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Association of anthracycline-related cardiac histological lesions with NADPH oxidase functional polymorphisms

Almudena Cascales1, Francisco Pastor-Quirante, Beatriz Sánchez-Vega

  • 1Centro Regional de Hemodonación, Murcia, Spain.

The Oncologist
|April 12, 2013
PubMed
Abstract

Insights

Anthracyclines cause heart lesions like fibrosis. Specific NADPH gene variants influence these cardiac changes, potentially aiding personalized cardiotoxicity prevention strategies.

Area of Science:

  • Cardiology
  • Oncology
  • Genetics

Background:

  • Anthracycline chemotherapy can lead to cardiac dysfunction.
  • The specific sequence of heart lesions induced by anthracyclines is not fully understood.
  • NADPH oxidase plays a role in anthracycline-induced cardiotoxicity.

Purpose of the Study:

  • To identify specific cardiac histological lesions caused by anthracycline treatment.
  • To investigate the role of NADPH oxidase genetic polymorphisms in the development of these lesions.

Main Methods:

  • Retrospective case-control study of 97 cancer patients (48 treated with anthracyclines).
  • Evaluation of cardiac histological lesions (myocytolysis, necrosis, fibrosis).
  • Analysis of NADPH oxidase gene polymorphisms (rs1883112, rs4673, rs13058338).

Main Results:

  • Anthracycline treatment was associated with myocytolysis, patched myocardial necrosis, and fibrosis.
  • NADPH polymorphism rs4673 showed a protective effect against focal myocardial necrosis.
  • NADPH polymorphism rs1883112 was strongly associated with cardiac fibrosis.

Conclusions:

  • Anthracyclines induce cardiac remodeling, notably interstitial or patched fibrosis.
  • NADPH polymorphisms rs1883112 and rs4673 contribute to anthracycline-related heart lesions.
  • These findings may enable personalized strategies for preventing anthracycline cardiotoxicity.

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