1 Our patient was not taking one, and he had 1:1 atrial flutter with a rapid ventricular response. 12, 13 Therefore, patients taking flecainide may also need an AV nodal-blocking agent to mitigate this risk if AF recurs. The estimated incidence of atrial proarrhythmic effects from class IC agents is 3.5% to 5%. 11 Hemodynamic compromise results when the atrial rate slows to enable 1:1 conduction through the AV node, 12 in the presence of rapid ventricular response. 11 Flecainide slows conduction through the atrial tissue more than it prolongs refractoriness, which enables organized AF activity and promotes atrial flutter. Atrial proarrhythmia has been described as the development of a persistent atrial arrhythmia that is either new or was previously paroxysmal. More notable, as in our patient's case, are the atrial arrhythmogenic properties of flecainide. 10 Because flecainide can cause life-threatening ventricular proarrhythmias in individuals who have structural heart disease, its use is now contraindicated in this patient population. 9 The extent to which flecainide delays cardiac conduction varies in different cardiac tissue its effects are more prominent in the atrial myocardium and the His-Purkinje system than in atrioventricular (AV) nodal tissue, thus giving rise to its antiarrhythmic actions and its proarrhythmic side effects. 5 – 8 Like other class IC antiarrhythmic agents, it selectively blocks sodium currents and inhibits potassium channels, thus prolonging cardiac conduction velocity and refractoriness. 4 Flecainide is well studied and is a safe therapy for AF. The first published ECG tracing of atrial flutter, in 1915, was from a patient whose ventricular rate was 270 beats/min. At 3-month follow-up, his ECG showed sinus rhythm, normal QRS duration, and no left bundle branch block ( Fig. Three months later, he underwent outpatient AF cryoablation. He tolerated the procedure without complication, remained in sinus rhythm, and was discharged from the hospital with instructions for outpatient cardiology follow-up. The day after hospital admission, the patient underwent radiofrequency catheter ablation across the cavotricuspid isthmus, to treat highly symptomatic atrial flutter. An echocardiogram confirmed the absence of structural heart disease. His only other prescribed medication was the anticoagulant rivaroxaban. After the second treatment, he had begun taking 100 mg of flecainide twice daily to maintain sinus rhythm. He had undergone 3 electrical cardioversions at 13 years, one year, and one week before the current presentation. ![]() The patient's medical history included refractory paroxysmal AF and atrial flutter, which had been diagnosed in 2004. The patient's 12-lead electrocardiogram on hospital arrival shows sinus rhythm and left bundle branch block, without ventricular tachycardia. The patient needed no cardiopulmonary resuscitation or intubation in the field, and he lost consciousness only temporarily after the first cardioversion. Subsequently, a 360-J shock restored sinus rhythm. However, as a result of the patient's rapid ventricular rate, the synchronized shock immediately precipitated VF secondary to the R-on-T phenomenon-also known as a “shock on T”-in which a premature beat of ventricular origin early after contraction causes persistent ventricular arrhythmia ( Fig. The patient was hemodynamically unstable, so the technicians attempted cardioversion with a direct-current, synchronized 100-J shock. The emergency medical technicians noted wide-complex tachycardia on telemetry (heart rate, 260 beats/min), consistent with atrial flutter with 1:1 conduction ( Fig. He had been in normal health until the morning of presentation, when he had sudden-onset dyspnea, palpitations, and a cough that produced pink sputum. In February 2019, a 59-year-old man arrived at our hospital by ambulance after being found in severe respiratory distress.
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