Abstract
PurposeThe aim of this proof-of-concept study is to introduce new high-dynamic ECG technique with potential to detect temporal-spatial distribution of ventricular electrical depolarization and to assess the level of ventricular dyssynchrony.Methods5-kHz 12-lead ECG data was collected. The amplitude envelopes of the QRS were computed in an ultra-high frequency band of 500–1000 Hz and were averaged (UHFQRS). UHFQRS V lead maps were compiled, and numerical descriptor identifying ventricular dyssynchrony (UHFDYS) was detected.ResultsAn electrical UHFQRS maps describe the ventricular dyssynchrony distribution in resolution of milliseconds and correlate with strain rate results obtained by speckle tracking echocardiography. The effect of biventricular stimulation is demonstrated by the UHFQRS morphology and by the UHFDYS descriptor in selected examples.ConclusionsUHFQRS offers a new and simple technique for assessing electrical activation patterns in ventricular dyssynchrony with a temporal-spatial resolution that cannot be obtained by processing standard surface ECG. The main clinical potential of UHFQRS lies in the identification of differences in electrical activation among CRT candidates and detection of improvements in electrical synchrony in patients with biventricular pacing.
Highlights
Pathological changes in the structure of cardiac ventricles often manifest themselves in electrical activity
An electrical UHFQRS maps describe the ventricular dyssynchrony distribution in resolution of milliseconds and correlate with strain rate results obtained by speckle tracking echocardiography
The effect of biventricular stimulation is demonstrated by the UHFQRS morphology and by the UHFDYS descriptor in selected examples
Summary
Pathological changes in the structure of cardiac ventricles often manifest themselves in electrical activity. The clinical 12lead ECG-based criteria for left ventricle (LV) dyssynchrony quantification and cardiac resynchronization therapy (CRT) implementation are based primarily on the duration and morphology of the QRS complex [1,2,3]. In 1981, Goldberger et al [10] reported the effect of myocardial infarction on lowvoltage high frequency (HF, 150–250 Hz) potentials in the QRS complex (HFQRS, HF-ECG). Studies dedicated to this topic [10,11,12] have shown that HFQRS potential morphology and amplitude reduction are modified by coronary occlusion or infarct-induced ischemia. The presented methodologies have focused predominantly on heart ischemia (single-lead HFQRS morphology), neglected the temporal-spatial properties (dyssynchrony), and analyzed ECG in a limited frequency range (up to 250 Hz) [12, 13]
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