Barra, SN

Nascimento, J

Providência, R

Name not available

Clinical correlates of early repolarization and J wave patterns...are they proarrhythmic on their own?

Repositório Institucional dos Hospitais da Universidade de Coimbra

T-wave window ever be moved the opposite way, and 3)could the T-wave window be shortened progressively, inorder to “unravel the contributions of different portions ofthe entire J–T interval, in rendering microvolt level T-wavealternans (MTWA) positive, in various patient populations”?To address the ﬁrst question, it should be noted that farfewer patients with structural heart disease have signiﬁcant QTprolongation than do patients in the long-QT population thatconstituted the basis of our study.1 Thus, it is likely that only asmall subset of patients referred for MTWA analysis willrequire adjustment of the T-wave window. However, in theseindividuals, appropriate T-wave window adjustment couldmean the difference between a negative and a nonnegative testresult. Modiﬁcation of the software to provide a picture ofwhere the T-wave window was positioned, as we havesuggested, would allow the interpreter to assess the adequacyof the study.Should the T-wave window ever be moved the oppositeway (to encompass more of the ST segment and/or QRScomplex)? Probably not, if MTWA analysis is being used toassess the risk of sudden cardiac death in patients with stablestructural heart disease. In this population, it is alternanswithin the T wave (and especially involving the apex of the Twave) that appears to predict life-threatening ventriculararrhythmia.2–5 Although it is theoretically possible thatpatients with pathologically short QT intervals might requirebackward adjustment of the T-wave window in order toencompass the T wave, the likelihood of this seems remote.Dr. Madias suggests that we manipulate the T-wavewindow in order to dissect out the contributions of thedifferent portions of the J–T interval to alternans in variouspopulations. Indeed, there is increasing interest in under-standing the different mechanisms by which various diseaseprocesses create alternans in the electrocardiogram. A recentsimulation study6 showed that action potential durationalternans produced maximum alternans at the peak of the Twave, whereas both action potential amplitude alternans andconduction block alternans produced alternans in the STsegment, and conduction delay alternans caused alternans atthe QRS complex. Through dissection of the J–T interval todetermine where alternans in occurring in a given diseaseprocess, together with further modeling studies, we may, inthe future, be able to determine the mechanism of a patient'salternans and tailor treatments to reduce the risk ofarrhythmia. We have only begun to explore the mechanismsand clinical utility of alternans.Elizabeth S. Kaufman, MDHeart and Vascular Research CenterMetroHealth Campus of Case Western Reserve UniversityCleveland, OH 44109-1998, USAE-mail address: ekaufman@metrohealth.orghttp://dx.doi.org/10.1016/j.jelectrocard.2012.10.019References1. Kaufman ES, Lewis SA, Leo P, Aswath G, Ziv O, Fendelander L.Microvolt-level T-wave alternans determination using the spectralmethod in patients with QT prolongation: value of adjusting the T-wave window. J Electrocardiol 2012 (Epub ahead of print).2. Rosenbaum DS, Jackson LE, Smith JM, Garan H, Ruskin JN, Cohen RJ.Electrical alternans and vulnerability to ventricular arrhythmias. N Engl JMed 1994;330:235.3. Narayan SM, Smith JM. Differing rate dependence and temporaldistribution of repolarization alternans in patients with and withoutventricular tachycardia. J Cardiovasc Electrophysiol 1999;10:61.4. Selvaraj RJ, Picton P, Nanthakumar K, Mak S, Chauhan VS. Endocardialand epicardial repolarization alternans in human cardiomyopathy:evidence for spatiotemporal heterogeneity and correlation with bodysurface T-wave alternans. J Am Coll Cardiol 2007;49:338.5. Narayan SM. T-wave alternans and the susceptibility to ventriculararrhythmias. J Am Coll Cardiol 2006;47:269.6. Rader F, Cutler MJ, Rosenbaum DS. Microvolt T-wave alternans: frommolecule to man. In: Dudley S, Kocheril AG, Sovari AA, editors.Ventricular arrhythmia: From principles to patients. Hauppauge, NY:Nova Science Publishers; 2012. in press.Clinical correlates of early repolarization and J wavepatterns…are they proarrhythmic on their own?We have read the manuscript by Lanza et al.1 entitled“Prevalence and clinical correlates of early repolarizationand J wave in a large cohort of subjects without overtheart disease,” in which the authors detail their prospectivestudy involving 4176 electrocardiograms of subjectswithout presumed structural heart disease. A differentiationbetween typical early repolarization (ER) and slurred ornotched J wave is emphasized, yet the authors concludethat neither the former nor the latter is associated withsymptoms potentially related to arrhythmias, such assyncope or palpitations.Their research adds new data to our current understandingof the clinical relevance of ER or J waves. To our knowledge,this study is among the very few that clearly differentiatestypical ER from J wave patterns and their conclusions areconsiderably robust, considering the very high number ofpatients included. The lack of association between those ECGpatterns and the occurrence of arrhythmia-related symptom-atology may contradict the ﬁndings of other studies that haveshown an increased risk of arrhythmic death during very long-term follow-up in asymptomatic adults with J waves N2 mmin amplitude,2 especially if combined with horizontal/descending ST segment.3 Increased transmural dispersion ofrepolarization potentiating the risk for phase 2 reentry andpolymorphic ventricular tachycardia/ventricular ﬁbrillation,or delayed depolarization of those segments with heteroge-neous remote scar tissue, irrespective of its etiology, creatingan anatomic/functional substrate for reentrant ventriculararrhythmias, are some of the mechanisms potentiallyassociated to the malignant role of J wave patterns withhorizontal/descending ST-segment.The ﬁndings of Lanza et al. deserve some additionalcomments:• It is possible that the occurrence of isolated J wavesor ER patterns does not increase arrhythmicmortality on its own, but only in the presence ofadditional proarrhythmic factors or triggers, such asacute myocardial ischaemia,4 neurohormonal andsympathetic activation in ischemic or non-ischemic73Letters to the Editor / Journal of Electrocardiology 46 (2013) 69–75chronic heart failure5 and severe hypokalemia.6Patients included in this study were presumablylow-risk patients, as they did not have any evidenceof structural heart disease according to clinicalhistory, ECG results and noninvasive cardiac inves-tigation, when required. Therefore, occurrence ofproarrhythmic triggers was probably rare, whichcould explain the lack of clinical correlation ofslurred or notched J wave pattern with ST segmentelevation. If the cohort had included patients with aknown cardiac condition, or older patients (evenwithout known cardiac disease), we might haveobtained contrasting results. However, this possibil-ity is unproven at present and should be clariﬁed byappropriately designed studies.• A diagnosis of ER has usually been based on thepresence of a typical concave, upsloping, ST-segmentelevation, often associated with low heart rate,suggestive of a vagal etiology. Independent predictorsof the occurrence of an ER/J wave pattern wereyounger age, male sex and lower heart rate, reinforcingits potential vagally mediated origin. Nevertheless, themechanism behind ER or J wave pattern in olderpatients may be of different electrogenic etiology.This should be further clariﬁed in the future. It wouldbe interesting if the authors could test the potentialassociation between ER/J wave and arrhythmia-related symptoms in elderly patients or in those witharterial hypertension and/or diabetes mellitus (morelikely to have endothelial dysfunction, subclinical ormanifest cardiovascular disease and, probably, a lowervagal tone).• A potential similarity between the Brugada and earlyrepolarization syndromes in terms of response toheart rate, pharmacologic agents and neuromodula-tion has been proposed. There might be a linkage intheir genetic7 or pathophysiological mechanisms.8 Infact, it has been suggested that the Brugadasyndrome (BS) may represent a more localized(right ventricular outﬂow tract) and pronouncedform of early repolarization/delayed depolarization.Sudden cardiac death is often the ﬁrst clinicalmanifestation of BS and the same phenomenonmight happen in the malignant variant of ER,provided additional proarrhythmic factors or triggersare present. Symptoms such as sustained palpitationsor syncope may as well occur only in the presence ofadditional arrhythmic triggers.• An association between ER and occurrence ofventricular arrhythmias has been shown in longitudi-nal studies. A potential relationship between ER or Jwave patterns and the occurrence of syncope and/orpalpitations is less likely to be detected in a cross-sectional study, such as the one by Lanza et al.In conclusion, ER or slurred/notched J wave patternsare not necessarily associated with higher arrhythmic riskin patients without structural heart disease or any potentialarrhythmic trigger such as myocardial ischemia, sympa-thetic activation or electrolyte disturbance. In fact, ER andall of its variants are relatively common in healthy youngmales with slower heart rates.9 However, given theconﬂictual and controversial currently available data onthis subject, we look forward to seeing the future analysisof Lanza and colleagues on the potential association ofER/J wave and long-term clinical outcome. Currently, wereinforce their suggestions concerning the need for detailedand standardized deﬁnitions and methods for measurementof ST elevation and J wave.Sérgio Nuno Craveiro Barra, MDRui Providência, MD, MScJosé Nascimento, MDCardiology DepartmentCoimbra's Hospital and University CentreCoimbra, PortugalE-mail address: sergioncbarra@gmail.comhttp://dx.doi.org/10.1016/j.jelectrocard.2012.10.004References1. Lanza GA, Mollo R, Cosenza A, Pinnacchio G, Careri G, Laurito M,Crea F. Prevalence and clinical correlates of early repolarization and Jwave in a large cohort of subjects without overt heart disease. JElectrocardiol 2012;45:404.2. Rosso R, Adler A, Halkin A, Viskin S. Risk of sudden death amongyoung individuals with J waves and early repolarization: putting theevidence into perspective. Heart Rhythm 2011;8:923 [Epub 2011 Feb 2].3. Rosso R, Glikson E, Belhassen B, Katz A, Halkin A, Steinvil A, ViskinS. Distinguishing “benign” from “malignant early repolarization”: thevalue of the ST-segment morphology. Heart Rhythm 2012;9:225 [Epub2011 Sep 10].4. Tikkanen JT, Wichmann V, Junttila MJ, et al. Association of earlyrepolarization and sudden cardiac death during an acute coronary event.Circ Arrhythm Electrophysiol 2012;5:714 [Epub 2012 Jun 22].5. Pei J, Li N, Gao Y, et al. The J wave and fragmented QRS complexes ininferior leads associated with sudden cardiac death in patients withchronic heart failure. Europace 2012;14:1180 [Epub 2012 Feb 2].6. Myojo T, Sato N, Nimura A, et al. Recurrent ventricular fibrillationrelated to hypokalemia in early repolarization syndrome. Pacing ClinElectrophysiol 2012;35:e234. http://dx.doi.org/10.1111/j.1540-8159.2012.03460.x [Epub 2012 Jun 26].7. Barajas-Martínez H, Hu D, Ferrer T, et al. Molecular genetic andfunctional association of Brugada and early repolarization syndromeswith S422L missense mutation in KCNJ8. Heart Rhythm 2012;9:548[Epub 2011 Nov 3].8. Di Grande A, Tabita V, Lizzio MM, et al. Early repolarization syndromeand Brugada syndrome: is there any linkage? Eur J Intern Med 2008;19:236 [Epub 2008 Jan 28].9. Panicker GK, Manohar D, Karnad DR, Salvi V, Kothari S, LokhandwalaY. Early repolarization and short QT interval in healthy subjects. HeartRhythm 2012;9:1265.Author's ResponseTo the Editor:We very much appreciate the interest of Barra et al. in ourstudy on the prevalence and clinical correlates of earlyrepolarization (ER) in apparently healthy subjects.174 Letters to the Editor / Journal of Electrocardiology 46 (2013) 69–75

Clinical correlates of early repolarization and J wave patterns...are they proarrhythmic on their own?

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