J-wave pattern on the ECG is characterized by >0.1 mV J-point elevation in two contiguous inferior or lateral leads and may manifest itself as either slurring or notching of the terminal portion of the QRS complex. On the other hand, fragmented QRS is characterized by more than one R-wave (i.e. R’) or notching of the R- or S-wave in two contiguous leads in subjects without complete or partial bundle branch block. Generally, the J-wave is considered an ECG manifestation of the transmural voltage gradient between epicardial and endocardial layers of myocardium during the early phase of repolarization. However, activation gradients may also contribute to J-waves. Regional activation delay or excitation failure can obscure the distinction between the QRS-complex and ST-segment, causing a deflection at the terminal part of the QRS-complex, which may be interpreted as a J-wave. Hence, currently there are two competing mechanistic explanations for the J-wave: one relating to abnormal repolarization, the other to abnormal depolarization. On the other hand, fragmented QRS is commonly believed to be a consequence of depolarization delay, i.e. a conduction abnormality. Thus, the genesis of these two ECG patterns may overlap, causing confusion in both clinical and experimental settings.
Both J-waves and fragmented QRS may be found in patients with lethal ventricular arrhythmias, however they are also seen in healthy subjects, and hence they cannot be solely responsible for fatal arrhythmic events, but rather constitute modulators of arrhythmic risk in patients with cardiac diseases.
In the context of arrhythmia risk, several questions arise:
(i) What is the relationship between J-wave and fragmented QRS?
(ii) How can we differentiate these two ECG patterns?
(iii) How can we recognize their malignant forms and what is their pathophysiological basis?
This Research Topic will cover all aspects concerning J-waves and fragmented QRS, and researchers dealing with these topics are welcomed to submit related manuscripts.
J-wave pattern on the ECG is characterized by >0.1 mV J-point elevation in two contiguous inferior or lateral leads and may manifest itself as either slurring or notching of the terminal portion of the QRS complex. On the other hand, fragmented QRS is characterized by more than one R-wave (i.e. R’) or notching of the R- or S-wave in two contiguous leads in subjects without complete or partial bundle branch block. Generally, the J-wave is considered an ECG manifestation of the transmural voltage gradient between epicardial and endocardial layers of myocardium during the early phase of repolarization. However, activation gradients may also contribute to J-waves. Regional activation delay or excitation failure can obscure the distinction between the QRS-complex and ST-segment, causing a deflection at the terminal part of the QRS-complex, which may be interpreted as a J-wave. Hence, currently there are two competing mechanistic explanations for the J-wave: one relating to abnormal repolarization, the other to abnormal depolarization. On the other hand, fragmented QRS is commonly believed to be a consequence of depolarization delay, i.e. a conduction abnormality. Thus, the genesis of these two ECG patterns may overlap, causing confusion in both clinical and experimental settings.
Both J-waves and fragmented QRS may be found in patients with lethal ventricular arrhythmias, however they are also seen in healthy subjects, and hence they cannot be solely responsible for fatal arrhythmic events, but rather constitute modulators of arrhythmic risk in patients with cardiac diseases.
In the context of arrhythmia risk, several questions arise:
(i) What is the relationship between J-wave and fragmented QRS?
(ii) How can we differentiate these two ECG patterns?
(iii) How can we recognize their malignant forms and what is their pathophysiological basis?
This Research Topic will cover all aspects concerning J-waves and fragmented QRS, and researchers dealing with these topics are welcomed to submit related manuscripts.