Fragmented QRS: A predictor of mortality and sudden cardiac death
Introduction
Several invasive and noninvasive tests for risk stratification of sudden cardiac death (SCD) have been studied,1 mostly in the context of structural heart disease such as coronary artery disease (CAD), cardiomyopathy, and heart failure. Except for left ventricular ejection fraction (LVEF), few markers of SCD can be utilized routinely in clinical practice. Tests such as microwave T-wave alternans (MTWA) and signal-averaged electrocardiogram (SAECG) have high negative predictive values in patients with myocardial infarction (MI) or cardiomyopathy. The major limitation of these tests is their lack of desirable positive predictive value for SCD.
Malignant ventricular arrhythmias such as sustained ventricular tachycardia (VT) and ventricular fibrillation (VF) are responsible for two-thirds of SCD.2 The initiation and maintenance of reentrant ventricular arrhythmias depend on the triggers and a vulnerable myocardial substrate. Focally initiated ventricular arrhythmias are also perpetuated by functional or anatomical reentry during VF. For reentry to occur, an abnormal repolarization of the tissues and/or disorder of impulse conduction are required. These can be detected as repolarization and depolarization abnormalities of the heart by various invasive and noninvasive tests. Repolarization abnormalities such as the MTWA and QT prolongation and dispersion are predictors of SCD. The major depolarization abnormality that predicts SCD is late potentials (LP) on SAECG.
Recently, we described the presence of a fragmented QRS complexes (fQRS) on a routine 12-lead ECG as another marker of depolarization abnormality.3 Our data suggest that the fQRS represents conduction delay caused by myocardial scar in patients with CAD. However, fQRS is not specific for CAD and also is encountered in other myocardial diseases such as cardiomyopathy and congenital heart disease. Recently, fQRS has been defined as a marker of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C)4 and Brugada syndrome.5 The purpose of this review is to discuss the potential role of fQRS in mechanisms and risk stratification of mortality and SCD.
Section snippets
fQRS: What we know so far
We defined fQRS on the routine 12-lead ECG (filter range, 0.15 to 100 Hz; AC filter, 60 Hz, 25 mm/s, 10 mm/mV) and includes various morphologies of the QRS wave with or without a Q wave.3 fQRS includes the presence of an additional R wave (R′) or notching in the nadir of the R wave or the S wave, or the presence of >1 R′ (fragmentation) in 2 contiguous leads, corresponding to a major coronary artery territory (Figure 1).3 Typical bundle branch block (BBB) pattern (QRS ≥ 120 ms) and incomplete
fQRS: A marker of myocardial scar in CAD
We showed that fQRS on a 12-lead ECG predicted myocardial scar in patients with CAD or suspected CAD.3 The presence of fQRS in ≥2 contiguous anterior leads (V1 to V5) predicted myocardial scar in anterior myocardial segments or in the left anterior descending territory. The presence of an fQRS in ≥2 contiguous lateral leads (I, aVL, and V6) predicted myocardial scar in lateral myocardial segments or left circumflex territory myocardial scar. Similarly, the presence of an fQRS in ≥2 contiguous
fQRS: A marker of arrhythmic events in nonischemic cardiomyopathy
The incidence of QRS fragmentation has not been fully studied in patients with nonischemic cardiomyopathy; however, it is a common finding on a 12-lead ECG in patients who receive an ICD for primary and secondary prophylaxis. In patients with nonischemic cardiomyopathy, QRS fragmentation has been recorded during wavelet ECG analysis recorded from 6 unipolar left precordial leads, using a high-precision amplifier.10 When compared with the control subjects with no heart disease, these wavelets
fQRS: A marker for ARVD/C
Recently, fQRS has been identified as a marker of ARVD/C by Peters et al.4 They studied the value of QRS fragmentation in a standard 12-lead ECG in 360 patients with ARVD/C (176 men, mean age: 47.3 ± 13.7 years) and compared its presence with the detection of the epsilon wave in highly amplified right precordial and modified limb leads in a subgroup of 207 patients. In this study, 52 phenotypically and genotypically nonaffected subjects from systematic family screening in 10 families with known
fQRS and other depolarization abnormalities in Brugada syndrome
Recently, Morita et al5 showed a 43% incidence of fQRS in 115 patients with Brugada syndrome (13 resuscitated from VF, 28 with syncope, and 74 asymptomatic) (Figure 4). The incidence of fQRS was significantly higher in the VF group as compared with the syncope or asymptomatic groups (incidence of fQRS: VF 85%, syncope 50%, and asymptomatic 34%, P < .01). Interestingly, the SCN5A mutation occurred more often in patients with fQRS (33%) than in patients without fQRS (5%). In patients with syncope
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Cited by (0)
Dr Zipes is a consultant to Medtronic, Inc.
Dr Das has no conflict of interest.
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This manuscript was independently reviewed.