Gender-affirming hormone therapy: effects on cardiovascular risk and vascular function

Area of Science:

• Cardiovascular Science
• Endocrinology
• Transgender Health

Background:

• Gender-affirming hormone therapy (GAHT) is crucial for aligning secondary sexual characteristics with affirmed gender in individuals with gender identity dysphoria.
• Understanding GAHT's vascular effects is essential for managing long-term health in transgender populations.
• The vasculature's response to GAHT requires detailed investigation due to potential cardiovascular implications.

Purpose of the Study:

• To systematically review existing literature on the mechanisms of GAHT's effects on the vasculature.
• To explore how GAHT influences cardiovascular disease (CVD) risk profiles in transgender individuals.

Main Methods:

• A comprehensive literature search was conducted across major databases (PubMed, Embase, Scopus, Lilacs) using keywords related to GAHT, CVD risk, and transgender health.
• Studies were screened by two independent reviewers, requiring comparison with cohorts either before GAHT, on GAHT, or cisgender populations.
• Quality assessment of included studies was performed using relevant Critical Skills Appraisal Programme (CASP) checklists.

Main Results:

• Out of 2,564 studies, 69 met inclusion criteria, revealing varied vascular effects of GAHT.
• Transgender women showed beneficial CVD risk profiles, including reduced hemoglobin, pro-inflammatory markers, and atheroprotective lipid changes.
• Transgender men exhibited negative CVD risk changes, such as atherogenic lipid profiles, increased hemoglobin, and heightened arterial stiffness and inflammation.

Conclusions:

• Current research on non-traditional CVD risk measures in transgender populations is limited.
• Heterogeneous study designs, follow-up loss, small sample sizes, and lack of diversity necessitate cautious interpretation of findings.
• Further research is imperative to clarify the mechanisms of increased CVD risk in transgender individuals and GAHT's role as a potential contributing factor.