Current Value of the Electrocardiogram in the 21st Century


Austin J Clin Cardiolog. 2014;1(2): 1009.

Current Value of the Electrocardiogram in the 21st Century

Andrés Ricardo Pérez-Riera1*, Raimundo Barbosa-Barros2, Adrian Baranchuk3

1Faculdade de Medicina do ABC - Fundação do ABCDisciplina de Cardiologia - Santo André - São Paulo-Brazil

2Coronary Center Hospital de Messejana Dr. Carlos Alberto Studart Gomes Fortaleza-Ceará-Brazil

3Heart Rhythm Service, Kingston General Hospital, Queen’s University, Kingston, Ontario, Canada

*Corresponding author: Andrés Ricardo Pérez-Riera, Rua Sebastião Afonso, 885-CEP: 04417-100 Jardim Miriam São Paulo- Brazil

Received: January 27, 2014; Accepted: February 20, 2014; Published: February 24, 2014


Surface 12–lead ECG remains in the 21 century, one of the diagnostic tools most extensively used in clinical practice. For the internist and the cardiologist, maintaining ECG interpretation skills is mandatory, as the ECG allows a rapid (and inexpensive) diagnosis of a large series of entities. The advances of new technologies have not replaced the ECG, which still is one of the most cost⁄effective tools in medicine. New imaging techniques allow us to further investigate the heart, once the surface ECG has revealed an abnormality. Several interventions (in the acute and chronic phases of a disease) are still guided by the proper analysis of the surface ECG.

We are delighted to provide a short updated review on the current value of the surface 12–lead ECG for this new clinical Journal. We selected few clinical scenarios that we believe all clinicians should be familiarized with. This is not intended as a systematic review but rather as a quick reminder on the value of the surface ECG in specific conditions.

In the following scenarios, the surface ECG is considered of “great help” to the physician:

Acute Coronary Syndrome (ACS):

The ECG is the first–line diagnostic tool in the assessment of patients with suspected ACS. Patients with ACS are, for the most part, dichotomised by whether significant ST–segment elevation is present or not (1). Patients without ST–segment elevation can subsequently be categorized to have unstable angina or non–ST elevation myocardial infarction (NSTEMI). Persistent ST–segment elevation (>20 min) in at least two contiguous leads and⁄or new left bundle branch block (LBBB) suggests STEMI and immediate action is taken based on the information provided by the ECG (percutaneous coronary intervention or thrombolytic drugs). Surface ECG provides the first diagnostic approach and has direct impact on the initial therapy.

The ECG not only helps in establishing the diagnosis of STEMI but also provides valuable information on infarct location, success or failure of reperfusion, as well as prognosis. The ECG is the first diagnostic tool that allows assessment of myocardial ischemia and despite multiple paradigm shifts in the management of ACS; it continues to be the pre–eminent test directing therapeutic management and prognostic stratification [1].

Pacing and Cardiac Resynchronization Therapy (CRT)

Paced rhythms became a “sub–specialty” of elecrocardiology. In addition to the recognition of pacemaker malfunctions (failure to capture, over and undersensing, noise, etc), surface 12–lead ECG helps in the recognition of the so–called “pacemaker pseudo–malfunctions” that refers to the recognition of sophisticated pacing algorithms in the surface ECG [2]. A wide QRS complex depicting LBBB pattern is a pre–requisite to become eligible for CRT in patients with refractory heart failure, however; 30% of patients do not benefit from CRT [3]. Patients are considered as responders when left ventricular ejection fraction (LVEF) increases by ≥5% and New York Heart Association class by ≥1 after 3 months of CRT. The presence of LBBB pattern with QRS duration ≥130 ms (men) and 140 ms (women) associated o a “notch” in at least 2 leads (V1–V2 or V5–V6, I and aVL) seems to identify patients with better response [3]. Lately, a QRS >150 ms was found to be associated with better response [4]. Strict LBBB criteria identified patients with greater mechanical dyssynchrony compared with patient’s only meeting non–strict LBBB criteria, whereas there was no significant difference between patients with non–strict LBBB criteria and non–LBBB [5–7].

Several algorithms to determine response to CRT after implantation were published in the last years, however; none has been completely validated so far. Narrowing of the QRS during CRT pacing does not predict outcome, however; on the other hand, widening of the QRS after CRT implant indicates poorer prognosis.

Inherited arrhythmic disorders (cardiac channelopathies)

These infrequent disorders are hereditary “ion channelopathies”, in which mutations in genes encode functional units of ion channels and⁄or their transporter–associated proteins in patients without apparent structural heart disease. The most frequent are: Brugada syndrome (BrS) [8], congenital long QT syndrome (LQTS) [9], congenital short QT syndrome (SQTS) [10,11], catecholaminergic polymorphic ventricular tachycardia (CPVT) [12] and early repolarization syndromes (ERS) [13]. The role of the surface ECG in the diagnosis, and sometimes prognosis of these conditions is of paramount importance. In Brugada Syndrome, the ECG is characterized by ST–segment elevation at least 2 mm coved to the top followed by a negative T–wave in the right precordial leads. The saddleback shaped ST elevation is non–diagnostic (Type 2 Brugada pattern) but raises concern as this entity associates with sudden cardiac death [8]. The Brugada ECG pattern is usually the first “red flag” of this condition. In congenital Long QT syndrome (LQTS), the ECG allows to speculate on the mechanism linking to life–threatening arrhythmias (torsades des pointes) depending on the morphology of the QT interval. It also allows classifying them into types 1, 2 and 3, and selecting appropriate treatment depending on the QT morphology [9]. Congenital short QT syndrome is a very rare channelopathy, characterized by very short QT⁄QTc interval, (QTc interval = 330 ms) and frequently associated with life–threatening arrhythmias[10,11]. Catecholaminergic polymorphic ventricular tachycardia (CPVT) is another rare entity characterized in the surface ECG by presenting a typical bidirectional ventricular tachycardia [12] and frequently associated with sudden cardiac death. Its rapid recognition links to proper treatment with either beta–blockers or ICDs. Early repolarization syndromes (ERS) can manifest in the surface ECG as Early Repolarization Pattern (ERP), consisting on J–point elevation and distinct J–wave with or without ST–segment elevation or slurring of the terminal part of the QRS. ERP was considered a benign ECG manifestation for decades. Later, a subgroup of patients with associated life–threatening arrhythmias was described calling attention to this new arrhythmic syndrome. Its correct identification will avoid warning people at no risk and at the same time prompt proper and rapid action for ones with the malignant forms of the disease [13,14].

Diagnosis and classification of cardiac arrhythmias

The surface ECG allows rapid recognition of the origin and electrophysiological mechanisms involved in the genesis of most cardiac arrhythmias [2]. ECG helps guiding further diagnosis and medical treatment. Narrow complex tachycardias, in 90% of the cases, correspond to supraventricular arrhythmias whereas 90% of wide complex tachycardias are ventricular in origin. The surface ECG remains irreplaceable for the diagnosis of cardiac rhythm disturbances [2].

Other Major contributions


These are only few but not all clinical scenarios where the ECG is still irreplaceable. We wanted to highlight that despite major advanced in medical technology, surface ECG remains as a useful tool that helps the cardiologist in many different clinical situations. Proper skill ECG interpretation should still be part of the medical curricula and new methods to teach and evaluate knowledge should be develop in order to avoid erosion of skills usually learnt at early stages of the medical career.


  1. Birnbaum Y, Wilson JM, Fiol M, de Luna AB, Eskola M, Nikus K. ECG Diagnosis and Classiication of Acute Coronary Syndromes. Ann Noninvasive Electrocardiol 2013; doi: 10.1111/anec.12130. [Epub ahead of print].
  2. Baranchuk A. Atlas of Advanced ECG Interpretation. Baranchuk A (ed); REMEDICA, London (UK), 2013
  3. Exner DV, Birnie DH, Moe G, Thibault B, Philippon F, Healey JS, et al. Canadian Cardiovascular Society guidelines on the use of cardiac resynchronization therapy: evidence and patient selection. Can J Cardiol, 2013; 29: 182-195.
  4. Goldenberg I, Moss AJ, Hall WJ, Foster E, Goldberger JJ, Santucci P, et al. Predictors of response to cardiac resynchronization therapy in the Multicenter Automatic Deibrillator Implantation Trial with Cardiac Resynchronization Therapy (MADIT-CRT). Circulation. 2011; 124: 1527-1536.
  5. Strauss DG. Differentiation between left bundle branch block and left ventricular hypertrophy: implications for cardiac resynchronization therapy. J Electrocardiol. 2012; 45: 635-639.
  6. Galeotti L, van Dam PM, Loring Z, Chan D, Strauss DG. Evaluating strict and conventional left bundle branch block criteria using electrocardiographic simulations. Europace. 2013; 15: 1816-1821.
  7. Andersson LG, Wu KC, Wieslander B, Loring Z, Frank TF, Maynard C, Gerstenblith G, et al. Left ventricular mechanical dyssynchrony by cardiac magnetic resonance is greater in patients with strict vs nonstrict electrocardiogram criteria for left bundle-branch block. Am Heart J. 2013; 165: 956-963.
  8. Bayés de Luna A, Brugada J, Baranchuk A, Borggrefe M, Breithardt G, Goldwasser D, et al. Current electrocardiographic criteria for diagnosis of Brugada pattern: a consensus report. J Electrocardiol. 2012; 45: 433-442.
  9. Modell SM, Lehmann MH. The long QT syndrome family of cardiac ion channelopathies: a HuGE review. Genet Med. 2006; 8: 143-155.
  10. Pérez Riera AR, Ferreira C, Dubner SJ, Schapachnik E, Soares JD, Francis J. et al. Brief review of the recently described short QT syndrome and other cardiac channelopathies. Ann Noninvasive Electrocardiol. 2005; 10: 371-377.
  11. Gollob MH, Redpath CJ, Roberts JD. The short QT syndrome: proposed diagnostic criteria. J Am Coll Cardiol. 2011; 57: 802-812.
  12. Femenia F, Barbosa-Barros R, Sampaio SV, Arce M, Perez-Riera A, Baranchuk A. Bidirectional ventricular tachycardia: a hallmark of catecholaminergic polymorphic ventricular tachycardia. Indian Pacing Electrophysiol J. 2012; 12: 65-68.
  13. Koncz I, Gurabi Z, Patocskai B, Panama BK, Szél T, Hu D, et al. Mechanisms underlying the development of the electrocardiographic and arrhythmic manifestations of early repolarization syndrome. J Mol Cell Cardiol. 2013 doi: 10.1016/j.yjmcc.2013.12.012. [Epub ahead of print].
  14. Antzelevitch C. J wave syndromes: molecular and cellular mechanisms. J Electrocardiol. 2013; 46: 510-518.
  15. Elliott PM, Poloniecki J, Dickie S, Sharma S, Monserrat L, Varnava A, et al. Sudden death in hypertrophic cardiomyopathy: identiication of high risk patients. J Am Coll Cardiol. 2000; 36: 2212-2218.
  16. Femenía F, Arce M, Van Grieken J, Trucco E, Mont L, Abello M, et al. Fragmented QRS as a Predictor of Arrhythmic Events in Patients with Hypertrophic Obstructive Cardiomyopathy. J Interv Card Electrophysiol. 2013; 38: 159-165.
  17. Marcus FI, McKenna WJ, Sherrill D, Basso C, Bauce B, Bluemke DA, et al. Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modiication of the task force criteria. Circulation. 2010; 121: 1533- 1541.
  18. Cardin G, Nava A, Canciani B, Bottero M, Zevallos JC, Buja GF. [Electro- vectorcardiographic behavior of right bundle branch block in endocardial cushion defects. Its probable relation to the so-called left anterior fascicular hemiblock]. Arch Inst Cardiol Mex. 1984; 54: 457-462.

Download PDF

Citation: Pérez-Riera AR, Barbosa-Barros R, Baranchuk A. Current Value of the Electrocardiogram in the 21st Century. Austin J Clin Cardiolog. 2014;1(2): 1009. ISSN 2381-9111

Journal Scope
Online First
Current Issue
Editorial Board
Instruction for Authors
Submit Your Article
Contact Us