Zusammenfassung
Die frühe Repolarisation tritt bei 1–9 % der Allgemeinbevölkerung auf und in 50–70 % der Fälle von idiopathischem Kammerflimmern. Bei der Mehrzahl der EKG-Befunde handelt es sich um eine harmlose EKG-Auffälligkeit und nur im Einzelfall sind die Veränderungen verantwortlich für das Auftreten lebensbedrohlicher Arrhythmien. Die Identifikation potenziell gefährdeter Personen stellt ein ungelöstes Problem dar. Leider erlaubt das Muster der frühen Repolarisation derzeit keine Risikoabschätzung. Insbesondere die Frage einer prophylaktischen ICD-Implantation kann nur vom Einzelfall abhängig gemacht werden. Das Konzept einer Repolarisationsreserve für das Long-QT-Syndrom ist auf die frühe Repolarisation übertragbar. Neben einem genetischen Hintergrund spielen hier insbesondere Faktoren wie das autonome Nervensystem, das Geschlecht, aber im Einzelfall vermutlich auch ein akute Ischämie eine Rolle. Ähnlich wie beim Long-QT-Syndrom ist es vorstellbar, dass auch hier erst durch das Zusammenspiel verschiedener Faktoren eine Schwelle für das Auftreten von Kammerflimmern überschritten wird. Der Übergang von benignen inferolateralen Zeichen einer frühen Repolarisation zu ausgedehnten frühen Repolarisationsveränderungen folgt dabei keinem Alles-oder-nichts-Gesetz. Kommen zu den EKG-Veränderungen, die für sich alleine genommen i. d. R. gutartig sind, besondere Trigger hinzu, kann eine elektrische Katastrophe entstehen, die zum Auftreten eines plötzlichen Herztodes führt.
Abstract
Early repolarization, involving infero-lateral ST segment elevation and prominent J waves at the QRS-ST junction has been considered a normal ECG variant for more than 80 years. More recent studies suggest that this phenomenon is not as benign as earlier believed and may represent a risk for subsequent ventricular fibrillation in patients with and without structural heart disease. However, based on current data it seems unjustified to consider these often accidental ECG findings a marker for high risk of sudden cardiac death. The concept of a reduced repolarization reserve developed for the Long QT syndrome can be transformed to early repolarization syndrome. In general a “fibrillation reserve” is relatively high but if triggers such as a genetic background, age, gender, influences of the autonomous nervous system, changes in body temperature, or an acute coronary syndrome act together ventricular fibrillation may occur. A combination of an “early repolarization ECG” with syncope and/or a positive family history of sudden cardiac death may justify defibrillator therapy just on an individual basis. This review intends to summarize actual aspects of early repolarizations syndrome and focuses on the dilemma of risk stratification.
Literatur
Abe A, Ikeda T, Tsukada T et al (2010) Circadian variation of late potentials in idiopathic ventricular fibrillation associated with J waves: insights into pathophysiology and risk stratification. Heart Rhythm 7:675–682
Antzelevitch C, Yan GX (2010) J wave syndromes. Heart Rhythm 7:549–558
Beniti B, Guasch E, Rivard L, Nattel S (2010) Clinical and mechanistic issues in early repolarization. J Am Coll Cardiol 56:1177–1186
Bianco M, Zeppilli P (2009) Early repolarization in the athlete. J Am Coll Cardiol 53:2199–2200
Bjornstad H, Storstein L, Meen HD, Hals O (1993) Electrocardiographic findings according to level of fitness and sport activity. Cardiology 83:268–275
Bruns HJ, Eckardt L, Vahlhaus C et al (2002) Body surface potential mapping in patients with Brugada syndrome: right precordial ST segment variations and reverse changes in left precordial leads. Cardiovasc Res 54:58–66
Cappato R, Furlanello F, Giovinazzo V et al (2010) J wave, QRS slurring and ST elevation in athletes with cardiac arrest in the absence of heart disease: Marker of risk or innocent bystander? (2010). Circ Arrhythm Electrophysiol 3:305–311
Corrado D, Pelliccia A, Heidbuchel H et al (2010) Recommendations for interpretation of 12 lead ECG in athletes. Eur Heart J 31:243–259
Gussak I, Antzelevitch C (2000) Early repolarization syndrome: clinical characteristics and possible cellular and ioic mechanisms. J Electrocardiol 44:299–309
Grant RP, Estes EH, Doyle JT (1951) Spacial vector and electrocardiography. The clinical charcateristics of ST and T vectors. Circulation 3:182–347
Haissaguerre M, Derval N, Sacher F et al (2008) Sudden cardiac arrest asscociated with early repolarization. N Engl J Med 358:20162023
Haissaguerre M, Sacher F, Nogami A et al (2009) Characteristics of recurrent ventricular fibrillation associated with inferolateral early repolarization role of drug therapy (2009). J Am Coll Cardiol 53:612–619
Huston TP, Puffer JC, Rodney WM (1985) The athlete heart syndrome. N Engl J Med 313:24–31
Köbe J, Reinke F, Meyer C et al (2013) Implantation and follow-up of totally subcutaneous versus conventional implantable cardioverter defibrillator: a multicenter case-control study. Heart Rhythm 10:29–36
Lebiedz P, Meiners J, Samol A (2012) Electrocardiographic changes during therapeutic hypothermia. Resuscitation 83:602–606
Merchant FM, Noseworthy PA, Weiner RP et al (2009) Ability of terminal QRS notching to distinguish benign from malignant electrocardiographic forms of early repolarization. Am J Cardiol 104:1402–1406
Mehta MC, Jain AC, Mehta A (1999) Early repolarization. Clin Cardiol 22:59
Milberg P, Tegelkamp R, Osada N et al (2007) Reduction of dispersion of repolarization and prolongation of postrepolarization refractoriness explain the antiarrhythmic effects of quinidine in a model of short QT syndrome. J Cardiovasc Electrophysiol 18:658–664
Nademanee K, Veerakul G, Chandanamattha P et al (2011) Prevention of ventricular fibrillation episodes in Brugada syndrome by catheter avblation over the anterior right ventricular outflow tract epicardium. Circulation 123:1270–1279
Nam GB, Kim YH, Antzelevitch C (2008) Augmentation of J waves and electrical storms in patients with early repolarization. N Engl J Med 358:20178–2079
Patel RB, Ilkhanoff L, Ng J (2012) Clinical characteristics and prevalence of early repolarization asscociated with ventricular arrhythmias following acute ST-elevation myocardial infarction. Am J Cardiol 110:615–620
Roden DM. Taking the “idio” out of “idiosyncratic”_predicting torsade des pointes. Pacinf Clin Electrophysiol 1998; 21:1029–1034
Rolf S, Bruns HJ, Wichter T et al (2003) The ajmaline challenge in Brugada syndrome: diagnostic impact, safety, and recommended protocol. Eur Heart J 24:1104–1112
Rollin A, Maury P, Bongard V (2012) Prevalence, prognosis, and identification of the malignant form of early repolarization pattern in an population based study. Am J Cardiol 110:1302–1308
Rosso R, Kogan E, Belhassen B et al (2008) J-point elevation in survivors of primary ventricular fibrillation and matched control subjects: Incidence and clinical significance. J Am Coll Cardiol 52:1231–1238
Rudic P, Veltmann C, Kuntz E et al (2012) Early repolarization pattern is associated with ventricular fibrillation in patients with acute myocardial infarction. Heart Rhythm 9:1295–1300
Shipley R, Hallaran W (1936) The four lead electrocardiogram in 200 normal men and women. Am Heart J 11:325–345
Tikkanen JT, Anttonen O, Junttila MJ et al (2009) Long-term outcome associated with early repolarization an electrocardiography. N Engl J Med 361:2529–2537
Tikkanen JT, Wichmann V, Juntitila MJ et al (2012) Association of early repolarization and sudden cardiac death during an acute coronary event. Circ Arrhythm Electrophysiol 5:714–718
Wasmer K, Köbe J, Pott C, Eckardt L (2010) The ICD as primary prevention. Rare indications. Herzschr Elektrophys 21:117–122
Interessenkonflikt.
Der korrespondierende Autor gibt für sich und seine Koautoren an, dass kein Interessenkonflikt besteht.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Eckardt, L., Wasmer, K., Köbe, J. et al. Frühe Repolarisation. Herzschr Elektrophys 24, 115–122 (2013). https://doi.org/10.1007/s00399-013-0270-x
Published:
Issue Date:
DOI: https://doi.org/10.1007/s00399-013-0270-x