Current Cardiology Reviews - Volume 10, Issue 3, 2014

Brugada syndrome is a genetically determined familial disease with autosomal dominant transmission and variable penetrance, conferring a predisposition to sudden cardiac death due to ventricular arrhythmias. The syndrome is characterized by a typical electrocardiographic pattern in the right precordial leads. This article will focus on the new electrocardiographic features recently agreed on by expert consensus helping to identify this infequent electrocardiographic pattern.

Interatrial block (IAB; P-wave duration ≥ 110 ms), which represents a delay in the conduction between the atria, is a pandemic conduction abnormality that is frequently underappreciated in clinical practice. Despite its comprehensive documentation in the medical literature, it has still not received adequate attention and also not adequately described and discussed in most cardiology textbooks. IAB can be of varying degrees and classified based on the degree of P-duration and its morphology. It can transform into a higher degree block and can also manifest transiently. IAB may be a preceding or causative risk factor for various atrial arrhythmias (esp. atrial fibrillation) and also be associated with various other clinical abnormalities ranging from left atrial dilation and thromboembolism including embolic stroke and mesenteric ischemia. IAB certainly deserves more attention and prospective studies are needed to formulate a standard consensus regarding appropriate management strategies.

T wave “memory” is a peculiar variety of cardiac remodeling caused by a transient change in the course of ventricular depolarization (due to ventricular pacing, rate-dependent intraventricular block, ventricular preexcitation or tachyarrhythmias with wide QRS complexes). It is usually manifested by inverted T waves that appears when normal ventricular activation is restored. This phenomenon is cumulative and occurs earlier if the ventricular myocardium has previously been exposed to the same conditioning stimuli. In this article the different conditions giving rise to “classical” T wave memory development are reviewed and also “another” type of T wave memory is described. It is also shown that cardiac memory may induce not only negative (pseudo-primary) T waves but also a reversal of primary and pseudoprimary T waves leading to “normalization” of ventricular repolarization. The knowledge of these dissimilar consequences of T wave memory is essential to assess the characteristics of ventricular repolarization.

True supernormality of excitability and conduction has been demonstrated in normal Purkinje fibers in in vitro studies. In the clinical setting, supernormality of conduction is manifested better than expected. This phenomenon is much more common than previously thought, particularly in the presence of certain clinical conditions. If a careful scanning of the cardiac cycle is performed on all patients with intermittent bundle branch block and second degree or advanced infranodal AV block, accessory pathways and mulfunctioning pacemakers, it is anticipated that a much larger amount of supernormal excitability and conduction will be unmasked.

Andersen - Tawil syndrome (ATS) is an autosomal - dominant or sporadic disorder characterized by ventricular arrhythmias, periodic paralysis, and distinctive facial and skeletal dysmorphism. Mutations in KCNJ2, which encodes the α-subunit of the potassium channel Kir2.1, were identified in patients with ATS. This genotype has been designated as type-1 ATS (ATS1). KCNJ2 mutations are detectable in up to 60 % of patients with ATS. Cardiac manifestations of ATS include frequent premature ventricular contractions (PVC), Q-U interval prolongation, prominent U-waves, and a special type of polymorphic ventricular tachycardia (PMVT) called bidirectional ventricular tachycardia (BiVT). The presence of frequent PVCs at rest are helpful in distinguishing ATS from typical catecholaminergic polymorphic ventricular tachycardia (CPVT). In typical CPVT, rapid PMVT and BiVT usually manifest during or after exercising. Additionally, CPVT or torsade de pointes in LQTS are faster, very symptomatic causing syncope or often deteriorate into VF resulting in sudden cardiac death. PVCs at rest are quite frequent in ATS1 patients, however, in LQTS patients, PVCs and asymptomatic VT are uncommon which also contributes to differentiating them. The article describes the new electrocardiographic criteria proposed for diagnosis of type-1 Andersen-Tawil syndrome. A differential diagnosis between Andersen-Tawil syndrome, the catecholamine polymorphic ventiruclar tachycardia and long QT syndrome is depicted. Special attention is paid on the repolarization abnormalities, QT interval and the pathologic U wave. In this article, we aim to provide five new electrocardiographic clues for the diagnosis of ATS1.

The electrocardiogram (ECG) findings in acute coronary syndrome should always be interpreted in the context of the clinical findings and symptoms of the patient, when these data are available. It is important to acknowledge the dynamic nature of ECG changes in acute coronary syndrome. The ECG pattern changes over time and may be different if recorded when the patient is symptomatic or after symptoms have resolved. Temporal changes are most striking in cases of ST-elevation myocardial infarction. With the emerging concept of acute reperfusion therapy, the concept STelevation/ non-ST elevation has replaced the traditional division into Q-wave/non-Q wave in the classification of acute coronary syndrome in the acute phase. Keypoints: In acute coronary syndrome, in addition to the traditional electrocardiographic risk markers, such as ST depression, the 12-lead ECG contains additional, important diagnostic and prognostic information. Clinical guidelines need to acknowledge certain high-risk ECG patterns to improve patient care.

The ECG is abnormal in most patients with arrhythmogenic right ventricular dysplasia (ARVD). Right ventricular parietal block, reduced QRS amplitude, epsilon wave, T wave inversion in V1-3 and ventricular tachycardia in the morphology of left bundle branch block are the characteristic changes that reflect the underlying genetic predetermined pathology and pathoelectrophysiology. Recognizing the characteristic ECG changes in ARVD will be of help in making a correct diagnosis of this rare disease.

Percutaneous pericardial access for epicardial mapping and ablation of ventricular arrhythmias has expanded considerably in recent years. After its description in patients with Chagas disease, the technique has provided relevant information on the arrhythmia substrate in other cardiomyopathies and has improved the results of ablation procedures in various clinical settings. Electrocardiographic criteria proposed for the recognition of the epicardial origin of ventricular tachycardias are mainly based on analysis of the first QRS components. Ventricular activation at the epicardium has a slow initial component reflecting the transmural activation and influenced by the absence of Purkinje system in the epicardium. Various parameters (pseudodelta wave, intrinsicoid deflection and shortest RS interval) of these initial intervals predict an epicardial origin in patients with scar-related ventricular tachycardias with right bundle branch block morphology. Using the same concept, the maximum deflection index was defined for the location of idiopathic epicardial tachycardias remote from the aortic root. Electrocardiogram criteria based on the morphology of the first component of the QRS (q wave in lead I) have been proposed in patients with nonischemic cardiomyopathy. All these criteria seem to be substrate-specific and have several limitations. Other information, including type of underlying heart disease, previous failed endocardial ablation, and evidence of epicardial scar on magnetic resonance imaging, can help to plan the ablation procedure and decide on an epicardial approach.

The traditional approach to the ECG diagnosis of left ventricular hypertrophy (LVH) is focused on the best estimation of left ventricular mass (LVM) i.e. finding ECG criteria that agree with LVM as detected by imaging. However, it has been consistently reported that the magnitude of agreement is rather low as reflected in the low sensitivity of ECG criteria. As a result, the majority of cases with true anatomical LVH could be misclassified by using ECG criteria of LVH. Despite this limitation, it has been reported that the ECG criteria for LVH provide independent information on the cardiovascular risk even after adjusting for LVM. Understanding possible reasons for the frequent discrepancy between common ECG LVH criteria and LVH by echo or MRI would help understanding the genesis of ECG changes that occur as a consequence of increased LV mass.

The differential diagnosis of a regular, monomorphic wide QRS complex tachycardia (WCT) mechanism represents a great diagnostic dilemma commonly encountered by the practicing physician, which has important implications for acute arrhythmia management, further work-up, prognosis and chronic management as well. This comprehensive review discusses the causes and differential diagnosis of WCT, and since the ECG remains the cornerstone of WCT differential diagnosis, focuses on the application and diagnostic value of different ECG criteria and algorithms in this setting and also provides a practical clinical approach to patients with WCTs.

Various noninvasive tests for risk stratification of sudden cardiac death (SCD) were studied, mostly in the context of structural heart disease such as coronary artery disease (CAD), cardiomyopathy and heart failure but have low positive predictive value for SCD. Fragmented QRS complexes (fQRS) on a 12-lead ECG is a marker of depolarization abnormality. fQRS include presence of various morphologies of the QRS wave with or without a Q wave and includes the presence of an additional R wave (R’) or notching in the nadir of the R’ (fragmentation) in two contiguous leads, corresponding to a major coronary artery territory. fQRS represents conduction delay from inhomogeneous activation of the ventricles due to myocardial scar. It has a high predictive value for myocardial scar and mortality in patients CAD. fQRS also predicts arrhythmic events and mortality in patients with implantable cardioverter defibrillator. It also signifies poor prognosis in patients with nonischemic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and Brugada syndrome. However, fQRS is a nonspecific finding and its diagnostic prognostic should only be interpreted in the presence of pertinent clinical evidence and type of myocardial involvement (structural vs. structurally normal heart).

The evaluation of every electrocardiogram should also include an effort to interpret the QT interval to assess the risk of malignant arrhythmias and sudden death associated with an aberrant QT interval. The QT interval is measured from the beginning of the QRS complex to the end of the T-wave, and should be corrected for heart rate to enable comparison with reference values. However, the correct determination of the QT interval, and its value, appears to be a daunting task. Although computerized analysis and interpretation of the QT interval are widely available, these might well over- or underestimate the QT interval and may thus either result in unnecessary treatment or preclude appropriate measures to be taken. This is particularly evident with difficult T-wave morphologies and technically suboptimal ECGs. Similarly, also accurate manual assessment of the QT interval appears to be difficult for many physicians worldwide. In this review we delineate the history of the measurement of the QT interval, its underlying pathophysiological mechanisms and the current standards of the measurement of the QT interval, we provide a glimpse into the future and we discuss several issues troubling accurate measurement of the QT interval. These issues include the lead choice, U-waves, determination of the end of the T-wave, different heart rate correction formulas, arrhythmias and the definition of normal and aberrant QT intervals. Furthermore, we provide recommendations that may serve as guidance to address these complexities and which support accurate assessment of the QT interval and its interpretation.