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Pharmacology · Antiarrhythmics: class IC drugs after myocardial infarction
Sample itemA 62-year-old man two weeks after anterior myocardial infarction with an ejection fraction of 35 percent has frequent asymptomatic ventricular premature beats. A colleague suggests 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
D. Class IC drugs increased mortality in post-infarction patients in the CAST trial
The Cardiac Arrhythmia Suppression Trial showed that flecainide and encainide, given to suppress ventricular ectopy after infarction, increased mortality through proarrhythmia in scarred myocardium. Class IC agents (flecainide, propafenone) are therefore avoided in structural heart disease and ischaemia. Beta-blockers improve outcome in this setting.
Option by option
A. Flecainide causes pulmonary fibrosis within weeks
Pulmonary fibrosis is a typical amiodarone adverse effect.
B. Flecainide acts as a class III agent that triggers torsades de pointes
Flecainide is a potent sodium channel blocker of class IC, not a class III potassium channel blocker.
C. Flecainide is ineffective against ventricular ectopy
Flecainide does suppress ventricular ectopy, which is why CAST tested it.
D. Class IC drugs increased mortality in post-infarction patients in the CAST trial (correct)
Correct. Suppressing ectopy with class IC drugs after infarction worsened survival.
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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