Conduction Time
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2021 ◽  
Vol 94 ◽  
pp. 24-31
Masahiro Funaba ◽  
Yasuaki Imajo ◽  
Hidenori Suzuki ◽  
Yuji Nagao ◽  
Takuya Sakamoto ◽  

Yoshiaki Kaneko ◽  
Tadashi Nakajima ◽  
Shuntaro Tamura ◽  
Hiroshi Hasegawa ◽  
Takashi Kobari ◽  

2021 ◽  
Kyoko Soejima ◽  
Yusuke Kondo ◽  
Shingo Sasaki ◽  
Kazumasa Adachi ◽  
Ritsushi Kato ◽  

Patrick Müller ◽  
Bob Weijs ◽  
Nadine M. A. A. Bemelmans ◽  
Andreas Mügge ◽  
Lars Eckardt ◽  

AbstractAtrial fibrillation (AF) is a major cause of cardiovascular morbidity and mortality. To early detect and to avoid AF-related complications, several cardiac imaging modalities and approaches aim to quantify the severity of the underlying atrial cardiomyopathy (i.e., the extent of atrial remodeling). However, most established cardiac imaging modalities just incorporate single components of atrial remodeling and do not reflect the complete multifactorial process, which may contribute to their limited predictive value. Echocardiography-derived PA-TDI duration is a sophisticated echocardiographic parameter to assess total atrial conduction time and directly reflects both electrical and structural changes to the atria. Therefore, PA-TDI duration provides a more comprehensive quantification of the extent of atrial remodeling than other imaging modalities. In this article we review the role of PA-TDI duration as a marker of atrial remodeling and summarize the available data on PA-TDI duration to identify patients at risk for AF, as well as to guide AF management. Moreover, we discuss how to assess PA-TDI duration and provide recommendations on the implementation of PA-TDI duration into routine clinical care. Graphic abstract

2021 ◽  
Vol 11 (1) ◽  
Ibrahim M. Moustafa ◽  
Aliaa A. Diab ◽  
Fatma Hegazy ◽  
Deed E. Harrison

AbstractA randomized controlled study was conducted to evaluate the effect of rehabilitation of the cervical sagittal configuration on sensorimotor integration and central conduction time in an asymptomatic population. Eighty (32 female) participants with radiographic cervical hypolordosis and anterior head translation posture were randomly assigned to either a control or an experimental group. The experimental group received the Denneroll cervical traction while the control group received a placebo treatment. Interventions were applied 3 × per week for 10 weeks. Outcome measures included radiographic measured anterior head translation distance, cervical lordosis (posterior bodies of C2–C7), central somatosensory conduction time (latency) (N13–N20), and amplitudes of potentials for spinal N13, brainstem P14, parietal N20 and P27, and frontal N30. Outcomes were obtained at: baseline, after 10 weeks of intervention, and at 3 months follow up. After 10 weeks and 3-months, between-group analyses revealed statistically significant differences between the groups for the following measured variables: lordosis C2–C7, anterior head translation, amplitudes of spinal N13, brainstem P14, parietal N20 and P27, frontal N30 potentials (P < 0.001), and conduction time N13–N20 (P = 0.004). Significant correlation between the sagittal alignment and measured variables were found (P < 0.005). These findings indicate restoration of cervical sagittal alignment has a direct influence on the central conduction time in an asymptomatic population.

2021 ◽  
Paheli Desai-Chowdhry ◽  
Alexander Brummer ◽  
Van Savage

Neurons are connected by complex branching processes - axons and dendrites - that collectively process information for organisms to respond to their environment. Classifying neurons according to differences in structure or function is a fundamental part of neuroscience. Here, by constructing new biophysical theory and testing against our empirical measures of branching structure, we establish a correspondence between neuron structure and function as mediated by principles such as time or power minimization for information processing as well as spatial constraints for forming connections. Specifically, based on these principles, we use undetermined Lagrange multipliers to predict scaling ratios for axon and dendrite sizes across branching levels. We test our predictions for radius and length scale factors against those extracted from neuronal images, measured for cell types and species that range from insects to whales. Notably, our findings reveal that the branching of axons and peripheral nervous system neurons is mainly determined by time minimization, while dendritic branching is mainly determined by power minimization. Further comparison of different dendritic cell types reveals that Purkinje cell dendrite branching is constrained by material costs while motoneuron dendrite branching is constrained by conduction time delay over a range of species. Our model also predicts a quarter-power scaling relationship between conduction time delay and species body size, which is supported by experimental data and may help explain the emergence of hemispheric specialization in larger animals as a means to offset longer time delays.

Sein H. Schmidt ◽  
Stephan A. Brandt

In this chapter, we survey parameters influencing the assessment of the size and latency of motor evoked potentials (MEP), in normal and pathological conditions, and methods to allow for a meaningful quantification of MEP characteristics. In line with the first edition of this textbook, we extensively discuss three established mechanisms of intrinsic physiological variance and collision techniques that aim to minimize their influence. For the first time, in line with the ever wider use of optical navigation and targeting systems in brain stimulation, we discuss novel methods to capture and minimize the influence of extrinsic biophysical variance. Together, following the rules laid out in this chapter, transcranial magnetic stimulation (TMS) can account for spinal and extrinsic biophysical variance to advance investigations of the central origins of MEP size and latency variability.

Ann‐Kathrin Kahle ◽  
Roberto G. Gallotti ◽  
Fares‐Alexander Alken ◽  
Christian Meyer ◽  
Jeremy P. Moore

Background Ultra‐high‐density mapping enables detailed mechanistic analysis of atrial reentrant tachycardia but has yet to be used to assess circuit conduction velocity (CV) patterns in adults with congenital heart disease. Methods and Results Circuit pathways and central isthmus CVs were calculated from consecutive ultra‐high‐density isochronal maps at 2 tertiary centers over a 3‐year period. Circuits using anatomic versus surgical obstacles were considered separately and pathway length <50th percentile identified small circuits. CV analysis was used to derive a novel index for prediction of postablation conduction block. A total of 136 supraventricular tachycardias were studied (60% intra‐atrial reentrant, 14% multiple loop). Circuits with anatomic versus surgical obstacles featured longer pathway length (119 mm; interquartile range [IQR], 80–150 versus 78 mm; IQR, 63–95; P <0.001), faster central isthmus CV (0.1 m/s; IQR, 0.06–0.25 versus 0.07 m/s; IQR, 0.05–0.10; P =0.016), faster non‐isthmus CV (0.52 m/s; IQR, 0.33–0.71 versus 0.38 m/s; IQR, 0.27–0.46; P =0.009), and fewer slow isochrones (4; IQR, 2.3–6.8 versus 6; IQR 5–7; P =0.008). Both central isthmus ( R 2 =0.45; P <0.001) and non‐isthmus CV ( R 2 =0.71; P <0.001) correlated with pathway length, whereas central isthmus CV <0.15 m/s was ubiquitous for small circuits. Non‐isthmus CV in tachycardia correlated with CV during block validation ( R 2 =0.94; P <0.001) and a validation map to tachycardia conduction time ratio >85% predicted isthmus block in all cases. Over >1 year of follow‐up, arrhythmia‐free survival was better for homogeneous CV patterns (90% versus 57%; P =0.04). Conclusions Ultra‐high‐density mapping‐guided CV analysis distinguishes atrial reentrant patterns in adults with congenital heart disease with surgical obstacles producing slower and smaller circuits. Very slow central isthmus CV may be essential for atrial tachycardia maintenance in small circuits, and non‐isthmus conduction time in tachycardia appears to be useful for rapid assessment of postablation conduction block.

2021 ◽  
Vol 11 (5) ◽  
pp. 648
Maurits Hoonhorst ◽  
Rinske Nijland ◽  
Cornelis Emmelot ◽  
Boudewijn Kollen ◽  
Gert Kwakkel

Background: Stroke affects the neuronal networks of the non-infarcted hemisphere. The central motor conduction time (CMCT) induced by transcranial magnetic stimulation (TMS) could be used to determine the conduction time of the corticospinal tract of the non-infarcted hemisphere after a stroke. Objectives: Our primary aim was to demonstrate the existence of prolonged CMCT in the non-infarcted hemisphere, measured within the first 48 h when compared to normative data, and secondly, if the severity of motor impairment of the affected upper limb was significantly associated with prolonged CMCTs in the non-infarcted hemisphere when measured within the first 2 weeks post stroke. Methods: CMCT in the non-infarcted hemisphere was measured in 50 patients within 48 h and at 11 days after a first-ever ischemic stroke. Patients lacking significant spontaneous motor recovery, so-called non-recoverers, were defined as those who started below 18 points on the FM-UE and showed less than 6 points (10%) improvement within 6 months. Results: CMCT in the non-infarcted hemisphere was prolonged in 30/50 (60%) patients within 48 h and still in 24/49 (49%) patients at 11 days. Sustained prolonged CMCT in the non-infarcted hemisphere was significantly more frequent in non-recoverers following FM-UE. Conclusions: The current study suggests that CMCT in the non-infarcted hemisphere is significantly prolonged in 60% of severely affected, ischemic stroke patients when measured within the first 48 h post stroke. The likelihood of CMCT is significantly higher in non-recoverers when compared to those that show spontaneous motor recovery early post stroke.

2021 ◽  
Vol 12 ◽  
Ryuichi Kambayashi ◽  
Hiroko Izumi-Nakaseko ◽  
Ai Goto ◽  
Kazuya Tsurudome ◽  
Hironori Ohshiro ◽  

Oseltamivir has been shown to prolong the atrial conduction time and effective refractory period, and to suppress the onset of burst pacing-induced atrial fibrillation in vitro. To better predict its potential clinical benefit as an anti-atrial fibrillatory drug, we performed translational studies by assessing in vivo anti-atrial fibrillatory effect along with in vivo and in vitro electropharmacological analyses. Oseltamivir in intravenous doses of 3 (n = 6) and 30 mg/kg (n = 7) was administered in conscious state to the persistent atrial fibrillation model dogs to confirm its anti-atrial fibrillatory action. The model was prepared by tachypacing to the atria of chronic atrioventricular block dogs for &gt; 6 weeks. Next, oseltamivir in doses of 0.3, 3 and 30 mg/kg was intravenously administered to the halothane-anesthetized intact dogs to analyze its in vivo electrophysiological actions (n = 4). Finally, its in vitro effects of 10–1,000 μM on IK,ACh, IKur, IKr, INa and ICaL were analyzed by using cell lines stably expressing Kir3.1/3.4, KV1.5, hERG, NaV1.5 or CaV1.2, respectively (n = 3 for IK,ACh and IKr or n = 6 for IKr, INa and ICaL). Oseltamivir in doses of 3 and 30 mg/kg terminated the atrial fibrillation in 1 out of 6 and in 6 out of 7 atrial fibrillation model dogs, respectively without inducing any lethal ventricular arrhythmia. Its 3 and 30 mg/kg delayed inter-atrial conduction in a frequency-dependent manner, whereas they prolonged atrial effective refractory period in a reverse frequency-dependent manner in the intact dogs. The current assay indicated that IC50 values for IK,ACh and IKr were 160 and 231 μM, respectively, but 1,000 µM inhibited INa, ICaL and IKur by 22, 19 and 13%, respectively. The extent of INa blockade was enhanced at faster beating rate and more depolarized resting membrane potential. Oseltamivir effectively terminated the persistent atrial fibrillation, which may be largely due to the prolongation of the atrial effective refractory period and inter-atrial conduction time induced by IK,ACh and IKr inhibitions along with INa suppression. Thus, oseltamivir can exert a powerful anti-atrial fibrillatory action through its ideal multi-channel blocking property; and oseltamivir would become a promising seed compound for developing efficacious and safe anti-atrial fibrillatory drugs.

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