The correct answer is C, he had acquired long QT syndrome and requires no genetic testing. So Stefan had a markedly prolonged QTC, over 800 milliseconds at the time of his cardiac arrest. There are multiple contributing factors. They include his hypokalemia and likely the three antibiotics that he was on that can each cause acquired long QT syndrome. Fluconazole, levofloxacin, and metronidazole. Stefan's electrocardiogram a month later off medicines and with a normal potassium had only borderline QTC prolongation at 450 milliseconds, making acquired long QT syndrome the most likely diagnosis. Acquired long QT syndrome is common and can be present in up to 2% of people who would be susceptible to it were they given the appropriate drug that can cause it. Now acquired long QT syndrome is not commonly associated with the mutations that cause inherited long QT syndrome and genetic testing in the absence of a family history or persistence of the QT prolongation off drugs is not recommended. Acquired long QT syndrome is caused by drugs binding to the HERG potassium channel and is thought to represent diminished repolarization reserve. In other words, it is thought that there are a group of people who have less repolarizing potassium current than most people do. And even the relatively small block by the offending drugs will prolong the QT interval. While hypokalemia likely contributed to the QTC prolongation and the arrest, it is not a sufficient cause and Stefan should continue to avoid QT prolonging drugs. And a list of those drugs can be found at the website that I've listed here.

cardiac arrest

long QT syndrome

hypokalemia

HERG potassium channel

QT-prolonging drugs