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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 ...
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 ...
Ventricular tachycardia (V-tach or VT) is a cardiovascular disorder in which fast heart rate occurs in the ventricles of the heart. [3] Although a few seconds of VT may not result in permanent problems, longer periods are dangerous; and multiple episodes over a short period of time are referred to as an electrical storm.
This tissue allows the electrical impulse, which stimulates the heartbeat, to happen very rapidly. Right ventricular outflow tract tachycardia is the most common type of ventricular tachycardia in otherwise healthy individuals. This defect is due to an electrical node in the right ventricle just before the pulmonary artery.
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).
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.
Early afterdepolarizations can result in torsades de pointes, tachycardia, and other arrhythmias. [3] 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.
However, ventricular tachycardia and ventricular fibrillation remain the most important causes of sudden death following spontaneous restoration of antegrade flow. [6] Prior to the modern practice of percutaneous coronary intervention for acute coronary syndrome , pharmacologic thrombolysis was more common and accelerated idioventricular ...
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