Cardiovascular disease is the leading cause of mortality among breast cancer survivors.
Anthracyclines and trastuzumab have been associated with an increased risk of cardiotoxicity,
requiring close follow-up for signs of clinical heart failure or asymptomatic left
ventricular systolic dysfunction. Whether neurohormonal antagonism with angiotensin-converting
enzyme inhibitor (ACE-I), angiotensin receptor blockers (ARBs), or β-blockers can
prevent the development of chemotherapy-induced cardiomyopathy in this population
remains unknown. We studied 459 women who were diagnosed with breast cancer at our
medical center from January 2014 to December 2021 and evaluated baseline characteristics,
oncologic treatment, and outcomes. The primary end point was the development of cardiotoxicity,
defined as symptomatic decline in ejection fraction of ≥5% below 55% or an asymptomatic
decline of ≥10% after treatment with chemotherapy. Patients who were exposed to neurohormonal
antagonists were more likely to have hypertension, hyperlipidemia, and diabetes. There
was an increased risk of cardiotoxicity noted for patients who were older (hazard
ratio [HR] 1.04, 95% confidence interval [CI] 1.01 to 1.1), smokers within the past
10 years (HR 2.54, 95% CI 1.41 to 4.6), or who received a combination of both trastuzumab
and anthracycline therapy (HR 2.52, 95% CI 1.01 to 6.3). Over a median follow-up of
12 months, there were no significant protective benefits noted for patients who were
taking ACE-I/ARBs (HR 0.49, 95% CI 0.17 to 1.4), β-blockers (HR 0.50, 95% CI 0.16
to 1.6), or both (HR 1.30, 95% CI 0.44 to 3.9). In conclusion, previous use of ACE-I/ARBs
and β-blockers, separately or in combination, was not associated with a reduction
in the development of cardiotoxicity in patients receiving anthracycline or trastuzumab
therapies. Older age, smoking, and combination chemotherapy were found to be associated
with an increased risk.
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Article info
Publication history
Published online: December 03, 2022
Received in revised form:
October 4,
2022
Received:
July 6,
2022
Footnotes
Funding: None.
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