A 49-year-old woman is brought to the emergency department with squeezing chest pain and profuse sweating for the last 2 hours. Medical history includes diet-controlled type 2 diabetes mellitus. ECG reveals ST-segment elevation in leads I, aVL, and V1-V4. The patient is immediately taken to the cardiac catheterization laboratory, where she is found to have complete occlusion of the left anterior descending coronary artery. The blockage is opened with percutaneous coronary intervention with stenting, but afterward she experiences recurrent and sustained episodes of ventricular arrhythmia. She is treated with an antiarrhythmic agent that preferentially binds to rapidly depolarizing and ischemic ventricular myocardial fibers and has minimal effect on normal ventricular myocardium. Which of the following agents was most likely used in this patient?
This patient sustained an anterolateral ST elevation myocardial infarction (MI) with successful reperfusion following percutaneous coronary intervention. Ventricular arrhythmias (premature beats, ventricular tachycardia/fibrillation) are common in the first 24-48 hours after MI and may be treated with antiarrhythmic medications (eg, amiodarone, lidocaine).
Class IB drugs like lidocaine are the weakest sodium channel blockers (dissociate the fastest) compared to other class I antiarrhythmics. They predominantly bind to sodium channels in the inactivated state, and dissociation from the channels occurs so rapidly that they have a negligible effect on QRS duration in normal cardiac tissues. Ischemic myocardium has higher than normal (less negative) resting membrane potential, which delays voltage-dependent recovery of sodium channels from the inactivated to the resting state. This allows increased binding of class IB agents; therefore, class IB antiarrhythmics are highly efficacious in inhibiting ischemia-induced ventricular arrhythmias.
(Choice A) Adenosine causes transient conduction delay through the atrioventricular (AV) node and is used in the acute treatment of paroxysmal supraventricular tachycardia; it is not indicated in ventricular arrhythmias.
(Choice B) Digoxin enhances vagal tone and leads to an increased effective refractory period and decreased conduction velocity through the AV node. These actions are useful in management of patients with supraventricular tachyarrhythmias.
(Choice C) Diltiazem is a class IV antiarrhythmic drug (calcium channel blocker) that slows the sinus rate, prolongs conduction through the AV node, and depresses myocardial contractility (ie, a negative inotropic effect). It is primarily used as a rate-control agent for the management of atrial tachyarrhythmias (eg, atrial flutter, atrial fibrillation).
(Choice D) Ibutilide is a class III antiarrhythmic drug (potassium channel blocker) and is occasionally used for acute termination of atrial flutter and fibrillation. It prolongs the QT interval and increases the risk of polymorphic ventricular tachycardia (torsades de pointes).
(Choice F) Metoprolol is a selective beta-1 receptor antagonist (class II antiarrhythmic) that acts as a negative inotropic and chronotropic agent (decreased myocardial contractility and heart rate). Beta blockers are frequently used in patients with acute or recent MI; they reduce the risk of ventricular arrhythmia by decreasing automaticity and reduce the size of ischemic myocardium by decreasing myocardial oxygen demand.
(Choice G) Class IA antiarrhythmic drugs (eg, procainamide, disopyramide) tend to bind to sodium channels in the open state and are more specific for suppressing arrhythmias arising from areas of normal automaticity (lidocaine is more specific to inactivated channels that are more predominant in ischemic myocardium). Class IA agents also have significant potassium channel-blocking activity, leading to prolongation of action potential and an increased risk of ventricular arrhythmias.
Educational objective:
Lidocaine is a class IB antiarrhythmic drug that tends to bind to inactivated sodium channels and rapidly dissociates. As a result, it is effective in suppressing ventricular tachyarrhythmias induced by rapidly depolarizing and ischemic myocardium.