Baseline and early changes in cardiac biomarkers as predictors of global longitudinal strain deterioration during breast cancer therapy: a PRADAII substudy
Aug 2026· European Heart Journal, Supplement· Vol 28· 0 citations
TL;DR
Baseline biomarker levels were not associated with GLS deterioration, and no biomarker–treatment interactions were observed (all p for interaction >0.27).Early post-anthracycline changes in hs-cTnI, hs-cTnT, or NT-proBNP were not predictive of subsequent GLS decline, nor were peak or persistent elevations (Table 1, Figure 1).
Abstract
Cardiac biomarkers are recommended for risk stratification before and during potentially cardiotoxic cancer therapy, but the prognostic value of baseline levels and early changes for subsequent left ventricular (LV) dysfunction remains unclear.
To evaluate wheter baseline and early changes in high-sensitivity cardiac troponins (hs-cTnI, hs-cTnT) and N-terminal pro–B-type natriuretic peptide (NT-proBNP) predict changes in global longitudinal strain (GLS) over 18 months.
In the randomized PRADAII, 138 women treated with anthracyclines (±trastuzumab) received sacubitril/valsartan or placebo and underwent serial biomarker sampling and cardiac imaging at baseline, post-anthracycline, and 18 months. Longitudinal changes in GLS and left ventricular ejection fraction (LVEF) were analyzed using adjusted linear mixed models, including exploratory analyses of combined, persistent, and peak biomarker elevations.
Mean age was 54.0±9.4 years. At baseline, no patients had hs-cTnI values above the sex-specific 99th percentile, 6 (4%) had hs-cTnT >99th percentile, and 16 (12%) had NT-proBNP >125 ng/L. Mean baseline GLS was −19.5±2.1% and CMR- and echocardiography-derived LVEF was 60.3±4.8% and 58.3±6.2%, respectively. GLS declined modestly over follow-up, with less deterioration in the sacubitril/valsartan group than in the placebo group (ΔΔ −1.26, 95% CI −2.19 to −0.33).
Both hs-cTnI and hs-cTnT increased markedly after anthracycline therapy, with 16.7% and 71.7% exceeding the sex-specific 99th percentile at peak, whereas NT-proBNP showed modest changes with wide inter-individual variability. Transient and persistent troponin elevation occurred in 60.1% and 11.6%, respectively; corresponding NT-proBNP elevations in 5.1% and 7.3%, and combined troponin and NT-proBNP elevation in 9.4%.
Baseline biomarker levels were not associated with GLS deterioration, and no biomarker–treatment interactions were observed (all p for interaction >0.27). Early post-anthracycline changes in hs-cTnI, hs-cTnT, or NT-proBNP were not predictive of subsequent GLS decline, nor were peak or persistent elevations (Table 1, Figure 1). No significant associations were observed between baseline or early biomarker levels and changes in LVEF assessed by echocardiography or CMR.
In our breast cancer cohort with preserved baseline LV function, baseline levels and early changes in hs-cTnI, hs-cTnT, and NT-proBNP were not associated with subsequent deterioration in GLS over 18 months. Larger studies including higher-risk patients and clinical endpoints are needed to clarify the role of cardiac biomarkers in individualized cardiotoxicity risk stratification.
Background:
Cardiotoxicity remains a major limitation in breast cancer treatment, especially with anthracyclines and radiotherapy. Early biomarkers may improve risk stratification.
Methods:
This retrospective cohort study included breast cancer patients treated between 2020 and 2023 with chemotherapy and/or radiotherapy. Troponin I (TPI) and N-terminal pro B-type natriuretic peptide (NT-proBNP) were measured at baseline and at three, six, 12, 18, 24, 30, and 36 months. Cardiotoxicity was defined per European Society of Cardiology (ESC) guidelines as a ≥10% drop in left ventricular ejection fraction (LVEF) to <53% or >15% relative reduction in global longitudinal strain (GLS). Receiver operating characteristic (ROC) analysis, logistic regression, and mixed-effects models assessed associations.
Results:
A total of 190 patients were included; 141 patients (74.2%) developed cardiotoxicity within 12 months. At six months, NT-proBNP (median: 212.6 pg/mL) and TPI (0.038 ng/mL) were significantly higher in the cardiotoxic group (
p
< 0.01). ROC area under the curve (AUC) for NT-proBNP at six months was 0.83 (95% CI: 0.77–0.89); for TPI, AUC = 0.79 (95% CI: 0.73–0.86). Multivariable regression showed both biomarkers remained independent predictors of cardiotoxicity after adjustment for GLS and cumulative anthracycline dose (NT-proBNP: OR 1.78 [95% CI 1.22–2.61],
p
= 0.003).
Conclusion:
In this real-world breast cancer cohort, serial NT-proBNP and TPI monitoring, particularly at 3 and 6 months, provided meaningful early prognostic information for subsequent cardiotoxicity beyond baseline assessment alone. When integrated with echocardiographic surveillance, these biomarkers may support earlier identification of high-risk patients, more tailored cardio-oncology follow-up, and timely cardioprotective intervention, although prospective external validation is required before routine implementation.
Benard Shehu, K. Shehu, B. Kraja et al.· Qatar medical journal· 0 citations
Purpose This study aimed to develop and validate a nomogram for predicting short-term LVEF decline in patients with DMD. Methods This was a single-center retrospective cohort study enrolling male patients diagnosed with DMD at Sun Yat-sen Memorial Hospital, Sun Yat-sen University, between 2015 and 2025. Data collected included patient age, cardiac troponin I (cTnI) levels, history of steroid therapy, baseline echocardiographic LVEF, and CMR data (including LGE and native T1 values). The primary outcome was the decline in LVEF (ΔLVEF ≤ −10%) during follow-up within 12 months. Least absolute shrinkage and selection operator (LASSO) logistic regression analysis was employed to identify independent risk factors and construct a nomogram-based predictive model. Model performance was assessed by the area under the receiver operating characteristic (ROC) curve and internally validated using bootstrap resampling (1000 repetitions). Results A total of 102 patients were included, of whom 38 (37.3%) exhibited a decline in LVEF. Multivariable analysis identified older age (OR 1.16, 95% CI 1.04–1.30, p = 0.009), abnormal cTnI (cTnI ≥ 0.04 ng/mL) (OR 7.27, 95% CI 1.46–36.28, p = 0.016), longer steroid duration (OR 1.72, 95% CI 1.09–2.71, p = 0.020, likely reflecting disease severity), the presence of LGE (OR 5.45, 95% CI 1.27–23.43, p = 0.023), and higher native T1 values (OR 1.02, 95% CI 1.01–1.04, p = 0.001) as independent risk factors. A higher baseline LVEF was protective (OR 0.81, 95% CI 0.72–0.91, p<0.001). The predictive model demonstrated excellent discrimination, with an AUC of 0.943 (95% CI 0.901–0.985). Internal validation yielded an optimism-corrected C-index of 0.922. Conclusion This study successfully established a comprehensive prediction model incorporating clinical and imaging variables, which can accurately identify DMD patients at risk for short-term LVEF decline. The model demonstrated high discriminative ability (AUC 0.943) in this retrospective, single-center cohort; however, these results are preliminary and require external validation.
Xue-Zhen Chen, Ruo-Hao Wu, Fang Zhang et al.· International Journal of Gen...· 0 citations
Background Early identification of patients at high risk of death following acute aortic dissection (AAD) remains a major clinical challenge because mortality is driven by multiple interacting pathophysiological mechanisms, including myocardial injury, hemodynamic stress, and activation of coagulation pathways. We aimed to develop and internally validate an integrated biomarker-based model for predicting 30-day mortality in patients with AAD. Methods We conducted a retrospective cohort study to develop and internally validate a multivariable prediction model for 30-day mortality in 572 consecutive patients with AAD. Admission levels of cardiac troponin I (cTnI), creatine kinase-MB (CK-MB), B-type natriuretic peptide (BNP), D-dimer, and fibrin/fibrinogen degradation products (FDP) were assessed. Multivariable logistic regression was performed after adjustment for age, Stanford classification, symptom-onset-to-admission time, systolic blood pressure, serum creatinine, and treatment strategy. Model performance was evaluated using discrimination, calibration, net reclassification improvement (NRI), and integrated discrimination improvement (IDI). Internal validation was conducted using bootstrap resampling with 1,000 iterations. Results Elevated cTnI (adjusted OR = 3.76, 95% CI: 1.87–7.56; P < 0.001), BNP (adjusted OR = 6.59, 95% CI: 2.76–15.76; P < 0.001), and D-dimer (adjusted OR = 2.70, 95% CI: 1.17–6.24; P = 0.020) were independently associated with 30-day mortality, whereas CK-MB and FDP were not independently associated with mortality after multivariable adjustment. The integrated prediction model incorporating cTnI, BNP, D-dimer, and clinical covariates demonstrated good discrimination, with an optimism-corrected AUC of 0.89 compared with 0.84 for the clinical model alone, representing a modest but statistically significant improvement (ΔAUC = 0.05). At the optimal probability threshold, the integrated model achieved a sensitivity of 76.2% and a specificity of 96.8%. It also significantly improved risk classification over the clinical model alone, with an NRI of 0.32 (P < 0.01) and an IDI of 0.11 (P < 0.01). A nomogram derived from the final multivariable model was developed to facilitate individualized estimation of 30-day mortality risk using routinely available clinical and laboratory variables. Conclusions An integrated model incorporating cTnI, BNP, D-dimer, and key clinical variables demonstrated good discrimination (optimism-corrected AUC 0.89) and statistically significant incremental value over clinical variables alone (NRI = 0.32, IDI = 0.11). However, the modest AUC improvement (ΔAUC = 0.05) and lack of head-to-head comparison with established risk scores (IRAD, Penn, GERAADA) warrant cautious interpretation and external validation before clinical implementation.
Yan-Fen Yao, Guo-Chen Li, Li Kong· Frontiers in Cardiovascular...· 0 citations
BACKGROUND
Preoperative hs-TnT (high-sensitivity cardiac troponin T) and NT-proBNP (N-terminal pro-B-type natriuretic peptide) are used for risk prediction in noncardiac surgery. While the European Society of Cardiology recommends hs-TnT, American Cardiology and European anesthesiology societies support NT-proBNP. Direct comparisons of their predictive performance are limited. This study compares preoperative hs-TnT and NT-proBNP in predicting cardiac events after noncardiac surgery.
METHODS
This secondary analysis pooled data from the METREPAIR (Metabolic Equivalents: Reevaluation for Perioperative Cardiac Risk) and MINSS (Myocardial Injury in Noncardiac Surgery in Sweden) studies involving patients with elevated cardiovascular risk undergoing elective noncardiac surgery. The primary end point was the incidence of 30-day major adverse cardiovascular events, with 30-day death as the secondary end point. Logistic regression models, including Revised Cardiac Risk Index (RCRI) and age, were augmented by biomarkers. Prediction was assessed using area under the receiver operating characteristic curve, calibration slopes, and Brier scores. Decision curve analysis was conducted at predefined thresholds for major adverse cardiovascular events and death.
RESULTS
Among 2251 patients, MACE occurred in 5.8% (131/2251) and death in 1.6% (37/2251). Both biomarkers were significantly associated with outcomes. Only hs-TnT improved discrimination for predicting death (area under the receiver operating characteristic curveRCRI+age+hsTnT=0.680 versus area under the receiver operating characteristic curveRCRI+age=0.674; Δ area under the curve: 0.006; P=0.047). Brier scores and calibration slopes showed good calibration for all models. Benefit equivalents of RCRI+hs-TnT versus RCRI+NT-proBNP were -0.06 per 1000 and -0.17 per 1000 for major adverse cardiovascular events and +0.06 per 1000 versus -0.08 per 1000 (5% threshold) and -0.35 per 1000 versus -0.06 per 1000 (10% threshold) for death. A literature review did not suggest differences between biomarkers.
CONCLUSIONS
Hs-TnT and NT-proBNP were associated with major adverse cardiovascular events and death, but their contribution to risk prediction over RCRI and age was limited. No significant difference was found between biomarkers.
Anna Kirkopoulos, J. Larmann, H. Gillmann et al.· Journal of the American Hear...· 0 citations
Cardiotoxicity remains a major limitation of contemporary anticancer therapies. Sodium–glucose cotransporter-2 inhibitors (SGLT2i) have demonstrated cardiovascular benefits, including reduced heart failure hospitalizations, and emerging evidence suggests potential additional benefits in oncology populations. Accurate baseline cardiovascular risk stratification and early initiation of cardioprotective therapy are essential for preventing cancer therapy–related cardiovascular toxicity (CTR-CVT).
We prospectively evaluated 256 patients with breast or lung cancer prior to initiation of anticancer therapy. Baseline cardiovascular assessment included echocardiography with biplane left ventricular ejection fraction (LVEF), global longitudinal strain (GLS), diastolic function, and measurement of cardiac biomarkers (troponin and NT-proBNP). Cardiovascular history, demographic data, and risk factors were collected. CTR-CVT risk was assessed using the HFA-ICOS Cardio-Oncology risk assessment tool.Seventy patients (29 men, 41 women; mean age 69.6 ± 8.0 years) were classified as high risk and initiated on cardioprotective therapy. Forty-seven patients (67.1%) received angiotensin-converting enzyme inhibitors, beta-blockers, statins, and SGLT2 inhibitors (SGLT2i group). Twenty-three patients (32.9%) had contraindications to SGLT2i therapy and received standard cardioprotective treatment. Outcomes were assessed at 6 months.
At 6-month follow-up, no statistically significant changes in systolic or diastolic function were observed in either group. In the SGLT2i group, LVEF and GLS remained stable between baseline and follow-up (median LVEF 60.0% vs. 53.0%, p>0.05; GLS −18.9% vs. −16.8%, p>0.05). Renal function showed a modest numerical decline (median eGFR 80.0 vs. 62.0 ml/min/1.73 m², p>0.05). In patients not receiving SGLT2i, no significant changes were detected in LVEF or GLS, while a numerically greater decline in renal function was observed (median eGFR 95.0 vs. 49.0 ml/min/1.73 m², p>0.05). Diastolic parameters remained stable in the SGLT2i group, whereas a numerical increase in E/e′ medial was observed in the non-SGLT2i group. No heart failure–related hospitalisations or cardiovascular deaths occurred.
In this 6-month longitudinal analysis of oncologic patients at high risk of CTR-CVT, inclusion of SGLT2 inhibitors in a cardioprotective regimen was not associated with adverse cardiac effects. Although statistical significance was not reached, trends toward more stable cardiac and renal parameters were observed. These findings are hypothesis-generating and support further investigation of SGLT2 inhibitors in cardio-oncology.Table showing the following parameters
M. Samardjieva, I. Simova, V. Petrusheva et al.· European Heart Journal, Supp...· 0 citations
Background/Objectives: Early circulating biomarkers capable of identifying patients at risk for impaired recovery of left ventricular (LV) systolic function after ST-segment elevation myocardial infarction (STEMI) remain limited. This exploratory study aims to determine whether serum follistatin measured within the first 24 h after coronary revascularization is associated with long-term LV systolic function, as assessed by cardiac magnetic resonance (CMR). Methods: In this prospective study, 31 patients with reperfused STEMI underwent serial CMR at 1 week and 6 months. Follistatin levels were measured within 24 h after revascularization. Associations between follistatin and CMR-derived LV systolic function were assessed using univariate and multivariable linear regression analyses. Results: Patients were stratified by median follistatin level (438 pg/mL) into below median (n = 15) and above median (n = 16). At 1 week, CMR-derived LV function, volumes, and structural indices were similar between groups. By 6 months, however, patients with follistatin above the median had higher LV ejection fraction (LVEF) [62 ± 9% vs. 54 ± 9%; p-value = 0.018] and lower LV end-systolic volume index (28 ± 12 vs. 41 ± 18 mL/m2; p-value = 0.037). In univariate analysis, follistatin was associated with 6-month LVEF (β = 0.027 per pg/mL; p-value = 0.004). After multivariable adjustment, follistatin remained independently associated with 6-month LVEF (β = 0.024 per pg/mL; p-value < 0.001) and with relative improvement in LVEF from 1 week to 6 months (β = 0.044 per pg/mL; p-value < 0.001). Conclusions: In reperfused STEMI patients, higher early follistatin levels were independently associated with more favorable LV systolic function at 6 months. These hypothesis-generating findings suggest that follistatin may represent a potential biomarker of subsequent systolic recovery after STEMI, warranting further validation in larger prospective studies.
J. Gavara, T. Molina-Garcia, E. de Dios et al.· Journal of Clinical Medicine· 0 citations
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