While women and men share the main leading causes of death (heart disease, cancer and stroke), most of the historical knowledge regarding their aetiology, progression and treatment has been derived from studies conducted exclusively in men.1 For decades, the medical community operated under the assumption that women were physiologically equivalent to men in terms of health, except for their reproductive function. This reductionist view has systematically overlooked the profound genetic, molecular, cellular and physiological differences between the sexes.
Moreover, there has been very little research into how motherhood impacts women’s long-term health.2 It has been suggested that pregnancy may act as a physiological stress test capable of exposing subclinical cardiovascular vulnerabilities that might otherwise remain latent for decades. During gestation, the maternal cardiovascular system undergoes profound haemodynamic adaptations, including a 50% increase in blood volume and cardiac output, alongside substantial metabolic shifts.
In particular, certain pregnancy complications, such as preterm birth (PTB), are considered early indicators of a higher risk of developing cardiovascular disease (CVD) in the future.3–6 PTB affects between 5% and 12.7% of pregnancies worldwide and has emerged as a significant reproductive factor associated with increased long-term cardiovascular risk in affected women. Epidemiological research has firmly established that PTB predisposes women to a host of cardiovascular risk factors, such as hypertension, type 2 diabetes (T2D), and dyslipidaemia, as well as to direct cardiovascular events, such as coronary heart disease, stroke and cardiovascular mortality.
Recent evidence, particularly from large-scale biobanks and registry analyses published in the last 3–5 years, suggests that this risk is not merely correlative but may share a genetic and pathophysiological basis with CVD. For example, data from the UK Biobank has elucidated the shared genetic liability between hypertensive disorders of pregnancy and coronary artery disease, suggesting a ‘common soil’ hypothesis in which PTB is a sentinel event for a pre-existing predisposition to vascular disease.7 Furthermore, updated longitudinal data from Scandinavian registries have clarified that these risks persist well into the seventh decade of life, challenging the notion that the impact of pregnancy complications fades after menopause.8,9
The recognition of PTB as an independent marker of future cardiovascular risk underscores the necessity to re-examine current risk assessment strategies in women and to incorporate obstetric history into preventive cardiology practices.10,11 This review aims to consolidate current scientific understanding by incorporating recent large-scale evidence, critically evaluating inconsistencies in the literature, discussing potential implicated mechanisms and providing a dedicated framework for clinical management aligned with the latest 2025 European Society of Cardiology (ESC) guidelines for the management of CVD and pregnancy.12,13
Pathophysiological Mechanisms
Although the exact biological mechanisms linking PTB to later CVD are not fully elucidated, several plausible pathways have been proposed based on both clinical and experimental evidence. One hypothesis is that PTB may serve as an early ‘stress test’ that exposes subclinical maternal cardiovascular dysfunction or predisposition to atherogenesis.3,14 Moreover, traditional cardiovascular risk factors such as obesity, insulin resistance, hypertension and dyslipidaemia may share common aetiological pathways with PTB. Pregnancy duration has been inversely associated with insulin resistance, blood pressure and low-grade inflammation in women years after delivery. Moreover, women with a history of PTB (excluding those with pre-eclampsia or small-for-gestational-age infants) have higher levels of atherogenic lipids and increased carotid artery wall thickness in the decade following delivery compared with women who delivered at term. These observations suggest that dysregulation of cardiometabolic factors, sharing common pathways with CVD, may help explain the association between PTB and later cardiovascular risk.15 However, in many instances, the occurrence of PTB precedes the manifestation of such metabolic abnormalities, suggesting that the pregnancy itself could unmask latent predispositions that later culminate in overt CVD (Figure 1 ).4,16–19
It is important to note that although postpartum development of conventional CVD risk factors such as hypertension and diabetes explains a portion of the increased risk, only a modest fraction (approximately 13–15%) of the elevated cardiovascular risk can be accounted for by these conditions.20,21 This residual unexplained risk points to additional, as yet undetermined, biological mechanisms (i.e. persistent low-grade inflammation, altered coagulation pathways and endothelial dysfunction) that may be triggered during the perinatal period and persist long after delivery.22
Moreover, lower gestational age at delivery is associated with a higher long-term maternal cardiovascular risk, indicating a direct relationship between the degree of prematurity and this risk.14 While certain mechanisms are suggested by associated conditions (such as hypertensive disorders of pregnancy or dyslipidaemia), others are supported by direct evidence, as described below.
Inflammatory and Oxidative Stress Pathways
Inflammatory processes, which are central to both spontaneous PTB and the pathogenesis of atherosclerosis, have been implicated, given that elevated levels of pro-inflammatory cytokines and oxidative stress markers during PTB might promote endothelial dysfunction and accelerated vascular ageing.23,24 Inflammation constitutes a fundamental process in the initiation of labour and is markedly exaggerated in many cases of PTB. Inflammatory signals characterised by the increased production of pro-inflammatory cytokines, including interleukins (IL-1β, IL-6, IL-8) and tumour necrosis factor-α (TNF-α), are frequently found in the maternal–fetal compartment during spontaneous PTB.23,25,26 These inflammatory mediators initiate a cascade leading to leukocyte recruitment, extracellular matrix (EM) degradation and activation of uterotonic pathways, thus promoting early cervical ripening and membrane rupture. Concurrently, the generation of reactive oxygen species (ROS) exceeds the capacity of antioxidant defences in PTB, leading to oxidative stress that damages cellular structures and augments inflammatory responses.24 This oxidative milieu contributes not only to premature uterine activation but also to endothelial dysfunction: a critical process implicated in the pathogenesis of CVD.27
In contrast, because of increased oxidative stress, ROS promotes the activation of transcription factors, such as nuclear factor κB (NF-κB), which then upregulate inflammatory mediators in the uterine and vascular tissues.24 This chronic inflammatory environment not only drives the premature initiation of labour, but also predisposes to long-term vascular inflammation and atherosclerosis, thereby establishing a mechanistic bridge between PTB and CVD.28
Under normal circumstances, a finely tuned balance of regulatory T-cells, tolerogenic dendritic cells and anti-inflammatory cytokines (such as transforming growth factor-β [TGF-β] and IL-10) maintains immune homeostasis at the maternal–fetal interface. In PTB this regulatory network is compromised, leading to an enhanced inflammatory response that contributes to both membrane rupture and uterine contractions.29 The release of damage-associated molecular patterns and cell-free fetal DNA during this process further activates toll-like receptors and the inflammasome complex, thereby amplifying the inflammatory cascade.30 This heightened inflammatory state not only triggers PTB but also establishes a chronic low-grade inflammation that may persist postpartum, predisposing women to endothelial dysfunction and atherosclerosis.15 Furthermore, maternal immune dysregulation, combined with genetic predispositions, could induce epigenetic modifications that influence both fetal development and long-term cardiovascular risk (Figure 2 ).
Disruption of Vascular Homeostasis
In both the onset of cardiovascular complications and PTB, the initial event seems to be a disruption of vascular homeostasis.
Endothelial Dysfunction
Endothelial dysfunction represents a central event in the development of CVD and is increasingly recognised in both PTB and its sequelae. Elevated levels of soluble adhesion molecules (e.g. including sICAM-1 [soluble intercellular adhesion molecule-1], sVCAM-1 [soluble vascular cell adhesion molecule-1] and soluble E-selectin) are indicative of endothelial activation and have been consistently associated with PTB.27 These molecules facilitate leukocyte adhesion and transmigration, triggering a pro-inflammatory state that damages vascular endothelium. Several human and murine studies have reported the presence of inflammatory neutrophils and macrophages in the uterus, decidua, cervix and fetal membranes during labour. The infiltration of these cells is facilitated by chemokines and cellular adhesion molecules.31 Inadequate conversion of the uterine spiral arteries during placentation (a hallmark of placental vascular lesions) is also observed in PTB and results in suboptimal uterine and placental perfusion.32,33 The resulting ischaemic environment further exacerbates oxidative stress and inflammatory signalling, thereby contributing to both PTB and the development of arterial stiffness and endothelial dysfunction in later life (Figure 2).
Vascular Remodelling
The persistent vascular remodelling that occurs in response to these early insults often includes alterations in the balance of EM components, such as elastin and collagen, as well as muscle cell proliferation. These structural changes predispose individuals to hypertension and coronary artery disease, and the molecular pathways governing such remodelling share many features with those activated during PTB.34
Remodelling of maternal spiral arteries is essential for adequate fetal blood supply and is mediated by extravillous trophoblast invasion. Extravillous trophoblast cells remodel the arteries through both interstitial and endovascular pathways, a process regulated by multiple factors including cytokines, growth factors, adhesion molecules, EM-modifying enzymes and local oxygen tension.35
Placental Dysfunction
Placental vascular lesions are the second-most-reported finding in PTB, after acute inflammation.36 These lesions, especially in medically indicated cases, may reflect underlying maternal vascular pathology: abnormalities such as placental insufficiency or vasculopathy are thought to be manifestations of microvascular disease, which is also a precursor to cardiovascular events.36,37 It has been proposed that in cases of severe uteroplacental ischaemia leading to decidual necrosis and subsequent haemorrhage, thrombin may act as a key mediator in the initiation of labour. Placental decidual cells express very high levels of tissue factor, one of the upstream precursors of thrombin, facilitating rapid activation of the clotting cascade during labour. However, while thrombin is produced to prevent haemorrhage, it paradoxically increases the risk of spontaneous PTB.36
Dysregulation of Angiogenic and Coagulation Pathways
Abnormal angiogenic signalling is another molecular mechanism that links PTB with CVD. In the context of preterm pre-eclampsia, elevated levels of soluble fms-like tyrosine kinase-1 (sFlt-1) and a corresponding reduction in placental growth factor have been identified. This leads to impaired angiogenesis and contributes to endothelial dysfunction and altered coagulation processes, key contributors to placental dysfunction and subsequent cardiovascular alterations in the mother.38 These angiogenic imbalances disrupt normal blood vessel formation and compromise endothelial integrity, which are also prominent features in CVD.
Similarly, elevated levels of thrombin, which converts fibrinogen into fibrin, forming blood clots, have been associated with premature rupture of membranes and therefore PTB. Indeed, prothrombin and thrombin have been postulated as markers of PTB.39,40 Moreover, genetic factors affecting coagulation, such as polymorphisms in thrombophilic genes, and the subsequent activation of the fibrinolytic cascade have been linked to both spontaneous PTB and maternal cardiovascular morbidity.41 The generation of thrombin during defective decidual haemostasis not only stimulates uterine contractility but also serves as a mediator of vascular remodelling and endothelial injury, drawing further parallels between the pathogenesis of PTB and CVD.28,42
Genetic and Epigenetic Contributions
Genetic predisposition plays an essential role in determining both the risk for PTB and the subsequent development of CVD. Genome-wide association studies and candidate gene analyses have identified variants in genes encoding for inflammatory cytokines, matrix metalloproteinases, components of the innate immune system and regulators of blood vessel function. For instance, polymorphisms in the genes encoding nitric oxide synthases (NOS2 and NOS3) affect the bioavailability of nitric oxide, a critical vasodilator, and are implicated in both PTB and cardiovascular pathologies due to their role in vascular tone regulation.42,43
Epigenetic modifications, including DNA methylation changes and altered microRNA (miRNA) expression profiles, have been observed in association with PTB and appear to ‘program’ long-term cardiovascular risk. PTB has been linked to notable molecular changes, including the upregulation of miRNAs, such as hsa-miR-150-5p, and the downregulation of others, such as hsa-miR-23b-5p, linked to key signalling pathways essential for pregnancy, such as TGF-β and p53 signalling, underscoring their potential roles in pregnancy complications.44 Furthermore, maternal stress and adverse intrauterine environments can lead to methylation changes in genes critical for the hypothalamic–pituitary–adrenal axis, such as the glucocorticoid receptor gene NR3C1, which in turn may predispose offspring to dysregulated cardiovascular responses and metabolic disorders later in life.45,46 One topic not addressed in this review is the impact of prematurity on the cardiovascular health of the child. Beyond the consequences of early birth itself, fetal reprogramming during a preterm pregnancy, driven by epigenetic modifications, must also be considered as a contributor to long-term cardiovascular risk. Environmental and maternal factors such as stress, nutrition and physiological immaturity can induce DNA methylation, histone modifications and changes in non-coding RNAs, which influence blood pressure regulation, vascular remodelling and endothelial function, predisposing the offspring to hypertension and other cardiovascular disorders later in life.47,48
Table 1 lists the proposed pathophysiological mechanisms underlying PTB, which share common pathways with the mechanisms driving CVD.
Epidemiological Evidence
Multiple observational studies and systematic reviews have consistently demonstrated that women with PTBs are at a higher risk for subsequent cardiovascular events compared with women with TB.15,49,50 The association appears robust across diverse populations and persists after adjustment for pre-pregnancy confounders, suggesting that PTB is not merely a bystander but a marker of specific vascular vulnerability.
Large cohort studies have reported hazard ratios for cardiovascular outcomes ranging from approximately 1.4 to over 2.0, depending on the gestational age at delivery and whether the PTB was spontaneous or medically indicated.49 The risk follows a distinct ‘dose–response’ pattern: the earlier the delivery, the higher the subsequent cardiovascular risk. In one extensive Danish cohort, women who delivered between 32 and 36 weeks had hazard ratios for T2D approaching 1.9, while deliveries before 27 weeks were associated with hazard ratios around 2.1, suggesting a graded association between the degree of prematurity and cardiovascular risk.51 Furthermore, meta-analytic evidence supports these findings, with pooled results indicating that the overall risk of CVD is increased by approximately 43% to over 100% in women with a history of PTB.15 Studies such as those conducted by Tanz et al. have demonstrated that even after extensive adjustments for pre-pregnancy lifestyle factors (diet, smoking, physical activity) and traditional cardiovascular risk factors, the increased risk persists. Notably, very early PTB (<32 weeks) was associated with a doubling of the risk of MI and other cardiovascular events later in life.14
Important large-scale studies published in the last 3–5 years have refined our understanding of these risks, using massive datasets from the UK Biobank and updated Scandinavian registries. These studies provide greater statistical power to analyse specific subtypes of CVD and explore potential genetic confounders. A nationwide Swedish cohort study of more than 2.1 million women found that any PTB was independently associated with a 72% higher risk of ischaemic heart disease in the first decade after delivery. Notably, this excess risk, while decreasing over time, remained significantly elevated even 30–46 years later.52 Complementing these findings, another analysis from the same Swedish cohort reported that PTB markedly increases the mother’s risk of heart failure (HF). Within 10 years postpartum, women who had any PTB had nearly a threefold higher risk of new-onset HF compared with those with full-term deliveries. This HF risk showed a clear gestational age gradient: mothers of extremely preterm infants (<28 weeks) had about a 12.8-fold higher HF risk, those with moderate preterm infants (28–33 weeks) a ~3.7-fold risk, and late preterm (34–36 weeks) about a 2.2-fold risk, all relative to full-term deliveries. Although the absolute incidence of maternal HF was low in early postpartum years, the elevated relative risk persisted decades later (HR ~ 1.5 even 30–40 years after a PTB).53
In addition to Scandinavian registry findings, analyses from the UK Biobank (a contemporary prospective cohort) have highlighted the broader context of female reproductive factors as it relates to cardiovascular health. While UK Biobank data suggest that specific pregnancy complications such as PTB may be underreported in that cohort, related reproductive factors have been linked to cardiovascular outcomes. For example, women who had their first childbirth at a younger age or who had higher parity had a significantly elevated risk of HF later in life. Also, having more than four children was associated with a 24% higher risk of developing HF compared with having one or two children.54 New systematic reviews have consolidated evidence on postpartum HF and coronary artery disease. A 2025 meta-analysis on peripartum cardiomyopathy relapses indicated a 32% risk of recurrence in subsequent pregnancies, often leading to PTB, thereby creating a cycle of cardiovascular compounding risk.55 Additionally, recent data indicate that women with PTB are specifically prone to HF with preserved ejection fraction later in life, likely to be mediated by chronic hypertension and endothelial dysfunction.56 Although some findings do not directly assess PTB, they reinforce the concept that a woman’s childbearing history (including factors often correlated with PTB) can shape her long-term cardiovascular risk profile. Taken together, the epidemiological evidence across diverse populations and study designs indicates that PTB is a powerful independent predictor of maternal CVD.
Clinical studies often adjust their results for covariates such as race and ethnicity, or even exclude participants based on these characteristics when they do not fall into the white or African-American categories.14,57 As a result, very few investigations have specifically examined differences in cardiovascular risk among women of diverse racial and ethnic backgrounds following PTB. Existing evidence, however, points to important disparities. For instance, research conducted in an Asian population reported that PTB was associated with a higher likelihood of subsequent stroke.58 In addition, analyses evaluating race and ethnicity as maternal cardiovascular risk factors for PTB have shown higher adjusted ORs for Hispanic, black, Asian and other ethnic groups compared with white women.59 The limited study of racial and ethnic diversity represents a clear gap in current knowledge, especially given that women from non-white racial and ethnic groups (including black, Asian, Native American, Native Hawaiian and other Pacific Islander populations) have higher rates of PTB.60,61 Supplementary Table 1 lists key clinical studies on CVD risk and PTB.
High-confidence evidence supports a robust association between a history of PTB and later maternal cardiometabolic disease and CVD across diverse study designs, including systematic reviews, meta-analyses and large population registries, with a consistent gestational age ‘dose–response’ gradient (earlier PTB conferring higher relative risk).17,50,51,57–59 The association is most consistently documented for chronic hypertension, T2D, ischaemic heart disease, stroke and HF, and importantly appears to persist for decades after the index pregnancy.4,8,9,62 Although residual confounding cannot be fully excluded, evidence from designs that partially address shared familial and environmental factors (e.g. co-sibling analyses) suggests that confounding alone is unlikely to explain the association.63 Key uncertainties remain regarding the degree to which postpartum emergence of conventional risk factors mediates later events; the generalisability of effect estimates beyond high-income settings and underrepresented racial/ethnic groups; and the extent to which PTB phenotypes should be modelled differently. In particular, while medically indicated PTB often shows stronger associations with cardiovascular outcomes compared to spontaneous PTB, available data also argue against considering spontaneous PTB ‘benign’, supporting the inclusion of PTB history in risk assessment while motivating phenotype-specific refinement.4,63
Evaluation of Inconsistencies and Recent Advances
While the association between PTB and maternal CVD is widely accepted, significant inconsistencies remain in the literature regarding the magnitude of risk, the specific cardiovascular endpoints affected and the role of confounding factors. This section critically evaluates these inconsistencies and integrates recent large-scale data to provide a nuanced understanding of the PTB–CVD association.
Heterogeneity in Preterm Birth Definitions
A major source of inconsistency lies in the definition and sub-classification of PTB. Many older studies aggregate all births <37 weeks into a single ‘preterm’ category, obscuring distinct pathophysiological pathways.
The pathophysiology of spontaneous PTB (often driven by infection or inflammation) differs distinctively from medically indicated PTB (often driven by placental dysfunction, pre-eclampsia, or intrauterine growth restriction). Studies that stratify these phenotypes often find stronger associations between medically indicated PTB and maternal CVD. This is probably because indicated PTB is frequently a downstream consequence of placental vascular pathology (e.g. pre-eclampsia), which shares direct pathophysiological mechanisms with adult atherosclerosis and hypertension (the ‘vascular phenotype’). However, recent data challenge the notion that spontaneous PTB is benign regarding cardiovascular risk; they have shown that women with spontaneous PTB had no improvement in arterial stiffness postpartum compared with term controls, suggesting that the inflammatory pathways inherent in spontaneous labour also produce lasting vascular damage.64
With the degree of prematurity, the ‘dose–response’ relationship is consistent, but the threshold varies. While extreme prematurity (<28 weeks) universally carries high risk, the risk associated with late PTB (34–36 weeks) is more variable across cohorts. Given that late PTB accounts for the majority of PTBs, clarifying this risk is vital. Recent large-scale studies suggest that even late PTB confers a modest but significant risk of hypertension and diabetes, which may accumulate over decades to drive overt CVD.8
Differences in Cardiovascular Endpoints
Inconsistencies also appear in specific CVD endpoints. While coronary heart disease is consistently linked to PTB, data on stroke have been more variable. Some earlier studies showed weak or null associations. However, recent large-scale registry data from Sweden have clarified this, showing robust associations with both ischaemic and haemorrhagic stroke.9,65 The discordance in older studies is likely to have stemmed from insufficient follow-up time, given that stroke typically occurs later in the life course than hypertension or metabolic syndrome. The 2025 analysis confirmed that this risk remains elevated into the sixth and seventh decades of life.63
The phenotype of HF also varies. Recent meta-analyses suggest a strong link, particularly for HF with preserved ejection fraction, which is closely tied to hypertension and endothelial dysfunction (sequelae common in women with a history of placental syndromes).56 Another long-term study further highlighted that in women with existing structural heart disease, PTB serves as a potent marker for accelerated deterioration, emphasising the need for specialised cardio-obstetric monitoring.5
Residual Confounding and Familial Factors
A pervasive challenge in observational research is residual confounding by shared environmental or genetic factors. Does PTB cause CVD, or do they share a common root cause? Low socio-economic status is a potent risk factor for both PTB and CVD.66 While most studies adjust for socio-economic status, it is difficult to fully capture the lifetime impact of social determinants. To address genetic and shared environmental confounding, recent studies have used co-sibling analyses, comparing women with PTBs with their sisters who had term births. They found that the association between PTB and coronary heart disease remained significant (albeit attenuated) in sibling comparisons.67 This suggests that while shared genetics and/or environment play a role, they do not fully explain the association. PTB itself (or the unique pregnancy physiology leading to it) is likely to exert a direct, independent effect on the cardiovascular trajectory. This ‘common soil’ hypothesis is further supported by UK Biobank data showing shared genetic liability between hypertensive disorders of pregnancy and coronary artery disease.
Future research should focus on further elucidating the biological mechanisms that underpin the observed associations. In particular, longitudinal studies using serial measurements of inflammatory markers, endothelial function and metabolic parameters could shed light on the temporal evolution of cardiovascular risk in women following PTB. Randomised controlled trials assessing the efficacy of early postpartum interventions, such as intensive lifestyle modification programmes or pharmacological therapies targeting endothelial dysfunction, may help determine whether the elevated cardiovascular risk in this population can be effectively mitigated.
Given that the majority of studies have been conducted in high-income countries, additional research in geographically and socio-economically diverse populations is needed to draw more generalisable conclusions. Furthermore, it will be important for future studies to explore the differences in cardiovascular outcomes among diverse ethnic and socio-economic groups, given that current data are predominantly derived from populations in developed countries with relatively homogenous demographics. Understanding these nuances could inform tailored risk assessment models and intervention strategies that are more broadly applicable across different populations.
Synthesising the sources of heterogeneity reviewed above, the most secure conclusions are that PTB is associated with increased long-term maternal cardiovascular risk and that risk scales with the degree of prematurity; these patterns are reproducible across outcomes (notably ischaemic heart disease, chronic hypertension, stroke and HF) and across long follow-up horizons.4,9 What remains uncertain is the optimal way to translate this evidence into calibrated prediction models, given persistent challenges in phenotype definition (misclassification of spontaneous versus indicated PTB; incomplete capture of concomitant placental syndromes), residual confounding by social determinants and limited mechanistic–longitudinal biomarker data.68,69 Importantly, current evidence does not support treating all PTB phenotypes as equivalent in cardiovascular risk stratification: medically indicated PTB (often linked to placental vascular dysfunction and hypertensive disorders) appears more consistently associated with later maternal CVD, whereas spontaneous PTB may carry more variable effect sizes but still demonstrates signals of persistent vascular dysfunction.70,71 Accordingly, the most evidence-aligned approach for risk models is to incorporate PTB as a risk-enhancing obstetric history while weighting risk by gestational age; recurrence; and phenotype (and co-occurring placental syndromes when available), rather than applying a uniform ‘PTB yes/no’ modifier.16,72
Clinical Implications and Actionable Recommendations
The robust association between PTB and maternal cardiovascular risk necessitates a paradigm shift in women’s health. The ESC consensus statement on women’s cardiovascular health, published as part of The Lancet Women and Cardiovascular Disease Commission: Reducing the Global Burden by 2030, highlighted several contributing factors, including differences in disease aetiology between women and men, the underrepresentation of women in clinical trials, limited awareness of sex-specific symptoms, and disparities in morbidity and mortality across countries.73 Among the priorities highlighted in the text, in order to close the gender gap in CVD health, this consensus calls for harmonisation of Europe-wide data regarding pregnancy-related CVD and peripartum cardiomyopathy in the EURObservational Research Programme. Given that PTB is associated with elevated long-term cardiovascular risk, obstetric history (particularly a history of PTB) should be integrated into cardiovascular risk assessments for women, thereby enabling earlier identification of those at heightened risk. Furthermore, the 2025 ESC guidelines for the management of CVD and pregnancy and recent American Heart Association (AHA) scientific statements provide a framework for this integration.12,13 On this basis, we propose clear and actionable recommendations with direct relevance for clinical practice and research.
Integrating Obstetric History into Cardiovascular Screening
Obstetric history, specifically the history of PTB (<37 weeks) and its phenotype (spontaneous versus indicated, recurrent versus singular), should be considered a clinically relevant, risk-enhancing obstetric factor for later maternal cardiometabolic and CVD. A history of PTB should be routinely elicited during primary care and cardiology visits. This history should be documented in the electronic health record and may be considered a risk-enhancing factor in guideline-based risk discussions (aligned with AHA/American College of Cardiology guidance). Where feasible, incorporating PTB history (and parity, when relevant) into risk assessment frameworks may improve identification of higher-risk younger women; however, the incremental predictive value and calibration across populations remain incompletely established.
Postpartum Follow-up: The ‘Fourth Trimester’ and Beyond
The postpartum period, especially the 6-week follow-up visit, is a critical window for cardiovascular risk screening and counselling. However, current care models frequently result in suboptimal transitions between obstetric and primary care services. A comprehensive cardiovascular risk assessment in the early postpartum period (e.g. within 3–6 months) should be considered, especially for higher-risk PTB phenotypes (very early, recurrent and/or medically indicated PTB with placental syndromes). At minimum, such an assessment should include:
- blood pressure: target <140/90 mmHg, with tighter control considered for those with end-organ damage or comorbidities, in accordance with the 2025 ESC guidelines; and
- metabolic screening: a full lipid panel and glucose screening (HbA1c or fasting glucose), given consistent associations between PTB history and subsequent metabolic risk, including T2D.
A structured transition of care from obstetrics to primary care and/or cardiology is recommended. Women with PTB, particularly medically indicated PTB and/or PTB accompanied by placental syndromes (e.g. pre-eclampsia and/or fetal growth restriction), should be considered for referral to a maternal heart team or specialised cardio-obstetrics clinic where available. Where such services are not available, periodic cardiovascular risk-factor monitoring in primary care is reasonable, with follow-up intensity tailored to PTB phenotype, gestational age, recurrence and comorbidities; an annual schedule may be considered for higher-risk phenotypes.
Preventive Strategies
Implementation of targeted preventive strategies may help attenuate the progression of CVD in this high-risk population.
- Lifestyle modifications: intensive lifestyle counselling can be initiated in the early postpartum period, as feasible. This includes support for breastfeeding, which has been associated with more favourable maternal cardiometabolic profiles. A heart-healthy diet and regular physical activity are important to mitigate the additive risk of post-pregnancy weight retention.
- Pharmacological interventions: in women with a history of PTB who develop stage 1 hypertension or borderline dyslipidaemia, clinicians may consider earlier initiation of pharmacological therapy within guideline frameworks when overall risk is borderline, treating obstetric history as a risk-enhancing context; decisions should be individualised given the absence of PTB-specific interventional trials.
Future Pregnancies
Women with a history of PTB have an increased risk of recurrence and for CVD complications in subsequent pregnancies. Pre-conception counselling, ideally involving a pregnancy heart team where available, by a pregnancy heart team is recommended to optimise cardiovascular health before a subsequent pregnancy. This aligns with the 2025 ESC guidelines, which emphasise the role of the pregnancy heart team in risk stratification (modified WHO 2.0 classification) and management of women with pre-existing risk factors.
From a public health perspective, these findings underscore the need for increased awareness among both clinicians and patients regarding the long-term cardiovascular risks associated with PTB. Educational initiatives and policy interventions could promote integration of obstetric history into routine cardiovascular risk assessments, potentially improving early detection and intervention rates.
Summary
What is supported with higher confidence (evidence-based):
- PTB is associated with higher long-term maternal cardiometabolic and CVD risk; risk increases with earlier gestational age and recurrence.
- Phenotype matters: medically indicated PTB (especially with placental and/or vascular syndromes) shows more consistent and stronger associations than spontaneous PTB, although spontaneous PTB is not benign.
- Document PTB (gestational age, phenotype, recurrence) and use it as a risk-enhancing context to intensify detection and guideline-based management of blood pressure, glycaemia, lipids, adiposity, smoking.
What remains based mainly on expert opinion/consensus:
- Follow-up schedules and testing intervals should be individualised (phenotype severity, comorbidities, resources).
- Selective referral (cardio-obstetrics and maternal heart team) and pre-conception counselling for higher-risk PTB phenotypes; universal referral is not established.
- No automatic lower drug thresholds solely for PTB history; treat within existing guideline frameworks and overall risk.
Conclusion
Extensive research, including recent large-scale observational studies and meta-analyses, has firmly established that PTB significantly increases a woman’s risk of future CVD, including coronary heart disease, stroke and cardiovascular mortality, beyond what is explained by traditional risk factors. Biological pathways such as inflammation, endothelial dysfunction and placental abnormalities are likely to contribute to this link, suggesting that PTB may expose underlying cardiovascular vulnerabilities. Given the strength of this association, it is crucial for healthcare providers to incorporate a history of PTB into cardiovascular risk assessments and to counsel women accordingly. Although guidelines are beginning to recognise adverse pregnancy outcomes as predictors of cardiovascular risk, further research is needed to refine risk models and develop targeted prevention strategies. Ultimately, integrating obstetric history into cardiovascular care offers an important opportunity to improve long-term health outcomes and reduce disease burden for women who have experienced PTB.