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Benign early repolarization


FieldValue
imageSemantic confusion early repolarization (CardioNetworks ECGpedia).svg
captionClassic and new definitions of early repolarization with end-QRS notching and end-QRS slurring
specialtycardiology
frequency1-13%
image2Benign early repolorization.jpg
caption2ECG of a benign early repolarization in a 15-year-old male

Benign early repolarization (BER) or early repolarization is found on an electrocardiogram (ECG) in about 1% of those with chest pain.

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:

  • Type 1 – BER pattern seen in lateral precordial leads.
  • Type 2 – BER pattern seen in inferior or inferolateral leads.
  • Type 3 – BER pattern seen globally (inferior, lateral, right precordial leads).

Associations with serious conditions

Research in the late 2000s has linked this finding to ventricular fibrillation, particularly in those who have fainted or have a family history of sudden cardiac death. 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. There has also been an association between early repolarization and short QT syndrome.

Risk factors

  • Male gender
  • J-point and horizontal or descending / downsloping ST segment (especially in inferior leads)
  • Elevation of ST segment by 2 mm
  • Elevation of a J-wave by 0.2 mV or more
  • J-point distribution globally
  • QRS longer than 110 ms
  • Longer duration of J wave, more than 60 ms

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. Studies have shown that higher testosterone levels in males result in an increased outward potassium currents causing J-point elevation.

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. 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.

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.

Genetics

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

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.

References

References

  1. (2018-11-27). "Early Repolarization Syndrome: Diagnostic and Therapeutic Approach". Frontiers in Cardiovascular Medicine.
  2. (1999). "Electrocardiographic manifestations: benign early repolarization". The Journal of Emergency Medicine.
  3. (2021-01-21). "'Benign' Early Repolarization Misnomer".
  4. (April 2011). "Rationale for the use of the terms J-wave syndromes and early repolarization". Journal of the American College of Cardiology.
  5. (April 2011). "Clinical aspects of the early repolarization syndrome: a 2011 update". Annals of Noninvasive Electrocardiology.
  6. (May 2008). "Sudden cardiac arrest associated with early repolarization". The New England Journal of Medicine.
  7. (May 2008). "Augmentation of J waves and electrical storms in patients with early repolarization". The New England Journal of Medicine.
  8. (October 2013). "Executive summary: HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes". Europace.
  9. (May 2010). "High prevalence of early repolarization in short QT syndrome". Heart Rhythm.
  10. (November 2012). "Clinical significance of variants of J-points and J-waves: early repolarization patterns and risk". European Heart Journal.
  11. (2016-06-30). "Early Repolarization Syndrome; Mechanistic Theories and Clinical Correlates". Frontiers in Physiology.
  12. (2014). "Early repolarisation and J wave syndromes". Indian Heart Journal.
  13. (March 2019). "Does early repolarization on ECG increase the risk of cardiac death in healthy people?". Cleveland Clinic Journal of Medicine.
  14. "Early Repolarization Syndrome".
  15. (2018). "Early Repolarization Syndrome: Diagnostic and Therapeutic Approach". Frontiers in Cardiovascular Medicine.
  16. (February 2015). "Long-term follow-up of early repolarization pattern in elite athletes". The American Journal of Medicine.
  17. (August 2011). "Early repolarization pattern in competitive athletes: clinical correlates and the effects of exercise training". Circulation: Arrhythmia and Electrophysiology.
  18. (2014). "Early repolarisation and J wave syndromes". Indian Heart Journal.
  19. (January 2009). "Ventricular fibrillation with prominent early repolarization associated with a rare variant of KCNJ8/KATP channel". Journal of Cardiovascular Electrophysiology.
  20. (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.
  21. (1936-03-01). "The four-lead electrocardiogram in two hundred normal men and women". American Heart Journal.
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