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Long QT syndrome (LQTS) is a condition affecting repolarization (relaxing) of the heart after a heartbeat, giving rise to an abnormally lengthy QT interval. [7] It results in an increased risk of an irregular heartbeat which can result in fainting, drowning, seizures, or sudden death. [1]
In addition, factors such as rapid infusion, concurrent use of more than one drug known to prolong QT interval, diuretic treatment, electrolyte derangements (hypokalemia, hypomagnesemia, or hypocalcemia), advanced age, bradyarrhythmias, and female sex have all been shown to be risk factors for developing drug-induced QT prolongation. [2]
The QT interval is a measurement made on an electrocardiogram used to assess some of the electrical properties of the heart.It is calculated as the time from the start of the Q wave to the end of the T wave, and approximates to the time taken from when the cardiac ventricles start to contract to when they finish relaxing.
Torsades de pointes is associated with long QT syndrome, a condition whereby prolonged QT intervals are visible on an ECG. Long QT intervals predispose the patient to an R-on-T phenomenon, wherein the R-wave, representing ventricular depolarization, occurs during the relative refractory period at the end of repolarization (represented by the ...
Long QT syndrome, or LQTS, is when somebody’s QT interval is longer than normal, which should typically be less than half of a cardiac cycle. In fact, for a heart rate of 60 beats per minute, the QT interval’s generally considered to be abnormally long when it’s greater than 440 milliseconds in males or 460 milliseconds in females.
The risk of arrhythmias is higher for those with Jervell and Lange-Nielsen syndrome than other forms of long QT syndrome. [10] Although this risk is dependent on the underlying genetic defect and degree of QT prolongation, without treatment more than 50% of those affected will die before the age of 15. [11]
Romano–Ward syndrome is a descriptive term for a group of subtypes of long QT syndrome, specifically subtypes LQT1-6 and LQT9-16. [8] Several subtypes of Romano–Ward syndrome have been described based on the underlying genetic variant. [5] These subtypes differ in clinical presentation and their response to treatment.
EADs can be triggered by hypokalemia and drugs that prolong the QT interval, including class Ia and III antiarrhythmic agents, as well as catecholamines. [1] Afterhyperpolarizations can also occur in cortical pyramidal neurons. There, they typically follow an action potential and are mediated by voltage gated sodium or chloride channels.