Abstract 14353: Feminizing Hormone Therapy and Subclinical Indicators of CVD Risk in Transgender Women With HIV

Abstract

Introduction: Transgender women (TW) are at higher risk of HIV infection compared to cisgender groups and HIV is associated with accelerated cardiovascular disease (CVD) complications. A high proportion of TW use feminizing hormone therapy (FHT), particularly estrogen. However, there is a scarcity of data about the cardiovascular impact of FHT in TW with HIV (TWH). Subclinical indicators of CVD risk, arterial stiffness and endothelial progenitor cells colony forming units (EPC-CFUs), were examined in TWH with and without FHT. Hypothesis: Estrogen use in FHT reduces arterial stiffness and induces EPC proliferation. Methods: This pilot included adults 20-60 years old, identifying as TW, with a documented HIV-1 diagnosis, stable ART ≥ 6 months, and without history of CVD. Sociodemographic questionnaire was completed prior to an in-person blood collection and applanation tonometry assessment. Groups were stratified by estrogen levels (normal: 1-82pg/ml vs high: >82pg/ml) and relationships with EPC-CFUs and arterial stiffness were examined using t-test and Pearson’s correlation. Results: Median age was 42 yrs. (IQR 34-52) with mean glucose 105.70 mg/dl (± 58.07), triglycerides 138.52 mg/dl (± 69.61), LDL 82.38 mg/dl (± 35.01), and CRP 3.45 mg/L (±3.57). TW with high (n=5) and normal (n=12) estrogen levels had similar values in EPC-CFUs counts (p=0.99), central augmentation index (cAIx; p=0.27), carotid to radial pulse wave velocity (CR-PWV; p=0.20), and carotid to femoral PWV (CF-PWV; p=0.87). A positive trend appeared in log-transformed estradiol across cAIx (r=0.32, p=0.21); negative trends in CR-PWV (r=-0.11, p=0.70) and CF-PWV (r=-0.19, p=0.48), and no relationship with EPC-CFUs (r=0.05, p=0.86). There were non-significant negative weak trends between EPC-CFUs and cAIx (r=-0.32, p=0.21), CR-PWV (r=-0.2, p=0.48), and CF-PWV (r =-0.29, p=0.27). Conclusions: An inverse correlation between EPC-CFUs and arterial stiffness measurements was observed. Considering these test modalities have a strong correlative potential with CVD risk, FHT does not appear to confer higher CVD risk through these mechanisms. Further research to understand the mechanisms underlying HIV related CVD pathophysiology is critically needed especially in TWH.