myocarditis; nonsustained ventricular arrhythmia; syncope; This is a literature report for the following literature source.  A 65-year-old female patient received BNT162b2 (BNT162B2), as dose 2, single (Batch/Lot number: unknown) for covid-19 immunisation. The patient's relevant medical history included: "hypertension" (unspecified if ongoing); "Left bundle branch block" (unspecified if ongoing). The patient's concomitant medications were not reported. Vaccination history included: Bnt162b2 (Dose 1), for COVID-19 immunization.The following information was reported: MYOCARDITIS (medically significant), outcome "recovering"; VENTRICULAR ARRHYTHMIA (medically significant), outcome "recovering", described as "nonsustained ventricular arrhythmia"; SYNCOPE (medically significant), 1 month after the suspect product(s) administration, outcome "recovering". The patient underwent the following laboratory tests and procedures: Angiocardiogram: demonstrated normal coronary arteries; Blood calcium: 8.4 mg/dl, notes: mildly low; Blood magnesium: 2.4 mg/dl, notes: normal; Blood potassium: 3.9 mmol/L, notes: normal; 2.7 mmol/L, notes: 3 hours later; Cardiac electrophysiologic study: demonstrated normal sinus node function, normal at, notes: atrioventricular node function, and mildly abnormal His-Purkinje system conduction with negative procainamide challenge; Echocardiogram: demonstrated a left ventricular ejection fraction, notes: of 45%-50% with left ventricular dyssynchrony and normal left ventricular wall thickness; Showed a reduced ejection fraction of 19%, notes: initial; Normalized to 50%, notes: after starting metoprolol succinate; Electrocardiogram: demonstrated sinus rhythm with left bundle branch, notes: block, premature atrial complexes, and premature ventricular complexes; demonstrated an accelerated idioventricular rhythm; demonstrated sinus rhythm with left bundle branch, notes: block; demonstrated progressive QT prolongation with a ma, notes: maximum QTc of 705 ms; Electrocardiogram QRS complex: 0.164 seconds; 0.160 seconds, notes: at baseline; 0.170 seconds, notes: increased, After completion of the procainamide infusion; 0.160 seconds; 0.170 seconds; Electrocardiogram QT interval: 0.454 seconds; 0.540 seconds; 0.780 seconds; 0.517 seconds; 0.525 seconds, notes: at baseline; 0.630 seconds, notes: increased, After completion of the procainamide infusion; 0.592 seconds; 0.705 seconds; Heart rate: 78, notes: beats per minute; 79, notes: beats per minute; 72, notes: beats per minute; 49, notes: beats/min; application of an automated external defibrillator: demonstrated ventricular fibrillation; HV interval: 0.065 seconds, notes: at baseline; 0.073 seconds, notes: prolonged, following procainamide 10 mg/kg intravenous infusion over 10 minutes; 0.380 seconds; 0.290 seconds; 0.330 seconds; 0.390 seconds, notes: increased, After completion of the procainamide infusion; 0.610 seconds; Magnetic resonance imaging head: demonstrated anoxic brain injury; SARS-CoV-2 test: negative, notes: on admission; Troponin I: 30 ng/L, notes: initial; 18697 ng/L, notes: rose, 10 hours later. Therapeutic measures were taken as a result of myocarditis, ventricular arrhythmia, syncope.  Clinical course: Introduction: Introduction Torsades de pointes is apolymorphic ventricular tachycardia that can cause syncope and lead to sudden cardiac death. This arrhythmia is initiated by early after depolarizations in the setting of prolonged ventricular repolarization, manifesting as QT prolongation on the12-leadelectrocardiogram (ECG). Common risk factors include QT-prolonging medications, electrolyte disturbances, bradycardia and certain inherited genetic mutations. We report a case of torsades de pointes that occurred shortly after vaccination for COVID-19. She had history of hypertension and left bundle branch block was referred to the electrophysiology clinic following a single episode of syncope. The episode occurred suddenly while sitting and was preceded by transient lightheadedness without palpitations. The cause of this patient cardiac arrest is not completely understood. The QT interval on presentation was significantly prolonged compared to baseline, even when accounting for the left bundle branch block. However, this case was unusual as it was not preceded by a pause, which typically initiates this arrhythmia. An alternative explanation for the observed arrhythmias ventricular fibrillation induced by a premature ventricular complex in the context of a mild non ischemic cardio myopathy. This could explain why the QT interval does not appear to be significantly prolonged on the loop recorder rhythm strip. The presence of myocarditis, which had been linked to the COVID-19 vaccine by Pfizer-BioNTech, may have also increased the risk of arrhythmogenesis. This was the first known case of polymorphic ventricular tachycardia in the setting of QT prolongation following COVID-19 vaccination.  Discussion: The ventricular arrhythmia recorded on the implantable loop recorder appears to be a polymorphic ventricular tachycardia with a twisting of points around a central axis, consistent with torsades de pointes, that rapidly degenerates into ventricular fibrillation. The QT interval on presentation was significantly prolonged compared to baseline, even when accounting for the left bundle branch block. However, this case was unusual as it was not preceded by a pause, which typically initiates this arrhythmia. An alternative explanation for the observed arrhythmia is ventricular fibrillation induced by a premature ventricular complex in the context of a mild nonischemic cardiomyopathy. This could explain why the QT interval does not appear to be significantly prolonged on the loop recorder rhythm strip. However, the QT interval at this precordial location may not necessarily appear prolonged owing to regional differences in the QT interval between leads on a 12-lead ECG. The presence of premature ventricular complexes on the presenting ECG also supports this arrhythmia mechanism following her initial syncopal episode prior to loop recorder implantation. The presence of myocarditis, which has been linked to the COVID-19 vaccine by Pfizer-BioNTech may have also increased the risk of arrhythmogenesis. Unfortunately, detailed cardiac imaging with positron emission tomography or magnetic resonance imaging were not performed, as they were unavailable at the treating facility. The mechanism is thought to be from a transmembrane shift in potassium from the vascular space into cells caused by either a neurohumoral response to the cardiac arrest itself, catecholamine therapy during the arrest, or rapid correction of metabolic acidosis from the administration of bicarbonate and mechanical ventilation.  Conclusion This is the first known case of polymorphic ventricular tachycardia in the setting of QT prolongation following COVID-19 vaccination. Whether this was an episode of torsades de pointes or ventricular fibrillation triggered by a premature ventricular complex is open for debate. Although this case does not prove a definitive causal link to the vaccine, continued data collection and adverse event reporting following vaccination is paramount to ensure safety of widespread vaccinations for the novel corona virus.; Sender's Comments: Based on available information , there is reasonable possibility of causal association between the events MYOCARDITIS , VENTRICULAR ARRHYTHMIA , SYNCOPE and the suspect drug BNT162b2 .,Linked Report(s) : US-PFIZER INC-PV202200032027 same patient/drug, different event;