Effective VA-ECMO Intervention for Severe Cardiotoxicity Induced by Neoadjuvant Paclitaxel and Cisplatin in Laryngeal Cancer: A Case Study - Report - MDSpire
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Effective VA-ECMO Intervention for Severe Cardiotoxicity Induced by Neoadjuvant Paclitaxel and Cisplatin in Laryngeal Cancer: A Case Study
Effective VA-ECMO for Severe Cardiotoxicity from Neoadjuvant Paclitaxel and Cisplatin
Overview
This case study reports a rare instance of fulminant myocarditis with cardiogenic shock and third-degree atrioventricular block induced by neoadjuvant paclitaxel and cisplatin chemotherapy in a laryngeal cancer patient. Prompt initiation of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) provided lifesaving mechanical circulatory support, enabling recovery from severe cardiotoxicity.
Background
Neoadjuvant chemotherapy with paclitaxel and cisplatin (TP regimen) is a standard treatment for locally advanced laryngeal cancer, improving locoregional control and survival. While mild cardiotoxic effects such as bradycardia and conduction abnormalities are known with paclitaxel, severe cardiotoxicity is uncommon. Cisplatin can cause cardiovascular complications including myocardial infarction and arrhythmias but fulminant myocarditis leading to cardiogenic shock is exceedingly rare. VA-ECMO offers temporary mechanical circulatory support in refractory cardiogenic shock and is emerging as a critical intervention for severe chemotherapy-induced cardiotoxicity.
Data Highlights
Parameter
Value
High-sensitivity Troponin I (hs-TnI)
> 27.533 ng/mL
Myoglobin
280.330 ng/mL
Creatine Kinase-MB
58.270 U/L
Leukocytes
10.5 × 10⁹/L
Neutrophils
8.2 × 10⁹/L
C-reactive Protein
114.45 mg/L
Creatinine
152.6 µmol/L
Lactate Dehydrogenase
7594 U/L
Aspartate Aminotransferase
3287 U/L
Alanine Aminotransferase
1733 U/L
Lactate
5.4 mmol/L
Potassium
5.7 mmol/L
Left Ventricular Ejection Fraction (LVEF)
< 30%
Key Findings
A 59-year-old male with laryngeal cancer developed fulminant myocarditis and cardiogenic shock after three cycles of neoadjuvant paclitaxel and cisplatin chemotherapy.
He presented with third-degree atrioventricular block, elevated cardiac biomarkers, and severely reduced left ventricular ejection fraction (<30%).
Coronary angiography ruled out obstructive coronary artery disease as the cause of cardiogenic shock.
Despite temporary pacing and vasopressor support, the patient’s condition deteriorated rapidly, necessitating VA-ECMO initiation.
VA-ECMO provided effective mechanical circulatory support, enabling stabilization and recovery from severe cardiotoxicity.
This case highlights a rare but life-threatening cardiac complication of the TP regimen and the critical role of VA-ECMO as rescue therapy.
Clinical Implications
Clinicians should be vigilant for rare but severe cardiotoxicity, including fulminant myocarditis and conduction blocks, in patients receiving paclitaxel and cisplatin chemotherapy. Early recognition and prompt initiation of VA-ECMO can be lifesaving in refractory cardiogenic shock secondary to chemotherapy-induced cardiac injury. Multidisciplinary management including cardiac monitoring and supportive therapies is essential for optimal outcomes.
Conclusion
Severe cardiotoxicity from neoadjuvant paclitaxel and cisplatin, though rare, can lead to fulminant myocarditis and cardiogenic shock. VA-ECMO serves as a critical rescue intervention, underscoring its emerging role in managing life-threatening chemotherapy-induced cardiac complications.
References
Clinical Case Report 2024 -- Effective VA-ECMO Intervention for Severe Cardiotoxicity Induced by Neoadjuvant Paclitaxel and Cisplatin in Laryngeal Cancer