Aug 2026· European Heart Journal, Supplement· 0 citations
TL;DR
In patients with low and moderate baseline CV risk, a statistically significant deterioration in lipid profile was observed during chemotherapy, which is consistent with the development of subclinical endothelial dysfunction and early vascular toxicity, despite the absence of overt clinical manifestations of vasculotoxicity.
Abstract
Current cardio-oncology surveillance strategies are primarily focused on patients with high or very high baseline cardiovascular (CV) toxicity risk. Patients with initially low risk are generally considered a clinically favorable group and therefore undergo less intensive monitoring. This approach may lead to underestimation of early, clinically silent vascular alterations developing during chemotherapy.
To assess changes in lipid profile parameters in oncohematological patients with low baseline cardiovascular toxicity risk and to determine their value for identifying early subclinical vascular toxicity and substantiating early initiation of cardioprotective therapy.
This study included 59 patients with B-cell hematological malignancies. According to ESC guidelines on cardio-oncology (2022), patients were stratified into low/moderate (n=42) and high/very high (n=17) CV toxicity risk groups. Lipid profiles were assessed at baseline and after three cycles of chemotherapy. Patients in the high/very high-risk group received standard cardioprotective therapy, including ACE inhibitors/ARBs, beta-blockers, and statins.
The median age in low risk group was 51.5 years [41.75; 63.00] (50% men), in high/very high risk group was 72 years [65.00; 75.00] (47.1% men). Most patients in both groups had traditional CV risk factors: obesity (n=11, 19%), smoking (n=12, 20%), diabetes mellitus (n=8, 13%), hypertension (n=24, 41%), and dyslipidemia (n=30, 51%), 8 patients in high/very high risk group were diagnosed with CAD. In patients with low and moderate baseline CV risk, a statistically significant deterioration in lipid profile was observed during chemotherapy, including increases in total cholesterol (4.54 vs. 5.43 mmol/L), low-density lipoprotein cholesterol (3.1 vs. 3.95 mmol/L), and triglycerides (0.86 vs. 1.01 mmol/L). All changes were highly significant (p<0.01). These findings are consistent with the development of subclinical endothelial dysfunction and early vascular toxicity, despite the absence of overt clinical manifestations of vasculotoxicity. In contrast, no significant changes in lipid parameters were observed in the high and very high-risk group, despite a greater baseline cardiovascular burden.
Patients with low baseline cardiovascular toxicity risk may develop early metabolic signs of subclinical vascular toxicity at the initial stages of chemotherapy. Dynamic assessment of lipid profile represents a simple and clinically applicable tool for early detection of vascular injury. The absence of high baseline cardiovascular risk does not preclude early vascular toxicity, supporting the rationale for considering earlier initiation of cardioprotective therapy in this patient population.
The regression analyses suggest that this phenotype is multifactorial, with echocardiographic indices capturing the functional component and circulating biomarkers reflecting complementary aspects of the underlying biological response.
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