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27 October 2026

13 Pages

Beyond Traditional Risk Scores: Precision Medicine for Comprehensive Cardiovascular Risk Assessment in Women and Men

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and
1
Department of Cardiology, Hospital Universitario Son Llatzer, 07198 Palma de Mallorca, Spain
2
Departamento de Medicina, University of the Balearic Islands, 07120 Palma de Mallorca, Spain
3
CIBEROBN (CIBER Physiopathology of Obesity and Nutrition CB12/03/30038), Carlos III Health Institute, 28029 Madrid, Spain
4
Department of Cardiology, Hospital Clínico San Carlos, 28040 Madrid, Spain
J. Clin. Med.2026, 15(21), 8365;https://doi.org/10.3390/jcm15218365
This article belongs to the Section Cardiovascular Medicine
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Abstract

Background and Objectives: Conventional 10-year cardiovascular risk estimation algorithms are insufficient because they fail to integrate non-traditional clinical, biological, reproductive, and psychosocial modifiers that exhibit marked sex differences. The objective of this position framework is to address this gap by developing structured, sex-stratified clinical checklists for routine clinical practice. Methods: An expert narrative review and literature screening were conducted across PubMed/MEDLINE, Embase, Cochrane, and 14 international clinical practice guidelines (2020–2026 window) to identify robust sex-stratified risk modifiers. The multidisciplinary working group (comprising cardiology, gynecology, and primary care) conducted iterative internal review rounds to synthesize evidence and structure two comprehensive clinical checklists across six operational domains. Results: Epidemiological evidence mandates a life-course prevention model starting prior to conception. In women, obstetric history (preeclampsia, gestational diabetes, preterm birth), gynecological milestones (PMOS, endometriosis), early menopause, and oncological therapies markedly elevate vascular risk. In men, persistent erectile dysfunction, functional hypogonadism, androgen deprivation therapy, and premature androgenetic alopecia serve as early indicators of vascular and metabolic risk. Advanced biomarkers (Lp(a) ≥ 50 mg/dL, ApoB > 100 mg/dL, persistent hs-CRP ≥ 2 mg/L) and social determinants of health further refine risk stratification. Conclusions: Incorporating these structured checklists into daily consultations complements validated population risk scores (SCORE2, PREVENT, QRISK3), mitigates systematic underdiagnosis—especially in women—and provides an actionable framework for personalized cardiovascular prevention.

1. Introduction and Objectives

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality globally, accounting for over 18 million annual deaths [1,2]. Despite decades of therapeutic advances, substantial under-recognition and under-treatment of cardiovascular risk persist worldwide. A primary driver of this clinical gap is a historical male-centric bias in clinical trial enrollment and diagnostic criteria, which has led to systematic diagnostic delays, lower therapeutic intensity, and poorer outcomes in women [3].
European and international guidelines advocate for systematic 10-year risk estimation in primary prevention using validated population engines such as SCORE2, SCORE2-OP, SCORE2-Diabetes, QRISK3, PREVENT, and LIFE-CVD2 [4,5,6]. However, these standard multivariable risk engines rely almost exclusively on classic major risk factors: age, biological sex, systolic blood pressure, smoking status, and blood lipid concentrations. Consequently, they routinely fail to capture critical non-traditional clinical, biological, reproductive, and psychosocial modifiers that exhibit profound sex-stratified impacts [7].
In women, the presentation of ischemic heart disease is frequently heterogeneous and atypical compared to men. Entities such as ischemia with non-obstructive coronary arteries (INOCA), myocardial infarction with non-obstructive coronary arteries (MINOCA), coronary microvascular dysfunction, and Takotsubo syndrome exhibit a substantially higher prevalence in women, challenging traditional obstructive coronary disease paradigms [3,7,8,9]. Furthermore, historical enrollment in major cardiovascular randomized controlled trials has averaged ≤37% female participation, leaving major evidence gaps regarding sex-specific therapeutic efficacy [10]. A recent multidisciplinary Delphi consensus among primary care physicians, cardiologists, and gynecologists confirmed persistent diagnostic and therapeutic inequities toward female patients across routine clinical settings [11].
Conversely, in men, standard primary care consultations also omit vital gender-specific vascular indicators. Routine examinations rarely evaluate erectile function, serum testosterone levels, hypogonadal symptoms, anabolic–androgenic steroid exposure, or androgen deprivation therapy (ADT) [12,13,14]. Yet these parameters provide early, highly sensitive markers of systemic endothelial dysfunction, microvascular damage, and cardiotoxic exposure. Additionally, psychosocial stressors—including depression, chronic anxiety, social isolation, intimate partner violence, and socioeconomic deprivation—exert profound cardiovascular impacts across both sexes, with distinct exposure patterns and vulnerability windows [3,15].

The New Paradigm: Life-Course Prevention

Historically, cardiovascular prevention has operated as a reactive, late-stage strategy aimed at mitigating overt vascular damage once classic risk factors manifest in middle age. Contemporary epidemiological and molecular evidence mandates a fundamental paradigm shift toward proactive, ‘cradle-to-grave’ life-course prevention [16,17]. Under this life-course framework, cardiovascular vulnerability begins prior to conception. Paternal obesity, metabolic dysfunction, and toxic exposures induce transmissible epigenetic modifications in sperm that alter offspring lipid metabolism and vascular structure from childhood. During pregnancy, the placenta serves as a real-time metabolic and vascular stress monitor; placental vascular lesions (e.g., acute atherosis of spiral arteries) directly mirror maternal cardiometabolic vulnerability and correlate with elevated maternal cardiovascular risk up to decades post-partum [15].
To bridge the critical gap between guideline recommendations and clinical implementation, we designed two comprehensive, sex-stratified clinical checklists. Operating as structured, non-competing adjuncts to established risk engines, these tools ensure systematic screening for non-traditional modifiers, enabling timely risk reclassification and personalized primary prevention [12].
To conceptualize this clinical challenge, cardiovascular risk assessment can be likened to an iceberg: standard risk engines evaluate only the visible tip, leaving major sex-specific modifiers submerged (Graphical Abstract).

2. Methodology

This work is structured as an Expert Narrative Review and Clinical Position Framework. Fourteen clinical practice guidelines and reference consensus documents from major international societies (including the European Society of Cardiology [ESC], American College of Cardiology/American Heart Association [ACC/AHA], European Atherosclerosis Society [EAS], and European Menopause and Andropause Society [EMAS]) were thoroughly evaluated [4,18,19,20,21,22].
A comprehensive literature search was conducted across PubMed/MEDLINE, Embase, and Cochrane databases covering the publication window from January 2020 to January 2026, while retaining foundational historical citations for essential clinical context. The Boolean search strings utilized included targeted combinations of medical subject headings (MeSHs) and text words: (‘cardiovascular risk’ OR ‘cardiovascular risk modifier’ OR ‘risk enhancer’) AND (‘sex differences’ OR ‘gender-specific’ OR ‘female-specific’ OR ‘male-specific’) AND (‘checklist’ OR ‘screening tool’ OR ‘risk reclassification’).
Study selection and eligibility criteria: inclusion criteria comprised prospective cohort studies, randomized controlled trials, systematic reviews, meta-analyses, and international practice guidelines evaluating non-traditional cardiovascular risk modifiers in adult populations. Pediatric populations (<10 years) were excluded, whereas late adolescents and young adults (15–19 years) presenting with early metabolic or reproductive transitions (e.g., polyendocrine metabolic ovarian syndrome [PMOS], early metabolic syndrome) were included to address early life-course vulnerability.
Consensus and checklist development process: the multidisciplinary working group—comprising 5 panel members representing cardiology, gynecology, and primary care—conducted iterative internal consensus rounds. Panelists systematically reviewed candidate variables retrieved from the literature, evaluating each item based on three explicit criteria: (1) strength of epidemiological association (hazard ratio or odds ratio), (2) biological plausibility, and (3) feasibility of rapid administration in routine primary care and outpatient consultations. Candidate items achieving consensus were synthesized into two sex-stratified clinical checklists (Supplementary Material).
Target population and applicability gate: both checklists are intended exclusively for primary prevention in adults without established atherosclerotic cardiovascular disease (ASCVD), familial hypercholesterolemia, severe chronic kidney disease (eGFR < 30 mL/min/1.73 m2), or diabetes mellitus with target organ damage. Patients with these high-risk conditions automatically require intensive preventive therapy, bypassing secondary risk reclassification.

3. Results

3.1. Checklist Architecture and Classic Risk Factors as the Essential Starting Point

To translate complex evidence into daily practice, the two clinical checklists were structured into six operational domains: (1) classic risk factors and population scores, (2) advanced biomarkers for reclassification, (3) sex-specific modifiers and reproductive/andrological milestones, (4) autoimmune and oncological comorbidities, (5) psychosocial and gender determinants, and (6) current symptom screening. The checklists employ a rapid binary format (‘Yes’, ‘No’, ‘Not Evaluated’) engineered for completion within an estimated 5 to 7 min during routine medical encounters.
Baseline evaluation incorporates standard multivariable parameters required by population risk engines (SCORE2, SCORE2-OP, SCORE2-Diabetes, QRISK3, PREVENT, LIFE-CVD2) [4,5,6,18,19]: age, biological sex, smoking status, systolic blood pressure, total cholesterol, HDL-C, LDL-C, non-HDL-C, eGFR, and urinary albumin-to-creatinine ratio (UACR). Glycemic screening explicitly differentiates prediabetes from type 2 diabetes (HbA1c %). Visceral adiposity is assessed via waist circumference using sex-specific pathological thresholds (≥88 cm in women, ≥102 cm in men). Physical activity, dietary quality, and history of recreational drug or anabolic–androgenic steroid use are systematically documented.
A comprehensive, unpooled synthesis of all non-traditional risk modifiers—including their meta-analytic effect sizes, evidence hierarchy tiers, and recommended primary care actions—is summarized in Table 1.
Table 1. Evidence hierarchy, effect sizes, and proposed actions for risk modifiers.

3.2. Advanced Biomarkers for Risk Reclassification

Advanced biomarkers identify subclinical atherogenesis and vascular inflammation in apparently low-to-moderate-risk individuals [4]. Lipoprotein(a) [Lp(a)] measurement at least once in a lifetime is mandated; values ≥ 50 mg/dL (or ≥105 nmol/L) constitute an independent, genetically determined risk enhancer [20]. Apolipoprotein B (ApoB) quantifies atherogenic particle burden more accurately than LDL-C in insulin-resistant and hypertriglyceridemic states; per the 2025 ESC/EAS Focused Update, ApoB > 100 mg/dL denotes elevated risk and >120 mg/dL indicates high risk [22,34,39,40]. Persistent low-grade vascular inflammation is captured by high-sensitivity C-reactive protein (hs-CRP ≥ 2 mg/L on two separate measurements in the absence of acute infection) [34]. In patients at borderline or intermediate calculated risk with therapeutic uncertainty, Coronary Artery Calcium (CAC) scoring serves as a Class IIb tie-breaker image test [4], noting that a CAC score of 0 in young women does not rule out soft, non-calcified atheromatous plaque or microvascular dysfunction. Additional metabolic markers include thyroid dysfunction [41], serum uric acid (sUA > 6.0 mg/dL in women, >7.0 mg/dL in men) [42], and metabolic cardioprotection with GLP1Ra/SGLT2i [43].

3.3. Female-Specific Risk Modifiers

Pregnancy represents a physiological vascular and metabolic stress test. Adverse pregnancy outcomes (APOs)—including preeclampsia and eclampsia (hazard ratio (HR) 1.8–2.2) [23,25], gestational hypertension, gestational diabetes (HR 1.8) [24], preterm birth (<37 weeks), recurrent miscarriages (≥2), fetal growth restriction, and placental abruption—unmask latent vascular vulnerability decades before clinical manifest disease. Gynecological conditions such as polycystic ovary syndrome (recently renamed polyendocrine metabolic ovarian syndrome [PMOS]) [26,44] and endometriosis (HR 1.2–1.4) [27] carry chronic metabolic and systemic inflammatory burdens. Additional critical female modifiers include history of infertility or assisted reproductive technology [28], cardiotoxic breast cancer therapies (anthracyclines, anti-HER2 agents, thoracic radiation) [32,45], autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis, antiphospholipid syndrome, psoriasis) [35], migraine with aura [25], early menopause (<45 years; HR 1.50) [29,30], surgical menopause (bilateral oophorectomy), nulliparity, lack of breastfeeding, and exogenous hormone exposure (combined oral contraceptives, menopausal hormone therapy) [46].

3.4. Male-Specific Risk Modifiers

In men, the checklist systematically screens for hidden endothelial and microvascular damage through andrological and oncological fields. Persistent erectile dysfunction (≥3 months) serves as an independent vascular predictor, preceding overt coronary artery disease by 2 to 5 years and offering an invaluable primary prevention window [31]. Functional hypogonadism—defined by low morning fasting total testosterone (<200–300 ng/dL [≈6.9–10.4 nmol/L]) or calculated free testosterone (<50–65 pg/mL [≈5.0–6.5 ng/dL])—correlates strongly with visceral obesity, insulin resistance, and endothelial dysfunction [12,13,14]. In prostate cancer management, androgen deprivation therapy (ADT) induces severe metabolic syndrome, dyslipidemia, and cardiotoxicity (HR 1.38–1.65) [32]. Male factor infertility, obstructive sleep apnea (HR 1.45) [38], chronic kidney disease progression, occupational shift work, and early-onset male androgenetic alopecia (<30 years) represent additional key male modifiers, with androgenetic alopecia serving as an early phenotypic marker of hyperinsulinemia and metabolic syndrome [33,47].

3.5. Psychosocial Factors, Mental Health and Gender Diversity

Psychosocial stressors and social determinants of health exert profound, independent effects on cardiometabolic morbidity [36,37]. It is essential to distinguish biological sex (chromosomal, hormonal, anatomical traits) from gender determinants (social constructs, caregiving burdens, gender roles, socioeconomic constraints). While gender constructs affect all individuals, economic deprivation, lower education levels, and chronic caregiving stress disproportionately burden women, accelerating vascular aging [48].
Severe mental illness, major depressive disorder, and chronic anxiety increase coronary event risk by 30% to 50% (HR 1.30–1.50) [15]. Brief validated primary care instruments (Goldberg Anxiety Scale ≥5, Depression Scale ≥ 2; or international alternatives PHQ-9 and GAD-7) are integrated into both checklists. Furthermore, both tools mandate sensitive evaluation of intimate partner violence (IPV) or trauma history using validated screening tools (HARK/HITS). Chronic post-traumatic stress induces sustained hypothalamic–pituitary–adrenal axis activation, resulting in autonomic dysregulation, systemic low-grade inflammation, and endothelial injury. IPV screening requires absolute privacy, strict confidentiality, and established institutional referral pathways.
Finally, a distinct clinical consideration involves individuals receiving exogenous Gender-Affirming Hormone Therapy (GAHT). While broader clinical and ethical debates regarding cross-sex hormonal interventions remain ongoing, from a cardiovascular perspective, long-term non-physiological hormone exposure introduces significant exogenous endocrine burdens—including heightened risks of venous thromboembolism, ischemic stroke, and metabolic dysregulation—necessitating strict, cautious vascular monitoring based on active pharmacological regimens and baseline risk profiles [45,46].

3.6. Current Clinical Assessment and Symptom Screening

Systematic symptom screening ensures that patients presenting with unrecognized angina or cardiovascular symptoms are not mismanaged under a primary prevention protocol. In patients reporting chest pain or exertional dyspnea, applying structured evaluation tools such as the ESC 2024 Symptom Score [18] allows rapid clinical triage. The presence of active symptoms immediately shifts the consultation focus from 10-year population risk scoring to urgent diagnostic workup for obstructive or non-obstructive CAD.

4. Implications for Clinical Practice and Implementation

Integrating sex-specific checklists standardizes medical history-taking and minimizes clinical variability across healthcare settings. Clinical application follows a structured three-phase workflow:
  • Phase 1: systematic recording of mandatory variables to compute baseline 10-year population risk scores (SCORE2, SCORE2-OP, SCORE2-Diabetes, QRISK3, PREVENT, or LIFE-CVD2).
  • Phase 2: comprehensive evaluation of sex-specific modifiers, reproductive/andrological milestones, and psychosocial determinants.
  • Phase 3: identification of critical risk enhancers to guide upward risk reclassification or selective imaging (CAC score) in borderline or low-to-moderate-risk scenarios.
Reclassification logic and avoidance of double-counting: non-traditional risk modifiers function as qualitative risk enhancers. When ≥1 major risk enhancer is identified in a patient categorized as low-to-moderate risk, clinicians should consider reclassifying the patient into a higher risk tier to initiate or intensify preventive interventions (e.g., lipid-lowering therapy or blood pressure optimization). To prevent double-counting or over-treatment, risk enhancers are evaluated qualitatively without adding cumulative points to baseline multivariable risk equations [4,48,49].

Challenges, Ethical Considerations, and Digitalization

Successful primary care implementation depends heavily on electronic health record (EHR) integration. Smart EHR systems utilizing conditional activation logic can automatically expand relevant domains—such as opening a post-partum surveillance tab when a history of preeclampsia is checked, or triggering an endothelial evaluation module when persistent erectile dysfunction is recorded. Ethical considerations are paramount: inquiring about intimate partner violence, mental health, or sexual function requires absolute privacy, clinician empathy, and clear institutional referral pathways [48,49].

5. Practical Proposal and Authors’ Recommendations

  • Dynamic risk scoring: use validated population engines (SCORE2, PREVENT, QRISK3) as the initial quantitative foundation, interpreting results dynamically alongside identified risk modifiers.
  • Comprehensive female screening: systematically document obstetric history (APOs), gynecological conditions (PMOS, endometriosis), menopausal age, and exogenous hormone exposure.
  • Mandatory male domain screening: systematically evaluate persistent erectile dysfunction (≥3 months), fasting morning testosterone (<200–300 ng/dL), ADT exposure, sleep apnea, and occupational shift work.
  • Biomarker reclassification: measure Lp(a) at least once in a lifetime (cut-off ≥50 mg/dL); evaluate ApoB (>100 mg/dL) and persistent hs-CRP (≥2 mg/L) in dyslipidemic or inflammatory states.
  • Selective imaging tie-breakers: utilize Coronary Artery Calcium (CAC) scoring in intermediate-risk patients when therapeutic decisions remain uncertain.
  • Psychosocial and mental health integration: screen for social determinants of health, depression/anxiety (PHQ-9/GAD-7), and intimate partner violence under strict confidentiality.

6. Future Research Directions and Limitations

6.1. Study Limitations and Implementation Feasibility

This work is an expert position proposal based on narrative review and consensus. Key limitations include: (a) the absence of prospective cohort validation regarding hard event reduction; (b) expert selection bias; (c) regional focus on European guidelines; and (d) potential risks of over-diagnosis. Feasibility evaluation indicates an item count of 25–30 fields with an estimated completion time of 5–7 min in primary care (optimizable via electronic health record conditional logic).

6.2. Staged Validation Roadmap

This position proposal provides a structured framework based on rigorous evidence synthesis and multidisciplinary expert consensus. Main limitations include the necessity for prospective validation in diverse primary care cohorts and the potential risk of over-diagnosis if reclassification rules are applied indiscriminately. A three-stage validation roadmap is outlined:
  • Stage 1 (feasibility and usability): assess completion times, electronic EHR integration, missing data rates, and inter-observer reliability in primary care pilot centers.
  • Stage 2 (process and patient-reported outcomes): measure appropriate preventive treatment initiation, patient-reported outcome measures (PROMs), quality of life improvement, and healthcare cost-effectiveness [48,49].
  • Stage 3 (prognostic net benefit): evaluate incremental discrimination (C-statistic), Net Reclassification Improvement (NRI), and long-term hard event reduction over standard risk scores alone.

7. Conclusions

Cardiovascular risk assessment must evolve from static estimation focused exclusively on classic risk factors (the visible tip) toward a comprehensive, structured, sex-sensitive, and psychosocial-aware model.
Specific clinical checklists for women and men bring critical, routinely omitted modifiers to light, structuring history-taking and advancing equitable precision medicine from guidelines into daily practice, subject to future prospective validation.

Supplementary Materials

The following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/jcm15218365/s1, S1: Checklist for cardiovascular risk assessment in women, S2: Checklist for cardiovascular risk assessment in men.

Author Contributions

Conceptualization, J.M.G. and D.V.; methodology, J.M.G. and D.V.; software, J.M.G. and D.V.; validation, J.M.G., D.V., M.G., V.P.-C. and M.A.S.-C.; formal analysis, J.M.G. and D.V.; investigation, J.M.G., D.V., M.G., V.P.-C. and M.A.S.-C.; resources, J.M.G. and D.V.; data curation, J.M.G. and D.V.; writing—original draft preparation, J.M.G. and D.V.; writing—review and editing, J.M.G., D.V., M.G., V.P.-C. and M.A.S.-C.; visualization, J.M.G. and D.V.; supervision, J.M.G.; project administration, J.M.G.; funding acquisition, J.M.G. All authors have read and agreed to the published version of the manuscript.

Funding

The project “Checklist for cardiovascular risk assessment in women and men” received unconditioned funding from Organon.

Institutional Review Board Statement

Not applicable.

Data Availability Statement

No new data were created or analyzed in this study. Data sharing is not applicable to this article.

Conflicts of Interest

The authors declare no conflicts of interest.

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