Korean Circ J.  2016 Sep;46(5):601-609. 10.4070/kcj.2016.46.5.601.

J Wave Syndromes: History and Current Controversies

• Liu T
• Zheng J
• Yan GX

• KMID: 2389614
• DOI: http://doi.org/10.4070/kcj.2016.46.5.601

Abstract

The concept of J wave syndromes was first proposed in 2004 by Yan et al for a spectrum of electrocardiographic (ECG) manifestations of prominent J waves that are associated with a potential to predispose affected individuals to ventricular fibrillation (VF). Although the concept of J wave syndromes is widely used and accepted, there has been tremendous debate over the definition of J wave, its ionic and cellular basis and arrhythmogenic mechanism. In this review article, we attempted to discuss the history from which the concept of J wave syndromes (JWS) is evolved and current controversies in JWS.

Keyword

Brugada syndrome; Sudden cardiac death; Ventricular fibrillation

MeSH Terms

Brugada Syndrome
Death, Sudden, Cardiac
Electrocardiography
Ventricular Fibrillation

Figure

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  Fig. 1 The sequence of ventricular activation influences the appearance of J wave in a transmural ECG recorded from coronary-perfused canine left ventricular wedge preparation. (A) Stimulation of the endocardial (Endo) surface causes the epicardial (Epi) surface to be activated last. In such case the J wave is aligned with Ito-mediated epicardial AP notch. (B) Stimulation of the epicardial surface activates it before the endocardial surface. This causes the epicardial AP notch to occur simultaneously with the QRS, hiding the J wave. Reproduced from Yan and Antzelevitch4) with permission. (C) Endocardial activation at different locations can cause the J wave to occur at the end of the QRS, manifesting as slurred (left panel) or notched (right panel) QRS. Reproduced from Badri et al.5) with permission.

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  Fig. 2 (A) Left panel: classical J waves with J-point and ST segment elevation that are likely mediated by Ito, Right panel: possible intraventricular conduction delay masquerading as pseudo J waves presented in the study by Tikkanen et al.40) Reproduced from Tikkanen et al.40) with permission. (B) Two examples of increased pseudo J wave amplitude after shorter RR intervals. (C) An example of right bundle branch block can cause pseudo J waves in inferior leads. IVCD: intraventricular conduction delay, RBBB: right bundle branch block.

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  Fig. 3 Cellular basis for the traditional ER. (A) Surface ECG (lead V5) recorded from a 17-year-old healthy African American man. Note the presence of a small J wave and upwardly concave ST segment elevation. (B) Simultaneous recording of transmembrane action potentials from epicardial (Epi) and endocardial (Endo) regions and a transmural ECG in an isolated arterially perfused canine left ventricular wedge. A J wave in the transmural ECG is present due to the action potential notch in the epicardium but not the endocardium. Perfusion of the preparation with pinacidil (2 µmol/L), an ATP-sensitive potassium channel opener, causes partial loss of the action potential dome in the epicardium that separates earlier from the endocardium during phase 2 plateau phase, resulting in upwardly concave ST segment elevation in the ECG resembling the traditional ER. Reproduced from Hlaing et al.12) with permission. ECG: electrocardiography.

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  Fig. 4 Frequency-dependent changes in epicardial notch and J wave amplitude. (A) Simultaneously recorded transmural ECG and transmembrane APs from an canine right ventricular wedge: during basic stimulation (S1-S2=4000 ms) there were associated prominent epicardial notch and J wave. Premature stimulation (S1-S2=300 ms) decreased the epicardial notch and J wave amplitude. (B) Plot of epicardial AP notch (□) and J wave (○) amplitude across a range of S1-S2 intervals. Epicardial AP notch and J wave amplitudes changed in parallel to changes in S1-S2 intervals. Reproduced from Yan and Antzelevitch4) with permission. (C) ECG tracings in lead V4-V5 recorded from a 34 year-old Chinese man with J wave syndromes showing prominent J waves that are more accentuated after a long (thick arrows) compared to short (thin arrows) R-R interval. (D) A J-wave-like deflection at the terminal potion of the QRS in a patient with intraventricular conduction delay. In contrary to the J wave in Fig. 4C, prolonged R-R interval allow more time for conduction, attenuating this terminal deflection (thin arrows) compared to the higher amplitude seen in the short R-R interval (thick arrows). Reproduced from Badri et al.5) with permission. ECG: electrocardiography.

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  Fig. 5 Ito-mediated J wave and ventricular fibrillation (VF) via phase 2 reentry. (A) VF in a male patient with J wave in lead II, note the larger amplitude of J wave in the beat preceding VF, following a longer R-R interval. (B) Phase 2 reentry predisposing to VF in a canine right ventricular wedge preparation in the presence of the K+ channel opener pinacidil. Loss of AP dome in Epi1 but not Epi2 caused propagation of the dome at Epi2 to Epi1, i.e. phase 2 reentry (solid arrows), which manifested a short-coupled R-on-T beats (open arrows) capable of triggering VF. Reproduced from Yan et al.35) with permission. ECG: electrocardiography.

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  Fig. 6 Example to demonstrate the counterparts of type 1 and 2 Brugada waves. (A) The bottom ECG tracing exhibiting prominent J waves in a left precordial lead V5 was obtained from a 34 year-old Chinese man who survived from idiopathic VF. The J wave wad accentuated after a pause, which was accompanied by a negative T wave. The upper ECG tracing was produced by turning the QRS complex in the bottom ECG tracing (V5) by 180 degree to simulate a pseudo V1 tracing. The upper tracing was then evaluated by 27 electrophysiologists, among whom 24 agreed that there were type 2 and type 1 Brugada waves in this tracing. (B) Type 2 Brugada wave equates J wave plus upwardly concave ST segment elevation in leads excluding V1 to V3; type 1 Brugada wave is the counterpart of a prominent J wave with a negative T wave in leads excluding V1 to V3. ECG: electrocardiography.

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