Monophasic action potential amplitude for substrate mapping

Although radiofrequency ablation has revolutionized the management of tachyarrhythmias, the rate of arrhythmia recurrence is a large drawback. Successful substrate identification is paramount to abolishing arrhythmia, and bipolar voltage electrogram’s narrow field of view can be further reduced for increased sensitivity. In this report, we perform cardiac mapping with monophasic action potential (MAP) amplitude. We hypothesize that MAP amplitude (MAPA) will provide more accurate infarct sizes than other mapping modalities via increased sensitivity to distinguish healthy myocardium from scar tissue. Using the left coronary artery ligation Sprague-Dawley rat model of ischemic heart failure, we investigate the accuracy of in vivo ventricular epicardial maps derived from MAPA, MAP duration to 90% repolarization (MAPD90), unipolar voltage amplitude (UVA), and bipolar voltage amplitude (BVA) compared with gold standard histopathological measurement of infarct size. Numerical analysis reveals discrimination of healthy myocardium versus scar tissue using MAPD90 ( P = 0.0158) and UVA ( P < 0.001, n = 21). MAPA and BVA decreased between healthy and border tissue ( P = 0.0218 and 0.0015, respectively) and border and scar tissue ( P = 0.0037 and 0.0094, respectively). Contrary to our hypothesis, BVA mapping performed most accurately regarding quantifying infarct size. MAPA mapping may have high spatial resolution for myocardial tissue characterization but was quantitatively less accurate than other mapping methods at determining infarct size. BVA mapping’s superior utility has been reinforced, supporting its use in translational research and clinical electrophysiology laboratories. MAPA may hold potential value for precisely distinguishing healthy myocardium, border zone, and scar tissue in diseases of disseminated fibrosis such as atrial fibrillation. NEW & NOTEWORTHY Monophasic action potential mapping in a clinically relevant model of heart failure with potential implications for atrial fibrillation management.

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Evidence for electrical remodelling of the atrial myocardium in patients with atrial fibrillation. A study using the monophasic action potential recording technique

Clinical Physiology and Functional Imaging ◽

10.1046/j.1475-097x.2002.00384.x ◽

2002 ◽

Vol 22 (1) ◽

pp. 8-12 ◽

Cited By ~ 13

Author(s):

Eva J. Hertervig ◽

Shiwen Yuan ◽

Jonas Carlson ◽

Ole Kongstad-Rasmussen ◽

S. Bertil Olsson

Keyword(s):

Atrial Fibrillation ◽

Action Potential ◽

Monophasic Action Potential ◽

Atrial Myocardium ◽

Recording Technique ◽

Potential Recording

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MONOPHASIC ACTION POTENTIAL AND SINUS RHYTHM STABILITY AFTER CONVERSION OF ATRIAL FIBRILLATION

Acta Medica Scandinavica ◽

10.1111/j.0954-6820.1971.tb07446.x ◽

2009 ◽

Vol 190 (1-6) ◽

pp. 381-387 ◽

Cited By ~ 66

Author(s):

S. Bertil Olsson ◽

Simion Cotoi ◽

E. Varnauskas

Keyword(s):

Atrial Fibrillation ◽

Action Potential ◽

Sinus Rhythm ◽

Monophasic Action Potential ◽

Rhythm Stability

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The Contribution of Monophasic Action Potential Recordings to the Understanding of Atrial Fibrillation

Cardiac Arrhythmias: The Management of Atrial Fibrillation ◽

10.1007/978-3-662-30492-1_3 ◽

1992 ◽

pp. 27-38 ◽

Cited By ~ 1

Author(s):

M. R. Franz ◽

B. Koller

Keyword(s):

Atrial Fibrillation ◽

Action Potential ◽

Monophasic Action Potential

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Acetylcholine release by a stimulus train lowers atrial fibrillation threshold

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.253.4.h863 ◽

1987 ◽

Vol 253 (4) ◽

pp. H863-H868 ◽

Cited By ~ 2

Author(s):

D. E. Euler ◽

P. J. Scanlon

Keyword(s):

Atrial Fibrillation ◽

Action Potential ◽

Right Atrium ◽

Single Pulse ◽

Monophasic Action Potential ◽

Adrenergic Blockade ◽

The Right ◽

Alpha Chloralose ◽

Electrical Stimuli ◽

Local Release

This study was designed to evaluate the importance of local release of autonomic neuromediators when electrical stimuli are applied to the right atrium to measure the atrial fibrillation threshold (AFT). Experiments were performed in 16 open-chest dogs anesthetized with alpha-chloralose. The dogs were denervated by bilateral transection of the stellates and cervical vagi. The AFT was determined in 11 dogs by delivering either a train of stimuli (14 pulses, 4 ms, 100 Hz) or a single stimulus (10 ms) to the right atrium during its vulnerable period. In eight dogs, beta-adrenergic blockade with timolol (0.1 mg/kg) had no effect on the AFT determined with either method. Atropine (0.2 mg/kg), given after timolol, significantly increased the train-of-pulses AFT from 4.7 +/- 0.4 to 32.3 +/- 4.6 mA (P less than 0.001). The single-pulse AFT increased from 16.5 +/- 1.5 to 17.8 +/- 1.5 mA (P less than 0.05). Atropine had a similar effect on the AFT when it was given in the absence of timolol (n = 3). In five additional dogs, a monophasic action potential was recorded while a 10-mA train was delivered to the atrium during its absolute refractory period. There was marked shortening of the monophasic action potential duration (55 +/- 6 ms) in the first beat after the train. The shortening was totally abolished by atropine (0.2 mg/kg). The results suggest that a train of stimuli liberates local stores of acetylcholine, which cause a shortening of atrial repolarization time and a profound decrease in the current necessary to evoke fibrillation.

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