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Acquired long QT syndrome. Many people with long QT syndrome have no signs or symptoms. When symptoms occur, they are generally caused by abnormal heart rhythms (arrhythmias), most commonly a form of ventricular tachycardia called Torsades de pointes (TdP).
Andersen–Tawil syndrome, also called Andersen syndrome and long QT syndrome 7, is a rare genetic disorder affecting several parts of the body. The three predominant features of Andersen–Tawil syndrome include disturbances of the electrical function of the heart characterised by an abnormality seen on an electrocardiogram (a long QT interval) and a tendency to abnormal heart rhythms ...
The term "torsades de pointes" is translated from French as "twisting of the peaks" because the complexes appear to undulate, or twist around, the EKG baseline. TdP can be acquired by inheritance of a congenital long QT syndrome, or more commonly from the ingestion of a pharmacologic drug. During TdP episodes, patients have a heart rate of 200 ...
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.
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.
Treatments used to prevent torsades in specific circumstances include beta blockers or mexiletine in long QT syndrome. [25] Occasionally a pacemaker may be used to accelerate the heart's own sinus rhythm, and those at risk of further torsades may be offered an implantable defibrillator to automatically detect and defibrillate further episodes ...
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]
Long QT syndrome, the most common form of cardiac channelopathy, is characterized by prolonged ventricular repolarization, predisposing to a high risk of ventricular tachyarrhythmias (e.g., torsade de pointes), syncope, and sudden cardiac death.
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