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

ABSTRACT:

Objective

Treatment with anthracyclines may cause cardiac dysfunction, but the sequence of anthracycline-induced heart lesions has been incompletely characterized. NADPH oxidase, a key mediator of oxidative cardiac damage and remodeling, modulates anthracycline clinical cardiotoxicity. Our aim was to determine which cardiac histological lesions are specifically induced by anthracycline treatment and to investigate the role of NADPH functional genetic polymorphisms in their development.

Patients and methods

Using a retrospective case-control design, we evaluated cardiac histological lesions and NADPH genotype (polymorphisms rs1883112, rs4673, and rs13058338) in 97 consecutive decedents with a cancer diagnosis (48 treated with anthracyclines).

Results

Myocytolysis (60%)

SUBMITTER: Cascales A 

PROVIDER: S-EPMC3639532 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature