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A Yu Filatova1, M V Vitsenya, A V Potekhina

  • 1FSBO National Medical research center of cardiology of the Ministry of healthcare of the Russian Federation. fake@neicon.ru.

Kardiologiia
|February 2, 2019
PubMed
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Cardiovascular toxicity is a concern in breast cancer treatment. Atherosclerosis progression, linked to T-lymphocyte activation and elevated lipoprotein(a), occurred in 60% of patients, with age and radiation therapy as risk factors.

Area of Science:

  • Oncology
  • Cardiology
  • Immunology

Background:

  • Cardiovascular toxicity is a significant clinical oncology problem.
  • Atherosclerosis progression is observed in cancer patients undergoing chemotherapy.
  • Evaluating vascular changes during anticancer therapy is crucial.

Purpose of the Study:

  • To assess vascular wall characteristics in breast cancer patients during anticancer therapy.
  • To identify predictors of atherosclerosis progression in brachiocephalic arteries.
  • To correlate vascular changes with immune and lipid parameters.

Main Methods:

  • Studied 43 breast cancer patients (II-III stage, HER2+) undergoing neoadjuvant therapy.
  • Assessed vascular stiffness (PWVcf, PWVsa), central pressure, CIMT, and brachiocephalic artery stenosis.

Related Experiment Videos

  • Measured lipid profile, lipoprotein(a), and autoantibodies before and during therapy.

    • Main Results:

    • Breast cancer patients showed increased vascular stiffness compared to healthy women.
    • T-lymphocyte activation correlated with increased vascular stiffness.
    • Atherosclerosis progression (60%) and CIMT increase (51%) were observed.
    • Elevated lipoprotein(a) (>12.8 mg/dl), age (>48 years), and radiation therapy were associated with progression.

    Conclusions:

    • Increased vascular stiffness in breast cancer patients is linked to T-lymphocyte activation.
    • Lipoprotein(a) levels, age, and radiation therapy are significant risk factors for atherosclerosis progression.
    • Further research is needed to understand the role of lipoprotein(a) in atherosclerosis progression.