J-Point Elevation in Survivors of Primary Ventricular Fibrillation and Matched Control Subjects: Incidence and Clinical Significance

https://www.heartrhythmjournal.com/article/S1547-5271(09)01377-0/pdf

J Wave Syndromes

https://www.cardiacep.theclinics.com/article/S1877-9182(10)00142-5/pdf

Overview of Basic Mechanisms of Cardiac Arrhythmia.

An early repolarization (ER) pattern in the ECG, distinguished by J-point elevation, slurring of the terminal part of the QRS and ST-segment elevation has long been recognized and considered to be a benign electrocardiographic manifestation. Experimental studies conducted over a decade ago suggested that some cases of ER may be associated with malignant arrhythmias. Validation of this hypothesis was provided by recent studies demonstrating that an ER pattern in the inferior or inferolateral leads is associated with increased risk for life-threatening arrhythmias, termed ER syndrome (ERS). Because accentuated J waves characterize both Brugada syndrome (BS) and ERS, these syndromes have been grouped under the term "J wave syndromes". ERS and BS share similar ECG characteristics, clinical outcomes and risk factors, as well as a common arrhythmic platform related to amplification of Ito-mediated J waves. Although BS and ERS differ with respect to the magnitude and lead location of abnormal J wave manifestation, they can be considered to represent a continuous spectrum of phenotypic expression. Although most subjects exhibiting an ER pattern are at minimal to no risk, mounting evidence suggests that careful attention should be paid to subjects with "high risk" ER. The challenge ahead is to be able to identify those at risk for sudden cardiac death. Here I review the clinical and genetic aspects as well as the cellular and molecular mechanisms underlying the J wave syndromes. (Circ J 2012; 76: 1054-1065)

Genetic, molecular and cellular mechanisms underlying the J wave syndromes.

https://www.heartrhythmjournal.com/article/S1547-5271(11)00076-2/pdf

Risk of sudden death among young individuals with J waves and early repolarization: Putting the evidence into perspective

We present an unusual case of a young Thai immigrant, symptom- atic, who had suffered prior episodes of syncope with strong family back- ground: male, first-degree relatives, younger than 45 years old who had died suddenly. The rest ECG, with the patient asymptomatic at the time, showed persistent ST-segment elevation, in inferior leads and "mirror" image in the anterior wall, which were not modified with sublingual nitrates, in absence of demonstrable structural heart disease by chest X-rays and echocardiogram, hypothermia, ischemia, or electrolytic disorders. Holter monitoring revealed at dawn, a short episode of polymorphic ventricular tachycardia of short onset extrasystole coupling, which evolved into asystole and sudden cardiac death. We believe this is a sudden unexplained death syndrome, although we did not have a chance to conduct a genetic study. Key words: Atypical Brugada Syndrome, Downsloping ST-segment elevation in inferior leads.

Electrocardiographic Curiosities Brugada Syndrome With Atypical ECG: Downsloping ST-Segment Elevation in Inferior Leads

Accelerated Idioventricular Rhythm (AIVR) is a ventricular rhythm consisting of three or more consecutive monomorphic beats, with gradual onset and gradual termination. It can rarely manifest in patients with completely normal hearts or with structural heart disease. It is usually seen during acute myocardial infarction reperfusion. This manuscript aims to review the history of the main discoveries that lead to the identification and comprehension of this fascinating arrhythmia.

Historical Review Accelerated Idioventricular Rhythm: History and Chronology of the Main Discoveries

The Brugada syndrome is a congenital syndrome displaying an autosomal dominant mode of transmission in patients with a structurally normal heart. The disease has been linked to mutations in SCN5A, a gene located on the short arm of chromosome 3 (p21-24) that encodes for the a subunit of the sodium channel. The syndrome is characterized by a dynamic ST-segment elevation (accentuated J wave) in leads V1 to V3 of the ECG followed by negative T wave. Right bundle-branch block of varying degrees is observed in some patients. The syndrome is associated with syncope and a relatively high incidence of sudden cardiac death secondary to the development of polymorphic ventricular tachycardia that may degenerate into ventricular fibrillation. An acquired form of the Brugada syndrome is also recognized, caused by a wide variety of drugs and conditions that alter the balance of currents active during the early phases of the action potential. Among patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia, there is a subpopulation with a clinical and electrocardiographic pattern similar to that of the Brugada syndrome. These cases of arrhythmogenic right ventricular cardiomyopathy/dysplasia are thought to represent an early or concealed form of the disease. This review examines the overlap between these 2 syndromes. D 2005 Elsevier Inc. All rights reserved.

An Invited Editorial Is there an overlap between Brugada syndrome and arrhythmogenic right ventricular cardiomyopathy/dysplasia?

The electrocardiogram (ECG) criteria for the left septal fascicular block (LSFB) are not universally accepted and many other denominations can be seen in literature: focal septal block, septal focal block, left septal fascicular block, left anterior septal block, septal fascicular conduction disorder of the left branch, left septal Purkinje network block, left septal subdivision block of the left bundle branch, anterior conduction delay, left median hemiblock, left medial subdivision block of the left bundle branch, middle fascicle block, block of the anteromedial division of the left bundle branch of His, and anteromedial divisional block. During exercise stress test, fascicular blocks (left anterior and posterior) seem to indicate severe coronary artery narrowing of left main coronary or proximal left anterior descending artery disease1 and transient exercise-induced left septal fascicular block has been reported a few times2,3.

 54-year-old male, with a history of essential arterial systemic hypertension, primary hyperlipidemia and six-month typical chest pain during exercise (Class II – Canadian Cardiovascular Society) underwent an exercise stress test. During the exercise stress test, ECG demonstrated abrupt prominent anterior forces, an increase in R wave amplitude from V1 to V4, extreme left axis deviation and minor ST segment depression in DII, DIII and aVF (Figure 1). The post-exercise period showed progressive return of the QRS axis in both frontal and horizontal planes and the ST depression worsened by 1 mm. Coronary angiogram (Figure 2A) showed a critical proximal left anterior descending artery lesion. An exercise stress test done three months after coronary artery bypass surgery grafting was normal (Figure 2B).

Interesting ECG Exercise-induced left septal fascicular block: an expression of severe myocardial ischemia

There are several papers in literature that prove in a conclusive and incontestable way, that the left branch of the His bundle, in most instances (85% of the cases) splits into three fascicles of variable morphological pattern, and not into two: left anterior fascicle (LAF), left posterior fascicle (LPF), and left septal fascicle (LSF). The abovementioned papers have anatomical, histological, anatomo-pathological, electrocardiographic, and vectocardiographic, body surface potential mapping or ECG potential mapping and electrophysiological foundation. Additionally, the mentioned papers have been performed both in animal models (dogs) and in the human heart. Several clinical papers have shown that the left septal fascicular block (LSFB) may occur intermittently or transitorily as a consequence of a temporary dromotropic alteration, constituting an aberrant ventricular conduction, rate-dependent or by the application of atrial extra-stimuli, or naturally during the acute phase of infarction when this involves the anterior descending artery, before the septal perforating artery that supplies the central portion of the septum, where the mentioned LSF runs.

Historical Review The History of Left Septal Fascicular Block: Chronological Considerations of a Reality Yet to be Universally Accepted

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