Altered Atrial Electrical Restitution and Heterogeneous Sympathetic Hyperinnervation in Hearts With Chronic Left Ventricular Myocardial Infarction

Abstract

Background-The substrates for the increased incidence of atrial fibrillation (AF) in hearts with chronic left ventricular myocardial infarction (MI) remain poorly defined. We hypothesized that chronic MI is associated with atrial electrical and neural remodeling that enhances AF vulnerability. Methods and Results-We created MI in 8 dogs by permanent occlusion of the left anterior descending (LAD) coronary artery. Seven dogs (3 with thoracotomy) that had no LAD occlusion served as controls. Eight weeks after surgery, the incidence and duration of pacing-induced AF in the open chest anesthetized state were significantly (PϽ0.05) higher in the MI than in control dogs. Multisite biatrial monophasic action potential (MAP) recordings showed increased heterogeneity of MAP duration (MAPD) and MAPD restitution slope. AF in the MI groups was preceded by significantly higher MAPD (PϽ0.01) and MAP amplitude (PϽ0.05) alternans in both atria compared with controls. Epicardial mapping using 1792 bipolar electrodes (1-mm spatial resolution) showed multisite wavebreaks of the paced wavefronts leading to AF in MI but not in control dogs. Multiple wavelets in MI dogs were associated with significantly higher incidence and longer duration of AF compared with control. The density of biatrial tyrosine hydroxylase (TH) and growth-associated protein43 (GAP43) nerves were 5-to 8-fold higher and were more heterogeneous in MI compared with control dogs. Conclusions-Chronic

Influences of Autonomic Nervous System on Atrial Arrhythmogenic Substrates and the Incidence of Atrial Fibrillation in Diabetic Heart

“…To investigate the distribution of sympathetic innervation in the RA, we examined the density of tyrosine hydroxylase (TH)-positive nerves using an immunohistochemical method 22,23) in control and DM rats (n = 7 in each group). Whole RA tissues were soaked in methanol with H 2 O 2 for 30 minutes.…”

Expression of tyrosine hydroxylase and growth-associated protein 43 in aging atrial fibrillation patients of Xinjiang Uygur and Han nationality

“…There are several possible reasons to explain why AF causes neural eruption and inhomogenous distribution, including: 1) electrical remodeling and structure reconstruction occurs during AF (Miyauchi et al, 2003), resulting in atrial enlargement, insufficient blood supply, and myocardial damage, which in turn impairs the nerve. GAP43 and b-NGF could help neural development and neural recovery, which promote the regeneration of impaired nerves in addition to promoting the growth of myocardial intact nerves; 2) atrial structure reconstruction in AF causes distribution disorder and regeneration of the nerves distributed in the atria, and the ANS distribution density intensifies, but is not even.…”

Abnormal Atrial Repolarization and Depolarization Contribute to the Inducibility of Atrial Fibrillation in Brugada Syndrome

“…The time course of restitution obtained by S 1 S 2 was fitted using a monoexponential equation and Origin 7.0 software (OriginLab Corp., Northampton, MA, USA), and the maximum slope of the APDR curve (slopemax) was obtained by the maximum value of the first derivative of the monoexponential equation fitting curve. [21][22][23][24] (Tables II and III). Electrophysiologic study: There was no significant difference between the groups in terms of the AH interval or the HV interval (Table IV).…”