Po-05-150 a case of quinidine responsive purkinje-mediated polymorphic ventricular tachycardia

Polymorphic ventricular tachycardia (PMVT) has several different etiologies including ischemic ventricular fibrillation (VF), VF in coronary artery disease without active ischemia, idiopathic VF, and Torsades De Pointes (TdP). To review a case of quinidine responsive Purkinje mediated PMVT and the importance of considering alternative formulations of quinidine. N/A A 74-year-old female with no cardiac history presented with an inferior STEMI. An echocardiogram showed LV ejection fraction of 25% with multiple regional wall motion abnormalities. Left heart catheterization revealed multivessel disease for which she underwent CABG x 2 (LIMA to LAD, SVG to PDA) with intraoperative course complicated by VT requiring lidocaine drip. Ventricular arrhythmias initially seemed responsive to lidocaine; however, 4 days after CABG the patient was noted to have increased ectopic burden on telemetry and ultimately developed PMVT that required defibrillation (Fig 1A, 1B). Repeat catheterization revealed patent stents. Telemetry and ECGs were typical for Purkinje-mediated PMVT, so the patient was started on quinidine sulfate IR 400 mg every 8 hours with successful lidocaine wean and improvement in ectopic burden, with cessation of PMVT. Unfortunately, approximately 9 days after quinidine sulfate initiation the patient was noted to have rising LFTs with a normal abdominal ultrasound, platelet count, and white blood cell count, prompting discontinuation of quinidine. Without quinidine she had recurrence of PVCs that triggered bouts of PMVT (Fig 1C). PVC ablation was considered, targeting short-coupled PVCs in the border zone of scar that could be triggers for the patient’s PMVT. However, it was felt that the patient was too tenuous for ablation. Ultimately, she was trialed on quinidine gluconate ER formulation. This was started as once daily dosing and titrated up to 12-hour dosing with suppression of PVCs/PMVT and no further LFT derangements. The patient ultimately underwent ICD implant for secondary prevention and was discharged home. Purkinje mediated PMVT can occur in patients with coronary artery disease without acute ischemia. We describe a case of quinidine mediated hepatitis that was overcome by switching formulation from quinidine sulfate IR to quinidine gluconate ER. It is essential that hospitals, particularly arrhythmia referral centers, keep quinidine supplies in stock because this medication can be lifesaving during arrhythmic storms.