Adverse pregnancy outcomes tied to increased maternal risk of subarachnoid haemorrhage

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Adverse pregnancy outcomes tied to increased maternal risk of subarachnoid haemorrhage

Women with a history of adverse pregnancy outcomes are at heightened risk of subarachnoid haemorrhage, as suggested in a study.

Researchers looked at 1,785,088 primiparous women (mean age 28.2 years) in the Swedish Medical Birth Register. They reviewed the women’s medical records to determine the history of adverse pregnancy disorders including hypertensive disorders of pregnancy, gestational diabetes, placental abruption, preterm birth, abnormal foetal growth, and stillbirth.

The primary outcome was subarachnoid haemorrhage, while secondary outcomes included aortic aneurysm rupture or dissection and spontaneous coronary artery dissection.

Over 50 years of follow-up, 759,722 women (42.6 percent) experienced at least one adverse pregnancy outcome, with the most common being abnormal foetal growth. There were 5,751 events of subarachnoid haemorrhage documented.

Women with vs without history of adverse pregnancy outcomes had elevated risk of subarachnoid haemorrhage. The risk increase was especially pronounced after placental abruption (hazard ratio [HR], 1.62, 95 percent confidence interval [CI], 1.29–2.04), hypertensive disorders of pregnancy (HR, 1.58, 95 percent CI, 1.41–1.77), gestational diabetes (HR, 1.40, 95 percent CI, 1.04–1.90), preterm birth (HR, 1.35, 95 percent CI, 1.24–1.47), and small for gestational age (HR, 1.34, 95 percent CI, 1.26–1.43).

Consistent associations were observed in sibship analyses.

Notably, the increase in the risk of subarachnoid haemorrhage was greatest in the first years after delivery and attenuated over time.

Increased risks of aortic aneurysm rupture or dissection were also seen in women with a history of hypertensive disorders of pregnancy, preterm birth, and severely large for gestational age (HR range, 1.43–1.66). No consistent associations were observed with spontaneous coronary artery dissection.

Stroke 2026;doi:10.1161/STROKEAHA.126.055347