Abstract
Epicardial high-density electrical mapping is a well-established experimental instrument to monitor in vivo the activity of the atria in response to modulations of the autonomic nervous system in sinus rhythm. In regions that are not accessible by epicardial mapping, noncontact endocardial mapping performed through a balloon catheter may provide a more comprehensive description of atrial activity. We developed a computer model of the canine right atrium to compare epicardial and noncontact endocardial mapping. The model was derived from an experiment in which electroanatomical reconstruction, epicardial mapping (103 electrodes), noncontact endocardial mapping (2048 virtual electrodes computed from a 64-channel balloon catheter), and direct-contact endocardial catheter recordings were simultaneously performed in a dog. The recording system was simulated in the computer model. For simulations and experiments (after atrio-ventricular node suppression), activation maps were computed during sinus rhythm. Repolarization was assessed by measuring the area under the atrial T wave (ATa), a marker of repolarization gradients. Results showed an epicardial-endocardial correlation coefficients of 0.80 and 0.63 (two dog experiments) and 0.96 (simulation) between activation times, and a correlation coefficients of 0.57 and 0.46 (two dog experiments) and 0.92 (simulation) between ATa values. Despite distance (balloon-atrial wall) and dimension reduction (64 electrodes), some information about atrial repolarization remained present in noncontact signals.
Highlights
Despite decades of investigations, many questions related to the mechanisms underlying the initiation and maintenance of atrial fibrillation remain open [1]
The origin of atrial fibrillation may be neurogenic, myogenic, or due to a combination of both [2]
In animal models reproducing the neurogenic form of atrial fibrillation, the identification of neurogenically-induced repolarization gradients in sinus rhythm is critical for understanding the mechanisms of arrhythmogenicity
Summary
Many questions related to the mechanisms underlying the initiation and maintenance of atrial fibrillation remain open [1]. Animal models have been developed to investigate the relation between atrial fibrillation and the autonomic nervous system [3]. In these models, atrial tachyarrhythmias could be induced by electrically stimulating the vagosympathetic trunks in the neck [4] or mediastinal nerves [5,6]. Heterogeneity of repolarization was created locally in various atrial areas depending on which nerve was stimulated. In animal models reproducing the neurogenic form of atrial fibrillation, the identification of neurogenically-induced repolarization gradients in sinus rhythm is critical for understanding the mechanisms of arrhythmogenicity
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