STEMI, Revascularization, and Peak Troponin by Adverse Pregnancy Outcomes in Women With Myocardial Infarction.

Background

Women with a history of adverse pregnancy outcomes have a higher risk of coronary heart disease. Emerging evidence suggests that women with a history of preeclampsia have a different pattern of overall coronary atherosclerosis and that they at the time of myocardial infarction (MI) more frequently present with ST-segment elevation MI (STEMI) compared to women with no such history.

Objectives

The purpose of this study was to determine whether among women with MI, those with a history of adverse pregnancy outcomes are more likely to present with STEMI or other clinical characteristics indicating a more severe myocardial injury.

Methods

The study sample consisted of 8,320 women aged ≤65 years with first MI in Sweden 2007 to 2022. Regression models were used to estimate the association between adverse pregnancy outcomes (hypertensive disorders of pregnancy [non-preeclamptic hypertension and preeclampsia], small for gestational age [SGA] infant, and preterm delivery) and STEMI, invasive revascularization, and high troponin, while considering known predictors of coronary heart disease.

Results

In total, 3,128 (38%) of women suffered STEMI. The adjusted OR of presenting with STEMI were higher in women with a history of preterm preeclampsia (OR: 1.40; 95% CI: 1.05-1.88), or an SGA infant (OR: 1.30; 95% CI: 1.13-1.50) compared to women with no such history, as well as for in-hospital revascularization. Stratified by infarct type, troponin levels did not differ by adverse pregnancy outcome history.

Conclusions

Among women with a first MI, a history of preterm preeclampsia or SGA infant were associated with STEMI and invasive revascularization.

Informations de copyright

© 2024 The Authors.

Déclaration de conflit d'intérêts

This work was supported by grants awarded to Dr Timpka from the 10.13039/501100004359Swedish Research Council (2019-02082), The 10.13039/501100003793Swedish Heart-Lung Foundation (20180312), Public research support via the Faculty of Medicine at 10.13039/501100003252Lund University (ALF: YF-ALF, ALF project), The 10.13039/501100007687Swedish Society of Medicine (SLS-885331), The Jeansson Foundations, Stockholm, Sweden, and Åke Wiberg Foundation, Stockholm, Sweden. Dr Gonҫalves received grants from the 10.13039/501100004359Swedish Research Council, the Swedish Heart and Lung Foundation, 10.13039/501100011077Skåne University Hospital funds and Lund University Diabetes Center (10.13039/501100004359Swedish Research Council - Strategic Research Area Exodiab Dnr 2009-1039, Linnaeus grant Dnr 349-2006-23 and the 10.13039/501100001729Swedish Foundation for Strategic Research Dnr IRC15-006). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.