Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice, occurring in 1% of the adult population of North America. Although AF does not typically lead to risk of immediate mortality, it is a potent risk factor for ischemic stroke. When left untreated AF reduces quality of life, functional status, cardiac performance and is associated with higher medical costs and an increased risk of death. Catheter ablation is a commonly used treatment method for those who suffer from drugrefractory AF. Prior to ablation, intra-cardiac mapping can be used to determine the activation sequence of cardiac tissue, which may be useful in deciding where to place ablation lesions. However, the electrical potential that is recorded during mapping is not a direct reflection of the current density across the tissue because the potential recorded at each point above the heart tissue is influenced by every cell in the tissue. This causes the recorded potential to be a blurred version of the true tissue current density. The potential that is observed can be described as the convolution of the true current density with a point spread function. Accordingly, deconvolution can, in principle, be used in order to improve the resolution of potential maps. However, because the number of electrodes which can be deployed transvenously is limited by practical restrictions, the recorded potential field is a sparsely sampled version of the actual potential field. Further, an electrode array cannot sample over the entire atrial surface, so the potential map that is observed is a truncated version of the global electrical activity. Here, we investigate the effects of electrode sampling density and edge extension on the ability of deconvolution to improve the resolution of measured electrical potentials within the atria of the heart. In particular, we identify the density of sensing electrodes that are required to allow deconvolution to provide improved estimation of the true current density when compared to the observed potential field.

No description available.

Ganglionated plexuses (GPs) are major constituents of the intrinsic cardiac nervous system, the final common integrator of regional cardiac control. We hypothesized that nicotinic stimulation of individual GPs exerts divergent regional influences, affecting atrial as well as ventricular functions. In 22 anesthetized canines, unipolar electrograms were recorded from 127 atrial and 127 ventricular epicardial loci during nicotine injection (100 mcg in 0.1 ml) into either the 1) right atrial (RA), 2) dorsal atrial, 3) left atrial, 4) inferior vena cava-inferior left atrial, 5) right ventricular, 6) ventral septal ventricular or 7) cranial medial ventricular (CMV) GP. In addition to sinus and AV nodal function, neural effects on atrial and ventricular repolarization were identified as changes in the area subtended by unipolar recordings under basal conditions and at maximum neurally-induced effects. Animals were studied with intact AV node or following ablation to achieve ventricular rate control. Atrial rate was affected in response to stimulation of all 7 GPs with an incidence of 50-95% of the animals among the different GPs. AV conduction was affected following stimulation of 6/7 GP with an incidence of 22-75% among GPs. Atrial and ventricular repolarization properties were affected by atrial as well as ventricular GP stimulation. Distinct regional patterns of repolarization changes were identified in response to stimulation of individual GPs. RAGP predominantly affected the RA and posterior right ventricular walls whereas CMVGP elicited biatrial and biventricular repolarization changes. Spatially divergent and overlapping cardiac regions are affected in response to nicotinic stimulation of neurons in individual GPs.

No description available.