Amir Jadidi1, Björn Müller-Edenborn2, Juan Chen3, Cornelius Keyl4, Reinhold Weber5, Jürgen Allgeier5, Zoraida Moreno-Weidmann6, Dietmar Trenk7, Franz-Josef Neumann2, Heiko Lehrmann5, Thomas Arentz5. 1. Department of Cardiology, University Heart Center Freiburg-Bad Krozingen, Bad Krozingen, Germany; Department of Electrophysiology, University Heart Center Freiburg-Bad Krozingen, Bad Krozingen, Germany. Electronic address: amir.jadidi@universitaets-herzzentrum.de. 2. Department of Cardiology, University Heart Center Freiburg-Bad Krozingen, Bad Krozingen, Germany. 3. Department of Electrophysiology, University Heart Center Freiburg-Bad Krozingen, Bad Krozingen, Germany; Cardiovascular Department, The First People's Hospital of Jingmen, Hubei, China. 4. Department of Anesthesiology, University Heart Center Freiburg-Bad Krozingen, Bad Krozingen, Germany. 5. Department of Cardiology, University Heart Center Freiburg-Bad Krozingen, Bad Krozingen, Germany; Department of Electrophysiology, University Heart Center Freiburg-Bad Krozingen, Bad Krozingen, Germany. 6. Department of Electrophysiology, University Heart Center Freiburg-Bad Krozingen, Bad Krozingen, Germany. 7. Department of Pharmacology, University Heart Center Freiburg-Bad Krozingen, Bad Krozingen, Germany.
Abstract
OBJECTIVES: Left atrial (LA) low-voltage substrate (LVS) potentially slows intra-atrial conduction, which might identify patients at risk for arrhythmia recurrence following pulmonary vein isolation (PVI). BACKGROUND: Up to 50% of patients with persistent atrial fibrillation (AF) have arrhythmia recurrence following PVI, mostly due to arrhythmogenic LA LVS. METHODS: Seventy-two patients with persistent AF underwent electrocardioversion to sinus rhythm and high-density voltage mapping of the left atrium. Invasively measured LA activation time and P-wave duration (PWD; total PWD and LA PWD [measured from -dV/dt in leads V1 and V2 until the end of the P-wave]) on amplified (40 to 50 mm/mV, 100 to 200 mm/s) digitized 12-lead electrocardiography (ECG) were compared with the extent of LA LVS (<0.5 and <1. 0mV). Freedom from arrhythmia following PVI was evaluated in 143 patients with persistent AF stratified according to amplified PWD before ablation. RESULTS: LA LVS resulted in regional conduction delay, which increased LA activation time (r = 0.79). LA PWD strongly correlated with LA activation time (r = 0.96) and LA LVS (r = 0.80). As the first (right atrial) portion of the P-wave (from P-wave beginning until -dV/dt in leads V1 and V2) was not affected by LA LVS, total PWD correlated with LA LVS (r = 0.84). PWD ≥150 ms identified advanced LA LVS with 94.3% sensitivity and 91.7% specificity. One-year arrhythmia freedom following PVI-only was significantly higher in patients with PWD <150 ms (n = 73) compared with those with prolonged PWD ≥150 ms (n = 70) (72.0% vs. 40.8%; p = 0.003). CONCLUSIONS: Advanced arrhythmogenic LVS is associated with significant intra-atrial conduction delay, which is accurately measurable by prolongation of PWD on amplified 12-lead ECG. PWD ≥150 ms during sinus rhythm measured prior to ablation identifies patients with persistent AF who are at increased risk for arrhythmia recurrence following PVI.
OBJECTIVES: Left atrial (LA) low-voltage substrate (LVS) potentially slows intra-atrial conduction, which might identify patients at risk for arrhythmia recurrence following pulmonary vein isolation (PVI). BACKGROUND: Up to 50% of patients with persistent atrial fibrillation (AF) have arrhythmia recurrence following PVI, mostly due to arrhythmogenic LA LVS. METHODS: Seventy-two patients with persistent AF underwent electrocardioversion to sinus rhythm and high-density voltage mapping of the left atrium. Invasively measured LA activation time and P-wave duration (PWD; total PWD and LA PWD [measured from -dV/dt in leads V1 and V2 until the end of the P-wave]) on amplified (40 to 50 mm/mV, 100 to 200 mm/s) digitized 12-lead electrocardiography (ECG) were compared with the extent of LA LVS (<0.5 and <1. 0mV). Freedom from arrhythmia following PVI was evaluated in 143 patients with persistent AF stratified according to amplified PWD before ablation. RESULTS: LA LVS resulted in regional conduction delay, which increased LA activation time (r = 0.79). LA PWD strongly correlated with LA activation time (r = 0.96) and LA LVS (r = 0.80). As the first (right atrial) portion of the P-wave (from P-wave beginning until -dV/dt in leads V1 and V2) was not affected by LA LVS, total PWD correlated with LA LVS (r = 0.84). PWD ≥150 ms identified advanced LA LVS with 94.3% sensitivity and 91.7% specificity. One-year arrhythmia freedom following PVI-only was significantly higher in patients with PWD <150 ms (n = 73) compared with those with prolonged PWD ≥150 ms (n = 70) (72.0% vs. 40.8%; p = 0.003). CONCLUSIONS: Advanced arrhythmogenic LVS is associated with significant intra-atrial conduction delay, which is accurately measurable by prolongation of PWD on amplified 12-lead ECG. PWD ≥150 ms during sinus rhythm measured prior to ablation identifies patients with persistent AF who are at increased risk for arrhythmia recurrence following PVI.
Authors: Martin Eichenlaub; Bjoern Mueller-Edenborn; Jan Minners; Nikolaus Jander; Martin Allgeier; Heiko Lehrmann; Simon Schoechlin; Juergen Allgeier; Dietmar Trenk; Franz-Josef Neumann; Thomas Arentz; Amir Jadidi Journal: Front Physiol Date: 2021-08-05 Impact factor: 4.566
Authors: Björn Müller-Edenborn; Jan Minners; Cornelius Keyl; Martin Eichenlaub; Nikolaus Jander; Sherif Abdelrazek; Christoph Ahlgrim; Jürgen Allgeier; Heiko Lehrmann; Franz-Josef Neumann; Thomas Arentz; Amir Jadidi Journal: Sci Rep Date: 2022-01-12 Impact factor: 4.379
Authors: Taiyuan Huang; Schurr Patrick; Louisa Katharina Mayer; Björn Müller-Edenborn; Martin Eichenlaub; Martin Allgeier; Jürgen Allgeier; Heiko Lehrmann; Christoph Ahlgrim; Marius Bohnen; Simon Schoechlin; Dietmar Trenk; Nikolaus Jander; Franz Josef Neumann; Thomas Arentz; Amir Jadidi Journal: J Clin Med Date: 2022-02-28 Impact factor: 4.241