Quinidine-Responsive Polymorphic Ventricular Tachycardia in Patients With Coronary Heart Disease

Abstract

Background: Polymorphic ventricular tachycardia (VT) without QT prolongation is well described in patients without structural heart disease (mainly idiopathic ventricular fibrillation and Brugada syndrome) and in patients with acute ST-elevation myocardial infarction. Methods: Retrospective study of patients with polymorphic VT related to coronary artery disease, but without evidence of acute myocardial ischemia. Results: The authors identified 43 patients in whom polymorphic VT developed within days of an otherwise uncomplicated myocardial infarction or coronary revascularization procedure. The polymorphic VT events were invariably triggered by extrasystoles with short (364±36 ms) coupling interval. Arrhythmic storms (4–16 events of polymorphic VT deteriorating to ventricular fibrillation) occurred in 23 (53%) patients. These arrhythmic storms were always refractory to conventional antiarrhythmic therapy, including intravenous amiodarone, but invariably responded to quinidine therapy. In-hospital mortality was 17% for patients with arrhythmic storm. Patients treated with quinidine invariably survived to hospital discharge. During long-term follow-up (of 5.6±6 years; range, 1 month to 18 years), 3 (16%) of patients discharged without quinidine developed recurrent polymorphic VT. There were no recurrent arrhythmias during quinidine therapy Conclusions: Arrhythmic storm with recurrent polymorphic VT in patients with coronary disease responds to quinidine therapy when other antiarrhythmic drugs (including intravenous amiodarone) fail.

Electrical storm after percutaneous coronary intervention: Ischemia, reperfusion injury, or channelopathy?

“…It remains unclear, however, whether ischemia–reperfusion injury would be enough to justify this clinical presentation, particularly outside the context of an acute coronary syndrome, or if a pre‐existing channelopathy could have been exacerbated after PCI. Interestingly, a recent case series suggested that CAD‐related but non‐ischemia‐driven drug‐refractory VAs may have a similar background to BrS (and other arrhythmogenic syndromes with a structurally normal heart) and display a remarkable response to quinidine, although in this study there is no mention of a BrP preceding the VAs 5 …”

Electrical storm 11 days after acute myocardial infarction: a case report

“…Viskin et al reported quinidine-responsive polymorphic VT in patients with coronary heart disease [10]. In their study, the polymorphic VT in patients with coronary heart disease shared important characteristics with idiopathic VF and Brugada syndrome; the characteristics are distinctive arrhythmia mode of onset by short-coupled extrasystoles and susceptibility to develop arrhythmic storms that are refractory to conventional antiarrhythmic drugs, including amiodarone.…”

Ventricular fibrillation after ablation of a benign arrhythmia. Angry Purkinje syndrome?

“…7 Once the electrotonic (suppressive) effects of the surrounding myocardium ceased, early-phase-2 afterdepolarizations (ubiquitous in Purkinje fibers) 8 could have propagated with unidirectional block and reentry within the Purkinje-myocardial junctions, causing very fast arrhythmias. 5,6 J o u r n a l P r e -p r o o f…”

“…Fearing the possibility of an arrhythmic storm of polymorphic VT, 4 we started quinidine therapy. 5,6 Intravenous quinidine gluconate (Quinidine Gluconate Injection, Lilly) at a rate of 15 mg/min led to immediate (within minutes) suppression of all ventricular ectopic activity; the infusion rate was then reduced by 50% every 15 minutes until a final dose 2 mg/min was achieved and maintained for a total dose of 800 mg intravenous quinidine gluconate over 4 hours. This was followed by oral hydroquinidine (Serecor, Sanofi) at a dose of 300 mg every 6 hours.…”