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QTc prolongation and monomorphic ventricular tachycardia: case report A 40-year-old woman developed QTc prolongation and monomorphic ventricular tachycardia following treatment with epirubicin and metoclopramide [durations of treatments to reactions onsets not stated]. The woman was identified to have congenital long QT syndrome (LQTS) type 2 with the mutation NM_000238.3 (KCNH2):c.2593-2A.G, which had been classified locally as pathogenic. She had been receiving metoprolol for more than 15 years. At a serial follow-up, she exhibited prolonged QTc (QT interval corrected for heart rate) of approximately 480ms. In 2019, she was diagnosed with left breast ductal cancer (T2 (38mm) pNX, luminal B, non-Her-2-amplified). Prior to a surgery, she was scheduled to receive neoadjuvant cytostatic chemotherapy including epirubicin infusion 75 mg/m2 [route not stated] and cyclophosphamide (EC75 chemotherapy). Prior to first dose of the chemotherapy, metoprolol dose was increased. At that time, she had normal serum potassium level. On day 1 of the chemotherapy, continuous telemetry monitoring was started. Subsequently, IV epirubicin 134mg was administered over 2 hours, which was followed by cyclophosphamide infusion over 1 hour. Additionally, she received metoclopramide [dosage and route not stated] and aprepitant for nausea prophylaxis and betamethasone. After start of the treatment, she developed palpitations associated with frequent premature ventricular complexes and episodes of repetitive nonsustained monomorphic ventricular tachycardias up to 8 complexes (heart rate 125 bpm). The rhythm comprised of the greater part of ectopic ventricular complexes separated by short periods of normal rhythm. The arrhythmias decreased but re-emerged. Therefore, the woman’s metoprolol dose was further increased and she received potassium and magnesium. After 24 hours, the arrhythmias decreased. She had a normal cardiac troponin-T test. During day 2 and day 3, telemetry showed singular and coupled ventricular complexes in the in decreasing frequency. On day 4, telemetry showed only singular ventricular complexes and she was discharged. During this period, her mean heart rate was 64 (±7) bpm. Prior to the treatment, her QTc (corrected by Bazett’s formula) was 474ms, which was increased during day 1 (QTc prolongation) and slowly decreased thereafter. The woman was scheduled to receive second dose of the chemotherapy 3 weeks later. One week prior to the second dose, she was switched from metoprolol to propranolol. Subsequently, she received second dose of the EC75 chemotherapy. She again received metoclopramide for nausea prophylaxis. She was monitored by continuous telemetry over 3 days. During or after the second treatment, no premature ventricular complexes or ventricular arrhythmias were noted. During this period, her mean heart rate was 67 (±6) bpm. After the second dose, she again exhibited increase in QTc, which was comparable to that during the first treatment. At that time, MRI showed no change in size of the tumor. Therefore, neoa