Revisiting October’s Insights: “Cardiovascular health and cardiometabolic risk in women”
The session provided a comprehensive exploration of the complexities surrounding cardiovascular health and cardiometabolic risk factors specifically in women. It emphasized the importance of a detailed assessment and stratification process to identify various risk factors, including those unique to or more prevalent in women. The discussion notably highlighted reproductive risk factors such as early menarche, polycystic ovary syndrome (PCOS), infertility, adverse pregnancy outcomes, and menopause, underscoring their significant impact on women’s cardiovascular health.
A critical part of the session was dedicated to addressing the disparities in cardiovascular care experienced by women. The dialogue stressed the urgent need for gender equality in healthcare provision and access, spotlighting the systemic barriers that contribute to these disparities. The session called for an integrated approach to healthcare that acknowledges and addresses the unique cardiovascular needs of women, promoting more equitable healthcare outcomes.
The session served as a crucial platform for advancing understanding and awareness of the unique cardiovascular and cardiometabolic challenges faced by women. It advocated for a more inclusive, equitable healthcare system that recognizes and addresses gender-specific health needs, aiming to improve cardiovascular health outcomes for women globally.
Erin D. Michos: So what’s the chicken versus the egg? Well, one of the biggest risk factors for an adverse pregnancy outcome is starting pregnancy in poor cardiometabolic health. This is why it’s so important to optimize pre-pregnancy cardiometabolic health, because this can clinically manifest these APOs, as pregnancy is nature’s free stress test.
But it’s also thought that these adverse pregnancy outcomes may contribute to future cardiovascular risk in a causal fashion. For example, in the setting of preeclampsia – the placenta is ischemic from adverse spiral artery remodeling. This sets off a cascade of hormonal changes, increased sFlt-1, increased sensitivity to Angiotensin II, that can lead to endothelial damage and future cardiovascular risk, perhaps in a causal fashion.
