Detection of Abnormal High-Frequency Components in the QRS Complex by the Wavelet Transform in Patients With Idiopathic Dilated Cardiomyopathy

Maehara, Kazuhira; Kokubun, Toshinori; Awano, Naoyuki; Taira, Kayano; Ono, Masahiro; Furukawa, Tatsuo; Shimizu, Yoshio; Maruyama, Yukio

doi:10.1253/jcj.63.25

Cited by 24 publications

(17 citation statements)

References 26 publications

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“…The fQRS has also been shown to be present in patients with dilated cardiomyopathy when wavelet analysis was performed on averaged QRS complexes obtained from the left precordial leads. 25 Similarly, myocardial scar may be present in patients with valvular heart disease, congenital heart disease, myocarditis, and rarer myocardial diseases (eg, Chagas disease, Kawasaki disease). The Q wave (without MI) may also be present in many of these conditions; therefore, we selected only those patients who underwent myocardial SPECT stress testing for evaluation of CAD.…”

Section: Limitationsmentioning

confidence: 99%

Significance of a Fragmented QRS Complex Versus a Q Wave in Patients With Coronary Artery Disease

et al. 2006

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Background-Q waves on a 12-lead ECG are markers of a prior myocardial infarction (MI). However, they may regress or even disappear over time, and there is no specific ECG sign of a non-Q-wave MI. Fragmented QRS complexes (fQRSs), which include various RSRЈ patterns, without a typical bundle-branch block are markers of altered ventricular depolarization owing to a prior myocardial scar. We postulated that the presence of an fQRS might improve the ability to detect a prior MI compared with Q waves alone by ECG. Methods and Results-A cohort of 479 consecutive patients (meanϮSD age, 58.2Ϯ13.2 years; 283 males) who were referred for nuclear stress tests was studied. The fQRS included various morphologies of the QRS (Ͻ120 ms), which included an additional R wave (RЈ) or notching in the nadir of the S wave, or Ͼ1 RЈ (fragmentation) in 2 contiguous leads, corresponding to a major coronary artery territory. The Q wave was present in 71 (14.8%) patients, an fQRS was present in 191 (34.9%) patients, and an fQRS and/or a Q wave was present in 203 (42.3%) patients. Sensitivity, specificity, and the negative predictive value for myocardial scar as detected by single photon emission computed tomography analysis were 36.3%, 99.2%, and 70.8%, respectively, for the Q wave alone; 85.6%, 89%, and 92.7%, respectively, for the fQRS; and 91.4%, 89%, and 94.2%, respectively, for the Q wave and/or fQRS. Conclusions-The fQRS on a 12-lead ECG is a marker of a prior MI, defined by regional perfusion abnormalities, which has a substantially higher sensitivity and negative predictive value compared with the Q wave.

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Section: Limitationsmentioning

confidence: 99%

Significance of a Fragmented QRS Complex Versus a Q Wave in Patients With Coronary Artery Disease

et al. 2006

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“…After the experiment, the QRS complex was digitized at 6 kHz, and the vector magnitude was averaged at approximately 20-40 consecutive beats as described previously. 13 Wavelet transform was obtained at 40, 100,160, 240, 320 and 400 Hz of the central frequency of the analyzing wavelet, and the area under the wavelet transform at each frequency was calculated as the increase in power with fine fractionation of the QRS complex reflecting inhomogeneous conduction. 13 …”

Section: Body Surface Ecg and Wavelet Analysismentioning

confidence: 99%

Comprehensive Analyses of Arrhythmogenic Substrates and Vulnerability to Ventricular Tachycardia in Left Ventricular Hypertrophy in Salt-Sensitive Hypertensive Rats

Kamei

Maehara

Kimura

et al. 2007

Circ J

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ypertensive left ventricular hypertrophy (LVH) is associated with an enhanced incidence of ventricular arrhythmia and an increased risk of sudden cardiac death. [1][2][3] Although in vitro studies of hypetensive LVH have proposed various electrophysiological abnormalities (ie, impulse formation 4,5 and conduction, 6-8 and repolarization abnormalities 9 ) as arrhythmogenic substrates, it remains unclear how these factors directly relate to the vulnerability to ventricular tachyarrhythmia in the in vivo whole heart. In other words, it remains poorly understood just how these electrophysiological abnormalities develop and increase the vulnerability to ventricular tachyarrhythmia with progression of LVH. The arrhythmogenic potential in hypertensive LVH may be multifactorial, but susceptibility to ventricular tachycardia (VT) induction has not been simultaneously investigated in the same LVH preparations, and therefore the relationships between various underlying arrhythmogenic mechanisms and VT attack have not been clarified. A clear understanding of this pathophysiological linkage is essential for determining the therapeutic target for prevention of fatal ventricular tachyarrhythmia. To investigate this issue, we used Dahl salt-sensitive hypertensive rats in which concentric LVH develops in a relatively short period. 10 Our preliminary study using this LVH model revealed that polymorphic VT was induced by programmed electrical stimulation, as shown by Coste et al in their clinical report. 11 Thus, the objectives of this study were first, to quantify the vulnerability of VT to programmed extrastimuli, and the changes it undergoes during the development of hypertensive LVH; second, to clarify how this vulnerability of VT relates to arrhythmogenic substrates (ie, conduction disturbances defined by a decrease in conduction velocity and an increase in the fractionation of QRS complex, and repolarization abnormalities defined by increases in the absolute refractory period and monophasic action potential (MAP) duration); and third, to examine how cellular electrophysiological remodeling relates to conduction and repolarization abnormalities of the whole heart during the progress of LVH. For these purposes, we performed programmed electrical stimulation to induce VT at 3 different observation periods in Dahl salt-sensitive (S) rats and -resistant (R) rats, and compared the vulnerability to VT with the conduction velocity and the degree of inhomogeneous conduction evaluated by wavelet analysis, 12,13 duration of MAP, 14 and absolute refractory period. In addition, myocytes were isolated from the same hearts, and patch-clamp analysis was performed for evaluation of resting membrane potential (RMP) and action potential (AP), as well as sodium (INa), calcium (ICa), and transient outward potassium currents (Ito). Background The contribution of conduction disturbances to susceptibility to ventricular tachycardia (VT) has not been directly examined in the process of left ventricular hypertrophy (LVH). Methods and ResultsDahl salt...

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“…Wavelet transform analysis is a novel timefrequency technique which is able to detect transient changes in an electrocardiogram even if they are superimposed on the high gain QRS complex. HFC in the QRS complex detected by this technique have been considered to reflect a conduction abnormality hidden in the QRS complex, which were observed in patients with structural heart diseases, such as prior myocardial infarction, 17) and hypertrophic or dilated cardiomyopathy, [18][19][20] and we previously reported the diagnostic importance of wavelet transformed ECG in Brugada syndrome. 21) As expected, HFC developed in MI patients, but not in normal controls.…”

Section: Discussionmentioning

confidence: 97%

Detection of Prior Myocardial Infarction Patients Prone to Malignant Ventricular Arrhythmias Using Wavelet Transform Analysis

et al. 2011

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SummaryVentricular tachycardia (VT) and ventricular fibrillation (VF) leading to sudden cardiac death remains responsible for significant mortality in patients with prior myocardial infarction (MI). The study population consisted of 50 normal controls and 50 patients with prior MI. The MI subjects were divided into 3 groups: VT/VF (-) group; 25 patients without ventricular tachyarrhythmia, VT group; 13 patients with sustained VT, and VF group; 12 patients with resuscitated VF. The parameters on the signal-averaged ECG and the frequency components recorded from the wavelet-transformed ECG were compared. The high-frequency components (HFC; 80-150 Hz) were developed in the MI group to a greater extent than those in the control group. Among the MI patients, the HFC were more developed in the VT and VF groups than in the VT/VF (-) group. In the VF group, the positive rate of LP was 50%. Meanwhile, when the peak power value at 150 Hz > 300 was defined as abnormal, the HFC was detected in 13 (100%) patients in the VT group and 12 (91.7%) in the VF group. The sensitivity of the abnormal HFC in identifying patients with VT/VF was higher than that of SAE-CG (96% versus 72%), although the specificity remained similar (68.5% versus 64.3%). Abnormal HFC recorded from the wavelet-transformed ECG may be a novel factor in detecting patients who are prone to VT/VF. (Int Heart J 2011; 52: 286-289) Key words: Wavelet transform, Electrocardiography, Ventricular fibrillation, Myocardial infarction V entricular tachycardia (VT) and ventricular fibrillation (VF) leading to sudden cardiac death remain responsible for significant mortality in patients with prior myocardial infarction (MI). The identification of patients at increased risk for VT/VF may reduce mortality in these patients. To date, late potentials (LP) by signal averaged electrocardiography (SAECG) have been studied and utilized to predict lethal ventricular arrhythmias in patients with previous MI.1-5) However, some patients with malignant ventricular arrhythmias did not demonstrate LP. In such patients, we found abnormal high frequency components (HFC) had developed in QRS complex using wavelet transform analysis. The purpose of this study was to assess the usefulness of the wavelet-transformed ECG (WTECG) in detecting post-MI patients who are prone to VT or VF. MethodsStudy population: This study is retrospective and consisted of 50 patients with prior MI and 50 sex and age-matched healthy individuals as normal controls (21 females and 29 males, 56.9 ± 13.8 years old). The MI subjects were divided into 3 groups: VT/VF (-) group; 25 patients without ventricular tachyarrhythmia, VT group; 13 patients with sustained VT, and VF group; 12 patients with resuscitated VF. All patients were referred to Nippon Medical School Main Hospital between December 1st, 1996 and December 31st, 2007. Sustained VT was defined as a tachycardia of ventricular origin, with a rate of ≥ 120 beats/ minute and lasting for ≥ 30 seconds. VF was defined as a polymorphic ventricular tachycardia with a ...

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Detection of Abnormal High-Frequency Components in the QRS Complex by the Wavelet Transform in Patients With Idiopathic Dilated Cardiomyopathy

Cited by 24 publications

References 26 publications

Significance of a Fragmented QRS Complex Versus a Q Wave in Patients With Coronary Artery Disease

Significance of a Fragmented QRS Complex Versus a Q Wave in Patients With Coronary Artery Disease

Comprehensive Analyses of Arrhythmogenic Substrates and Vulnerability to Ventricular Tachycardia in Left Ventricular Hypertrophy in Salt-Sensitive Hypertensive Rats

Detection of Prior Myocardial Infarction Patients Prone to Malignant Ventricular Arrhythmias Using Wavelet Transform Analysis

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