Cardiotoxicity of antitumor therapy: a clinical case and cardioprotection strategies

This article presents a clinical case of a 63-year-old female patient with multiple myeloma (IgG variant, stage IIA by Durie–Salmon, stage I by ISS) who received polychemotherapy (PCT) according to the VCD regimen (bortezomib, cyclophosphamide, dexamethasone). After 6 cycles of PCT, rapid progression of cardiac abnormalities was documented: over 19 days, left ventricular ejection fraction dropped from 60 % to 49–53 %, mitral regurgitation progressed from grade 1–2 to grade 2–3, tricuspid regurgitation advanced from grade 1 to a gradient of 37 mm Hg, and zones of myocardial hypokinesis appeared. Holter ECG monitoring revealed one paroxysm of ventricular tachycardia and 21 episodes of supraventricular tachycardia. Cardiotoxicity remains a major challenge in modern oncology, particularly in patients receiving proteasome inhibitors and alkylating agents. Cardiomyocyte damage is mediated by oxidative stress, mitochondrial dysfunction, and apoptosis. In the present case exogenous phosphocreatine – a mitochondrial metabolic cardioprotector – was used for the prevention and management of cardiotoxic manifestations. The drug was administered intravenously as a short course (1.0–2.0 g) 4–5 days before each PCT cycle. Phosphocreatine is an endogenous substance that ensures rapid ATP resynthesis in cardiomyocytes, stabilizes cell membranes, and protects mitochondria from injury. According to current evidence, phosphocreatine-based cardioprotection exerts beneficial effects on the functional status of the cardiovascular system, prevents cardiac arrhythmias and the development of heart failure, and improves patients’ quality of life. Exogenous phosphocreatine is regarded as an effective cardioprotective agent that has shown efficacy in reversing antitumor-therapy-induced cardiotoxicity. The use of exogenous phosphocreatine becomes particularly valuable in situations where interruption of life-saving PCT is not feasible and the risk of further cardiac deterioration is high. In the described case, phosphocreatine administration allowed continuation of specific therapy under cardioprotective support.