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Pharmacology · Cardiovascular drugs: class IC antiarrhythmics
Sample itemA 62-year-old man with a previous myocardial infarction and an ejection fraction of 35% has frequent ventricular premature beats. A colleague proposes flecainide to suppress them. Why is this inappropriate?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Use-dependent sodium channel block in structural heart disease increases proarrhythmic mortality
In the Cardiac Arrhythmia Suppression Trial, encainide and flecainide suppressed ventricular ectopy after infarction but increased mortality. Class IC drugs markedly slow conduction and can provoke fatal re-entrant ventricular arrhythmias in scarred myocardium. They are used only in patients without structural heart disease, for example for atrial fibrillation or supraventricular tachycardia.
Option by option
A. It prolongs the QT interval through IKr block and causes torsades
Flecainide acts chiefly by widening the QRS through sodium channel block; torsades from marked QT prolongation is the typical hazard of class IA and III agents.
B. Use-dependent sodium channel block in structural heart disease increases proarrhythmic mortality (correct)
Correct. Slowed conduction in scar tissue favours lethal re-entry.
C. It causes severe bradycardia through beta-adrenergic blockade
Flecainide has no important beta-blocking action.
D. It causes pulmonary fibrosis with long-term use
Pulmonary fibrosis is characteristic of amiodarone.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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