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This article describes for the first time in the domestic literature a clinical case of the therapeutic effect of neuromodulation on the permanent form of atrial fibrillation and chronic heart failure in an elderly patient with spinal stenosis which led to the development of pain syndrome and movement disorders. For the treatment of neurological pathology, at the beginning epidural administration of drugs was applied, followed by spinal cord stimulation trial and implantation of permanent neurostimulator. At each stage of treatment conducted by a functional neurosurgeon the patient had a spontaneous restoration of sinus rhythm, and during continuous neurostimulation a stable retention of sinus rhythm and regression of heart failure symptoms have been observed throughout a long observation period. The article also presents the data of a few experimental and clinical studies on the use of neuromodulation in cardiology, describes the method of implantation of spinal electrodes and analyzes possible mechanisms of modulation of the autonomic innervation of the heart, implemented by spinal cord stimulation.

Aims: Use of a non-invasive electrocardiographic mapping system may aid in rapid diagnosis of atrial or ventricular arrhythmias or the detection of ventricular dyssynchrony. The aim of the present study was to validate the mapping accuracy of a novel non-invasive epi- and endocardial electrophysiology system (NEEES)., Methods and Results: Patients underwent pre-procedural computed tomography or magnetic resonance imaging of the heart and torso. Radiographic data were merged with the data obtained from the NEEES during pacing from implanted pacemaker leads or pacing from endocardial sites using an electroanatomical mapping system (CARTO 3, Biosense Webster). The earliest activation as denoted on the NEEES three-dimensional heart model was compared with the true anatomic location of the tip of the pacemaker lead or the annotated pacing site on the CARTO 3 map. Twenty-nine patients [mean age: 62 ± 11 years, 6/29 (11%) female, 21/29 (72%) with ischaemic cardiomyopathy] were enrolled into the pacemaker verification group. The mean distance from the non-invasively predicted pacing site to the anatomic reference site was 10.8 ± 5.4 mm for the right atrium, 7.7 ± 5.8 mm for the right ventricle, and 7.9 ± 5.7 mm for the left ventricle activated via the coronary sinus lead. Five patients [mean age 65 ± 4 years, 2 (33%) females] underwent CARTO 3 verification study. The mean distance between non-invasively reconstructed pacing site and the reference pacing site was 7.4 ± 2.7 mm for the right atrium, 6.9 ± 2.3 mm for the left atrium, 6.5 ± 2.1 mm for the right ventricle, and 6.4 ± 2.2 for the left ventricle, respectively., Conclusion: The novel NEEES was able to correctly identify the site of pacing from various endo- and epicardial sites with high accuracy., (© The Author 2015. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Patient P., 50 years old, male, with type I Brugada syndrome was examined. The patient had aborted sudden death event (2006) in his clinical history, ICD Gem III VR was implanted in 2006, ICDLumax DR was reimplanted in 2012. The patient had coved type pattern in right precordial ECG-leads. The p.E553X mutation in SCN5A gene, whish encodes the sodium channel -subunit, was found. Noninvasive electrocardiographic mapping was performed. Significant changes of local unipolar electrograms including QRS fragmentation, ST segment elevation and late ventricular potentials were identified in the epicardium of the right ventricle outflow tract. Thus, the presented case demonstrates that noninvasive electrocardiographic mapping methodology allows to determine and visualize arrhythmogenic substrate.

Patient P., 50 years old, male, with type I Brugada syndrome was examined. The patient had aborted sudden death event (2006) in his clinical history, ICD Gem III VR was implanted in 2006, ICDLumax DR was reimplanted in 2012. The patient had coved type pattern in right precordial ECG-leads. The p.E553X mutation in SCN5A gene, whish encodes the sodium channel α-subunit, was found. Noninvasive electrocardiographic mapping was performed. Significant changes of local unipolar electrograms including QRS fragmentation, ST segment elevation and late ventricular potentials were identified in the epicardium of the right ventricle outflow tract. Thus, the presented case demonstrates that noninvasive electrocardiographic mapping methodology allows to determine and visualize arrhythmogenic substrate in patients with inherited channelopathies.