Electrophysiological Studies Research Articles

Real-world battery longevity of implantable loop recorders implanted for unexplained syncope: Results from a large single-center registry.

Implantable loop recorders (ILR) are increasingly used in cardiac rhythm monitoring and diagnostic work-up of unexplained syncope. ILR battery longevity, according to manufacturers' product performance specifications, typically ranges between 2 and 4 years, but real-world data in this population are lacking. This monocentric, prospective, observational study included consecutive patients with unexplained syncope undergoing ILR implantation between October 2007 and 2019. The main purpose was to determine real-world battery longevity of ILRs. Diagnostic yield and relationship between arrhythmogenic diagnosis and duration of ILR monitoring were explored. The study included 309 patients (59 years [38-73], 49% female) with ILR implantation for unexplained syncope. Median battery longevity was 42 [40-45] months. A total of 99.5% of ILRs reached prespecified battery longevity. The time to end-of-life varied by up to 33 months among the same ILR models. Overall arrhythmogenic diagnostic yield counted 27% (73% sick sinus syndrome, 20% atrioventricular block, and 7% ventricular tachycardia). Median time to diagnosis was 10 [2-25] months, with the latest event at 43 months. The cumulative diagnostic yield for arrhythmogenic event explaining syncope was 4.2%, 6.1%, 9.4%, 14.6%, 19.4%, and 26.7% at 1, 2, 6, 12, 24, and 48 months, respectively. In univariate analysis, first degree AV block and prolonged HV time on EP study were predictors of diagnosis, while QRS duration abnormality borderline missed significance. Real-world battery longevity of ILRs matched industry projected longevity in 99.5% of patients implanted with ILR for unexplained syncope. A battery longevity of minimum 3.5 years is recommended to maximize the diagnostic yield in this population.

A p75 neurotrophin receptor-sparing nerve growth factor protects retinal ganglion cells from neurodegeneration by targeting microglia.

Retinal ganglion cells (RGCs) are the output stage of retinal information processing, via their axons forming the optic nerve (ON). ON damage leads to axonal degeneration and death of RGCs, and results in vision impairment. Nerve growth factor (NGF) signalling is crucial for RGC operations and visual functions. Here, we investigate a new neuroprotective mechanism of a novel therapeutic candidate, a p75-less, TrkA-biased NGF agonist (hNGFp) in rat RGC degeneration, in comparison with wild type human NGF (hNGFwt). Both neonate and adult rats, whether subjected or not to ON lesion, were treated with intravitreal injections or eye drops containing either hNGFp or hNGFwt. Different doses of the drugs were administered at days 1, 4 or 7 after injury for a maximum of 10days, when immunofluorescence, electrophysiology, cellular morphology, cytokine array and behaviour studies were carried out. Pharmacokinetic evaluation was performed on rabbits treated with hNGFp ocular drops. hNGFp exerted a potent RGC neuroprotection by acting on microglia cells, and outperformed hNGFwt in rescuing RGC degeneration and reducing inflammatory molecules. Delayed use of hNGFp after ON lesion resulted in better outcomes compared with treatment with hNGFwt. Moreover, hNGFp-based ocular drops were less algogenic than hNGFwt. Pharmacokinetic measurements revealed that biologically relevant quantities of hNGFp were found in the rabbit retina. Our data point to microglia as a new cell target through which NGF-induced TrkA signalling exerts neuroprotection of the RGC, emphasizing hNGFp as a powerful treatment to tackle retinal degeneration.

Mirror movements in multiple sclerosis -a clinical, electrophysiological, and imaging study

BackgroundMirror movements (MM) are commonly caused by a defect of interhemispheric pathways also affected in multiple sclerosis (MS), particularly the corpus callosum. We investigated the prevalence of MM in MS in relation to functional and morphological callosal fiber integrity by transcranial magnetic stimulation (TMS), magnetic resonance imaging (MRI), as well as fatigue.MethodsIn 21 patients with relapsing–remitting MS and 19 healthy controls, MM were assessed and graded (Woods and Teuber scale: MM 1—4) using a bedside test. Fatigue was evaluated using the Fatigue Scale for Motor and Cognitive Functions (FSMC) questionnaire. TMS measured ipsilateral silent period latency and duration. MRI assessed callosal atrophy by measuring the normalized corpus callosum area (nCCA), corpus callosum index (CCI), and lesion volume.ResultsMS patients had significantly more often and pronounced MM compared to healthy controls (p = 0.0002) and nCCA was significantly lower (p = 0.045) in MRI studies. Patients with higher MM scores (MM > 1 vs. MM 0/1) showed significantly more fatigue (higher FSMC sum score, p = 0.04, motor score, p = 0.01). In TMS and MRI studies, no significant differences were found between patients with MM 0/1 and those with MM > 1 (ipsilateral silent period measurements, CCA, CCI and lesion volume).ConclusionsMM are common in MS and can easily be detected through bedside testing. As MM are associated with fatigue, they might indicate fatigue in MS. It is possible that other cerebral structures, in addition to the corpus callosum, may contribute to the origin of MM in MS.

Comparison of Neural Recovery Effects of Botulinum Toxin Based on Administration Timing in Sciatic Nerve-Injured Rats.

This study aimed to assess the effects of the timing of administering botulinum neurotoxin A (BoNT/A) on nerve regeneration in rats. Sixty 6-week-old rats with a sciatic nerve injury were randomly divided into four groups: the immediately treated (IT) group (BoNT/A injection administered immediately post-injury), the delay-treated (DT) group (BoNT/A injection administered one week post-injury), the control group (saline administered one week post-injury), and the sham group (only skin and muscle incisions made). Nerve regeneration was assessed 3, 6, and 9 weeks post-injury using various techniques. The levels of glial fibrillary acid protein (GFAP), astroglial calcium-binding protein S100β (S100β), growth-associated protein 43 (GAP43), neurofilament 200 (NF200), and brain-derived neurotrophic factor (BDNF) in the IT and DT groups were higher. ELISA revealed the highest levels of these proteins in the IT group, followed by the DT and control groups. Toluidine blue staining revealed that the average area and myelin thickness were higher in the IT group. Electrophysiological studies revealed that the CMAP in the IT group was significantly higher than that in the control group, with the DT group exhibiting significant differences starting from week 8. The findings of the sciatic functional index analysis mirrored these results. Thus, administering BoNT/A injections immediately after a nerve injury is most effective for neural recovery. However, injections administered one week post-injury also significantly enhanced recovery. BoNT/A should be administered promptly after nerve damage; however, its administration during the non-acute phase is also beneficial.

Genome-Wide Association Study of Accessory Atrioventricular Pathways.

Understanding of the genetics of accessory atrioventricular pathways (APs) and affiliated arrhythmias is limited. To investigate the genetics of APs and affiliated arrhythmias. This was a genome-wide association study (GWAS) of APs, defined by International Classification of Diseases (ICD) codes and/or confirmed by electrophysiology (EP) study. Genome-wide significant AP variants were tested for association with AP-affiliated arrhythmias: paroxysmal supraventricular tachycardia (PSVT), atrial fibrillation (AF), ventricular tachycardia, and cardiac arrest. AP variants were also tested in data on other heart diseases and measures of cardiac physiology. Individuals with APs and control individuals from Iceland (deCODE Genetics), Denmark (Copenhagen Hospital Biobank, Danish Blood Donor Study, and SupraGen/the Danish General Suburban Population Study [GESUS]), the US (Intermountain Healthcare), and the United Kingdom (UK Biobank) were included. Time of phenotype data collection ranged from January 1983 to December 2022. Data were analyzed from August 2022 to January 2024. Sequence variants. Genome-wide significant association of sequence variants with APs. The GWAS included 2310 individuals with APs (median [IQR] age, 43 [28-57] years; 1252 [54.2%] male and 1058 [45.8%] female) and 1 206 977 control individuals (median [IQR] year of birth, 1955 [1945-1970]; 632 888 [52.4%] female and 574 089 [47.6%] male). Of the individuals with APs, 909 had been confirmed in EP study. Three common missense variants were associated with APs, in the genes CCDC141 (p.Arg935Trp: adjusted odds ratio [aOR], 1.37; 95% CI, 1.24-1.52, and p.Ala141Val: aOR, 1.55; 95% CI 1.34-1.80) and SCN10A (p.Ala1073Val: OR, 1.22; 95% CI, 1.15-1.30). The 3 variants associated with PSVT and the SCN10A variant associated with AF, supporting an effect on AP-affiliated arrhythmias. All 3 AP risk alleles were associated with higher heart rate and shorter PR interval, and have reported associations with chronotropic response. Associations were found between sequence variants and APs that were also associated with risk of PSVT, and thus likely atrioventricular reentrant tachycardia, but had allele-specific associations with AF and conduction disorders. Genetic variation in the modulation of heart rate, chronotropic response, and atrial or atrioventricular node conduction velocity may play a role in the risk of AP-affiliated arrhythmias. Further research into CCDC141 could provide insights for antiarrhythmic therapeutic targeting in the presence of an AP.

Sensory dysfunction in SMA type 2 and 3 - adaptive mechanism or concomitant target of damage?

BackgroundThe motor neuron survival protein performs numerous cellular functions; hence, spinal muscular atrophy (SMA) is considered to be a multi-organ disease with possible sensory system damage. The controversy surrounding the presence of sensory disturbances, prompted us to conduct standard electrophysiological studies and assess the sensory thresholds for different modalities in adults with SMA types 2 and 3. The study group consisted of 44 adult SMA patients (types 2 and 3). All patients underwent neurological examination using the Hammersmith Functional Motor Scale – Expanded (HFMSE). Standard sensory electrophysiological studies in the ulnar nerve and the estimation of vibratory, temperature, and warm- and cold-induced pain thresholds with temperature dispersion assessment were performed using quantitative sensory testing (QST).ResultsThe most repeatable result was the high amplitude of the sensory nerve action potentials (SNAP) in SMA patients compared to controls. This was higher in type 2 patients compared to type 3a and 3b patients and patients with low HFSME scores. Patients with SMA, especially type 3b presented a longer sensory latency and slower conduction velocity than did controls. Cold pain threshold was higher and warm dispersion larger in SMA. The vibratory limit was higher in patients with high HFSME scores.ConclusionsA high SNAP amplitude suggests sensory fibre hyperactivity, which may be based on overactivation of metabolic pathways as an adaptive mechanism in response to SMN protein deficiency with additionally coexisting small C- and A-delta fibre damage. SMA patients seem to have a concomitant, mild demyelinating process present at the early SMA stage.

Incidentally Induced Atrial Fibrillation During Programmed Electrical Stimulation in Patients With Depressed Left Ventricular Systolic Function After an Acute Myocardial Infarction.

The aim of this study was to investigate the clinical implication of incidentally induced atrial fibrillation (AF) during programmed electrical stimulation (PES) in patients with left ventricular systolic dysfunction (≤40%) after an acute myocardial infarction (MI). In this study, we included 231 patients from the Cardiac Arrhythmias and RIsk Stratification after Myocardial InfArction (CARISMA) study with left ventricular ejection fraction ≤40% and no prior history of AF. These patients underwent PES 6 weeks post-MI as part of the study protocol. Patients all received an implantable cardiac monitor (ICM) 3-21 days post-MI and were continuously monitored for cardiac arrhythmias for 2 years. Induction of AF was unwanted but reported if this incidentally occurred. A total of 61 patients (26%) developed AF within 2 years of follow-up, in which n = 10 (29%) had incidental AF during PES at baseline. The overall risk of AF was not significantly increased in patients with incidental AF (n = 34) during PES compared to patients without incidental AF (n = 197) (HR 1.6 [0.9-3.0], p = 0.14). The risk of bradyarrhythmia (HR = 0.2 [0.0-1.2], p = 0.07), ventricular arrhythmias (HR = 0.7 [0.1-5.8], p = 0.77), and major cardiovascular events (MACE) (HR 0.5 [0.2-1.7], p = 0.28) was not significantly different in patients with versus without incidental AF. Incidentally induced AF during PES in post-MI patients with reduced LVEF was not significantly associated with a higher risk of long-term atrial fibrillation, other cardiac arrhythmias, or major cardiac events. NCT00145119.

Efficacy and safety of early postoperative ablation in patients with congenital heart disease

BackgroundPostoperative arrhythmias are most often transient and medically treated, but some patients may require electrophysiology study (EPS) and ablation. ObjectiveThe purpose of this study was to describe the efficacy and safety of early postoperative ablation. MethodsThis study presents a retrospective series of patients who underwent EPS within 12 months of surgery for congenital heart disease between 2000 and 2021. The procedural outcome included complete or partial success, empirical ablation or failure, and complications. The long-term outcome included arrhythmia recurrence and burden according to a 12-point clinical arrhythmia severity score (documented arrhythmia, arrhythmia severity, cardioversion, and antiarrhythmic medication). ResultsAmong 28,902 operations during the study period, 24 patients (0.1%) underwent EPS within 3 months of surgery and 26 (0.1%) 3–12 months after surgery. Most patients had great (n = 27 [50%]) or moderate (n = 21 [42%]) congenital heart disease complexity. Mechanisms of arrhythmias included intra-atrial reentrant tachycardia (n = 23 [46%]), ectopic atrial tachycardia (n = 13 [26%]), accessory pathway (n = 6 [12%]), atrioventricular nodal reentrant tachycardia (n = 7 [14%]), twin atrioventricular node (n = 1 [2%]), atrial fibrillation (n = 1 [2%]), junctional ectopic tachycardia (n = 1 [2%]), and ventricular tachycardia (n = 2 [4%]). The procedure was acutely successful in 41 patients (82%), empirical in 5 (10%), and unsuccessful in 4 (8%). Complications occurred in 4 (8%) patients (major in 1, moderate in 1, and minor in 2). The recurrence of arrhythmia was documented in 27 patients (54%), although the burden of arrhythmia was significantly reduced. ConclusionA minority of patients require early postoperative EPS and ablation. For those, the procedure can be performed with reasonable acute success and manageable morbidity even in critically ill patients with complex surgical anatomy.

The Neural and Computational Architecture of Feedback Dynamics in Mouse Cortex during Stimulus Report.

Conscious reportability of visual input is associated with a bimodal neural response in the primary visual cortex (V1): an early-latency response coupled to stimulus features and a late-latency response coupled to stimulus report or detection. This late wave of activity, central to major theories of consciousness, is thought to be driven by the prefrontal cortex (PFC), responsible for "igniting" it. Here we analyzed two electrophysiological studies in mice performing different stimulus detection tasks and characterized neural activity profiles in three key cortical regions: V1, posterior parietal cortex (PPC), and PFC. We then developed a minimal network model, constrained by known connectivity between these regions, reproducing the spatiotemporal propagation of visual- and report-related activity. Remarkably, while PFC was indeed necessary to generate report-related activity in V1, this occurred only through the mediation of PPC. PPC, and not PFC, had the final veto in enabling the report-related late wave of V1 activity.

A proposed algorithm for management of patients with left bundle branch block post-TAVR: 1-year follow-up

BackgroundTAVR has revolutionized the management of aortic stenosis and has become the standard of care across a broad spectrum of patients with aortic stenosis. However, it is still associated with high incidence of conduction abnormalities, particularly new LBBB. Management of these patients remains a challenge. ObjectiveTo assess the clinical outcomes of patients with post-TAVR conduction disorders managed according to a pre-specified institutionally developed algorithm. MethodsA retrospective analysis including all patients undergoing TAVR in our institute between October-2018 to December-2022 was performed. Patients with new LBBB were managed according to the algorithm comprising QRS width and electrophysiology study. In-hospital and one-year clinical outcomes were assessed. ResultsA total of 230 patients were included in the present analysis. Seventy patients (30.4%) developed new LBBB after TAVR. Overall, 44 patients (19.1%) required permanent pacemaker implantation (PPM): 20 patients (8.7%) with Mobitz II, complete AV block or alternating bundle branch block, 21 patients (9.1%) with persistent new LBBB, and 3 others (1.3%) per physician discretion. During 1-year follow-up, only 3 patients required late PPM, of whom only 1 patient with new LBBB. There was no difference in mortality or heart failure hospitalizations between the PPM and No PPM groups. Multivariable analysis identified atrial fibrillation, chronic kidney disease, and pre-TAVR RBBB as independent predictors for PPM following TAVR. ConclusionOur findings suggest that the presented algorithm may serve as a safe and efficacious strategy for management of patient with post-TAVR LBBB, although the PPM rate may be further reduced.

The importance of medial plantar nerve conduction study in detectıon of polyneuropathy in inflammatory bowel disease

Background & Objective: Peripheral neuropathy is the most frequent neurologic complication of inflammatory bowel disease (IBD). We aimed to evaluate the clinical utility of medial plantar nerve conduction study (NCS) in the detection of distal sensory polyneuropathy in IBD patients. Methods: The study was performed with 21 Crohn’s disease (Group 1) patients, 24 Ulcerative Colitis (Group 2) patients without clinical peripheral neuropathy and 28 healthy participants (Group 3). Each patient group underwent electrophysiological conduction studies. The findings were analyzed statistically. Results: Abnormal medial plantar nerve conduction was present on both sides in 11 (24.4 %) patients with IBD; 5 (11.1 %) patients had low sural nerve amplitude, and 5 (11.1 %) had low superficial peroneal nerve amplitude bilaterally. There were significant differences between the IBD groups (Group 1 and 2) and Group 3 in the mean sensory nerve action potential amplitude of the right medial plantar nerve (p<0.024), and in the mean sensory nerve action potential amplitude of the left medial plantar nerve (p<0.025). The polyneuropathy pattern was mostly of the sensory axonal type in patients with IBD. Conclusions: These electrophysiologic findings indicate that peripheral neuropathy is more prevalent in IBD. In IBD patients the amplitudes of the medial plantar nerve were abnormal more than in the sural and superficial peroneal nerves.

Neuroimaging and electrophysiology techniques unveiling the mystery of disorders of consciousness: a narrative review

The diagnosis and prognosis of disorders of consciousness pose challenges for clinics because human consciousness is still a mysterious and unknown phenomenon. Scientists and clinicians are seeking evidence from neuroimaging and electrophysiology to explore the biological and pathological mechanisms of human consciousness. They attempt to provide new insights into the neuronal foundations of consciousness injury and recovery. These findings have improved the accuracy of the clinical diagnosis and prognosis of disorders of consciousness to some extent. However, they are still not clearly sorted out. Herein, we structure the available knowledge on the basis of neuroimaging (including positron emission tomography, functional magnetic resonance imaging, and functional near-infrared spectroscopy) and electrophysiology (spontaneous electroencephalography, event-related potentials, brain–computer interfaces, and transcranial magnetic stimulation-evoked electroencephalography) studies and their associations with disorders of consciousness-relevant clinical practice. Our aim is to promote their translation into the clinical management of patients with disorders of consciousness.

Coactivation of the Laryngeal Muscles in Pigs Without External Neural Control Indicates Existence of an Intrinsic Neuronal Network

Electrophysiological studies of the larynx expose the mechanisms by which voice production is controlled. Previous studies have revealed certain phenomena during laryngeal oscillations that suggest a complex control mechanism.Starting from the principle of agonist-antagonist muscular pairing, the aim of this study was to gain a deeper insight into the function of the cricothyroid and thyroarytenoid muscles, both central to voice production.Electromyographic recordings were used to determine the response of the two muscles to different stimulation situations in an ex-vivo animal model of the denervated larynx of pigs (n=26).Using a set of different experiments, it was shown that when one muscle (cricothyroid or thyroarytenoid muscle) was electrically stimulated, a response was observed in the other muscle, which in the otherwise denervated larynx was caused only by the applied stimulation and exhibited the characteristics of compound action potentials. This response was reproducible in all larynxes examined and was present bidirectionally. No response was registered in the absence of stimulation.Results show the existence of coactivation of the cricothyroid and thyroarytenoid muscles in the absence of external innervation hinting at the presence of a localized neuronal network of the larynx that has not been described previously. Further morphological investigation is needed to determine the presence of this internal laryngeal neuronal network.

Two Arrhythmias, One Diagnosis, All from Surface ECGs

A 48-year-old male with known supraventricular tachycardia presented with wide complex tachycardia and he was cardioverted. The patient was initially diagnosed with both ventricular tachycardia and supraventricular tachycardia. After reviewing electrocardiograms, a correct diagnosis of orthodromic atrioventricular reciprocating tachycardia with left-sided accessory pathway was made which was confirmed and successfully ablated in subsequent electrophysiological study. Not all wide complex tachycardias are ventricular tachycardia. If the rate of narrow complex supraventricular tachycardia becomes slower with the development of a bundle branch block, it is diagnostic for the presence and participation of the ipsilateral accessory pathway, which is called Coumel’s law

Poration of mitochondrial membranes by amyloidogenic peptides and other biological toxins.

Mitochondria are essential organelles known to serve broad functions, including in cellular metabolism, calcium buffering, signaling pathways and the regulation of apoptotic cell death. Maintaining the integrity of the outer (OMM) and inner mitochondrial membranes (IMM) is vital for mitochondrial health. Cardiolipin (CL), a unique dimeric glycerophospholipid, is the signature lipid of energy-converting membranes. It plays a significant role in maintaining mitochondrial architecture and function, stabilizing protein complexes and facilitating efficient oxidative phosphorylation (OXPHOS) whilst regulating cytochrome c release from mitochondria. CL is especially enriched in the IMM and at sites of contact between the OMM and IMM. Disorders of protein misfolding, such as Alzheimer's and Parkinson's diseases, involve amyloidogenic peptides like amyloid-β, tau and α-synuclein, which form metastable toxic oligomeric species that interact with biological membranes. Electrophysiological studies have shown that these oligomers form ion-conducting nanopores in membranes mimicking the IMM's phospholipid composition. Poration of mitochondrial membranes disrupts the ionic balance, causing osmotic swelling, loss of the voltage potential across the IMM, release of pro-apoptogenic factors, and leads to cell death. The interaction between CL and amyloid oligomers appears to favour their membrane insertion and pore formation, directly implicating CL in amyloid toxicity. Additionally, pore formation in mitochondrial membranes is not limited to amyloid proteins and peptides; other biological peptides, as diverse as the pro-apoptotic Bcl-2 family members, gasdermin proteins, cobra venom cardiotoxins and bacterial pathogenic toxins, have all been described to punch holes in mitochondria, contributing to cell death processes. Collectively, these findings underscore the vulnerability of mitochondria and the involvement of CL in various pathogenic mechanisms, emphasizing the need for further research on targeting CL-amyloid interactions to mitigate mitochondrial dysfunction.

Resting human trabecular meshwork cells experience tonic cation influx.

The trabecular meshwork (TM) regulates intraocular pressure (IOP) by converting biochemical and biomechanical stimuli into intracellular signals. Recent electrophysiological studies demonstrated that this process is mediated by pressure sensing ion channels in the TM plasma membrane while the molecular and functional properties of channels that underpin ionic homeostasis in resting cells remain largely unknown. Here, we demonstrate that the TM resting potential is subserved by a powerful cationic conductance that disappears following Na+ removal and substitution with choline or NMDG+. Its insensitivity to TTX, verapamil, phenamil methanesulfonate and amiloride indicates it does not involve voltage-operated Na+, Ca2+ and epithelial Na+ (ENaC) channels or Na+/H+ exchange while a modest hyperpolarization induced by SEA-0440 indicates residual contribution from reversed Na+/Ca2+ exchange. Tonic cationic influx was inhibited by Gd3+ and Ruthenium Red but not GsMTx4, indicating involvement of TRP-like but not Piezo channels. Transcriptional analysis detected expression of most TRP genes, with the canonical transcriptome pool dominated by TRPC1 followed by the expression ofTRPV1, TRPC3 and TRPC5. TRPC3 antagonist Pyr3 and TRPC1,4,5 antagonist Pico1,4,5 did not affect the standing current, whereas the TRPC blocker SKF96365 promoted rather than suppressed, Na+ influx. TM cells thus maintain the resting membrane potential, control Na+ homeostasis, and balance K+ efflux through a novel constitutive monovalent cation leak current with properties not unlike those of TRP channels. Yet to be identified at the molecular level, this novel channel sets the homeostatic steady-state and controls the magnitude of pressure-induced transmembrane signals.

Prognostic value of electroanatomic-guided endomyocardial biopsy in patients with myocarditis, arrhythmogenic cardiomyopathy and non dilated left ventricular cardiomyopathy

A wide variety of non-invasive and invasive techniques for SCD risk stratification in non ischemic cardiomyopathy (NICM) have been proposed, including left ventricular (LV) ejection fraction, QRS duration, late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) and invasive electrophysiologic study with or without three-dimensional electroanatomic mapping (3D-EAM), to identify and characterize the arrhythmogenic substrate. There is still no clear consensus on the risk stratification in this clinical setting.The aim of our study is to characterize the 3D-EAM substrate in patients with the same clinical presentation of unexplained complex VAs and NICM using CMR, three-dimensional electranatomic mapping (3D-EAM) in association with endomyocardial biopsy (EMB) and genetic screening, as a more precise and early diagnostic assessment may provide important subsequent prognostic impact. The study was designed as a prospective multi-center observational evaluation and the patient follow-up was scheduled at 6 months interval. We enrolled 125 patients distinct into four different group by complete diagnostic work-up: myocarditis, non-dilated left ventricular cardiomyopathy, arrhythmogenic cardiomyopathy and control group. The four groups were compared in terms of clinical, imaging and 3D-EAM data. At multivariate analysis sustained VT/VF on admission [HR: 3.64 (1.79–7.4), p < 0.001], total bipolar scar area of left and right ventricle detected by 3D-EAM [HR: 2.24 (1.13–4.49), p = 0.02], histological diagnosis of myocarditis by 3D-EAM guided endomyocardial biopsy (EBM) [HR: 2.79 (1.04–7.44), p = 0.01] were independent predictors of complex VAs or death at follow-up. 3D-EAM guided EMB represent not only a valid diagnostic tool to identify the arrhythmogenic substrate in patients with NICM and ventricular arrhythmic phenotype but also an important predictor of complex Vas at long term follow-up.

Enhanced Place Specificity of the Parallel Auditory Brainstem Response: An Electrophysiological Study

PurposeThis study investigates the effect of parallel stimulus presentation on the place specificity of the auditory brainstem response (ABR) in human listeners. Frequency-specific stimuli do not guarantee a response from the place on the cochlea corresponding only to that characteristic frequency — especially for brief and high-level stimuli. Adding masking noise yields responses that are more place specific, and our prior modeling study has suggested similar effects when multiple frequency-specific stimuli are presented in parallel. We tested this hypothesis experimentally here, comparing the place specificity of responses to serial and parallel stimuli at two stimulus frequencies and three stimulus rates.MethodsParallel ABR (pABR) stimuli were presented alongside high-pass filtered noise with a varied cutoff frequency. Serial presentation was also tested by isolating and presenting single-frequency stimulus trains from the pABR ensemble. Latencies of the ABRs were examined to assess place specificity of responses. Response bands were derived by subtracting responses from different high-pass noise conditions. The response amplitude from each derived response band was then used to determine how much individual frequency regions of the auditory system were contributing to the overall response.ResultsWe found that parallel presentation improves place specificity of ABRs for the lower stimulus frequency and at higher stimulus rates. At a higher stimulus frequency, serial and parallel presentations were equally place specific.ConclusionParallel presentation can provide more place-specific responses than serial for lower stimulus frequencies. The improvement increases with higher stimulus rates and is in addition to the pABR’s primary benefit of faster test times.

Impact of Urethral Sphincter Electrophysiology on Botulinum Toxin A Treatment in Women with Non-Neurogenic Dysfunctional Voiding.

Dysfunctional voiding (DV) is an abnormal urethral sphincter activity during voiding in neurologically normal individuals. Urethral sphincter botulinum toxin A (BoNT-A) injection has been used to treat DV, but the results have not been completely satisfactory. This study investigated the neurological characteristics of women with DV using the lower urinary tract electrophysiology (EP) study and the therapeutic efficacy of BoNT-A injection. In total, 48 women with DV and 16 women with normal voiding were included. Videourodynamic studies were conducted to diagnose DV before BoNT-A injection. EP studies, including urethral sphincter electromyography, bulbocavernosus reflex, and pudendal nerve conduction velocity, were conducted. Polyphasic motor unit action potentials suggestive of reinnervation were detected in 58.3% of patients with DV and 18.8% of controls (p = 0.001). Significant improvement in the corrected maximum flow rate (cQmax) was observed in patients with reinnervation at 1 and 3 months after BoNT-A injections into the urethral sphincter. Urethral sphincter denervation or reinnervation activity was commonly noted in 62.5% of women with DV. Repeated BoNT-A injections into the urethral sphincter provided effective treatment in 47.9% of patients, with mild improvement in cQmax observed in patients with urethral sphincter reinnervation. However, the improvement was not superior to those without reinnervation.

Association of induced atrial fibrillation in the electrophysiology laboratory with endothelial dysfunction and documented atrial fibrillation

ObjectiveAtrial fibrillation (AF) is a common arrhythmia that increases morbidity and mortality, as well as healthcare costs. The induction of AF (IAF) during programmed atrial pacing in an electrophysiological study (EPS) is a prevalent phenomenon that has been underappreciated by electrophysiologists. Despite extensive research on AF, only a few studies have focused on this phenomenon. The aim of our study was to investigate the association between history of AF and IAF and the underlying pathophysiological factors such as arterial stiffness, subclinical atherosclerosis, and impaired endothelial function. MethodsThis cross-sectional and observational study included 87 patients who had palpitations and were scheduled for EPS. Patients underwent biochemical investigations, transthoracic echocardiography, carotid ultrasound, carotid-femoral artery pulse wave velocity (PWV), and flow-mediated dilatation (FMD) measurements before EPS. Patients were divided into two groups, AF-induced and non-induced in EPS, for further statistical analysis. ResultsAF was induced in 16 of 87 patients (18.3%) included in the analysis. The FMD (%) was significantly lower (16.01 ± 10.1 vs. 8.7 ± 5.7, P = 0.022) and, remarkably, the proportion of patients with a history of AF was significantly higher (2.8% vs. 37.5%, P < 0.001) in the IAF group. ROC analysis showed that a documented AF and FMD predicted IAF, with AUC of 0.741 (p = 0.012) and 0.740 (p = 0.001), respectively. Logistic regression analysis revealed that FMD and history of AF were strong predictors of IAF (odds ratio [OR], 0.853; 95% confidence interval [CI] 0.737–0.988; P = 0.034, OR: 10.1, 95% CI 4.9–20.5; P = 0.003, respectively). ConclusionEndothelial dysfunction and documented AF were associated with IAF during EPS.