**Core Concept**
Prolonged QT interval is a cardiac electrical conduction abnormality characterized by a delay in the repolarization phase of the ventricular action potential. This can increase the risk of torsades de pointes, a potentially life-threatening arrhythmia.

**Why the Correct Answer is Right**
The correct answer is related to the pathophysiology of QT interval prolongation. Type 1a anti-arrhythmic drugs (e.g., quinidine, disopyramide) can prolong the QT interval by blocking potassium channels (specifically, the I_Kr and I_Ks channels) and thereby reducing the repolarization of the ventricular myocardium. This is in contrast to Type 1c anti-arrhythmic drugs, which primarily block sodium channels. The prolongation of the QT interval can lead to torsades de pointes, a polymorphic ventricular tachycardia.

**Why Each Wrong Option is Incorrect**
* **Option A:** Hypercalcemia can actually shorten the QT interval, not prolong it, by increasing the influx of calcium ions during the plateau phase of the action potential.
* **Option C:** Torsades de pointes is a consequence of QT interval prolongation, not a cause. It is a type of arrhythmia that can occur in the setting of prolonged QT intervals.
* **Option D:** Atrial fibrillation is a type of supraventricular tachycardia, not a direct consequence of QT interval prolongation.

**Clinical Pearl / High-Yield Fact**
When managing patients with prolonged QT intervals, it's essential to avoid administering Type 1a anti-arrhythmic drugs and to closely monitor for signs of torsades de pointes, such as polymorphic ventricular tachycardia.

**Correct Answer:** B. Type la anti arrythmic drugs