Reduction of Ultra-High-Frequency ECG Components Following Sodium Channel Blockade by Propafenone: Evidence for Their Electrophysiological Origin

Radovan Smisek1, Pavel Leinveber2, Josef Halamek3, Magdalena Matejkova4, Martin Pesl5, Ivo Viscor6, Pavel Jurak6, Filip Plesinger6, Zdenek Starek7
1Institute of Scientific Instruments of the CAS, v. v. i., 2International Clinical Research Center, St. Anne’s University Hospital, Brno, Czech Republic, 3Institute of Scientific Instruments, CAS, CZ, 4International Clinical Research Center, St. Anne's University Hospital, Brno, Czech Republic, 5Department of Biology, Faculty of Medicine, Masaryk University, Brno, Czech Republic 2 ICRC, St. Anne’s University Hospital, Brno, Czech Republic 3 1st Department of Internal Medicine, Cardio-Angiology, Faculty of Medicine, Masaryk University, Brno, Czech Republic, 6Institute of Scientific Instruments of the CAS, 7Department of Internal Medicine, Cardioangiology, St. Anne's University Hospital in Brno

Abstract

Ultra-high-frequency ECG (UHF-ECG) is an advanced non-invasive technique for assessment of heart ventricular electrical dyssynchrony. The origin of UHF components in the ECG signal remains uncertain. It is hypothesized that rapid changes in membrane voltage during the opening of sodium channels (Phase 0 in the action potential) create these UHF components. The objective of this study was to evaluate changes in the amplitude of UHF components following the administration of propafenone, a sodium channel blocker.

We analyzed data from 12 patients; 7 received 300 mg of propafenone three times daily, and 5 received 150 mg three times daily. For each patient, amplitude data from 8 precordial leads (V1–V8) were analyzed across 76 frequency bands ranging from 150 to 1000 Hz (bandwidth: 100 Hz; frequency window shift: 10 Hz). For each lead and frequency band, the amplitude ratio before and after propafenone administration was calculated and subsequently averaged. Statistical significance was assessed using a paired t-test.

Our results show that 11 out of 12 patients exhibited a reduction in UHF component amplitudes following sodium channel blockade. On average, UHF amplitudes before propafenone administration were 1.61 times higher than after (p < 0.01).

This study demonstrates that the blockade of sodium channels reduces the amplitude of the UHF components in the ECG signal. This finding supports the hypothesis that the UHF components in the ECG are caused by the rapid opening of sodium channels.