The cardiac QT interval (QTc) determines the time elapsed between contraction and relaxation of the cardiac ventricles. It may be shortened at faster heart rates, or lengthened at slower rates without further consequences, however, abnormalities in this interval may trigger clinical implications.
The QT interval represents the duration of systole or ventricular contraction (the set of ventricular depolarization and repolarization), and is visualized on an electrocardiogram as the period between the beginning of the Q wave and the end of the T wave. This value can vary in physiological situations inversely proportional to the value of the heartbeat without major consequences. However, there are different clinical conditions that trigger the abnormal increase or decrease of this interval in individuals who may be genetically predisposed.
An abnormally long QTc is considered when it exceeds 440 milliseconds (ms) in men and 460 ms in women. This increase in clinical QTc may be due to acquired situations of low blood levels of potassium (hypokalemia), magnesium (hypomagnesemia), calcium (hypocalcemia), in cases of hypothermia, myocardial ischemia, increased intracranial pressure, or due to the presence of a high blood pressure (hypokalemia).In cases of hypothermia, myocardial ischemia, increased intracranial pressure, or due to the use of certain drugs such as some antipsychotics, antiarrhythmics or antibiotics, as well as congenital forms in the case of Long QT syndrome. Long QT syndrome is a congenital structural channelopathy of cardiac calcium and/or sodium channels or proteins involved in the modulation of ionic currents. The most relevant manifestations include episodes of syncope that can lead to cardiac arrest and sudden cardiac death. In some cases it may be associated with extracardiac manifestations such as deafness or neurodevelopmental disorders among others.
An abnormally short QTc is considered when it does not reach <350ms. This decrease can also be acquired in association with elevated levels of calcium in the blood (hypercalcemia), or potassium (hyperkalemia) to the use of the antiarrhythmic digoxin, as well as the congenital form of short QT syndrome. This hereditary pathology consists of a potassium channel disorder associated with an increased risk of paroxysmal atrial and ventricular fibrillation and sudden cardiac death. Most patients present manifestations such as atrial fibrillation, palpitations or fainting.
In any case, follow-up is recommended in cases of suggestive electrocardiograms, family history of sudden death, and personal histories of syncope or fibrillation of unknown origin.
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