Pulmonary Vein Isolation Without Left Atrial Mapping

Background: One of the crucial points during in most approaches developed for ablation of atrial fibrillation (AF) is the ability to identify the pulmonary vein (PVs) and to accurately locate their ostia. Objectives: The purpose of this case series was to investigate a simplified method for fusion of the multislice computer tomography (CT) derived 3D dataset with the electroanatomical map in order to facilitate the mapping procedure. Methods: In 5 consecutive patients (4 male) referred for catheter ablation of symptomatic drug-refractory paroxysmal atrial fibrillation contrast enhanced computer tomography was performed before the procedure and imported into an electroanatomical mapping system (Carto XP) using CartoMerge Image Integration Module. During the procedure a multipolar mapping catheter (Quick Star DS, Biosense Webster, Diamond Bar, CA, USA) was introduced to the coronary sinus (CS) to align the CSCT shell to the proper position. The CS potentials provided information to identify the ostium of the CS to achieve a more accurate fusion of the images. No mapping points were taken in the left atrium. The feasibility of the method was characterized by the distance of mapping points. Mapping, registration and outcome data were compared with a cohort of patients undergoing MRI image integration. Result: The mean distance between the mapping points taken in the CS by the Quick Star catheter and the CS CT surface was suitable (mean±SD, 1.4±0.3 mm). Full electrical isolation of the pulmonary veins could be achieved in all patients. The mean procedure and fluoroscopy time were 39 ± 22 and 134 ±38 min respectively, significantly decreased as compared to the MRI cohort. Conclusions: Highly accurate CT image and the electroanatomical map (EAM) fusion can be obtained by the Carto 3D electromanatomical mapping system using CS as the key anatomical structure for registration. Using this technique the mapping time of the left atrium can be reduced

The sigma-1 receptor enhances brain plasticity and functional recovery after experimental stroke.

Stroke leads to brain damage with subsequent slow and incomplete recovery of lost brain functions. Enriched housing of stroke-injured rats provides multi-modal sensorimotor stimulation, which improves recovery, although the specific mechanisms involved have not been identified. In rats housed in an enriched environment for two weeks after permanent middle cerebral artery occlusion, we found increased sigma-1 receptor expression in peri-infarct areas. Treatment of rats subjected to permanent or transient middle cerebral artery occlusion with 1-(3,4-dimethoxyphenethyl)-4-(3-phenylpropyl)piperazine dihydrochloride, an agonist of the sigma-1 receptor, starting two days after injury, enhanced the recovery of lost sensorimotor function without decreasing infarct size. The sigma-1 receptor was found in the galactocerebroside enriched membrane microdomains of reactive astrocytes and in neurons. Sigma-1 receptor activation increased the levels of the synaptic protein neurabin and neurexin in membrane rafts in the peri-infarct area, while sigma-1 receptor silencing prevented sigma-1 receptor-mediated neurite outgrowth in primary cortical neuronal cultures. In astrocytic cultures, oxygen and glucose deprivation induced sigma-1 receptor expression and actin dependent membrane raft formation, the latter blocked by sigma-1 receptor small interfering RNA silencing and pharmacological inhibition. We conclude that sigma-1 receptor activation stimulates recovery after stroke by enhancing cellular transport of biomolecules required for brain repair, thereby stimulating brain plasticity. Pharmacological targeting of the sigma-1 receptor provides new opportunities for stroke treatment beyond the therapeutic window of neuroprotection