An 11-year-old male neutered Birman cat was referred for investigation of pyelonephritis. On physical examination, gallop sounds and bradycardia were noted. There was mild azotaemia and marked neutrophilia, attributed to the pyelonephritis. Transthoracic echocardiography revealed a non-specific cardiomyopathy phenotype with biatrial enlargement. Electrocardiography showed wide QRS complexes, bradycardia and synchronous dissociation between atrial and ventricular activity. During the first examination, the synchronisation appeared mostly fixed, with consistent PR intervals, on subsequent evaluations, the PR intervals appeared to vary on a beat-to-beat basis. The diagnosis was of isorhythmic atrioventricular dissociation type I, with an initial long phase of fixed synchronisation, mimicking an isorhythmic atrioventricular dissociation type II, and concomitant ventricular depolarisation with a left bundle branch block morphology.

Wolff-Parkinson-White syndrome, though previously diagnosed and without prior arrhythmic events, may remain clinically quiescent until atrial fibrillation with rapid antegrade conduction over an accessory pathway precipitates a potentially life threatening arrhythmia. We present a teaching case of a 46-year-old man who developed abrupt onset wide-complex tachycardia with ventricular rates exceeding 280 beats per minute on postoperative day three following thoracic surgery. Electrocardiography demonstrated an irregularly irregular rhythm with marked beat-to beat QRS variability and very short RR intervals, favoring atrial fibrillation with preexcitation rather than ventricular tachycardia or rate-related aberrancy. This case is used to illustrate key electrocardiographic features that distinguish pre-excited atrial fibrillation from other causes of wide-complex tachycardia and to review evidence based management principles in hemodynamically stable patients, including the selection of therapies that target accessory pathway conduction while avoiding atrioventricular nodal blockade.

Hereditary transthyretin (TTR) cardiac amyloidosis is a rare infiltrative cardiomyopathy. Involvement of the cardiac conduction system may lead to atrioventricular block. Left bundle branch area pacing (LBBAP) represents an emerging pacing strategy. We report a case of hereditary TTR amyloidosis with 2:1 atrioventricular block (second-degree), a wide QRS escape rhythm, and reduced ejection fraction, in which LBBAP improved symptoms and hemodynamic parameters. To our knowledge, this is the first documented case of Ser43Asn TTR amyloidosis managed with LBBAP.

Diphenhydramine overdose can cause life-threatening ventricular dysrhythmias through sodium channel blockade, similar to tricyclic antidepressant (TCA) toxicity. Current management guidelines recommend sodium bicarbonate as first-line therapy, with class Ib antiarrhythmics such as lidocaine considered in refractory cases, though this recommendation is largely extrapolated from TCA data. Clinical reports describing lidocaine use in diphenhydramine toxicity remain exceedingly rare. We report a case where a 16-year-old female who ingested approximately 315 tablets of diphenhydramine and developed pulseless ventricular tachycardia during emergency department resuscitation. Return of spontaneous circulation was achieved after sodium bicarbonate, amiodarone and defibrillation, but recurrent wide-complex tachycardia occurred shortly thereafter. She was treated with a lidocaine bolus and continuous infusion, resulting in progressive QRS narrowing and rhythm stabilization. Diphenhydramine exposure was confirmed with toxicology testing. The lidocaine infusion was weaned, and patient was discharged home without further dysrhythmias. Experimental data demonstrates that diphenhydramine binds preferentially to open sodium channels and dissociates slowly, suggesting a mechanistic basis for lidocaine's therapeutic effect. This case provides additional clinical evidence supporting the use of lidocaine as an adjunct for refractory ventricular dysrhythmias in diphenhydramine induced sodium channel blockade and highlights the important of early recognition and consultation with a poison center in severe antihistamine toxicity.

The initial electrocardiogram (ECG) of a 5-month-old infant with complex congenital heart disease (pulmonary valvular stenosis, ventricular septal defects, and patent ductus arteriosus) revealed a regular wide QRS tachycardia at 169 bpm, initially suggestive of ventricular tachycardia (VT) or supraventricular tachycardia (SVT) with aberrant conduction. However, a subsequent ECG obtained during spontaneous heart rate deceleration to 143 bpm showed narrow QRS complexes with discernible sinus P waves and a markedly prolonged PR interval (300 ms). These findings establish the diagnosis of sinus rhythm with biatrial enlargement and first-degree atrioventricular (AV) block. Comparative analysis of these ECGs revealed that the initial tracing did not represent a true wide QRS complex but rather a "pseudo-wide QRS complex" tachycardia. This phenomenon occurs when profound PR prolongation results in concealed sinus P waves overlapping the terminal portion of the preceding QRS complex, thereby mimicking a wide QRS complex. The significant PR interval prolongation, reflecting first-degree AV block, is likely attributable to underlying anatomical abnormalities leading to atrial enlargement and consequent impaired AV nodal conduction. This case report highlights the critical importance of meticulously identifying concealed sinus P waves within wide QRS rhythms to prevent misdiagnosis and inappropriate interventions.

Electrocardiogram interpretation is critical in neonatal care, as artefacts may mimic life-threatening arrhythmias. We report the case of a preterm newborn girl, delivered at 31 weeks of gestation due to acute fetal distress, who developed tachycardia shortly after birth. The initial ECG showed chaotic electrical activity, initially raising suspicion of artifact; however, a subsequent tracing confirmed a life-threatening arrhythmia with wide QRS complexes, prolonged QTc, and torsades de pointes. As the patient remained haemodynamically stable, intravenous lidocaine and magnesium sulphate were administered, achieving pharmacological cardioversion. Propranolol was subsequently initiated, and the lidocaine infusion was tapered and replaced with oral mexiletine. Serial electrocardiograms showed QTc interval improvement, left ventricular function normalised, and the patient was discharged on the 39th postnatal day following stabilisation and supportive care for prematurity. Genetic testing identified a de novo SCN5A c.796C > G (p.L266V) mutation associated with Long QT syndrome type 3. At 1 year of age, the patient remains stable and asymptomatic while receiving combined therapy with propranolol and mexiletine.

A 55-year-old male from El Salvador presented to an emergency department in the northeastern United States with diarrhea, vomiting, dizziness, and melena. Shortly after arrival, the patient's heart rate increased to 235 beats/min with a narrow QRS complex, which subsequently degenerated into a wide complex ventricular tachycardia (VT). Initial workup revealed severe transaminitis, reduced systolic function, and an anomalous right coronary artery. After extensive diagnostic workup, including cardiac magnetic resonance imaging and serologies, a diagnosis of Chagas cardiomyopathy was made. Given the presence of arrhythmogenic substrate and a high Rassi score for sudden cardiac death, the patient underwent placement of an implantable cardioverter-defibrillator (ICD) for secondary prevention of VT. This case underscores the increasing importance of considering Chagas disease in patients in the United States coming from endemic countries and the decision-making process regarding ICD placement in a patient with underlying Chagas-related cardiomyopathy.

Idiopathic right ventricular outflow tract tachycardia (RVOT) of the Gallavardin type is a form of repetitive monomorphic ventricular tachycardia that typically occurs under adrenergic stimulation. Herein, we describe a typical presentation in a healthy, physically active man.The patient reported intermittent retrosternal tightness, palpitations and weakness during intense physical exertion. A 12-lead Holter-ECG repeatedly showed exercise-induced wide QRS-complex tachycardia with an inferior axis, left bundle branch block morphology and a presumed origin in the RVOT. After exclusion of structural heart disease by echocardiogram and unsuccessful antiarrhythmic therapy with verapamil, an electrophysiological study followed by catheter ablation was successfully performed. The patient remained asymptomatic.

Abnormal patterns of ventricular repolarisation are thought to contribute to lethal arrhythmias in various cardiac conditions, including inherited and acquired channelopathies, cardiomyopathies, and ischaemic heart disease. However, methods to detect these repolarisation abnormalities are limited. In this study, we introduce and assess a novel simulation-based method to infer ventricular activation and repolarisation times from the 12-lead electrocardiogram (ECG) and magnetic resonance-derived ventricular anatomical reconstruction, applicable for the first time to both healthy controls and cases with abnormal repolarisation. First, ventricular activation times were reconstructed through iterative refinement of early activation sites and conduction velocities, until the model and target QRS complexes matched. Then, ventricular repolarisation times were reconstructed through iterative refinement of ventricular action potential durations and an action potential shape parameter until the model and target T waves matched, including regularisation. Repolarisation inference was evaluated against 18 benchmark simulations with known repolarisation times, including both control and hypertrophic cardiomyopathy (HCM) cases with abnormal repolarisation. Inferred repolarisation times showed good agreement with the ground truth in control and HCM (Spearman r=0.63±0.11 and 0.65±0.19, respectively), with the inferred model T waves closely matching the target T waves (r=0.81±0.05 and 0.78±0.08, respectively). The method further demonstrated flexibility in reconstructing the macroscopic patterns of delayed repolarisation across a range of abnormal ventricular repolarisation sequences, demonstrating applicability to a wide range of pathological scenarios. Simulation-based inference can accurately reconstruct repolarisation times from the 12-lead ECG in cases with both normal and abnormal repolarisation patterns.