Step 1: Separate congenital from acquired long QT.
Torsades de pointes can occur in two settings: acquired long QT (from drugs, low potassium or magnesium, or bradycardia) and congenital long QT, present from birth due to an inherited ion channel defect. The management of the two overlaps for the emergency but differs for ongoing prevention.
Step 2: Recall acute, general treatment of torsades.
Any episode of torsades de pointes, congenital or acquired, is treated acutely with IV magnesium sulphate first, since it stabilises the cardiac membrane regardless of the cause. Overdrive pacing and isoproterenol are used mainly in acquired, pause-dependent torsades, where speeding up the heart rate shortens the QT interval and breaks the arrhythmia.
Step 3: Note why isoproterenol is wrong here.
Isoproterenol is a beta agonist. In congenital long QT syndrome, especially the common LQT1 type, sympathetic (catecholamine) surges are what trigger torsades in the first place. Giving isoproterenol to a patient with congenital long QT can worsen the arrhythmia rather than help it, so it is avoided here even though it helps in acquired, bradycardia-related torsades.
Step 4: Recall the mainstay for congenital long QT.
For patients with congenital long QT syndrome, the definitive, guideline-backed treatment to prevent torsades is a beta-blocker, traditionally propranolol, though metoprolol is also used, since it blunts the sympathetic trigger that provokes the arrhythmia in this inherited condition.
Step 5: Rule out magnesium and pacing as the specific answer.
Magnesium sulphate and overdrive pacing treat the acute rhythm disturbance but are not the answer suited to managing a lifelong, inherited channelopathy going forward.
Step 6: Final answer.
For a patient with congenital long QT syndrome, the beta-blocker metoprolol is the appropriate choice.
\[ \boxed{\text{Metoprolol}} \]