Anterior Fascicle Research Articles

Clinical observation of radiofrequency ablation for premature ventricular contractions originating from uncommon His-Purkinje sites

BackgroundRadiofrequency catheter ablation (RFCA) of premature ventricular contractions (PVCs) originating from common locations such as the proximal and middle fascicles of the His-Purkinje system (HPS) has been established as an effective therapy. This report aims to highlight the electrophysiological properties and RFCA of PVCs originating from uncommon locations of the HPS.MethodsAmong 57 patients with fascicular PVCs, 3 with fascicular PVCs originating from uncommon sites were retrospectively analyzed.ResultsWe identified three patients with PVCs originating separately from diseased fascicles, the dead-end tract (DET), and the distal fascicle. In contrast to PVCs originating from the proximal and medial fascicles, the fascicular potentials could not be recorded at the target sites of patients with PVCs originating from diseased fascicles or the distal fascicle during sinus rhythm. However, these PVCs were successfully ablated from the HPS, guided by recording their earliest fascicular potentials in PVCs. PVCs originating from the DET are morphologically consistent with those originating from the proximal left anterior fascicle or the distal left bundle branch. The corresponding tiny sharp potential of the DET could be mapped, and RFCA of the right coronary cusp achieved successful suppression of PVCs.ConclusionsThe knowledge of the different electrophysiological characteristics of fascicular PVCs originating from uncommon locations can contribute to precise mapping and ablation. For such arrhythmia, the target site for successful ablation should be identified by earliest fascicular potential.

Abstract 10579: Prevalence and Morphology of Premature Ventricular Contractions on Routine Athletic Electrocardiogram Screening

Introduction: The clinical implications of incidental premature ventricular contractions (PVCs) are poorly understood. Though controversial, athletes often receive electrocardiograms (ECGs) during pre-participation exams. The prevalence and morphologies of PVCs in this cohort have not been widely reported. Recent studies have defined benign PVC morphologic patterns in athlete populations that may guide clinical evaluations. Methods: Digital ECGs were obtained from 10,728 screened athletes aged 14 to 35 at school and professional team screenings in California. Captured PVCs were analyzed using simultaneous frontal and horizontal plane leads, displaying each standard ECG lead in full-length, allowing for morphologic categorization. PVCs were coded for morphology and benign status using recommended criteria outlined in Figure 1. Results: Twenty-six of 10,728 athletes (0.24%) had at least one PVC (Figure 1); 7 of those (27%) had bigeminy and 3 of those (12%) had trigeminy. Overall, participants were 43% female, 62% White, 12% Black, 9% Asian, and 8% Hispanic. Of those with PVCs, 50% were female, 65% were White, 23% were Black, 8% were Asian, and 4% were Hispanic. Twenty-four ECGs (92%) had PVCs with benign patterns, including 17 with right ventricular outflow tract, 5 with left anterior fascicle, and 2 with left posterior fascicle morphology. Two ECGs had non-benign PVCs with left bundle branch patterns and superior axes. Both of these athletes had normal echocardiograms and exercise testing and are being followed closely. Conclusions: We found a low prevalence of PVCs on routine ECG screening of young athletes, although evaluation of PVC prevalence and frequency are limited by the short duration of an ECG. Most incidental PVCs among young athletes had benign patterns. This study also demonstrates the value of digital ECG recorders to display simultaneous frontal and horizontal plane leads for the morphologic categorization of PVCs which may guide further workup.

Modulations in motor unit discharge are related to changes in fascicle length during isometric contractions.

The integration of electromyography (EMG) and ultrasound imaging has provided important information about the mechanisms of muscle activation and contraction. Unfortunately, conventional bipolar EMG does not allow an accurate assessment of the interplay between the neural drive received by muscles, changes in fascicle length and torque. We aimed to assess the relationship between modulations in tibialis anterior muscle (TA) motor unit (MU) discharge, fascicle length, and dorsiflexion torque using ultrasound-transparent high-density EMG electrodes. EMG and ultrasound images were recorded simultaneously from TA using a 32-electrode silicon matrix while performing isometric dorsiflexion contractions at two ankle joint positions (0° or 30° plantar flexion) and torques (20% or 40% of maximum). EMG signals were decomposed into MUs and changes in fascicle length were assessed with a fascicle-tracking algorithm. MU firings were converted into a cumulative spike train (CST) that was cross-correlated with torque (CST-torque) and fascicle length (CST-length). High cross-correlations were found for CST-length (0.60, range: 0.31-0.85) and CST-torque (0.71, range: 0.31-0.88). Cross-correlation delays revealed that the delay between CST-fascicle length (∼75 ms) was smaller than CST-torque (∼150 ms, P < 0.001). These delays affected MU recruitment and de-recruitment thresholds since the fascicle length at which MUs were recruited and de-recruited was similar but MU recruitment-de-recruitment torque varied. This study demonstrates that changes in TA fascicle length are related to modulations in MU firing and dorsiflexion torque. These relationships allow assessment of the interplay between neural drive, muscle contraction and torque, enabling the time required to convert neural activity into movement to be quantified.NEW & NOTEWORTHY By employing ultrasound-transparent high-density EMG electrodes, we show that modulations in tibialis anterior muscle motor unit discharge rate were related to both changes in fascicle length and resultant torque. These relationships permitted the quantification of the relative delays between fluctuations in neural drive, muscle contraction, and transfer of torque via the tendon during sustained isometric dorsiflexion contractions, providing information on the conversion of neural activity into muscle force during a contraction.

Connecting Fibers Between ATFL's Inferior Fascicle and CFL Transmit Tension Between Both Ligaments

Category: Basic Sciences/Biologics; Ankle Introduction/Purpose: The lateral ligament complex of the ankle has been extensively studied. Recently an anatomical study described a connection between anterior talofibular ligament inferior fascicle (ATFLif) and calcaneofibular ligament (CFL). The applicability and the mechanical role of these connections have not yet been studied and need to be clarified. The purpose of this study is to evaluate the connection between ATFLif and CFL through a dynamic measurement analysis. Methods: An anatomical study was performed in 13 fresh-frozen below-the-knee ankle specimens. Each specimen was dissected in a protocolized manner until the lateral ligaments were exposed. A complete injury to both ATFL's fascicles was created in the proximal third of the ligament. A displacement transducer specifically design was inserted in the CFL and in the lateral part of the calcaneus to test its lengthening. A traction of 1 kg weight (9.8 N) was applied to ATFLif while the transducer measured the lengthening that this force created in the CFL. Results: A total of 13 ankle specimens were carefully dissected. One specimen with signals of a prior traumatic injury of the ATFLif was excluded. A total of 12 specimens were included, 7 females and 5 males with an average age of 74 years (52-88 years). The right ankle was dissected in 6 specimens. ATFL was identified as a two-fascicled ligament in all cases. The fibers connecting the ATFLif and CFL were observed in all specimens. The displacement transducer showed lengthening in the CFL in all measurements with a median of 0.59 mm (SD 0.34). Conclusion: Connecting fibers between ATFLif and CFL are robust enough to transmit tension from one structure to the other.In the case of associated proximal lesions of the ATFLif and CFL, ligaments repair with a single suture may be considered. This can be applied in surgical procedures in patients with lateral ankle instability.

3D Light Scanner Analysis of the Lateral Collateral Ligaments of the Ankle: An Anatomical Study

Category: Basic Sciences/Biologics; Ankle Introduction/Purpose: Recently an anatomical study described a medial connection between the anterior talofibular ligament inferior fascicle (ATFLif), calcaneofibular ligament (CFL) and posterior talofibular ligament (PTFL). Therefore, there is no research evaluating the lateral ligaments and their relationships through a three-dimensional view achieved by a digital marking of their foot prints. The authors hypothesize that a three-dimensional analysis made only by an accurately digital analysis can clarify the lateral collateral ligaments (LCL) connections and their foot prints relations. This work aims to carry out an anatomical study in cadaveric pieces in which the lateral ankle ligaments were dissected and evaluated by a tridimensional scanner that allows a digitally and three-dimensional assessment of their foot prints and connections. Methods: An anatomical study was performed in 11 fresh-frozen ankle specimens. Each ankle was dissected to achieve the amputation of the calcaneus, talus and fibula, keeping the inserts of the footprints of LCL. After that, each bone piece with the insertion remnants of the LCL was submitted to an evaluation by a scanner machine. Surface scans for these bones were collected using a structured light scanner. Each bone piece was set on a 3D automatic turntable to capture a 360° scan and was scanned in two orientations, with 6 scans per orientation. Finally, all the scans were aligned and final fused models were created using the HP DAVID software package and exported to a wavefront 3D object file. The 3D models were imported into Geomagic Studio to calculate surface area of the LCL foot prints. Results: A total of 11 units of each, talus, fibula and calcaneus were dissected from 11 ankles specimens. The ATFL was identified as a two-fascicled ligament and the fibers connecting fibers between the ATFLif and CFL was present in all specimens. In two talus there was only one insertion of the ATFL. After scanning the bones, the authors observed that the foot prints of ATFLif, CFL and PTFL were contiguous at medial side of the fibula, with an average of the surface area of 486,7 mm2. The foot print of the CFL on the calcaneus was located at the junction of a vertical line tangent to the highest point of the posterior subtalar with a horizontal line extending from the sinus tarsi in all specimens. Conclusion: This study demonstrated by a 3D analysis that the LCL of the ankle share the same foot print at medial side on the fibula and are all connected since the foot prints of the ATFL inf, CFL and PTFL were contiguous. In the case of associated proximal lesions of the ATFLif and CFL, ligaments repair with a single suture may be considered. This can be applied in surgical procedures in patients with lateral ankle instability.fig

Terminal end of retro-aortic root branch: An unrecognized origin for "proximal left anterior fascicle" premature ventricular complexes with narrow QRS duration.

Premature ventricular complexes (PVCs) with narrow QRS duration, inferior frontal plane QRS axis, and right bundle branch block (RBBB) pattern generally originate from the proximal segment of the left anterior fascicle (LAF). The purpose of this study was to investigate the exact origin of this category of PVCs. Twenty-two patients with assumed proximal LAF-PVCs were enrolled in the study. Detailed mapping of fascicular potentials (FPs) was performed during sinus rhythm (SR) and PVCs. During SR, a cluster of FPs could be found at the most superior portion of the left ventricle (LV). These FPs represented the terminal end of a discrete branch of the left fascicular system, which we named the "retro-aortic root branch" (RARB). The shortest distance between the proximal LAF and the terminal end of the RARB was 13.5 ± 4.2 mm. The earliest activation site (EAS) of PVCs in all patients were confirmed at the terminal end of the RARB, where the FP-V interval was 35.1 ± 4.3 ms during PVCs. The shortest distance from the right coronary cusp (RCC) to the EAS was 5.3 ± 3.5 mm. PVCs could be eliminated by ablation from the RCC in 45.5% (10/22) cases, in the remaining cases, ablation at the EAS in the LV endocardium successfully abolished PVCs. The terminal end of the retro-aortic root branch was the actual origin site for PVCs with inferior frontal plane axis, RBBB pattern and narrow QRS duration. Ablation in the RCC or at the EAS in the LV could both eliminate PVCs safely with high efficacy.

Inflammatory infiltration of the cardiac conduction system in acute lymphocytic myocarditis.

A 53-year-old man with prior history of bone marrow transplant after acute myeloblastic leukaemia was admitted in the acute cardiac care unit due to suspected acute myocarditis. At admission, his electrocardiogram (ECG) showed right bundle branch block and left anterior fascicular block (Panel A). Previously, he had been assessed regularly in a dedicated cardio-oncology clinic, with normal ECG and transthoracic echocardiography (see Supplementary material online, Videos S1 and S2). Despite high-dose pulses of methylprednisolone, he developed both complete atrio-ventricular (AV) block and progressive left ventricular systolic dysfunction (see Supplementary material online, Videos S3 and S4), leading to cardiogenic shock requiring temporary transvenous pacing and mechanical circulatory support with VA-ECMO. However, he died on day 9 due to multiorgan failure. Gross examination of the heart (Panel B) was normal, but histopathology and immunohistochemistry showed significant infiltration of the ventricular myocardium (Panel C), AV node (Panel D) left anterior fascicle (Panel E), and right bundle branch (Panel F) by mononuclear CD3 + T cells, consistent with the diagnosis of lymphocytic myocarditis. High-definition images S1-S8 are included in the Supplementary material online.

Biomechanical Study of Arthroscopic All-Inside Anterior Talofibular Ligament Suture Augmentation Repair, Plus Suture Augmentation Repair and Anterior Tibiofibular Ligament's Distal Fascicle Transfer Augmentation Repair.

Objective: To explore the biomechanical efficacy of arthroscopic all-inside anterior talofibular ligament (ATFL) suture augmentation repair, plus suture augmentation repair and anterior tibiofibular ligament-distal fascicle (ATiFL-DF) transfer augmentation repair, so as to provide a basis for the accurate selection of ATFL repair in clinical practice. Methods: Twenty-four (12 pairs) fresh frozen human cadaver ankle specimens were used. Six of the ankle specimens were set as the normal group, and the other 18 ankle specimens were used to establish ATFL injury models. The ATFL was then repaired using arthroscopic all-inside ATFL suture augmentation repair (suture augmentation group), plus suture augmentation repair (plus suture augmentation group) and ATiFL-DF transfer augmentation repair (biological augmentation group), respectively. After the repaired ATFL was separated, the ankle specimens were fixed on an electronic universal testing machine with a customized fixture for the tensile test, and the ultimate failure load (N) and stiffness (N/mm) of the ankle specimens were compared. Results: The ultimate failure load of the plus suture augmentation group (229.3 ± 66.7 N) was significantly higher than that in the normal group (148.2 ± 39.4 N, p = 0.045) and the biological augmentation group (131.3 ± 38.8 N, p = 0.013). There was no statistical difference in ultimate failure load between the suture augmentation group (167.2 ± 47.2 N), the normal group and the biological augmentation group. The stiffness of the plus suture augmentation group (26.2 ± 8.2 N/mm) was significantly higher than that in the normal group (12.1 ± 3.8 N/mm, p = 0.005) and the biological augmentation group (12.7 ± 5.2 N/mm, p = 0.007). The stiffness of the suture augmentation group (23.6 ± 7.0 N/mm) was significantly higher than that in the normal group (p = 0.024) and the biological augmentation group (p = 0.033). There was no statistical difference in stiffness between the plus suture augmentation group and the suture augmentation group, and no statistical difference in stiffness between the normal group and the biological augmentation group. Conclusions: The tensile strength and rigidity of plus suture augmentation repair were significantly better than those of normal ATFL, suture augmentation repair and ATiFL-DF transfer augmentation repair. Suture augmentation repair can obtain tensile strength similar to normal ATFL and ATiFL-DF transfer augmentation repair, and suture augmentation repair can obtain rigidity significantly better than normal ATFL and ATiFL-DF transfer augmentation repair. ATiFL-DF transfer augmentation repair can obtain tensile strength and rigidity similar to normal ATFL.

Peripheral Nerve Innervation in Bilateral Cleft Hand Syndrome Elucidated by Ultrasound.

Bilateral cleft hand syndrome is a rare congenital malformation with complex anatomy. Previous reports have mainly focused on the description of bone and soft tissue abnormalities, but information about innervation is scarce. Knowledge of the peripheral nerve anatomy is helpful for surgical treatment, optimizing the reconstruction, and preventing iatrogenic damage. Following clinical assessment and conventional radiologic imaging, we used high-resolution ultrasound of both hands and forearms to image the peripheral nerves in a patient with severe bilateral cleft hand syndrome. The patient presented with two ulnar digits, a deformed thumb on the right, and a rudimentary thumb appendage on the left. In keeping with the tissue elements present and absent, we found a severe bilateral nerve size reduction of the median nerves, sparing the anterior interosseous nerve fascicles. The radial nerve and end branches were intact, and a slightly smaller ulnar nerve was found that ended in two digital branches to a single digit. Our study shows that in cleft hand syndrome the peripheral nervous system anatomy exactly reflects the presence and absence of the corresponding muscle and skin innervation areas. This information is helpful for planning a surgical-reconstructive approach and suggests a potential role for nerve ultrasound in the assessment of complex limb malformations.

Group beating bradycardia due to two level AV junctional conduction block including combined Wenckebach and Mobitz 2 fascicular block

A case of a complex advanced two level AV junctional conduction block is described with electrocardiographic features consistent with the combination of incompletely concealed Wenckebach in the left anterior fascicle of the left bundle branch, and most probably in the right bundle branch and with Mobitz type II in the left posterior fascicle of the left bundle branch, resulting in intermittent trifascicular block.

Premature Ventricular Contractions From the Left Anterior Fascicle: Electrocardiographic and Electrophysiological Characteristics, Mapping Strategy, and Immediate and Long-Term Catheter Ablation Results

BackgroundLeft anterior fascicle (LAF) premature ventricular contractions (PVC) are rarely reported. We described the electrocardiographic and electrophysiological characteristics of PVCs originating from LAF and evaluated the results of catheter ablation.MethodsThe baseline AH and HV intervals were recorded during normal sinus rhythm (NSR), and the HV interval of LAF-PVC was measured during the procedure. During the index procedure, the conduction interval from the earliest Purkinje potential (PP) site to the His was labeled as time A, the conduction interval from the earliest site to the onset of the QRS as time B, then the HV interval during NSR (HVNSR) is A + B, and the HV interval during PVC (HVPVC) is B-A; a predicted PP time was calculated using HVNSR and HVPVC. The calculated formula is as follows: Predicted target PP = (HVNSR + HVPVC)/2. During the repeat procedure, the mapping strategy only focuses on the earliest retrograde PP due to the injury or block of LAF sustained at the index procedure.ResultsNotably, 24 patients with LAF-PVC were included. The ECG characteristics of PVC exhibited right bundle branch block (RBBB) morphology with right-axis deviation (RAD) in 18 patients and only RAD in 6 patients. The QRS durations of NSR and PVC were 78.8 ± 7.9 and 106.8 ± 12.3 ms, respectively. There was no significant difference between the predicted and mapped PP site (31.5 ± 8.1 vs. 30.6 ± 7.8 ms; P = 0.17). There was a significant difference between the mean axis deviation before and after ablation (46.3 ± 25.4° vs. 18.3 ± 44.1°; P = 0.001); however, only 10 patients had a complete LAF block. Eight patients had a recurrence, the QRS morphology of LAF-PVC became narrower (95.9 ± 17.2 vs. 105.3 ± 16.9 ms, P = 0.003), and 4 patients’s PVC QRS morphology was similar to NSR. During the repeat procedure, the earliest retrograde PP interval was longer than the index procedure in four patients (12.0 ± 1.9 vs. 37.8 ± 1.1 ms; P < 0.001).ConclusionThe target PP site for ablation of the LAF region can be calculated using the HV interval during NSR and PVC at the index procedure. The mapping strategy at repeat procedures focused on the earliest retrograde PP interval.

A Rhythmic Electrocardiographic Pattern in an Older Adult With Chest Pain.

Scenario: An 87-year-old woman with a history of atrial fibrillation, hypertension, and hyperlipidemia came to the emergency department with substernal chest pain that was not relieved with nitroglycerin. She was found to be in atrial fibrillation with rapid ventricular response and had dynamic troponin levels that were concerning for myocardial infarction. Left-sided cardiac catheterization revealed severe coronary disease with about 80% occlusion of the left main and left anterior descending coronary arteries; however, percutaneous coronary intervention (PCI) was not done because of the patient’s hemodynamic instability. After the catheterization, she continued to have substernal chest pain for 2 days and was taken back for emergent PCI with temporary mechanical ventricular support. Two drug-eluting stents were placed. Her bedside electrocardiography (ECG) strip after the emergent PCI is shown here.Atrial bigeminy with a sinus rate of 35 beats per minute and right bundle branch block (RBBB).This patient exhibited multiple deficits in conduction due to acute occlusion of the left main and left anterior descending (LAD) coronary arteries leading to infarction of the surrounding myocardium. The left main coronary artery arises from the aorta, passes between the pulmonary trunk and the left atrial appendage, and bifurcates into the LAD and the left circumflex coronary artery. The LAD, of interest in this example, supplies oxygenated blood to the interventricular septum and left ventricle. Occlusion of both the left main and LAD coronary arteries likely led to the atrial bigeminy and RBBB seen here.Occlusion of the left main coronary artery can induce ischemia in the left atrium and left atrial appendage, propogating atrial bigeminy, a regularly irregular rhythm where a premature atrial contraction (PAC) follows each normal sinus beat (N). Ischemia propagates spontaneous electrical activity such as PACs and disrupts normal conduction. When another region of the atria depolarizes before the sinoatrial node, PACs occur; the PACs may be sporadic or patterned (eg, bigeminy, trigeminy). On an ECG, PACs may show a P wave morphology different from the sinus beat or no P wave preceding the QRS complex. If the P wave preceding the QRS complex is not visible, the P wave is most likely embedded in the preceding T wave. Both PACs and sinus beats travel down the same conduction pathway to the ventricle, producing a morphologically similar QRS complex; this feature differentiates PACs from premature ventricular contractions, which have grossly different morphologies, unless there is an existing BBB (as here), which makes distinguishing PACs from premature ventricular contractions challenging.The wide QRS complexes with slurred qRs morphology in lead V1 and the discordant T waves are due to RBBB, most likely caused by the occlusion of the LAD. In about 90% of patients, the proximal LAD septal perforators perfuse the right bundle branch and the anterior fascicle of the left bundle branch. Thus, occlusion of the LAD may have caused subsequent ischemia in the intraventricular septum, slowing conduction through the bundle branches and inducing an RBBB in this patient. Importantly, an RBBB does not preclude assessment of ST-segment elevation indicative of transmural ischemia due to coronary occlusion, but since it is unknown if the RBBB was preexisting, it is best to review a previous ECG tracing.After emergent PCI, the patient developed atrial bigeminy and remained in the irregular rhythm for 6 hours. She did not develop new ischemic symptoms and did not require more interventions. She remained clinically unstable with a bradycardic sinus rate in atrial bigeminy, but no signs or symptoms of hypoperfusion were noted. The bedside nurse closely monitored the patient and the ECG because atrial bigeminy can progress to atrial fibrillation. Optimal guideline-based therapies for acute coronary syndrome, including dual antiplatelet therapy, are indicated to maintain stent patency. Careful monitoring of the ST segments for ischemia is indicated.

Axis deviation in nonischemic cardiomyopathy with left bundle branch block: Insights from left bundle branch pacing.

Biventricular pacing has shown excellent results in patients with heart failure and left bundle branch block (LBBB). Studies have shown that the patients with abnormal axis deviation may benefit less from cardiac resynchronization therapy (CRT) as compared to those with the normal axis. The exact reason for left axis deviation (LAD) in LBBB is not known but could be due to diseased left anterior fascicle, left ventricular enlargement, or due to advanced electrical remodeling. The aim of the study was to analyze the incidence of LAD in nonischemic cardiomyopathy (NICM) with LBBB and the clinical outcomes following left bundle branch pacing (LBBP). We have included 64 consecutive patients with NICM and LBBB, who underwent successful LBBP. Patients were divided into two groups-Group I with baseline normal axis (n = 40; 63%) and Group II with LAD (n = 24; 37%). The mean axis changed from +23.6 ± 28.8° at baseline to +16.5 ± 35.1° and from -40.4 ± 10.3° at baseline to 7.08 ± 41.1° after LBBP in Group I and Group II, respectively. LBBP retained the normal axis in 93% of Group I patients and normalized the axis in 75% of Group II patients. The percentage changes in QRS duration, left ventricular ejection fraction, and left ventricular end-diastolic diameter were similar in both the groups (+40% vs. +32%; p = .52, +64% vs. +50%; p = 0.34, -8% vs. -6%; p = .76, respectively). Capturing the proximal LBB would correct the LAD by recruitment of left anterior fascicles and pacing proximal to the site of the septal breakthrough of the right bundle branch activation wavefront during LBBB. LBBP as an alternative strategy for CRT could result in similar improvement in LBBB patients with LAD as in those with the normal axis.

Selective proximal left anterior fascicle pacemapping for guiding narrow QRS premature ventricular complex ablation from the right coronary cusp

A 38-year-old woman with a structurally normal heart was referred for catheter ablation due to symptomatic, monomorphic, high burden (12%) premature ventricular complexes (PVC) refractory to medical therapy. The PVC's ECG morphology suggested an origin in the proximal left anterior fascicle (LAF). During procedure PVCs were mechanically suppressed. Consequently, selection of the ablation target site was based on pace-mapping. This case illustrates how ablation from the right coronary cusp (RCC) for PVC arising from the proximal LAF could be accurately guided by pace-mapping. At this location, pacing can result in both a selective and a non-selective capture of the proximal LAF.

DYNAMIC LBBB AND T WAVE INVERSIONS IN A CASE OF PREGABALIN OVERDOSE

TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: New or presumed new-onset LBBB on an ECG may represent acute myocardial ischemia. However, in rare situations, a new left bundle branch block pattern can be drug induced. In this report, we present a patient with presumed substance overdose from Pregabalin who presented with this exact phenomenon. CASE PRESENTATION: A 58-year-old Caucasian female with past medical history anxiety and depression presented with Pregabalin overdose. She had no cardiac complaints. Initial ECG showed a normal sinus rhythm, heart rate of 86 beats per minute, and a new LBBB pattern. Serial high sensitivity troponin was normal and CPK was 62. Echocardiogram did not show any wall motion abnormalities. After supportive treatment, repeat ECG revealed resolution of bundle branch pattern, however a sinus rhythm with deep negative T-wave inversions in the anterior leads was noted. Interestingly, as her heart rate increased beyond 90 beats per minute, a rate-related LBBB developed, with subsequent resolution as the heart rate decreased. Patient underwent a stress test which did not reveal evidence of myocardial ischemia. DISCUSSION: We report a case of a patient who presented with varying ECG findings in the setting of a drug overdose. A left bundle branch block (LBBB) is an ECG finding which is a result of an injury to the anterior and posterior fascicles as well as the His-Purkinje system (1). It is often considered an ST segment equivalent based on the clinical presentation, but can also be associated with chronic underlying structural disease, fibrotic changes of the conduction systems, and progressive heart failure (1). Pregabalin is used for treatment of seizures and neuropathic pain. It works to release various neurotransmitters by acting on calcium channels, which may play a role in cardiac strain and cause unexpected cardiac excitation (2). This patient's varying ECG findings in the setting of a drug overdose were suggestive of a finding known as cardiac memory, which is defined as persistent T-wave changes occurring as a result of a widened QRS (3). This is a rare phenomenon which describes remodeling of the heart as a result of an electrical conduction alteration. Our case was unique as the electrical abnormalities occurred secondary to a medication which has the potential to cause cardiac toxicity. The onset of a new LBBB and T-wave changes raises major concerns for acute coronary events, however additional etiologies may play a role in such cases, such as a Pregabalin overdose. CONCLUSIONS: Pregabalin overdose was associated with a new onset LBBB pattern, which may mimic an acute coronary event. Resolution of LBBB with subsequent development of T wave inversion may mimic dynamic ischemic changes, however, it is important to consider the phenomenon of cardiac memory as a potential etiology of T wave inversions. REFERENCE #1: Scherbak D, Hicks GJ. Left Bundle Branch Block. [Updated 2020 Aug 15]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482167/ REFERENCE #2: Taylor CP, Angelotti T, Fauman E. Pharmacology and mechanism of action of pregabalin: the calcium channel alpha2-delta (alpha2-delta) subunit as a target for antiepileptic drug discovery. Epilepsy Res. 2007 Feb;73(2):137-50. doi: 10.1016/j.eplepsyres.2006.09.008. Epub 2006 Nov 28. PMID: 17126531. REFERENCE #3: Shvilkin, A., Alexei Shvilkin From the Department of Medicine/Cardiology Division, Huang, H., Henry D. Huang From the Department of Medicine/Cardiology Division, Josephson, M., Mark E. Josephson From the Department of Medicine/Cardiology Division, & Shvilkin, C. (2015, April 01). Cardiac memory. Retrieved April 30, 2021, from https://www.ahajournals.org/doi/full/10.1161/circep.115.002778. DISCLOSURES: No relevant relationships by Tapan Buch, source=Web Response No relevant relationships by Pranav Karambelkar, source=Web Response No relevant relationships by Kashyap Kela, source=Web Response No relevant relationships by Pooja Kharbanda, source=Web Response No relevant relationships by jacob miller, source=Web Response No relevant relationships by Princy Shah, source=Web Response

Straight Form of Calcaneofibular Ligament as a Three-Dimensional Magnetic Resonance Imaging Sign in Diagnosis of Calcaneofibular Ligament and Anterior Talofibular Ligament Inferior Fascicle Injury

The present study was performed to investigate the morphological characteristics of the calcaneofibular ligament (CFL) and evaluate its relationship to the anterior talofibular ligament (ATFL) in patients with lateral ankle ligament injury using 3-dimensional magnetic resonance imaging (3D-MRI). This retrospective study involved 35 patients with lateral ankle ligament injury and 24 patients without a history of ankle trauma and a bone abnormality as controls. Reconstructed 3D-MRI was used to classify the form of the CFL as curved, wavy, or straight. The presence/absence of continuity between the fibula and CFL was evaluated in the 35 patients with injury, who were divided into 2 groups (continuity and discontinuity groups). The number of fascicles in the ATFL and the continuity between the distal end of the fibula and the proximal end of the ATFL were then evaluated. Among the patients with injury, 54.3% had the curve type of CFL, 34.3% had the wave type, and 11.4% had the straight type. In the control group, 62.5% had the curve type, 37.5% had the wave type, and none had the straight type. Continuity between the fibula and CFL was seen in 88.6%, and discontinuity was seen in 11.4%. Additionally, 85.7% had double fascicles in the ATFL. Inferior fascicle discontinuity between the ATFL and fibula was found in 13.3% with a double-fascicle ATFL; in all of these patients, the form of the CFL was straight and exhibited inferior fascicle discontinuity. The straight form of CFL could be a 3D-MRI sign in the diagnosis of CFL and ATFL inferior fascicle injury.

Purkinje triggers of ventricular fibrillation in patients with hypertrophic cardiomyopathy.

Ventricular fibrillation (VF) is the main mechanism of sudden cardiac death in patients with hypertrophic cardiomyopathy (HCM). The origin of VF and the success of catheter ablation to eliminate recurrent episodes in this population are poorly understood. From 2010 to 2014, five patients with HCM (age 21 ± 9 years, three female) underwent invasive electrophysiological studies and ablation at our center after resuscitation from recurrent (9 ± 7) episodes of VF. Ventricular premature beats (VPBs), seen to initiate VF in certain cases, were recorded noninvasively before the ablation procedure. Postprocedural computed tomography (CT) was performed to correlate ablation sites with myocardial hypertrophy in three patients. Outcomes were assessed by clinical follow-up and implantable cardioverter-defibrillator interrogations. VPB triggers were localized invasively to the distal left Purkinje conduction system (left posterior fascicle [2], left anterior fascicle [1], and both fascicles [2]). All targeted VF triggers were successfully eliminated by radiofrequency ablation in the left ventricle. Among patients with postablation CT imaging, 93 ± 12% of ablation sites corresponded to hypertrophied segments. Over 50 ± 38 months, four of five patients were free from primary VF without antiarrhythmic drug therapy. One patient who had 13 episodes of VF before ablation had a single recurrence. In our study of patients with HCM and recurrent VF, VF was not initiated from the myocardium but rather from Purkinje arborization. These sources colocalized with the hypertrophic substrate, suggesting electromechanical interaction. Focal ablation at these sites was associated with a marked reduction in VF burden.

A single premature stimulation from the para-Hisian region unmasked negative involvement of the left anterior fascicle in the verapamil-sensitive ventricular tachycardia with a right bundle branch block and right-axis deviation

A 33-year-old man had verapamil-sensitive ventricular tachycardia (VT) with a right bundle branch block (RBBB) and right axis deviation. Programmed stimulation from the para-Hisian region induced ventricular tachycardias (VT1 or VT2). VT1 was entrained during pacing from the para-Hisian region. A single para-Hisian stimulation antidromically captured the proximal portion of the left anterior fascicle (LAF), but the cycle length of VT2 remained unchanged. This observation indicated that the upper limb of the LAF was a bystander of the reentry circuit. We have clarified this mechanism with applying a single premature stimulation from the para-Hisian region.

Premature ventricular contraction originating from the distal left anterior fascicle: The usefulness of a multipolar catheter with small electrodes in mapping presystolic Purkinje potential and pace mapping

Mapping and localizing presystolic Purkinje potentials are crucial for determining the optimal ablation site for fascicular premature ventricular contractions (PVCs). Here we present a case of PVCs originating from the distal left anterior fascicle (LAF). Activation mapping using a multipolar catheter with small electrodes demonstrated early presystolic Purkinje potentials during the PVCs. A moderately good pace-map match was also obtained near the successful ablation site. This case demonstrates the activation pattern of PVCs originating from the distal LAF and the usefulness of multipolar catheters with small electrodes for the mapping of fascicular PVCs.

The change of cardiac axis deviation in catheter ablation of verapamil-sensitive idiopathic left ventricular tachycardia.

The underlying mechanism of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) has been postulated to be reentrant activation in the Purkinje fiber network of the left posterior fascicle or the left anterior fascicle (LAF). However, changing of cardiac axis deviation in sinus rhythm (SR) or during ILVT after radiofrequency catheter ablation (RFCA) has been rarely analyzed. Of the 232 patients with sustained ILVT induced and surface electrocardiogram (ECG) in SR recorded before and after RFCA, the changes of ECG morphology in SR and during ILVT were analyzed. The surface ECG in SR changed in 114 (49.1%) patients after RFCA. ILVT could still be induced in 27 (23.7%) patients. In comparison with the original ILVT, three forms of ECG morphology were observed. In eight patients, the ILVT morphology was unchanged. In the 13 patients with ILVT axis deviation conversion after ablation, the successful target was more proximal. In the six patients with ILVT morphology change but without axis deviation conversion after ablation, the successful ablation site was more distal. Among 15 patients with recurrent ILVT during follow-up, seven patients had previous axis deviation changes in SR after RFCA, the changes maintained in four patients and recovered in three patients. The morphology changes on surface ECG in SR after RFCA would not be a necessary prerequisite or a good endpoint for ILVT ablation. To analyze ILVT morphology changes after ablation would help to further clarify an appropriate approach for catheter ablation of ILVT.