This is the case:

Case 13 15 Minutes An 18-year-old high school student has seen a cardiologist regularly since it was discovered that she had symptoms of the long QT (LQT) syndrome 3 years ago. At that time, she experienced several episodes of light-headedness during a soccer game. Her family physician performed an analysis of systems, which found everything normal except for some electrocardiographic abnormalities. She was referred to the cardiologist whose examination included an ECG. The cardiologist reported a patient in normal sinus rhythm with a heart rate of 71 beats/min. Other ECG data were a PR interval of 0.14 s, QRS duration of 0.10 s, and a QT interval of 475 ms. The QT interval, even when corrected for heart rate, is abnormally long. Analysis of DNA revealed that the patient had a mutation in a gene linked to a cardiac potassium channel. The mutation results in less outward repolarizing current and therefore, a longer ventricular action potential. The phenotype of her syndrome is designated LQT1. The cardiologist had the patient walk around the office for light exercise. Immediately after exercising, her heart rate was increased and her QT interval had decreased, as expected. The cardiologist advised her not to participate in competitive athletics and prescribed a ?adrenergic antagonist (atenolol) to be taken daily. She has followed this regimen and has remained symptom-free since first diagnosed.

This is my question:

How does a voltage-gated K+ channel differ from voltage-gated Na+ channel structurally and functionally?