Dynamic cardiac toxicity monitoring in hematological tumor patients based on time thresholds and chemotherapy stratification

Background Early detection of cardiotoxicity in cancer treatment requires quantitative assessment of time effects and regimen specificity. This prospective study analyzed 43 hematologic malignancy patients (lymphoma 58.1%, myeloma 27.9%, leukemia 14.0%) receiving receiving chemotherapies to explore subclinical cardiac dysfunction evolution patterns. Methods A paired pre-post treatment design was implemented. Core parameters included GLS (absolute value), right ventricular (RV) strain (absolute value), left atrial (LA) strain, EF, average E/E', and myocardial work index. Statistical analysis employed Wilcoxon signed-rank tests, Spearman correlation for time-interval effects, and subgroup analyses by chemotherapy toxicity stratification (anthracyclines/proteasome inhibitors/BTK inhibitors/hypomethylating agents) and diagnostic groups. All p-values underwent Holm-Bonferroni correction. Results Overall analysis revealed significant GLS worsening (median decline: 0.5%, p=0.028) and RV strain impairment (median decline: 1.3%, p=0.009), while LA strain showed compensatory enhancement (median increase: 0.7%, p=0.038). EF and E/E' remained stable. Critical time effects emerged: Patients with >2-month treatment intervals exhibited 73.7% GLS deterioration rate, representing a 2.92-fold increased risk versus ≤2-month group (41.7%; OR=3.92, 95%CI:1.24-12.41) Each additional treatment month accelerated GLS decline by 0.16% (ρ=-0.41, p=0.003) and worsened RV impairment (ρ=-0.44, p=0.001) Chemotherapy-specific patterns were identified: Anthracyclines: Most severe GLS deterioration (median Δ=+1.2%) with highest time-sensitivity (ρ=-0.52). Proteasome inhibitors: Predominant RV strain damage (median Δ=+0.8%). Diagnosis-based compensation mechanisms differed: Lymphoma: Highest GLS deterioration rate (68.0%) with preserved EF. Myeloma: Activated LA strain compensation (p=0.019). Leukemia: Significant myocardial efficiency reduction (p=0.047). Conclusion This study establishes 2 months as the critical time threshold for cardiotoxicity monitoring and constructs a chemotherapy-specific risk stratification: High-risk anthracyclines require ≤2-month surveillance. Diagnosis-tailored strategies are proposed: prioritize GLS tracking in lymphoma and assess LA compensation in myeloma. Clinical Implications Quantifying the 0.16% monthly GLS deterioration slope, defining anthracycline >0.8%/cycle as high-risk threshold, and uncovering myeloma’s LA compensatory mechanism revolutionize precision monitoring in cardio-oncology.