Clinical Mechanistic Insights Into Polymorphic Ventricular Tachycardia: Infection-Triggered Unmasking of Long QT Syndrome

A 63-year-old woman presented with fever, cough, and recurrent presyncope following a lower respiratory tract infection. Initial telemetry demonstrated intermittent complete atrioventricular block with ventricular premature complexes. Despite correction of electrolyte abnormalities and withdrawal of QT-prolonging medications (prescribed for cough), she developed repetitive episodes of polymorphic ventricular tachycardia triggered by R-on-T phenomena, requiring electrical cardioversion and suppression with overdrive pacing after magnesium and phenytoin proved ineffective. A nasopharyngeal bio fire panel identified Mycoplasma pneumoniae, prompting initiation of targeted antibiotic therapy along with propranolol. Cardiac magnetic resonance imaging demonstrated myocardial edema with biventricular dysfunction, consistent with acute myocarditis. With clinical stabilization, resolution of infection, and restoration of sinus rhythm following 2 weeks of antibiotic therapy, atrioventricular conduction improved; however, the QTc remained persistently prolonged on serial electrocardiograms. This persistent QT prolongation beyond the acute inflammatory phase prompted genetic testing, which revealed an autosomal dominant loss-of-function mutation in KCNH2, consistent with long QT syndrome type 2. Following further stabilization, a dual-chamber permanent pacemaker was implanted to prevent bradycardia-mediated arrhythmogenic triggers. The patient has remained free of recurrent ventricular arrhythmias at 1-year follow-up. In conclusion, this case illustrates a rare convergence of infectious, structural, and genetic substrates producing a potent arrhythmogenic milieu, in which Mycoplasma myocarditis unmasked an underlying severe long QT syndrome 2 (LQT2) phenotype and precipitated malignant polymorphic ventricular tachycardia.