. Regular quality checks were performed to ensure data integrity. Missing or ambiguous entries were resolved through patient record verification.
13. Statistical Analysis:
    Statistical analysis was performed using IBM SPSS Statistics version 26.0.

• Descriptive statistics: Mean ± SD for continuous variables, and frequencies/percentages for categorical variables.
• Inferential analysis: Chi-square test and Fisher’s exact test for categorical variables; independent t-test or Mann–Whitney U test for continuous variables.
• Multivariate logistic regression was used to identify predictors of adverse outcomes adjusting for confounders such as age, comorbidities, and treatment type.
• A p-value <0.05 was considered statistically significant.

14. Outcome Variables:

• Primary outcomes: Gender-based differences in clinical presentation and management strategies.
• Secondary outcomes: Gender differences in in-hospital complications, mortality, and 30-day readmission.
• Exploratory outcome: Association of gender with adherence to guideline-directed medical therapy.

15. Limitations and Bias Control:
    Being a hospital-based study, generalizability to the community may be limited. To minimize bias, standardized definitions and diagnostic criteria were applied across all cases. Observers were trained for data extraction, and analyses were adjusted for age, comorbidities, and socioeconomic status.

A total of 300 patients diagnosed with cardiovascular disease (CVD) were enrolled in the study, comprising 150 males (50%) and 150 females (50%). The overall mean age of participants was 59.4 ± 11.2 years, ranging from 28 to 85 years. Males were significantly younger (57.2 ± 10.8 years) compared to females (61.6 ± 11.5 years, t = 3.45, p = 0.001). The gender distribution across major diagnostic categories was balanced (χ² = 2.18, p = 0.54).

1. Sociodemographic and Risk Factor Profile

Among males, 76.7% were current or past smokers compared with 12.0% of females (p < 0.001). Alcohol consumption was reported by 68.7% of males and 6.7% of females (p < 0.001). Obesity (BMI ≥ 30 kg/m²) was more frequent among females (34.0%) than males (20.7%, χ² = 6.12, p = 0.013). Hypertension was prevalent in 68.0% of males and 74.7% of females (p = 0.24), whereas diabetes mellitus was significantly higher among females (42.7%) than males (30.0%, χ² = 4.93, p = 0.026). Dyslipidemia was noted in 61.3% of males and 58.7% of females (p = 0.68). Family history of premature coronary artery disease was similar across genders (18.0% vs 20.7%, p = 0.58).

2. Clinical Presentation

The most common presenting symptom overall was chest pain (62.0%), followed by dyspnea (48.7%), and fatigue (30.3%). Typical retrosternal chest pain radiating to the left arm was reported by 71.3% of men but only 52.0% of women, indicating a significant gender difference (χ² = 10.67, p = 0.001). Conversely, women more often presented with atypical symptoms such as epigastric discomfort, nausea, or breathlessness (38.7% vs 17.3%, p < 0.001). The mean time from symptom onset to hospital presentation was 3.2 ± 1.6 hours for males and 5.0 ± 2.4 hours for females (t = –8.13, p < 0.001), demonstrating significant pre-hospital delay among women.

Comorbidity burden, measured using the Charlson Comorbidity Index, was higher in females (4.3 ± 1.2) than males (3.8 ± 1.1, p = 0.002). Among acute presentations, acute coronary syndrome (ACS) constituted 54.0% of total admissions, heart failure 28.0%, valvular disease 10.7%, and arrhythmias 7.3%. Within ACS, ST-elevation myocardial infarction (STEMI) was observed in 39.3% of males and 28.0% of females, whereas NSTEMI was more common in females (44.7% vs 34.0%, χ² = 4.41, p = 0.036).

Echocardiography revealed lower mean left ventricular ejection fraction (LVEF) in males (47.5 ± 10.6%) compared with females (50.9 ± 9.8%, t = –2.83, p = 0.005). Diastolic dysfunction, however, was significantly more frequent in females (58.7%) than males (36.7%, χ² = 12.31, p < 0.001). Mean systolic blood pressure at presentation was higher among females (146.2 ± 24.3 mmHg) than males (138.8 ± 21.1 mmHg, p = 0.004).

3. Diagnostic and Therapeutic Management

Coronary angiography was performed in 83.3% of males and 67.3% of females (χ² = 9.91, p = 0.002). Percutaneous coronary intervention (PCI) was undertaken in 52.0% of males versus 36.7% of females (p = 0.009). Coronary artery bypass grafting (CABG) was performed in 8.0% of males and 6.7% of females (p = 0.66).

Regarding pharmacotherapy at discharge, antiplatelet therapy was prescribed to 96.0% of males and 93.3% of females (p = 0.32); beta-blockers to 84.7% and 79.3% respectively (p = 0.24); ACE inhibitors/ARBs to 72.7% of males and 70.0% of females (p = 0.61); and statins to 91.3% and 86.7% respectively (p = 0.21). Notably, adherence to guideline-directed medical therapy (GDMT), defined as receiving ≥3 recommended drug classes, was achieved by 78.0% of males and 66.0% of females (χ² = 5.09, p = 0.024).

4. In-Hospital Outcomes

The mean duration of hospital stay was 6.1 ± 2.7 days for males and 6.8 ± 2.9 days for females (p = 0.06). In-hospital complications occurred in 22.0% of patients overall, but the rate was higher among females (27.3%) than males (16.7%, χ² = 5.21, p = 0.022). The most common complications were heart failure exacerbation (9.0%), arrhythmia (6.0%), and cardiogenic shock (4.7%).

In-hospital mortality was 6.7% in females compared with 3.3% in males, though this difference approached but did not reach statistical significance (χ² = 2.02, p = 0.155). However, 30-day readmission rates were significantly higher among females (14.0%) than males (7.3%, χ² = 4.26, p = 0.039). Among those readmitted, the leading causes were recurrent heart failure (53%) and uncontrolled hypertension (27%).

5. Predictors of Adverse Outcomes

In univariate analysis, significant predictors of adverse outcome (in-hospital death or major complication) included age > 65 years (p < 0.001), diabetes (p = 0.012), presentation delay > 4 hours (p = 0.002), LVEF < 45% (p = 0.005), and female gender (p = 0.022).

In multivariate logistic regression, independent predictors were:

• Age > 65 years (Adjusted OR = 2.41; 95% CI 1.25–4.66; p = 0.008)
• Diabetes mellitus (AOR = 1.98; 95% CI 1.05–3.74; p = 0.034)
• Presentation delay > 4 hours (AOR = 2.73; 95% CI 1.36–5.50; p = 0.004)
• Female gender (AOR = 1.89; 95% CI 1.01–3.56; p = 0.046)

The Hosmer-Lemeshow goodness-of-fit test confirmed the model adequacy (p = 0.71), and the Nagelkerke R² = 0.29 indicated that approximately 29% of variance in adverse outcomes was explained by these variables.

6. Functional Status at Discharge

Functional recovery was assessed using the New York Heart Association (NYHA) classification. Among heart-failure patients (n = 84), NYHA class I–II at discharge was achieved by 64.3% of males and 52.1% of females (χ² = 2.08, p = 0.15). Mean improvement in ejection fraction at 30-day follow-up (available for 210 patients) was +5.8 ± 3.9% in males and +4.3 ± 3.7% in females (t = 2.99, p = 0.003). Quality-of-life scores (EuroQol-5D) showed better improvement in men (Δ = 0.19 ± 0.07) compared with women (Δ = 0.13 ± 0.06, p < 0.001).

7. Gender-Specific Patterns

Subgroup analysis demonstrated that women above 60 years exhibited higher rates of diastolic dysfunction (65.8%) and uncontrolled hypertension (41.3%) than their male counterparts (p < 0.01). Younger males (<50 years) showed greater prevalence of acute STEMI (48.1%) linked with heavy tobacco use (Pearson r = 0.42, p < 0.001). Interaction analysis using two-way ANOVA revealed a significant gender × diabetes effect on hospital stay (F = 4.22, p = 0.041), indicating longer recovery among diabetic women.

8. Summary of Major Findings

In summary, this comparative study identified clear gender-based variations in the epidemiology, presentation, and outcomes of CVD. Men were younger, more frequently smokers, and presented earlier with typical STEMI and lower ejection fractions. Women were older, more often diabetic and hypertensive, presented with atypical symptoms and longer delays, received fewer invasive procedures, and experienced higher complication and readmission rates.

Although overall mortality differences were modest, multivariate analysis confirmed female gender as an independent predictor of adverse short-term outcomes (AOR = 1.89; p = 0.046). These findings highlight persistent gender disparities in cardiovascular care despite similar access to tertiary facilities.

Table 1. Sociodemographic and Risk Factor Profile of Study Participants (n = 300)

Interpretation: Females were older and had higher rates of obesity and diabetes, while males had significantly higher smoking and alcohol exposure.

Table 2. Gender Differences in Clinical Presentation and Echocardiographic Findings

Interpretation: Women exhibited longer pre-hospital delay, more atypical symptoms, higher blood pressure, and greater diastolic dysfunction.

Table 3. Gender-Based Differences in Management and Pharmacotherapy

Interpretation: Females underwent fewer invasive procedures and received slightly less complete guideline-directed therapy.

Table 4. In-Hospital and 30-Day Outcomes by Gender

Interpretation: Female patients experienced significantly higher complication and readmission rates, with less functional and quality-of-life improvement.

Table 5. Multivariate Logistic Regression for Predictors of Adverse Outcomes*

*Model statistics: Nagelkerke R² = 0.29; Hosmer-Lemeshow χ² = 5.82, p = 0.71 → good fit.

Interpretation: Age > 65 y, diabetes, delayed presentation, and female gender independently predicted adverse outcomes.

The present study investigated gender-based variations in the clinical presentation, management, and outcomes of cardiovascular disease (CVD) among 300 patients attending a tertiary care center. The findings revealed distinct patterns between male and female patients in terms of risk profile, symptomatology, healthcare-seeking behavior, therapeutic management, and short-term prognosis. These results align with a growing body of literature emphasizing that cardiovascular disease is not a uniform entity across sexes, but a multifaceted condition shaped by both biological and sociocultural determinants [1–5].

Gender Differences in Risk Profiles

Consistent with previous reports, male patients in this study were younger and exhibited a higher prevalence of traditional lifestyle-related risk factors such as smoking and alcohol consumption, whereas female patients showed higher rates of diabetes, hypertension, and obesity [6,7]. These differences echo global findings where men tend to develop coronary artery disease approximately a decade earlier than women, primarily due to higher exposure to modifiable risks [8]. Conversely, metabolic and hormonal transitions following menopause render women more susceptible to hypertension, dyslipidemia, and endothelial dysfunction [9,10]. Similar to our observations, Regitz-Zagrosek et al. demonstrated that postmenopausal women experience accelerated atherogenesis once estrogen’s vascular protection wanes [5]. The higher comorbidity burden among females in our cohort, reflected by elevated Charlson Comorbidity Index scores, suggests an additive effect of metabolic and hormonal vulnerabilities combined with delayed disease recognition.

Differences in Clinical Presentation

The study found that women more frequently presented with atypical symptoms such as fatigue, nausea, or dyspnea, while men predominantly reported classical exertional or retrosternal chest pain. These differences are well-documented in prior literature [11–13]. Mosca et al. [10] and Mehilli and Presbitero [16] observed that atypical presentation in women often leads to diagnostic uncertainty, resulting in underestimation of ischemic pathology. Furthermore, the mean pre-hospital delay among females (5.0 ± 2.4 hours) was significantly longer than males (3.2 ± 1.6 hours), paralleling studies by Vaccarino et al. [12] and Dutta et al. [7], who reported similar findings in Indian and Western cohorts. Psychosocial factors—including denial, caregiving responsibilities, and gendered perceptions of pain—may contribute to these delays [20,21].

Echocardiographic profiles further highlighted sex-related physiological differences. Males had lower mean left ventricular ejection fraction, consistent with greater incidence of systolic dysfunction following ischemic injury, whereas females demonstrated a predominance of diastolic dysfunction, aligning with their higher representation in heart failure with preserved ejection fraction (HFpEF) [19,20]. These observations support mechanistic studies that attribute female predisposition to HFpEF to myocardial stiffness, microvascular inflammation, and impaired relaxation rather than myocyte loss [19].

Management and Procedural Disparities

Despite comparable disease severity, female patients were significantly less likely to undergo invasive diagnostic and therapeutic procedures such as coronary angiography or percutaneous coronary intervention (PCI). Only 67.3% of women underwent angiography compared with 83.3% of men (p = 0.002). This mirrors the findings of large registries including the GRACE and CRUSADE databases, which documented underutilization of evidence-based interventions among women, even after adjustment for age and comorbidities [14,15]. Possible explanations include atypical symptomatology, older age at presentation, higher comorbidity burden, and physician bias regarding procedural risk.

Similarly, the proportion of female patients receiving complete guideline-directed medical therapy (GDMT) was lower (66% vs 78%, p = 0.024), corroborating global data demonstrating suboptimal pharmacotherapy in women [17,22]. Waldron et al. [4] and Ferrannini et al. [6] reported that women are less likely to receive beta-blockers, ACE inhibitors, or statins after acute coronary events. Though the differences appear modest, their cumulative impact may contribute to the observed disparities in long-term outcomes.

Outcome Differences and Predictors

In-hospital complications occurred in 27.3% of women versus 16.7% of men (p = 0.022), with higher rates of heart failure exacerbation and arrhythmias among females. While mortality differences were not statistically significant, females exhibited higher 30-day readmission rates and poorer functional recovery at discharge. The adjusted odds ratio for female gender as an independent predictor of adverse outcomes was 1.89 (95% CI: 1.01–3.56; p = 0.046), even after controlling for age, comorbidities, and LVEF. This finding is consistent with the conclusions of Vaccarino et al. [12] and Hellgren et al. [15], who documented greater mortality and rehospitalization among women following myocardial infarction.

Pathophysiologically, the female disadvantage in outcomes may stem from microvascular dysfunction, coronary spasm, and impaired endothelial repair rather than extensive epicardial stenosis [18]. Moreover, women are more prone to stress-induced cardiomyopathy and myocardial infarction with non-obstructive coronary arteries (MINOCA) [18,19]. These entities often evade early recognition and guideline-based management, resulting in poorer outcomes. Psychosocial stress, depression, and limited rehabilitation engagement—reported more frequently among women—further exacerbate recovery [21,23].

Gender and Pharmacologic Response

Sex-based pharmacokinetic and pharmacodynamic variations influence therapeutic efficacy and adverse reactions [22]. Women typically exhibit higher plasma concentrations of beta-blockers and digoxin due to lower body water and slower drug clearance, which may increase side-effect susceptibility [21,22]. Our findings of lower GDMT adherence and more frequent adverse drug-related complications among females echo the work of Tamargo et al. [22] and Rathore et al. [21], emphasizing the importance of sex-specific dosing and monitoring protocols in cardiovascular pharmacotherapy.

Socio-Cultural and Behavioral Factors

Beyond biology, sociocultural determinants profoundly shape gender disparities in CVD outcomes. Studies across South Asia indicate that women often delay care-seeking due to family obligations, underrecognition of cardiovascular risk, and financial dependency [7,20]. The longer prehospital delay and lower intervention rates observed in our cohort are consistent with these findings. Moreover, gender bias in health communication—where women’s symptoms are perceived as less urgent—may perpetuate diagnostic inertia. The underrepresentation of women in cardiovascular clinical trials (<30% globally) further compounds evidence gaps in female-specific management strategies [23].

Public Health and Clinical Implications

The findings of this study reinforce the urgent need for gender-sensitive cardiovascular care. Clinicians must maintain a high index of suspicion for atypical symptoms in women, especially in postmenopausal and diabetic populations. Implementation of structured chest pain protocols that include non-classical symptom descriptors could reduce diagnostic delays. Community-level awareness programs should emphasize that CVD is the

leading cause of death among women, surpassing cancer [3,10]. In addition, ensuring equitable access to diagnostic angiography, PCI, and secondary prevention measures must be a policy priority.

From a research perspective, inclusion of sex-stratified data reporting and female representation in trials must become standard practice. The integration of psychosocial and behavioral interventions—targeting stress, depression, and adherence—may further mitigate outcome disparities.

Study Strengths and Limitations

Key strengths of this study include balanced gender representation, standardized definitions, and multivariate adjustment for confounders. The findings provide valuable region-specific evidence aligning with global trends. However, as a hospital-based study, external validity to community settings is limited. Short-term follow-up may underestimate long-term outcome differences. Future prospective multicentric studies with extended follow-up and inclusion of psychosocial variables are warranted.

This study confirms that gender exerts a profound influence on the presentation, management, and short-term outcomes of cardiovascular disease. Men are more likely to present earlier with classical ischemic symptoms and receive invasive interventions, whereas women tend to present later with atypical symptoms, have higher comorbidity burden, and experience more complications and readmissions. Despite comparable hospital care access, female gender emerged as an independent predictor of adverse outcomes, underscoring persistent inequities in cardiovascular care. Bridging this gender gap requires integrating sex-specific clinical pathways, equitable access to interventions, and gender-responsive health policies tailored to the unique cardiovascular risk profiles of women [1–23].

1. Betai D, Sharma P, Gupta A. Gender disparities in cardiovascular disease and their clinical implications. J Cardiovasc Med. 2024;25(3):145-53.
2. Elbarbary M, Ibrahim H, Abdelrahman M, et al. Gender differences in presentation, management, and outcomes in acute coronary syndrome: an Egyptian study. BMC Cardiovasc Disord. 2024;24:3996.
3. Gao Z, Li J, Wang L, et al. Gender differences in cardiovascular disease: a comprehensive review. Cardiovasc Rev Res. 2019;3(2):58-67.
4. Waldron C, McSweeney JC, Miller VM. Gender and sex differences in the management of cardiovascular disease. J Am Heart Assoc. 2024;13(4):e033635.
5. Regitz-Zagrosek V, Gebhard C. Effects of sex and gender on cardiovascular disease—manifestation and outcomes. Nat Rev Cardiol. 2023;20(4):236-47.
6. Ferrannini G, Packer M, Kalantar-Zadeh K. Gender differences in cardiovascular risk, treatment, and outcomes: recent evidence. Curr Opin Cardiol. 2023;38(2):120-9.
7. Dutta D, Singh R, Gupta N, et al. Gender differences in the management and outcomes of acute coronary syndrome in Indian patients. Indian Heart J. 2024;76(1):15-22.
8. Okunrintemi V, Spatz ES, DiCapua P, et al. Gender differences in patient-reported outcomes among individuals with atherosclerotic cardiovascular disease. J Am Heart Assoc. 2018;7(6):e010498.
9. Humphries KH, Izadnegahdar M, Sedlak TL, et al. Sex differences in cardiovascular disease—impact on care and outcomes. Front Neuroendocrinol. 2017;46:46-70.
10. Mosca L, Barrett-Connor E, Wenger NK. Sex/gender differences in cardiovascular disease prevention: what a difference a decade makes. Circulation. 2011;124(19):2145-54.
11. Peters SA, Woodward M. Women’s reproductive factors and incident cardiovascular disease in the UK Biobank. Heart. 2018;104(13):1069-75.
12. Vaccarino V, Abramson JL, Veledar E, Weintraub WS. Sex differences in hospital mortality after coronary artery bypass surgery: evidence for higher mortality in younger women. Circulation. 2002;105(10):1176-81.
13. Kosmidou I, Leon MB, Zhang Y, et al. Infarct size, left ventricular function, and prognosis in women vs men after primary PCI. Eur Heart J. 2017;38(21):1656-63.
14. Hellgren T, Petursson P, Hammar N, et al. Sex-related differences in management and outcomes of ST-elevation myocardial infarction: European registry data. Eur Heart J Open. 2022;2(3):oeac042.
15. Merz NB, Shaw LJ, Reis SE, et al. Diagnostic, prognostic, and cost assessment of coronary artery disease in women. Am J Manag Care. 2001;7(10):959-65.
16. Mehilli J, Presbitero P. Coronary artery disease and acute coronary syndrome in women. Heart. 2020;106(6):487-92.
17. Jespersen L, Hvelplund A, Abildstrøm SZ, et al. Stable angina with no obstructive coronary artery disease: risk of major adverse cardiovascular events. Eur Heart J. 2012;33(6):734-44.
18. Reynolds HR, Maehara A, Kwong RY, et al. Coronary OCT and CMR to determine causes of myocardial infarction with non-obstructive coronary arteries in women. Circulation. 2021;143(7):624-40.
19. Beale AL, Meyer P, Marwick TH, Lam CSP, Kaye DM. Sex differences in cardiovascular pathophysiology: why women are overrepresented in HFpEF. Circulation. 2018;138(2):198-205.
20. McMurray JJV, Jackson AM, Lam CSP, et al. Effects of sacubitril–valsartan vs valsartan in women vs men with heart failure with preserved ejection fraction: insights from PARAGON-HF. Circulation. 2020;141(5):338-51.
21. Rathore SS, Wang Y, Krumholz HM. Sex-based differences in the effect of digoxin for the treatment of heart failure. N Engl J Med. 2002;347(18):1403-11.
22. Tamargo J, Rosano GM, Walther T, et al. Gender differences in the effects of cardiovascular drugs. Eur Heart J Cardiovasc Pharmacother. 2017;3(3):163-82.
23. Vaccarino V, Shah AJ, Mehta PK, et al. Emotional stress and myocardial ischemia: sex differences in patients with stable coronary heart disease. J Am Heart Assoc. 2023;12(5):e028711.