LEFT VENTRICULAR GLOBAL LONGITUDINAL STRAIN FOR EARLY DETECTION OF ANTHRACYCLINE-INDUCED CARDIOTOXICITY IN ADULT BREAST CANCER PATIENTS: A SYSTEMATIC REVIEW
Aug 2026· International Journal of Innovative Technologies in Social Science· 0 citations· 15 references
TL;DR
LV GLS appears to be a sensitive and clinically useful echocardiographic marker for the early detection of anthracycline-induced cardiotoxicity in adult breast cancer patients and may improve identification of subclinical cardiac dysfunction before a measurable decline in left ventricular ejection fraction occurs.
Abstract
Introduction: Anthracycline-based chemotherapy remains an important component of breast cancer treatment, but its use is limited by the risk of cardiotoxicity, including subclinical left ventricular dysfunction and cancer therapy-related cardiac dysfunction. Conventional monitoring based on left ventricular ejection fraction may detect myocardial injury relatively late. Left ventricular global longitudinal strain (LV GLS), assessed by speckle-tracking echocardiography, has emerged as a more sensitive parameter for identifying early myocardial impairment. This systematic review summarizes current evidence on the role of LV GLS in the early detection of anthracycline-induced cardiotoxicity in adult breast cancer patients.
Methods: A systematic literature review was performed using PubMed/MEDLINE. The search strategy combined terms related to breast cancer, anthracyclines, global longitudinal strain, speckle-tracking echocardiography, and cardiotoxicity. Original English-language studies focused on adult breast cancer patients receiving anthracycline-based chemotherapy and undergoing strain echocardiographic assessment were considered eligible. After title, abstract, and full-text screening, seven studies were included in the qualitative synthesis.
Results: The included studies consistently suggested that LV GLS detects subclinical myocardial dysfunction earlier than conventional left ventricular ejection fraction assessment in breast cancer patients treated with anthracyclines. Several studies reported early impairment in myocardial deformation parameters during or shortly after chemotherapy, even in the presence of preserved ejection fraction. The reviewed evidence also indicated that changes in GLS may have diagnostic and prognostic relevance for subsequent cardiotoxicity and later decline in cardiac function. More recent studies additionally supported the value of integrating GLS with other echocardiographic parameters in the assessment of cancer therapy-related cardiac dysfunction.
Conclusions: LV GLS appears to be a sensitive and clinically useful echocardiographic marker for the early detection of anthracycline-induced cardiotoxicity in adult breast cancer patients. Its use may improve identification of subclinical cardiac dysfunction before a measurable decline in left ventricular ejection fraction occurs. Further studies are needed to clarify optimal cutoff values, monitoring intervals, and the role of GLS within standardized cardio-oncology surveillance protocols.
A significant decline in right ventricular function is demonstrated during anthracycline-based cardiotoxic therapy and persisting up to one year after treatment completion, even in patients with low cardiotoxic risk, despite changes being subclinical and largely within normal ranges.
I. Gigovska Dimova, G. Petkovska, I. Ismaili et al.· European Heart Journal, Supp...· 0 citations
GLS and LVEF were the most sensitive echocardiographic parameters for differentiating between groups with and without cardiotoxicity, showing consistent changes throughout the study.
R. D. De Sousa, V. Fonseca, M. Henriques et al.· European Heart Journal, Supp...· 0 citations
It is suggested that RV strain assessment provides information complementary to conventional LV–based cardiotoxicity criteria and may occur in the absence of concurrent changes in conventional LV cardiotoxicity parameters as currently defined.
Z. Tlegenova, A. Amanova, S. Balmagambetova et al.· European Heart Journal, Supp...· 0 citations
Anthracyclines remain cornerstone agents in oncology, yet their cardiotoxic potential poses a substantial clinical challenge. Up to 30% of treated patients develop some degree of cardiac dysfunction, with overt heart failure occurring in 2–5% of cases. Current surveillance relies on serial ejection fraction measurements, which detect damage only after significant myocardial injury has occurred. Histopathological evidence consistently shows that the subendocardial layer suffers earliest and most severely from anthracycline exposure—often weeks before any decline in global ventricular function becomes apparent. This temporal gap represents a missed opportunity for timely cardioprotective intervention.
We designed the CARDIAC-STRAIN study to determine whether layer-specific strain analysis by cardiac magnetic resonance can identify subclinical cardiotoxicity substantially earlier than conventional echocardiographic surveillance, potentially enabling earlier initiation of cardioprotective treatment.
This prospective single-centre diagnostic cohort study will recruit 120 consecutive patients scheduled for anthracycline-based chemotherapy (sample size calculated to detect 20% sensitivity difference, power 80%, α=0.05). Eligible participants are aged 18–75 years with preserved baseline ejection fraction (≥50%) and no prior anthracycline exposure or known cardiomyopathy. Each patient undergoes blinded comprehensive cardiac evaluation at four timepoints: baseline, after the fourth chemotherapy cycle, four weeks post-treatment, and at six months' follow-up. The protocol includes 1.5T cardiac MRI with cine sequences, native and post-contrast T1 mapping, T2 mapping, and late gadolinium enhancement. Layer-specific strain is quantified at subendocardial, midmyocardial, and subepicardial levels using dedicated feature-tracking software. Parallel assessments include three-dimensional echocardiography and cardiac biomarkers (troponin, NT-proBNP). Primary endpoints: ejection fraction decline >10% to below 50%, decline >15% with preserved function, or layer-specific strain deterioration >15% from baseline.
Study hypothesis: We hypothesize that layer-specific strain analysis will detect subclinical myocardial injury approximately 2–4 weeks earlier than conventional ejection fraction monitoring, with significantly improved diagnostic sensitivity compared to standard surveillance protocols.
Expected outcomes: If layer-specific strain analysis proves capable of reliably identifying subclinical cardiotoxicity before irreversible damage occurs, this approach may help shift clinical practice from heart failure treatment to early prevention in cardio-oncology. The study received ethics committee approval in November 2025, and patient recruitment is underway.
N. Kavelashvili, N. Sharashidze, F. Schiedat et al.· European Heart Journal, Supp...· 0 citations
Cancer therapy–related cardiac dysfunction (CTRCD) remains a major limitation of anthracycline and anti-HER2 therapy, and most monitoring focuses on left ventricular (LV) function. Data on the role of right ventricular (RV) function as an early marker of CTRCD are limited.
To evaluate the association between echocardiographic RV parameters - TAPSE, tricuspid S’ velocity and RV free-wall longitudinal strain (RV-FWLS) - and the development of CTRCD in patients treated with anthracyclines and/or anti-HER2 therapy.
Retrospective, single-center observational study including patients treated with anthracyclines and/or anti-HER2 agents and followed in Cardio-oncology consultation in a district hospital. CTRCD was defined according to contemporary cardio-oncology criteria based on LV ejection fraction and global longitudinal strain. RV function was evaluated by TAPSE, tricuspid S’ and RV-FWLS.
We included 65 women, mean age 60±10 years. Chemotherapy regimens comprised anthracyclines only in 45%, anti-HER2 therapy only in 10% and combined anthracyclines plus anti-HER2 in 45%. According to the HFA-ICOS tool, 34% were at low, 37% at moderate, 17% at high and 12% at very high cardiovascular risk at baseline. Over a median follow-up of 36 months (IQR 23–70), CTRCD occurred in 15 patients (23%). 9 patients (14%) died, including 2 cardiovascular deaths.
At baseline, TAPSE and tricuspid S’ were similar in patients with and without CTRCD (TAPSE 22±2.7 vs 23±2.1mm, p=0.19; S’ 12.5±1.9 vs 12±1.8cm/s, p=0.30), whereas RV-FWLS was significantly less negative in those who subsequently developed CTRCD (−23.6±3.1% vs −26.1±2.8%, p=0.02).
During follow-up, patients with CTRCD showed a greater decline in RV function, with larger reductions in TAPSE (−2±1.9 vs −0.5±1.5mm, p=0.01) and RV-FWLS (+4.8±3.7 vs +2.9±3%, p=0.04). A relative reduction in RV-FWLS ≥15% occurred in 60% of patients with CTRCD versus 20% of those without (p=0.01).
In univariable logistic regression, baseline RV-FWLS was associated with higher odds of CTRCD (OR per 1% less negative strain 1.17, 95% CI [1.03–1.28], p=0.01).
In this cohort of women treated with anthracyclines and anti-HER2 therapy, RV-FWLS identified patients who developed CTRCD, supporting RV strain as a useful tool for early risk stratification and refinement of cardio-oncology surveillance strategies.
B. Andrade, N. Cotrim, C. Coelho et al.· European Heart Journal, Supp...· 0 citations
Cancer therapy-induced left ventricular diastolic dysfunction (LVDD) is gaining research attention as a potential early marker of cardiotoxicity. Radiotherapy, chemotherapy, and targeted agents may cause cardiomyocyte energy depletion, cardiac fibrosis, and microvascular dysfunction—known mechanisms of diastolic dysfunction. Heart failure (HF) with preserved ejection fraction and LVDD remain understudied in oncological settings.
We aimed to assess the changes in LV diastolic function caused by cancer treatment.
We prospectively enrolled 60 adults planned for chemotherapy (CT) for breast (n = 50) or gastrointestinal (n = 10) cancers. Exclusion criteria were fewer than 3 visits, a poor acoustic window, or pre-existing cardiac or chronic pulmonary disease. We performed 2D echocardiography at baseline and 1, 3, 6, 9, 12, and 18 months after CT initiation. Left ventricular ejection fraction (LVEF) was considered abnormal if it dropped by over 10% to below 50%. Longitudinal LV systolic dysfunction was defined as a decrease of over 15% to below 7 cm/s in systolic tissue S′ velocity, averaged from septal and lateral S′. We assessed LVDD using the 2025 American Society of Echocardiography algorithm and the parameters: indexed left atrial volume (LAVi); early (E) and late (A) mitral inflow velocities; E/A ratio; isovolumic relaxation time (IVRT); pulmonary artery systolic pressure (PASP); early diastolic tissue e′ velocity (average of septal and lateral e′) (LVe′); and E/e′ ratio. The temporal parameters' changes were estimated using generalised estimating equations (GEE) regression. Correlations were examined using the Spearman and chi-squared tests and Goodman-Kruskal's gamma (γ) statistic.
The mean patient age was 53 years (SD 11.6), with 91.7% female. Half (n = 30) received anthracycline-based CT, either with or without trastuzumab; the remainder received non-anthracycline CT, with or without trastuzumab. The median CT duration was 98 days (IQR: 64, 112). Twenty-seven patients (45%) had radiotherapy. Over a median follow-up of 381 days (IQR: 187, 464), LVE/e' and LVe' declined significantly in the third month. Both parameters showed moderate correlation with LVS’ (Figure 1). Six patients had baseline LVDD; in one, it progressed from grade 1 to grade 2. New-onset LVDD occurred in 6 patients (10%), all grade 1 (Figure 2). Among them, two had transient LVDD; in two cases, LVDD advanced to grade 2, and one patient showed symptoms of HF (NYHA class II). There was a trend toward LVDD at the first and sixth months (Figure 2). No new-onset LVDD patient developed abnormal LVEF, although two had concurrent longitudinal systolic dysfunction. LVDD and longitudinal systolic dysfunction showed a positive association (ꭓ² = 5.2, p = 0.022; Kruskal’s γ = 0.64).
Cancer therapy-related LVDD may develop early and present as either a transient or persistent condition. Its clinical implications need further investigation.
S. Slavcheva, A. Angelov· European Heart Journal, Supp...· 0 citations
