OC.15.3 SAFETY OF OMOM CAPSULE ENDOSCOPY IN PATIENTS WITH PACEMAKERS AND IMPLANTABLE CARDIAC DEFIBRILLATORS: AN “IN VIVO” ELECTROPHYSIOLOGICAL STUDY

2014 ◽  
Vol 46 ◽  
pp. S33-S34
Author(s):  
D. Moneghini ◽  
A. Lipari ◽  
G. Missale ◽  
R. Bozzi ◽  
L. Minelli ◽  
...  
2016 ◽  
Vol 4 (2) ◽  
pp. 216-220 ◽  
Author(s):  
Dario Moneghini ◽  
Alessandro Lipari ◽  
Guido Missale ◽  
Luigi Minelli ◽  
Gianpaolo Cengia ◽  
...  

2011 ◽  
Vol 73 (4) ◽  
pp. AB454-AB455 ◽  
Author(s):  
Dario Moneghini ◽  
Alessandro Lipari ◽  
Guido Missale ◽  
Luigi Minelli ◽  
Gianpaolo Cengia ◽  
...  

2016 ◽  
Vol 38 (2) ◽  
pp. 487-501 ◽  
Author(s):  
Stella Petric ◽  
Sofia Klein ◽  
Lisa Dannenberg ◽  
Tillman Lahres ◽  
Lukas Clasen ◽  
...  

Background/Aims: Pannexin-1 (Panx1) is an ATP release channel that is ubiquitously expressed and coupled to several ligand-gated receptors. In isolated cardiac myocytes, Panx1 forms large conductance channels that can be activated by Ca2+ release from the sarcoplasmic reticulum. Here we characterized the electrophysiological function of these channels in the heart in vivo, taking recourse to mice with Panx1 ablation. Methods: Cardiac phenotyping of Panx1 knock-out mice (Panx1-/-) was performed by employing a molecular, cellular and functional approach, including echocardiography, surface and telemetric ECG recordings with QT analysis, physical stress testing and quantification of heart rate variability. In addition, an in vivo electrophysiological study entailed programmed electrical stimulation using an intracardiac octapolar catheter. Results: Panx1 deficiency results in a higher incidence of AV-block, delayed ventricular depolarisation, significant prolongation of QT- and rate corrected QT-interval and a higher incidence of atrial fibrillation after intraatrial burst stimulation. Conclusion: Panx1 seems to play an important role in murine cardiac electrophysiology and warrants further consideration in the context of hereditary forms of atrial fibrillation.


2005 ◽  
Vol 100 (8) ◽  
pp. 1728-1731 ◽  
Author(s):  
Jonathan A. Leighton ◽  
Komandoor Srivathsan ◽  
Elizabeth J. Carey ◽  
Virender K. Sharma ◽  
Russell I. Heigh ◽  
...  

2014 ◽  
Vol 21 (7) ◽  
pp. 905-915 ◽  
Author(s):  
Chenyu Wang ◽  
David Paling ◽  
Luke Chen ◽  
Sean N Hatton ◽  
Jim Lagopoulos ◽  
...  

Objective: The objective of this paper is to inform the pathophysiology of medial longitudinal fasciculus (MLF) axonal dysfunction in patients with internuclear ophthalmoplegia (INO) due to multiple sclerosis (MS), and develop a composite structural-functional biomarker of axonal and myelin integrity in this tract. Methods: Eighteen patients with definite MS and clinically suspected INO underwent electrical vestibular stimulation and search-coil eye movement recording. Components of the electrically evoked vestibulo-ocular reflex (eVOR) were analyzed to probe the latency and fidelity of MLF axonal conduction. The MLF and T2-visible brainstem lesions were defined by high-resolution MRI. White matter integrity was determined by diffusion-weighted imaging metrics. Results: eVOR onset latency was positively correlated with MLF lesion length (left: r = 0.66, p = 0.004; right: r = 0.75, p = 0.001). The mean conduction velocity (±SD) within MLF lesions was estimated at 2.72 (±0.87) m/s. eVOR onset latency correlated with normalized axial diffusivity ( r = 0.66, p < 0.001) and fractional anisotropy ( r = 0.44, p = 0.02) after exclusion of cases with ipsilateral vestibular root entry zone lesions. Conclusions: Axonal conduction velocity through lesions involving the MLF was reduced below levels predicted for natively myelinated and remyelinated axons. Composite in vivo biomarkers enable delineation of axonal from myelin processes and may provide a crucial role in assessing efficacy of novel reparative therapies in MS.


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