Benign early repolarization

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Benign early repolarization
Semantic confusion early repolarization (CardioNetworks ECGpedia).svg
Classic and new definitions of early repolarization with end-QRS notching and end-QRS slurring
Benign early repolorization.jpg
ECG of a benign early repolarization in a 15-year-old male
Specialty Cardiology
Frequency1-13% [1]

Benign early repolarization (BER) or early repolarization is found on an electrocardiogram (ECG) in about 1% of those with chest pain. [2] It is diagnosed based on an elevated J-point / ST elevation with an end-QRS notch or end-QRS slur and where the ST segment concave up. It is believed to be a normal variant. [2]

Contents

Benign early repolarization that occurs as some patterns is associated with ventricular fibrillation. The association, revealed by research performed in the late 2000s, is very small.

Types

Benign early repolarization, very prevalent in younger people and healthy male athletes, can be divided into 3 subtypes: [3] [4]

Associations with serious conditions

Research in the late 2000s has linked this finding when found as some patterns to ventricular fibrillation, particularly in those who have fainted or have a family history of sudden cardiac death. [5] [6] [7] Although there is a significant relationship between ventricular fibrillation and some early repolarization's patterns, the overall lifetime occurrence of idiopathic ventricular fibrillation is exceptionally rare. [8] There has also been an association between early repolarization and short QT syndrome. [9]

Risk factors

Electrocardiography

On an electrocardiogram (EKG or ECG), benign early repolarization may produce an elevation of the J-point and ST segment in 2 or more leads, similar to that observed in heart attacks (myocardial infarction). However, with benign early repolarization, the ST segment is usually concave up, rather than concave down (as with heart attacks), and there is a notable absence of reciprocal changes suggestive of ischemia on the EKG.

Causes

It is thought that the mechanism causing early repolarization is a more excitable ion channel system, which causes a faster myocardium contraction. [13] Studies have shown that higher testosterone levels in males result in an increased outward potassium currents causing J-point elevation. [15]

Epidemiology

Benign early repolarization occurs in about 1 to 13 percent of the general population with a significant increase in occurrence within athletes and adolescents. [1] In one study, an occurrence of early repolarization was observed in 31.6% of elite athletes while in another study occurrence was observed in 25.1% of athletes. [16] [17]

Being a male is strongly associated with early repolarization ECG pattern, and 70% of subjects with early repolarization are males. Prevalence of early repolarization declines in males from early adulthood until middle-age which could suggest a hormonal influence on its presence. Early repolarization patterns are more common in physically active younger individuals, athletes and Africans. [18]

Genetics

Genes associated with ER and ATP sensitive potassium current channel mutations are KCNJ8, ABCC9 [11] [19] [20] Others associated with transient outward potassium current - KCNE5, DPP10, L-type voltage gated calcium current - CACNA1C, CACNB2B, CACNA2D1, sodium current - SCN5A, SCN10A. [14]

History

Early repolarization with ST segment elevation was first described in 1936 by R.A. Shipley and W.R. Hallaran in a study of 200 healthy 20–35 year old people. [14] [21]

Related Research Articles

<span class="mw-page-title-main">Electrocardiography</span> Examination of the hearts electrical activity

Electrocardiography is the process of producing an electrocardiogram, a recording of the heart's electrical activity through repeated cardiac cycles. It is an electrogram of the heart which is a graph of voltage versus time of the electrical activity of the heart using electrodes placed on the skin. These electrodes detect the small electrical changes that are a consequence of cardiac muscle depolarization followed by repolarization during each cardiac cycle (heartbeat). Changes in the normal ECG pattern occur in numerous cardiac abnormalities, including:

<span class="mw-page-title-main">Brugada syndrome</span> Heart conduction disease

Brugada syndrome (BrS) is a genetic disorder in which the electrical activity of the heart is abnormal due to channelopathy. It increases the risk of abnormal heart rhythms and sudden cardiac death. Those affected may have episodes of syncope. The abnormal heart rhythms seen in those with Brugada syndrome often occur at rest. They may be triggered by a fever.

<span class="mw-page-title-main">Ventricular fibrillation</span> Rapid quivering of the ventricles of the heart

Ventricular fibrillation is an abnormal heart rhythm in which the ventricles of the heart quiver. It is due to disorganized electrical activity. Ventricular fibrillation results in cardiac arrest with loss of consciousness and no pulse. This is followed by sudden cardiac death in the absence of treatment. Ventricular fibrillation is initially found in about 10% of people with cardiac arrest.

<span class="mw-page-title-main">Premature ventricular contraction</span> Skipped beat with ventricular origin

A premature ventricular contraction (PVC) is a common event where the heartbeat is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node. PVCs may cause no symptoms or may be perceived as a "skipped beat" or felt as palpitations in the chest. PVCs do not usually pose any danger.

<span class="mw-page-title-main">Long QT syndrome</span> Medical condition

Long QT syndrome (LQTS) is a condition affecting repolarization (relaxing) of the heart after a heartbeat, giving rise to an abnormally lengthy QT interval. It results in an increased risk of an irregular heartbeat which can result in fainting, drowning, seizures, or sudden death. These episodes can be triggered by exercise or stress. Some rare forms of LQTS are associated with other symptoms and signs including deafness and periods of muscle weakness.

<span class="mw-page-title-main">Wolff–Parkinson–White syndrome</span> Medical condition

Wolff–Parkinson–White syndrome (WPWS) is a disorder due to a specific type of problem with the electrical system of the heart involving an accessory pathway able to conduct electrical current between the atria and the ventricles, thus bypassing the atrioventricular node. About 60% of people with the electrical problem developed symptoms, which may include an abnormally fast heartbeat, palpitations, shortness of breath, lightheadedness, or syncope. Rarely, cardiac arrest may occur. The most common type of irregular heartbeat that occurs is known as paroxysmal supraventricular tachycardia.

<span class="mw-page-title-main">Short QT syndrome</span> Medical condition

Short QT syndrome (SQT) is a very rare genetic disease of the electrical system of the heart, and is associated with an increased risk of abnormal heart rhythms and sudden cardiac death. The syndrome gets its name from a characteristic feature seen on an electrocardiogram (ECG) – a shortening of the QT interval. It is caused by mutations in genes encoding ion channels that shorten the cardiac action potential, and appears to be inherited in an autosomal dominant pattern. The condition is diagnosed using a 12-lead ECG. Short QT syndrome can be treated using an implantable cardioverter-defibrillator or medications including quinidine. Short QT syndrome was first described in 2000, and the first genetic mutation associated with the condition was identified in 2004.

<span class="mw-page-title-main">Cardiac conduction system</span> Aspect of heart function

The cardiac conduction system transmits the signals generated by the sinoatrial node – the heart's pacemaker, to cause the heart muscle to contract, and pump blood through the body's circulatory system. The pacemaking signal travels through the right atrium to the atrioventricular node, along the bundle of His, and through the bundle branches to Purkinje fibers in the walls of the ventricles. The Purkinje fibers transmit the signals more rapidly to stimulate contraction of the ventricles.

<span class="mw-page-title-main">Torsades de pointes</span> Type of abnormal heart rhythm

Torsades de pointes, torsade de pointes or torsades des pointes is a specific type of abnormal heart rhythm that can lead to sudden cardiac death. It is a polymorphic ventricular tachycardia that exhibits distinct characteristics on the electrocardiogram (ECG). It was described by French physician François Dessertenne in 1966. 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 receive QT-prolonging antiarrhythmic drugs.

<span class="mw-page-title-main">Ventricular tachycardia</span> Medical condition of the heart

Ventricular tachycardia is a cardiovascular disorder in which fast heart rate occurs in the ventricles of the heart. 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. Short periods may occur without symptoms, or present with lightheadedness, palpitations, shortness of breath, chest pain, and decreased level of consciousness. Ventricular tachycardia may lead to coma and persistent vegetative state due to lack of blood and oxygen to the brain. Ventricular tachycardia may result in ventricular fibrillation (VF) and turn into cardiac arrest. This conversion of the VT into VF is called the degeneration of the VT. It is found initially in about 7% of people in cardiac arrest.

<span class="mw-page-title-main">QT interval</span> Measurement made on an electrocardiogram

The QT interval is a measurement made on an electrocardiogram used to assess some of the electrical properties of the heart. It is calculated as the time from the start of the Q wave to the end of the T wave, and approximates to the time taken from when the cardiac ventricles start to contract to when they finish relaxing. An abnormally long or abnormally short QT interval is associated with an increased risk of developing abnormal heart rhythms and sudden cardiac death. Abnormalities in the QT interval can be caused by genetic conditions such as long QT syndrome, by certain medications such as sotalol or pitolisant, by disturbances in the concentrations of certain salts within the blood such as hypokalaemia, or by hormonal imbalances such as hypothyroidism.

<span class="mw-page-title-main">Supraventricular tachycardia</span> Abnormally fast heart rhythm

Supraventricular tachycardia (SVT) is an umbrella term for fast heart rhythms arising from the upper part of the heart. This is in contrast to the other group of fast heart rhythms – ventricular tachycardia, which start within the lower chambers of the heart. There are four main types of SVT: atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia (PSVT), and Wolff–Parkinson–White syndrome. The symptoms of SVT include palpitations, feeling of faintness, sweating, shortness of breath, and/or chest pain.

<span class="mw-page-title-main">Repolarization</span> Change in membrane potential

In neuroscience, repolarization refers to the change in membrane potential that returns it to a negative value just after the depolarization phase of an action potential which has changed the membrane potential to a positive value. The repolarization phase usually returns the membrane potential back to the resting membrane potential. The efflux of potassium (K+) ions results in the falling phase of an action potential. The ions pass through the selectivity filter of the K+ channel pore.

<span class="mw-page-title-main">T wave</span> Repolarization of the ventricles in a human heart

In electrocardiography, the T wave represents the repolarization of the ventricles. The interval from the beginning of the QRS complex to the apex of the T wave is referred to as the absolute refractory period. The last half of the T wave is referred to as the relative refractory period or vulnerable period. The T wave contains more information than the QT interval. The T wave can be described by its symmetry, skewness, slope of ascending and descending limbs, amplitude and subintervals like the Tpeak–Tend interval.

SCN5A Protein-coding gene in the species Homo sapiens

Sodium channel protein type 5 subunit alpha, also known as NaV1.5 is an integral membrane protein and tetrodotoxin-resistant voltage-gated sodium channel subunit. NaV1.5 is found primarily in cardiac muscle, where it mediates the fast influx of Na+-ions (INa) across the cell membrane, resulting in the fast depolarization phase of the cardiac action potential. As such, it plays a major role in impulse propagation through the heart. A vast number of cardiac diseases is associated with mutations in NaV1.5 (see paragraph genetics). SCN5A is the gene that encodes the cardiac sodium channel NaV1.5.

<span class="mw-page-title-main">Catecholaminergic polymorphic ventricular tachycardia</span> Medical condition

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 or ventricular fibrillation. Those affected may be asymptomatic, but they may also experience blackouts or even sudden cardiac death.

<span class="mw-page-title-main">KCNE5</span> Protein-coding gene in the species Homo sapiens

KCNE1-like also known as KCNE1L is a protein that in humans is encoded by the KCNE1L gene.

<span class="mw-page-title-main">Arrhythmia</span> Group of medical conditions characterized by irregular heartbeat

Arrhythmias, also known as cardiac arrhythmias, heart arrhythmias, or dysrhythmias, are irregularities in the heartbeat, including when it is too fast or too slow. A resting heart rate that is too fast – above 100 beats per minute in adults – is called tachycardia, and a resting heart rate that is too slow – below 60 beats per minute – is called bradycardia. Some types of arrhythmias have no symptoms. Symptoms, when present, may include palpitations or feeling a pause between heartbeats. In more serious cases, there may be lightheadedness, passing out, shortness of breath, chest pain, or decreased level of consciousness. While most cases of arrhythmia are not serious, some predispose a person to complications such as stroke or heart failure. Others may result in sudden death.

<span class="mw-page-title-main">Cardiac transient outward potassium current</span> Ion current

The cardiac transient outward potassium current (referred to as Ito1 or Ito ) is one of the ion currents across the cell membrane of heart muscle cells. It is the main contributing current during the repolarizing phase 1 of the cardiac action potential. It is a result of the movement of positively charged potassium (K+) ions from the intracellular to the extracellular space. Ito1 is complemented with Ito2 resulting from Cl− ions to form the transient outward current Ito.

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). QT prolongation is an established side effect of antiarrhythmics, but can also be caused by a wide range of non-cardiac medicines, including antibiotics, antidepressants, antihistamines, opioids, and complementary medicines. On an ECG, the QT interval represents the summation of action potentials in cardiac muscle cells, which can be caused by an increase in inward current through sodium or calcium channels, or a decrease in outward current through potassium channels. By binding to and inhibiting the “rapid” delayed rectifier potassium current protein, certain drugs are able to decrease the outward flow of potassium ions and extend the length of phase 3 myocardial repolarization, resulting in QT prolongation.

References

  1. 1 2 Bourier F, Denis A, Cheniti G, Lam A, Vlachos K, Takigawa M, et al. (2018-11-27). "Early Repolarization Syndrome: Diagnostic and Therapeutic Approach". Frontiers in Cardiovascular Medicine. 5: 169. doi: 10.3389/fcvm.2018.00169 . PMC   6278243 . PMID   30542653.
  2. 1 2 Brady WJ, Chan TC (1999). "Electrocardiographic manifestations: benign early repolarization". The Journal of Emergency Medicine. 17 (3): 473–478. doi:10.1016/S0736-4679(99)00010-4. PMID   10338242.
  3. ↑ Buttner R, Cadogan M (2021-01-21). "'Benign' Early Repolarization Misnomer". Life in the Fast Lane • LITFL. Retrieved 2021-12-25.
  4. ↑ Antzelevitch C, Yan GX, Viskin S (April 2011). "Rationale for the use of the terms J-wave syndromes and early repolarization". Journal of the American College of Cardiology. 57 (15): 1587–1590. doi:10.1016/j.jacc.2010.11.038. PMC   3073061 . PMID   21474038.
  5. ↑ Stern S (April 2011). "Clinical aspects of the early repolarization syndrome: a 2011 update". Annals of Noninvasive Electrocardiology. 16 (2): 192–195. doi:10.1111/j.1542-474X.2011.00429.x. PMC   6932469 . PMID   21496171.
  6. ↑ Haïssaguerre M, Derval N, Sacher F, Jesel L, Deisenhofer I, de Roy L, et al. (May 2008). "Sudden cardiac arrest associated with early repolarization". The New England Journal of Medicine. 358 (19): 2016–2023. doi: 10.1056/NEJMoa071968 . PMID   18463377.
  7. ↑ Nam GB, Kim YH, Antzelevitch C (May 2008). "Augmentation of J waves and electrical storms in patients with early repolarization". The New England Journal of Medicine. 358 (19): 2078–2079. doi:10.1056/NEJMc0708182. PMC   2515862 . PMID   18463391.
  8. ↑ Priori SG, Wilde AA, Horie M, Cho Y, Behr ER, Berul C, et al. (October 2013). "Executive summary: HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes". Europace. 15 (10): 1389–1406. doi:10.1093/europace/eut272. PMID   23994779.
  9. ↑ Watanabe H, Makiyama T, Koyama T, Kannankeril PJ, Seto S, Okamura K, et al. (May 2010). "High prevalence of early repolarization in short QT syndrome". Heart Rhythm. 7 (5): 647–652. doi:10.1016/j.hrthm.2010.01.012. PMID   20206319.
  10. 1 2 3 Junttila MJ, Sager SJ, Tikkanen JT, Anttonen O, Huikuri HV, Myerburg RJ (November 2012). "Clinical significance of variants of J-points and J-waves: early repolarization patterns and risk". European Heart Journal. 33 (21): 2639–2643. doi:10.1093/eurheartj/ehs110. PMID   22645193.
  11. 1 2 Mercer BN, Begg GA, Page SP, Bennett CP, Tayebjee MH, Mahida S (2016-06-30). "Early Repolarization Syndrome; Mechanistic Theories and Clinical Correlates". Frontiers in Physiology. 7: 266. doi: 10.3389/fphys.2016.00266 . PMC   4927622 . PMID   27445855.
  12. ↑ Sethi, Kamal K.; Sethi, Kabir; Chutani, Surendra K. (2014). "Early repolarisation and J wave syndromes". Indian Heart Journal. 66 (4): 443–452. doi:10.1016/j.ihj.2014.06.002. ISSN   0019-4832. PMC   4150048 . PMID   25173204.
  13. 1 2 3 4 Sayedahmad Z, Darmoch F, Al-Khadra Y, Kabach A, Alraies MC (March 2019). "Does early repolarization on ECG increase the risk of cardiac death in healthy people?". Cleveland Clinic Journal of Medicine. 86 (3): 165–166. doi: 10.3949/ccjm.86a.17032 . PMID   30849033. S2CID   73467268.
  14. 1 2 3 "Early Repolarization Syndrome". American College of Cardiology. Retrieved 2021-12-25.
  15. ↑ Bourier, Felix; Denis, Arnaud; Cheniti, Ghassen; Lam, Anna; Vlachos, Konstantinos; Takigawa, Masateru; Kitamura, Takeshi; Frontera, Antonio; Duchateau, Josselin; Pambrun, Thomas; Klotz, Nicolas (2018). "Early Repolarization Syndrome: Diagnostic and Therapeutic Approach". Frontiers in Cardiovascular Medicine. 5: 169. doi: 10.3389/fcvm.2018.00169 . ISSN   2297-055X. PMC   6278243 . PMID   30542653.
  16. ↑ Serra-Grima R, Doñate M, Álvarez-García J, Barradas-Pires A, Ferrero A, Carballeira L, et al. (February 2015). "Long-term follow-up of early repolarization pattern in elite athletes". The American Journal of Medicine. 128 (2): 192.e1–192.e9. doi: 10.1016/j.amjmed.2014.06.017 . PMID   24979742.
  17. ↑ Noseworthy PA, Weiner R, Kim J, Keelara V, Wang F, Berkstresser B, et al. (August 2011). "Early repolarization pattern in competitive athletes: clinical correlates and the effects of exercise training". Circulation: Arrhythmia and Electrophysiology. 4 (4): 432–440. doi:10.1161/CIRCEP.111.962852. PMC   3700366 . PMID   21543642.
  18. ↑ Sethi KK, Sethi K, Chutani SK (2014). "Early repolarisation and J wave syndromes". Indian Heart Journal. 66 (4): 443–452. doi:10.1016/j.ihj.2014.06.002. PMC   4150048 . PMID   25173204.
  19. ↑ Haïssaguerre M, Chatel S, Sacher F, Weerasooriya R, Probst V, Loussouarn G, et al. (January 2009). "Ventricular fibrillation with prominent early repolarization associated with a rare variant of KCNJ8/KATP channel". Journal of Cardiovascular Electrophysiology. 20 (1): 93–98. doi:10.1111/j.1540-8167.2008.01326.x. PMID   19120683. S2CID   21002962.
  20. ↑ Medeiros-Domingo A, Tan BH, Crotti L, Tester DJ, Eckhardt L, Cuoretti A, et al. (October 2010). "Gain-of-function mutation S422L in the KCNJ8-encoded cardiac K(ATP) channel Kir6.1 as a pathogenic substrate for J-wave syndromes". Heart Rhythm. 7 (10): 1466–1471. doi:10.1016/j.hrthm.2010.06.016. PMC   3049900 . PMID   20558321.
  21. ↑ Shipley RA, Hallaran W (1936-03-01). "The four-lead electrocardiogram in two hundred normal men and women". American Heart Journal. 11 (3): 325–345. doi:10.1016/S0002-8703(36)90417-9.

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