Abstract P1100: Risk of Incident Heart Failure by Gender Identity among US Veterans

Abstract

Background: Disparities in heart failure (HF) are driven in part by social and structural determinants of health. Rates of HF among transgender and gender diverse (TGD) individuals relative to cisgender (cis) peers are not well described. Methods: We used EHR data from the Veterans Healthcare Administration (VHA) to identify veterans with >2 outpatient encounters from 2010-2019. Gender identity was ascertained using natural language processing in combination with gender-affirming hormone therapy (GAHT) and a validated algorithm utilizing ICD codes and VHA data. Among 1,103,923 veterans, 42,157 were classified as TGD. We examined sample characteristics by gender identity and used Cox regression to assess the association of gender identity with incident HF. Results: TGD veterans’ mean age was 46 years (cis females=40; cis males=53). Median follow-up was 9.41 years. There were 107,766 incident HF events (3,078 among TGD veterans). The HF rate among TGD veterans was 8.19 [95% CI: 7.90-8.48] per 1,000 person-years compared to 13.05 [12.97-13.13] and 3.87 [3.76-3.98] among cis male and cis female veterans, respectively. Adjusting for age, race, Hispanic ethnicity, and sexual minority identity, TGD veterans had 1.51 [1.44-1.58] and 0.89 [0.86-0.92] times the risk of HF compared to cis females and cis males, respectively. Results remained statistically significant with adjustment for additional social, clinical, and structural factors ( Table ). When stratified by gender identity, trans feminine veterans (HR [95% CI]: 1.19 [1.07-1.33]) were at higher HF risk than cis females; trans masculine (HR [95% CI]: 0.79 [0.72-0.86]) and trans feminine veterans (HR [95% CI]: 0.80 [0.72-0.89]) were at lower HF risk than cis males. Conclusion: Trans feminine veterans experienced greater HF risk than cis females, while trans feminine and trans masculine veterans’ HF risk was less than cis males. Future studies should consider the underlying mechanisms of these associations, HF subtypes (HFrEF and HFpEF), and the role of GAHT on HF risk.