Step 1: Read the key phrase in the question.
"Prolonged QT interval since birth" signals congenital long QT syndrome, an inherited channelopathy, not a drug or electrolyte problem picked up later in life.
Step 2: Split the four options by mechanism.
Magnesium sulphate calms the heart membrane in any torsades episode. Overdrive pacing and isoproterenol both work by raising heart rate, which shortens a QT interval that is long because of bradycardia or a pause, the pattern typical of acquired long QT from drugs or electrolyte problems. Metoprolol, a beta-blocker, works by blunting the effect of adrenaline on the heart.
Step 3: Match mechanism to congenital disease.
In congenital long QT syndrome, especially the LQT1 subtype, exercise and emotional stress, meaning adrenaline surges, are the classic triggers for torsades. A drug like isoproterenol that mimics adrenaline would make this worse, not better, so it is unsuitable here even though it is useful in acquired, bradycardia-driven torsades.
Step 4: Confirm the beta-blocker link.
Because adrenaline drive is the problem in congenital LQTS, blocking it with a beta-blocker is the standard preventive treatment recommended for these patients, cutting the risk of future torsades and sudden death.
Step 5: State the answer.
The suitable drug for this patient with lifelong QT prolongation is the beta-blocker $metoprolol$.
\[ \boxed{\text{Metoprolol}} \]