Heart failure (HF) in cardio-oncology patients during anticancer therapy is usually regarded as an accelerated form of classical HF, which restricts early diagnosis and timely pathogenetically based treatment. Myocardial decompensation in these patients appears to involve distinct molecular mechanisms detectable before overt HF, and metabolomic profiling may help identify a specific cardio-oncological HF phenotype.
To characterize the metabolomic profile of HF in cardio-oncology patients versus HF patients without cancer and assess its utility for early cardiotoxicity detection and justification of early personalized cardioprotective therapy.
The study enrolled 102 patients. The cardio-oncology group (Onco, n=59) included patients with hematological malignancies (34 lymphomas, 25 multiple myeloma) examined before treatment and after three cycles of anticancer therapy; baseline risk was stratified using ESC-ICOS tools (24 low, 17 intermediate, 12 high, 6 very high). Various forms of cardiotoxicity were documented in 15 patients (left ventricular dysfunction n=8, arterial hypertension n=4, arrhythmias n=2, pulmonary embolism n=1). The control HF group comprised 43 patients with chronic HF without cancer (left ventricular ejection fraction 56%, NT-proBNP >968 pg/mL). All patients underwent targeted metabolomic analysis.
Significant differences in metabolomic profiles were found between Onco and HF patients. Arginine levels were higher in the Onco group (89.15 ± 33.89 vs. 73.27 ± 17.84; p=0.002), while ADMA and homoarginine did not differ significantly. No intergroup differences were seen for tryptophan, kynurenine, or kynurenic acid, whereas quinolinic acid and tryptamine were higher in the Onco group (p<0.005 and p<0.011), indicating a shift of kynurenine pathway activity toward a pro-inflammatory branch. All analyzed markers of mitochondrial fatty acid oxidation (C14-OH, C16:1-OH, C18:1-OH, C18-OH, C5-DC, cytidine) differed significantly (p<0.05), consistent with more pronounced impairment of mitochondrial β-oxidation in the HF group.
HF in cardio-oncology patients exhibits a distinct metabolomic phenotype that differs from classical HF and reflects key pathogenetic mechanisms of myocardial injury, enabling detection of subclinical cardiotoxicity. Metabolomic profiling opens new possibilities for early, pathogenetically oriented, personalized cardioprotective therapy, including pharmacological strategies targeting these metabolic alterations.
R. Alieva, K. Fozilov, M. Yakhyoeva et al.· European Heart Journal, Supp...· 0 citations
Anthracyclines remain a cornerstone of therapy for lymphoproliferative diseases eratie(LPD) but are associated with cardiovascular toxicity (CVT). While myocardial injury is well studied, anthracycline-induced vascular toxicity and endothelial dysfunction as early manifestations of cardiovascular damage remain insufficiently explored, particularly in patients with low or intermediate baseline CVT-risk, who do not meet criteria for cardioprotective therapy according to current guidelines. Identification of early biomarkers of subclinical vascular injury is, therefore, of major importance in cardio-oncology.
To assess the diagnostic and prognostic value of endothelin-1 (ET-1) for detection and progression of endothelial dysfunction in lymphoma patients with low and intermediate CVT-risk receiving anthracycline-based chemotherapy.
This prospective study included 37 patients with newly diagnosed LPDs (median age 46 [34–62] years) treated with anthracycline-containing chemotherapy. Baseline CVT-risk was assessed using HFA-ICOS scores; all patients were classified as low or intermediate risk and did not require cardioprotective therapy. Serum ET-1 levels were measured by ELISA before treatment initiation and after 3 chemotherapy cycles (cumulative anthracycline dose 270 mg/m²). Endothelial function was evaluated using digital photoplethysmography (ANGIOSCAN-01), assessing phase shift (PS) and occlusion index (OI). ROC analysis was performed to evaluate prognostic performance.
Baseline ET-1 levels were elevated and increased significantly after 3 cycles of chemotherapy (5.39 [4.6–7.21] vs 7.19 [5.9–11.6] pg/mL; p = 0.003). This was accompanied by a significant decline in endothelial function parameters: PS (normal >10 ms) decreased from 8.6 [7.2–10.2] to 6.3 [5.2–9.8] ms (p = 0.014), and OI (normal >1.8) decreased from 1.7 [1.4–1.9] to 1.5 [1.2–1.9] (p = 0.004). ROC analysis demonstrated good prognostic performance of ET-1 for endothelial dysfunction: AUC 0.772 for PS (95% CI: 0.582-0.962, p=0.031) and 0.743 for OI (95% CI: 0.532-0.954, p=0.048).
Endothelin-1 is a promising early diagnostic and prognostic biomarker of subclinical anthracycline-induced vascular toxicity in lymphoma patients with low and intermediate CVT-risk. ET-1 assessment may facilitate early risk reclassification and optimization of cardio-oncology surveillance strategies.
R. Alieva, K. Fozilov, M. Yakhyoeva et al.· European Heart Journal, Supp...· 0 citations
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