Cardiovascular Impacts of Maternal Hypertensive Disorders

Maternal hypertensive disorders—including chronic hypertension, gestational hypertension and preeclampsia—are among the most common complications of pregnancy worldwide. Beyond immediate obstetric risks such as placental insufficiency, foetal growth restriction and preterm birth, these conditions programme long-term cardiovascular health in both mother and offspring. In affected mothers, endothelial activation, oxidative stress and dysregulation of the renin-angiotensin-aldosterone system accelerate vascular dysfunction and heighten the risk of future hypertension, ischaemic heart disease and stroke. In the offspring, in utero exposure to elevated maternal blood pressure and antiangiogenic factors alters cardiac morphology, promotes arterial stiffening and primes the endothelium towards a proinflammatory state. These changes manifest during childhood and adolescence as higher resting blood pressure, impaired vasodilatory responses and subtle concentric remodelling of the left ventricle. Epigenetic modifications—including altered DNA methylation and microRNA profiles—further embed susceptibility to atherosclerosis and metabolic dysregulation. Recognising these intergenerational effects underlines the need for early screening, targeted prevention in women of childbearing age and long-term cardiovascular surveillance of exposed children.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Cardiovascular Impacts of Maternal Hypertensive Disorders publication trend

The graph below shows the total number of articles in cardiovascular impacts of maternal hypertensive disorders across all publications each year (not limited to Nature Index journals).

Technical terms

Preeclampsia: New-onset hypertension after 20 weeks’ gestation with proteinuria or organ dysfunction.

Gestational hypertension: Elevated blood pressure first detected after 20 weeks’ gestation without proteinuria or end-organ injury.

Arterial stiffness: Reduced elasticity of arterial walls, measured by pulse wave velocity, associated with increased cardiac afterload.

Endothelial dysfunction: Impaired endothelium-dependent vasodilation due to disrupted nitric oxide signalling and heightened inflammatory responses.

Vasculogenic capacity: The ability of endothelial progenitor cells to proliferate and form new microvessels, reflecting vascular repair potential.

References

1. Blood pressure, arterial stiffness, and cardiovascular risk profiles in 8–12-year-old children following preeclampsia (FINNCARE-study). Journal of Hypertension (2023).
2. The Molecular Basis of the Augmented Cardiovascular Risk in Offspring of Mothers with Hypertensive Disorders of Pregnancy. International Journal of Molecular Sciences (2024).
3. Maternal hypertensive disorder of pregnancy and offspring early-onset cardiovascular disease in childhood, adolescence, and young adulthood: A national population-based cohort study. PLOS Medicine (2021).
4. Hypertensive Disorders of Pregnancy and Offspring Cardiac Structure and Function in Adolescence. Journal of the American Heart Association (2016).