<unk>  QT<unk>  results from an inherited abnormality in the ion channels of the heart, most commonly potassium channels and sodium channels.  In<unk>  QT<unk> , mutations in the potassium channels lead to a decrease in the potassium efflux during repolarization, whereas gain of function in the sodium channels cause a slow sodium influx during depolarization.  The different mutations involved in<unk>  QT<unk>  culminate in a similar outcome which is the prolongation of both the action potential and the QT interval.  Arrhythmia in<unk>  QT<unk>  involve an abnormal repolarization of the heart.
Long QT Syndrome pathophysiology
Short QT syndrome pathophysiology
Sick sinus syndrome pathophysiology
Sinoatrial arrest pathophysiology
Pacemaker syndrome pathophysiology
Short QT syndrome risk factors
Brugada syndrome pathophysiology
Dextrocardia pathophysiology