Cardiac structural and hemodynamic changes following cancer therapy in patients with hypertrophic cardiomyopathy

Introduction

Cardiotoxicity of cancer therapy is increasingly recognized as a critical determinant of long-term clinical outcome. However, evidence on cardiac structural and hemodynamic effects of oncological treatment in patients with hypertrophic cardiomyopathy (HCM) remains scarce.

Purpose

The aim of our study was to evaluate myocardial and functional changes after cancer treatment in patients with HCM and to assess treatment tolerability.

Methods

We retrospectively analyzed consecutive patients with HCM who underwent oncological treatment between January 2000 and December 2024 at our institution. All patients had a baseline echocardiogram performed within 1 year prior to initiation of cancer therapy and at least one post-treatment echocardiogram up to maximum of 40 months out from start of cancer therapy.

Results

A total of 115 patients were included, of which 80 (69.6%) underwent oncological surgery, 14 (12.2%) chest radiation therapy, 29 (25.2%) chemotherapy, 24 (20.9%) hormonal therapy, and 18 (15.7%) immunotherapy. The median age at HCM and cancer diagnosis was 63.0 (57.3–69.9) and 68.6 (60.6–75.2) years, respectively. Obstructive HCM was present in 69 patients (60%). Prior to cancer therapy, 2 (1.7%) of these patients had undergone heart transplantation, 3 (2.6%) alcohol septal ablation, and 33 (28.7%) septal myectomy.

Following treatment, 5 (4.3%) patients developed new onset left ventricular (LV) systolic dysfunction (defined as LV ejection fraction (EF) <50% or ≥5% decline if baseline LVEF <50%), and 2 (1.7%) additional patients exhibited a relative global longitudinal strain (GLS) reduction of ≥15%. No patient developed clinical heart failure or discontinued cancer therapy due to cardiovascular complications.

The median echocardiographic follow-up interval was 16.1 (10.8–22.9) months. Neither in the overall cohort, nor in the subcohorts of patients undergoing surgery, chest radiation, hormonal therapy, or immunotherapy significant changes were observed in LVEF, GLS, ventricular septal or posterior wall thickness, or LVOT gradients.

Among chemotherapy-treated patients, those who received platinum-containing combination chemotherapy demonstrated significant increases in LVOT gradient (baseline 5.8 (5.0-42.0) vs. post-treatment 31.0 (4.8-74.0), p=0.031, n=7), while LVEF remained preserved. In contrast, patients receiving non-platinum-containing chemotherapy showed a significant reduction in LVOT gradient (baseline 8.4 (4.0-37.5) vs. post-treatment 6.3 (4.0-25.8), p=0.007, n=20) and posterior wall thickness (baseline 11.38 ± 2.16 vs. post-treatment 10.39 ± 2.71, p=0.040, n=16), without a significant change in septal thickness.

Conclusions

Patients with hypertrophic cardiomyopathy generally demonstrate good tolerance to oncological therapy. However, platinum combination chemotherapy may be associated with worsening or new-onset LVOT obstruction, whereas other chemotherapy regimens may have the oppositive effect.