Pregnancy imposes substantial haemodynamic and metabolic demands that act as a natural physiological stress test for the maternal cardiovascular system. When pregnancy is complicated by adverse pregnancy outcomes (APOs), latent susceptibility to future cardiovascular disease (CVD) can be unmasked. This Review shifts focus from cardiovascular events occurring during pregnancy to the long-term cardiovascular implications of APOs after delivery, emphasising the opportunity to identify women at elevated lifelong risk earlier in the life course.
Key APO phenotypes associated with increased long-term cardiovascular risk are hypertensive disorders of pregnancy (HDP), gestational diabetes, and preterm birth (delivery before 37 weeks' gestation). Epidemiological data demonstrate that women who experience these complications face substantially higher long-term risks of cardiovascular morbidity and mortality compared with those without APOs. The Review synthesises evidence across these major phenotypes, noting that APO history identifies a population in whom cardiovascular risk trajectories are accelerated and disease may present earlier than in women without APOs.
The excess cardiovascular risk observed after APOs likely reflects multiple overlapping pathways. First, pre-existing cardiometabolic and genetic susceptibility may predispose some women to both APOs and later CVD. Second, the haemodynamic and metabolic stressors of pregnancy can accelerate trajectories of traditional risk factors (for example, blood pressure dysregulation, impaired glucose tolerance, dyslipidaemia) and produce relative impairment in endothelial and microvascular function that persists after delivery. These combined effects can promote earlier onset of clinical cardiovascular disease.
Emerging evidence links maternal APO history with adverse cardiometabolic trajectories in offspring. The Review summarises epidemiological findings supporting associations between parental APOs and offspring cardiovascular risk markers and disease indicators in early adulthood. These data suggest potential intergenerational transmission of cardiometabolic risk, although detailed mechanistic and long-term outcome data remain an area for further research.
The authors summarise existing guidelines and consensus-informed recommendations for short-term and long-term follow-up after APOs. These recommendations aim to recognise APOs as actionable risk indicators and to guide surveillance and management of cardiometabolic risk factors after pregnancy. Specifics of guideline content and timing were described in the source but vary by organisation and clinical context. The Review highlights the need for consistent implementation and for care pathways that bridge obstetric and primary/cardiovascular care.
Practical approaches to incorporating APO history into cardiovascular risk assessment are proposed. Positioning APOs as early, sex-specific indicators of increased cardiovascular risk creates a window of opportunity to shift prevention upstream. The Review underlines the importance of recognising APOs within lifelong risk stratification and of linking obstetric history to guideline-directed prevention strategies across the female life course. Limitations of current risk-stratification tools to fully capture APO-related risk are emphasised.
Several important knowledge gaps are identified. Optimal follow-up models after APOs are uncertain: the best timing, responsible clinicians, and modalities of surveillance remain to be defined. Existing cardiovascular risk tools have limitations in accounting for APO history, and there is an absence of clinical trials testing APO-specific prevention strategies. The authors call for mechanistic research to clarify causal pathways, implementation studies to define effective follow-up models, and intervention trials to test targeted prevention in women with APO histories.
The Review concludes that recognising adverse pregnancy outcomes as early, sex-specific markers of cardiovascular risk presents an opportunity to intervene earlier in the disease process and improve long-term outcomes for women. By synthesising epidemiological links, outlining plausible mechanisms, summarising guideline recommendations, and highlighting implementation and research priorities, the authors advocate for integrating APO history into cardiovascular risk assessment and preventive care. They recommend advancing mechanistic and implementation research to close current evidence gaps and to develop APO-specific prevention trials.