Beyond ejection fraction: cardiac magnetic resonance imaging in anthracycline cardiotoxicity

TL;DR

This paper reviews how cardiac MRI can detect early heart damage caused by cancer drugs called anthracyclines, offering better monitoring than traditional methods.

Contribution

The study systematically evaluates the role of cardiac MRI in detecting early and late cardiotoxic effects of anthracyclines.

Findings

CMR detects early declines in left ventricular ejection fraction before echocardiography can detect changes.

Tissue mapping techniques reveal myocardial injury through increased T1, T2, and extracellular volume.

Persistent strain and ECV abnormalities in long-term survivors highlight lasting cardiotoxic effects.

Abstract

Anthracyclines are a cornerstone of cancer therapy, yet they carry a significant risk of cardiotoxicity, which may present as subclinical myocardial injury or overt heart failure. Timely detection is essential to prevent irreversible cardiac dysfunction and safeguard long-term quality of life. Cardiac magnetic resonance (CMR) imaging—capable of quantifying myocardial structure, function, and tissue characteristics—has emerged as a leading modality in this context. This systematic review evaluates the role of CMR in detecting both early and late cardiotoxic changes after anthracycline exposure.

We conducted a systematic search in accordance with PRISMA 2020 guidelines, searching PubMed, Embase, Scopus and Web of Science for studies involving CMR assessment in patients treated with anthracyclines. We extracted data on changes in functional parameters, volumetric indices, strain measurements, and tissue characterization before, during, and after anthracycline therapy in patients receiving active chemotherapy, and differences of these parameters compare to healthy adults or their pretreatment CMR scan in long term cancer survivors.

Across the 26 eligible studies, CMR consistently identified early declines in left ventricular ejection fraction, often before changes were detectable on echocardiography. More sensitive markers, including increases in the left ventricular end-systolic volume and alterations in strain parameters, provided early signs of subclinical dysfunction. Tissue mapping techniques revealed significant increases in native T1, T2, and extracellular volume (ECV), correlating with diffuse myocardial injury, even in the absence of late gadolinium enhancement. In long-term survivors, persistent abnormalities in strain and ECV were observed, highlighting the enduring nature of anthracycline induced cardiotoxicity. Right ventricular and left atrial remodeling, while less frequently assessed, emerged as clinically relevant and prognostically significant.

CMR is a promising noninvasive tool that enables early detection and monitoring of anthracycline-induced cardiotoxicity, aiding risk stratification and timely cardioprotective interventions in cancer patients.

The online version contains supplementary material available at 10.1186/s12880-025-02027-y.

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