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Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited genetic disorder that predisposes those affected to potentially life-threatening abnormal heart rhythms or arrhythmias. The arrhythmias seen in CPVT typically occur during exercise or at times of emotional stress, and classically take the form of bidirectional ...
Ventricular tachycardia can occur due to coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte problems (e.g., low blood levels of magnesium or potassium), inherited channelopathies (e.g., long-QT syndrome), catecholaminergic polymorphic ventricular tachycardia, arrhythmogenic right ventricular dysplasia, alcohol withdrawal ...
It is a polymorphic ventricular tachycardia that exhibits distinct characteristics on the electrocardiogram (ECG). It was described by French physician François Dessertenne in 1966. [ 3 ] Prolongation of the QT interval can increase a person's risk of developing this abnormal heart rhythm, occurring in between 1% and 10% of patients who ...
QT prolongation is a measure of delayed ventricular repolarisation, which means the heart muscle takes longer than normal to recharge between beats. It is an electrical disturbance which can be seen on an electrocardiogram (ECG). Excessive QT prolongation can trigger tachycardias such as torsades de pointes (TdP).
[5] [6] The overload of the sarcoplasmic reticulum may cause spontaneous Ca 2+ release after repolarization, causing the released Ca 2+ to exit the cell through the 3Na + /Ca 2+-exchanger. This results in a net depolarizing current. The classical feature is Bidirectional ventricular tachycardia.
But ventricular tachycardia’s different than, say, a fast heart rate from exercising, which is called as “sinus tachycardia”. Normally, the electrical signals that generates each heart beat starts in the right atrium, at the sinus node, also known as the sinoatrial node or the SA node, if the rate goes over 100 bpm and originates in the ...
Re-entry ventricular arrhythmia is a type of paroxysmal tachycardia occurring in the ventricle where the cause of the arrhythmia is due to the electric signal not completing the normal circuit, but rather an alternative circuit looping back upon itself. [1] There develops a self-perpetuating rapid and abnormal activation.
Although many of those with Brugada syndrome do not have any symptoms, Brugada syndrome may cause fainting or sudden cardiac death due to serious abnormal heart rhythms, such as ventricular fibrillation or polymorphic ventricular tachycardia. [9] Blackouts may be caused by brief abnormal heart rhythms that revert to a normal rhythm spontaneously.
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