QT Intervals

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.

Number of observed variants

13.5 million variants

Number of loci analyzed

34 loci

Genes analyzed

ANKRD9 ATP1B1 ATP2A2 AZIN1 CAV1 CCT6B CDC23 CREBBP ELP6 EXOG FADS1 GBF1 GMPR KCNH2 KCNJ2 KCNQ1 KLF12 LITAF MATN2 MRTFB NCOA2 NOS1AP PLN PRKCA RPL22 SETD6 SLC4A4 SLC8A1 SMARCAD1 SP3 SPATS2L TTN USP50 ZNF436

Bibliography

ECG library [May 2022].

Al-Azaam B et al. Atrial Fibrillation in Inherited Channelopathies. Card Electrophysiol Clin. 2021 Mar;13(1):155-163.

Schwartz PJ et al. Inherited cardiac arrhythmias. Nat Rev Dis Primers. 2020;6(1):58.

Loussouarn G et al. Diversity in human hair growth, diameter, colour and shape. An in vivo study on young adults from 24 different ethnic groups observed in the five continents. Eur J Dermatol 2016; 26(2): 144-54.

Arking DE et al. Genetic association study of QT interval highlight’s role for calcium signaling pathways in myocardial repolarization. Nature Genetics, 22 Jun 2014, 46(8):826-836.

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