Oral Abstract
Fabian Muehlberg, MD
Professor of Cardiology & Deputy Head of Department
Charité Berlin / HELIOS, Germany
Fabian Muehlberg, MD
Professor of Cardiology & Deputy Head of Department
Charité Berlin / HELIOS, Germany
Jonathan Gavrysh, MD
Clinical Scientist
Charité/Helios Berlin-Buch, Germany
Markus Kornfeld
HELIOS Hospital Berlin-Buch, Germany
Christine Mau, MD
Obstrectrics & Gynaecology Attending
Helios Hospital Berlin-Buch, Germany
Michael Untch, MD
Head of Obstrectrics & Gynaecology
Helios Hospital Berlin-Buch, Germany
Jeanette Schulz-Menger, MD
Head Working Group Cardiac MRI
Charité/ University Medicine Berlin and Helios, Germany
Anti-HER2 therapy has greatly improved the long-term prognosis of patients with HER2-positive breast cancer, however, regularly induces therapy-induced cardiomyopathy. We evaluated if early changes in myocardial tissue characteristics may predict subsequent Anti-HER2-related cardiomyopathy.
Methods:
Patients with HER2-positive breast cancer and planned dual Anti-HER2 therapy with trastuzumab/pertuzumab were included. All patients received 240mg/m2 doxorubicin therapy before Anti-HER2 therapy. Hence, four cardiac MRI (CMR) scans were performed – before anthracycline therapy, before start of trastuzumab/pertuzumab, after the first dose and after four doses of trastuzumab/pertuzumab. Therapy-induced cardiomyopathy was defined as absolute drop of ≥10% of left ventricular ejection fraction (LVEF) and below 55%. CMR was performed on 1.5T AvantoFit® (SIEMENS Healthineers®, Erlangen, Germany). CMR protocol included cine-SSFP sequences (LAX/SAX package), midventricular native and post-contrast T1 mapping (MOLLI), motion-corrected T2 mapping and late gadolinium enhancement using a segmented PSIR sequence (7mm slice thickness/0mm gap SAX). Strain analysis was performed on SSFP-cine images using 4-chamber-view, 3-chamber-view, and 2-chamber-view. Individuals received 0.2mmol/kg gadoteridol contrast intravenously. All post-processing was done with CVI42® (Circle cardiovascular imaging, Calgary, Canada).
Results:
Thirty patients were initially included; four patients were excluded due to early disease progress and therapy switch (n=2) or patient wish (n=2). Patient characteristics are displayed in table 1.
Three patients developed anthracycline-associated cardiomyopathy (aCMP). Of the remaining 23 patients, n=7 patients developed trastuzumab/pertuzumab-related cardiomyopathy (tCMP) after four doses of trastuzumab/pertuzumab (LVEF before therapy 56.7±10.6% vs. 45.5 ±8.6% after four doses, p< 0.01) (Figure 1).
In these tCMP individuals, T2 mapping showed an increase of 4.4±1.7ms after the first dose of trastuzumab/pertuzumab (49.6±1.7ms vs. 54.0±3.7ms, p=0.028), which was not detectable in patients without subsequent cardiomyopathy (51.7±3.9ms vs. 51.6±3.3ms, p >0.05) (Figure 1).
Native T1 times and extracellular volume did not change significantly in any group or time point (Figure 2). No new late gadolinium enhancement was detected in any individual.
Strain analysis showed decreased global longitudinal strain (GLS) in patients with tCMP (-14.8±3.3% before therapy vs. 13.1±1.6% after four doses), while patients without tCMP showed no change in GLS. (Figure 3)
Conclusion:
Early myocardial edema assessed by T2 mapping after the first dose of Anti-HER therapy may predict subsequent development of cardiomyopathy in breast cancer patients with sequential anthracycline and dual Anti-HER2 therapy with trastuzumab/pertuzumab.
Figure 1 - LVEF and T2 development
SCMR2025_HER2_Figure1.pdf
Figure 2 - Tissue characterization
SCMR2025_HER2_Figure2.pdf
Figure 3 - Strain analysis
SCMR2025_HER2_Figure3.pdf
