Key result
Aromatase inhibitor therapy in postmenopausal breast cancer survivors was associated with a significant decline in endothelial function at six months, with the median EndoPAT ratio decreasing from 2.18 to 1.12.
Why the study?
Studies show mixed results on the impact of aromatase inhibitors on cardiovascular events, creating a need to understand their impact on blood vessels and cardiovascular risk.
Does aromatase inhibitor therapy cause endothelial dysfunction in postmenopausal breast cancer survivors?
Observational (n=14)
No
Does aromatase inhibitor therapy cause endothelial dysfunction in postmenopausal breast cancer survivors?
Effect estimate: Median change -0.16
Absolute Event Rate: 1.12% vs 2.18%
p-value: p=0.045
Aromatase inhibitor therapy in postmenopausal breast cancer survivors is associated with early development of endothelial dysfunction at 6 months, a potential precursor to adverse cardiovascular events.
Endothelial decline may warrant closer CV surveillance in breast cancer survivors; hypothesis-generating for aromatase inhibitor cardiotoxicity.
Background: Aromatase inhibitors (AIs) are recommended as adjuvant treatment for estrogen-receptor positive breast carcinoma in postmenopausal women. Studies demonstrate mixed results as to the impact of AIs on cardiovascular (CV) events and overall survival. With the increasing number of pre- and postmenopausal women on AIs for five to ten years, understanding the long-term impact of AIs on blood vessels and CV risk in cancer survivors is vital. Methods: A single arm longitudinal study of 14 postmenopausal women with ER+ breast cancer prescribed adjuvant AIs at the University of Minnesota. Subjects with a history of tobacco use, hypertension, or hyperlipidemia were excluded. Participants underwent routine labs, blood pressure assessments, and vascular testing at baseline (prior to starting AIs) and at six months. Vascular assessment was performed using the EndoPAT 2000 and HDI/PulseWave CR-2000 Cardiovascular Pro ling System and pulse contour analysis on two occasions as previously described. Vascular measurements were conducted by one trained vascular technician. Assessments were performed in triplicate, and the mean indices were used for analyses. All subjects were on an AI at the follow-up visit. The protocol was approved by the UMN Institutional Review Board and all participants were provided written informed consent. Baseline and follow-up characteristics were compared using Wilcoxon signed-rank tests. Analyses were performed using R version 3.6.1 (R Foundation for Statistical Computing, Vienna, Austria). Results: and change in estradiol level (p=0.91). There were no statistically significant changes in small or large arterial elasticity. Conclusion: Endovascular dysfunction is an early sign for atherosclerosis and vascular impairment. This study suggests that postmenopausal breast cancer survivors on aromatase inhibitor therapy develop endothelial dysfunction as early as six months which is a predictor of adverse CV disease. We hypothesize that long-term use of AIs can lead to persistent endothelial dysfunction. It is unclear if these changes are reversible once AI use is discontinued and further investigation is necessary.
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Shaaban et al. (2023) conducted an observational in Estrogen-receptor positive breast cancer (n=14). Aromatase inhibitors vs. Baseline (pre-treatment) was evaluated on EndoPAT ratio (endothelial function) (Median change -0.16, p=0.045). Aromatase inhibitor therapy in postmenopausal breast cancer survivors was associated with a significant decline in endothelial function at six months, with the median EndoPAT ratio decreasing from 2.18 to 1.12.
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