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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]
The QTc interval is longer in females, as well as having a stronger response to IKr-blocking agents. In males, the presence of testosterone upregulates IKr channels and therefore decreases QT interval. [2] Stated otherwise, estrogens prolong the QT interval, while androgens shorten it and decrease the response to IKr-blocking agents. [citation ...
Jervell and Lange-Nielsen syndrome causes severe sensorineural hearing loss from birth, affecting both ears. Those affected have a prolonged QT interval on an electrocardiogram and are at risk of abnormal heart rhythms (arrhythmias), which can cause dizziness, blackouts, or seizures. [2]
There’re at least 10 specific gene mutations that are known to be linked to Long QT syndrome, which are referred to as, for example, LQT1, LQT2, and so on, all of which have some effect on one or more ion channels. Aside from congenital causes though, sometimes the QT interval can be prolonged by certain medications which affect ion channels.
QT interval dispersion (QTd) is the maximum QT interval minus the minimum QT interval, and is linked with ventricular repolarization. [40] A QTd over 80 ms is considered abnormally prolonged. [ 41 ] Increased QTd is associated with mortality in type 2 diabetes. [ 41 ]
Torsades occurs as both an inherited (linked to at least 17 genes) [6] and as an acquired form caused most often by drugs and/or electrolyte disorders that cause excessive lengthening of the QT interval. [7] Common causes for torsades de pointes include drug-induced QT prolongation and less often diarrhea, low serum magnesium, and low serum ...
Romano–Ward syndrome is principally diagnosed by measuring the QT interval corrected for heart rate (QTc) on a 12-lead electrocardiogram (ECG). Romano–Ward syndrome is associated with a prolonged QTc, although in some genetically proven cases of Romano–Ward syndrome this prolongation can be hidden, known as concealed Long QT syndrome. [13]
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.