Pacemaker Malfunction Research Articles

Stereotactic Ablative Radiotherapy for Early-stage Lung Cancer in Patients With Left Ventricular Assist Device: A Case Series.

Radiotherapy-induced malfunction of pacemakers and cardiac defibrillators has been reported, and corresponding guidelines have been developed in various countries. Although several studies have reported the effects of radiotherapy in patients with implantable left ventricular assist device (LVAD), its safety remains unclear. Herein, we report three cases of stereotactic ablative radiotherapy (SABR) using CyberKnife for early-stage lung cancer in patients with implantable LVAD. Three patients in their 50s or 60s, including two women and one man, who had LVADs due to dilated or ischemic cardiomyopathy and performance status of 0 or 1, were diagnosed with stage IA2 lung cancer (cT1bN0M0) by imaging only. All three patients were deemed inoperable due to cardiac comorbidity and underwent SABR at the Osaka University Hospital. The total radiation dose was 42-52 Gy, administered in four fractions. All treatment plans were designed to keep the LVAD dose below 2 Gy. In all patients, SABR was completed without acute adverse events or LVAD malfunction. During the follow-up period of 3-29 months, no disease progression or chronic adverse events were observed in any of the patients. This case series indicated that SABR using CyberKnife is a safe treatment option for early-stage lung cancer in patients with LVAD by reducing the dose to the LVAD.

Assessment of current pediatric electrocardiogram (ECG) interpretation practices

BackgroundDespite improvements in digital electrocardiograms (ECGs), current standard of care requires physician confirmation. Mismatched expectations between ordering providers and ECG readers, often pediatric cardiologists and electrophysiologists (EPs), are common, especially since there are no standardized practices for pediatric ECG reading. ObjectivesThe aim of this study was to understand current practices in pediatric ECG reading. MethodsAn electronic survey was sent to members of the Pediatric and Congenital Electrophysiology Society (PACES). Participation was optional; results were recorded from 12/19/22–1/9/23. Only complete and non-duplicate entries were included. ResultsA total of 127 responses were received, 93 were analyzed. Most responses were from centers in North America (n = 65, 70 %), including the US (n = 58, 62 %), Canada (n = 6, 6 %), and Mexico (n = 1, 1 %). The remaining were from Europe (n = 18, 19 %), Asia (n = 7, 8 %), Australia (n = 2, 2 %), and South America (n = 1, 1 %). Most (n = 46, 49 %) were from small centers (0–25 ECGs read per day), 27 respondents (29 %) were from medium centers (26–50 ECGs read per day), 20 respondents (22 %) were from large centers (>50 ECGs read per day). The majority (n = 65, 70 %) reported >3 readers/day for inpatient and emergency department ECGs. 49 % (n = 46) of centers read ECGs >2 times/day on weekdays with more variable practice on weekends. For critical/time sensitive findings, most centers (n = 90, 97 %) used verbal communication +/− the EMR. There was consensus (≥50 % agreement) that the following findings are critical/time sensitive: QTc >500 ms, T-wave alternans, narrow complex tachycardia, wide complex tachycardia, pre-excited atrial fibrillation, focal ischemic changes, second degree heart block type II, complete heart block, and pacemaker malfunction. ConclusionReading practices are variable. Critical/time sensitive findings are most often communicated verbally, however, there is no agreed upon standard. There was consensus in critical/time-sensitive findings. Improved understanding of common practices and resource allocation may lead to increased consistency in pediatric ECG reading.

Anesthetic Considerations for a Patient with Prosthetic Valves, AF, and PPM Undergoing Surgery for Misplaced Dental Implant in Paranasal Sinuses: A Case Report

Managing pts with DVR, PPM, AF and HTN is a challenge to anesthesiologist because of risk due to endocarditis, bleeding, thromboembolism, malfunction of pacemaker and MI. Displacement of dental implant in paranasal sinus is not very rare but it primarily occurs in patient with severe pneumatization of maxillary sinus/or defect of alveolar process. The present case report highlights the anaesthetic management of a patient with double valve replacement (DVR), atrial fibrillation (AF) and permanent pacemaker (PPM) for misplaced dental implant in the paranasal sinuses. Successful non-cardiac surgeries in patients who have heart disease depends on good preoperative assessment, intraoperative and post-operative management.

Prevention of Pacemaker Malfunctions in Patients With Bradyarrhythmia: Results of a Single-Center Follow-up

Objective: To evaluate results of surgical treatment in patients with bradyarrhythmia and risk factors for pacemaker (PM) malfunctions using improved preventive measures.Materials and methods: Our study consisted of two stages. At stage I, we retrospectively analyzed histories and outpatient medical records of 948 patients with various forms of bradiarrhythmias who underwent surgery in the clinic between 2006 and 2021 to identify PM malfunctions that occurred both in the early and late postoperative periods. Based on the data on the most common types of PM malfunctions and possible risk factors for their development, preventive measures were improved in this cohort of patients and were further used at stage II (pilot) to select patients for surgery.During stage II (pilot), 188 patients were operated on between 2019 and 2021: risk factors for malfunctions were identified in 72 (38.3%) cases at the preoperative stage. All the patients underwent surgery with the proposed and improved preventive measures. Follow­up was during the hospital stay and in 6 and 12 months.Results: At stage I (retrospective analysis), 78 (8.23%) patients had signs of PM malfunction. The most common malfunctions were endocardial electrode displacement (30.8%), increased stimulation threshold (25.6%), a change in the endocardial electrode impedance (17.9%), and impaired sensitivity (10.3%). In addition, premature battery depletion and PM syndrome were present in 9% and 6.4% of the patients, respectively.The correlation analysis revealed that the most common findings associated with malfunctions were enlarged right chambers of the heart due to valvular defects and dilated cardiomyopathy, myocardial remodeling caused by chemotherapy and radiation therapy, postinfarction cardiosclerosis in the electrode implantation area, untimely and inadequate PM programming, as well as increased levels of blood uric acid, urea, and creatinine, and prolonged and uncontrolled use of steroid drugs and bronchodilators.At stage II, there were no PM malfunctions requiring changes in the pacing parameters during the hospitalization period. Six months postsurgery, 1 (1.4%) patient had an increase in impedance (to 2843 ohms) caused by the uncontrolled intake of high doses of corticosteroids due to decompensation of chronic obstructive pulmonary disease. After correction of the corticosteroids dose, the ventricular electrode impedance returned to the normal level. Twelve months postsurgery, 2 (2.8%) patients had a decrease in impedance to 215 and 143 ohms, respectively, caused by the ventricular electrode displacement. After correcting the electrode position, normal pacing parameters were restored. No cardiac complications due to malfunctions were observed. Morphofunctional parameters of the heart did not significantly differ when compared with preoperative ones.Conclusions: Surgical treatment of patients with bradyarrhythmia and risk factors for PM malfunctions who underwent surgery with the proposed preventive measures demonstrated high efficiency in reducing the number of malfunctions and cardiac complications associated with inadequate stimulation in the long­term follow­up.

Abstract 13000: Twiddler’s Syndrome - A Rare Cause of Pacemaker Malfunction

Description of Case: A 76-year-old female with a past medical history of chronic atrial fibrillation and symptomatic tachycardia and bradycardia status-post dual-chamber pacemaker with right atrial and ventricular leads who presented with dyspnea on exertion. TTE showed normal biventricular function and no significant valvular abnormalities. Upon further evaluation of her pacemaker, she was found to have a very high ventricular capture threshold suggesting RV lead failure. The patient underwent RV lead replacement. The inspection of the pacemaker pocket during the procedure showed manual dislodgement of both tie-down sleeves and the pacemaker leads required untangling. A new RV lead was subsequently placed. Upon further imaging review, displacement of the previous RV lead was evident from initial placement. In addition, the patient had previously had a history of interval diaphragmatic stimulation as well. Overall, the presentation was felt to be consistent with Twiddler’s Syndrome. Discussion: Twiddler’s or Reel Syndrome occurs when conscious or subconscious self-manipulation and spinning of the pulse generator result in lead dislodgement and loss of pacing and pacemaker malfunction. The reeling of the leads around the generator can also cause stimulation of the brachial plexus or phrenic nerve stimulation and subsequent rhythmic arm twitching or diaphragmatic pacing, respectively. It has previously been reported in cases of single- and dual-chamber ICDs, deep brain stimulators, and spinal nerve stimulators with varying presentation. The diagnosis requires clinical suspicion based on history, physical exam, imaging, or surgical inspection suggesting the displacement of leads with evidence of coiling of the wires around the pacemaker. Treatment often requires revision and focus should be maintained on patient education for both primary and secondary prevention of Twiddler’s Syndrome.

P256 AN UNUSUAL CASE OF PACEMAKER MALFUNCTION WITH NON COMMON ELCTROCARDIOGRAPHIC PRESENTATION AND UNEXPECTED ECHOCARDIOGRAPHIC FINDING

Abstract This clinical case shows the diagnostic challenge and the management of a 79 y–o male with recent hospitalization for infero–lateral STEMI undergoing primary PCI of Right Coronary Artery with 2 DES and following DDDR MRI PM (pacemaker) implantation due to the development of persistent 2:1 Atrio–Ventricular Block. One month later, admission at Emergency Department for syncope. Normal parameters were found at laboratory analyses. The electro–stimulator activity evaluation showed a PM malfunction with ventricular capture failure. Thus, the increase of PM output up to electric ventricular capture (8 Volt/120 msec) was performed, but the following Electrocardiogram showed a PM–induced rhythm with RBBB–morphology. Then, the bedside Echocardiogram showed an apparent presence of a linear hyper–echogenic image into left ventricle with no inter–ventricular septal defect neither inter–ventricular shunt, inter–atrial septal hypermobility with no evident inter–atrial shunt at rest; while a chest Radiography identified the atrial and ventricular leads with no accurate individuation of their position. The patient was admitted in Intensive Cardiac Care Unit with confirmation of intermittent failure to ventricular capture and RBBB–morphology during PM–induced rhythm at telemetry monitoring. Due to Electrocardiographic and Echocardiographic findings, a strong suspect of abnormal position of the ventricular lead into left ventricle through a possible PFO has been raised. A chest Computed Tomography was performed confirming the anomalous position of the ventricular lead: it reached the left atrium through an inter–atrial defect/patent foramen ovale (PFO), then crossing the mitral valve up to left ventricle. The PM–lead repositioning was scheduled two days after. After positioning of temporary stimulator lead in right ventricle, the ventricular lead has been withdrawn from left–side chambers and positioned into septal–apical right ventricle; furthermore, the position of right atrial lead has been optimized (because of frequent spontaneous passage to the left atrium through the PFO, during manual maneuvers) thus obtaining good stability of the device. During the following days, the telemetry monitoring showed a PM–induced rhythm, without capture nor sensing failure. The chest Radiography confirmed the correct position of leads and the pre–discharge Echocardiography showed a LVEF 57% with no valvular pathology and with atrial and ventricular leads into right–side chambers.

Multidisciplinary Management of Opioid Use-Related Infective Endocarditis: Treatment, QTc Values, and Cardiac Arrests due to Ventricular Fibrillation.

(1) Background: The opioid epidemic has led to an increase in cardiac surgery for infective endocarditis (IE-CS) related to injection use of opioids (OUD) and other substances and a call for a coordinated approach to initiate substance use disorder treatment, including medication for OUD (MOUD), during IE-CS hospitalizations. We sought to determine the effects of the initiation of a multi-disciplinary endocarditis evaluation team (MEET) on MOUD use, electrocardiographic QTc measurements and cardiac arrests due to ventricular fibrillation (VF) in patients with OUD. (2) Methods and Results: A historical group undergoing IE-CS at Yale-New Haven Hospital prior to MEET initiation, Group I (43 episodes of IE-CS, 38 patients) was compared to 24 patients undergoing IE-CS after MEET involvement (Group II). Compared to Group l, Group II patients were more likely to receive MOUD (41.9 vs. 95.8%, p < 0.0001), predominantly methadone (41.9 vs. 79.2%, p = 0.0035) at discharge. Both groups had similar QTcs: approximately 30% of reviewed electrocardiograms had QTcs ≥ 470 ms and 17%, QTcs ≥ 500 ms. Cardiac arrests due to VF were not uncommon: Group I: 9.3% vs. Group II: 8.3%, p = 0.8914. Half occurred in the 1-2 months after surgery and were contributed to by pacemaker malfunction/ management and half were related to opioid use. (3) Conclusions: MEET was associated with increased MOUD (predominantly methadone) use during IE-CS hospitalizations without an increase in QTc prolongation or cardiac arrest due to VF compared to Group I, but events occurred in both groups. These arrests were associated with pacemaker issues or a return to opioid use. Robust follow-up of IE-CS patients is essential, as is further research to clarify the longer-term effects of MEET on outcomes.

262 AN UNUSUAL CAUSE OF PACEMAKER MALFUNCTION WITH NON-COMMON ELECTROCARDIOGRAPHIC PRESENTATION AND UNEXPECTED ECHOCARDIOGRAPHIC FINDING

Abstract This clinical case shows the diagnostic challenge and the management of a 79 y-o male with arterial hypertension, tabagism, obesity and a recent hospitalization for infero-lateral STEMI undergoing primary PCI of Right Coronary Artery with 2 DES and following DDDR MRI PM (pacemaker) implantation (through left cephalic vein) due to the development of persistent 2:1 AV block (atrio-ventricular block). One month later, admission at Emergency Department for syncope. The admission therapy included Aspirin plus Clopidogrel, Ramipril, Atorvastatin. Normal parameters were found at laboratory analyses. The electro-stimulator activity evaluation showed a PM malfunction with ventricular capture failure. Thus, the increase of PM output up to electric ventricular capture (8 Volt/120 msec) was performed, but the following Electrocardiogram (ECG) showed a PM-induced rhythm with RBBB-morphology. Then, the bedside Echocardiogram showed an apparent presence of a linear hyper-echogenic image (lead?) into left ventricle with no inter-ventricular septal defect neither inter-ventricular shunt, inter-atrial septal hypermobility with no evident inter-atrial shunt at rest; while a chest Radiography identified the atrial and ventricular leads with no accurate individuation of their position. The patient was admitted in Intensive Cardiac Care Unit with confirmation of intermittent failure to ventricular capture and RBBB-morphology during PM-induced rhythm at telemetry monitoring. Due to Electrocardiographic and (above all) Echocardiographic findings, a strong suspect of abnormal position of the ventricular lead into left ventricle through a possible PFO has been raised. A chest Computed Tomography was performed confirming the anomalous position of the ventricular lead: the atrial lead was in the right atrium whereas the ventricular lead reached the left atrium through an inter-atrial defect/patent foramen ovale (PFO), then crossing the mitral valve up to left ventricle. The PM-lead repositioning was scheduled two days after. With intra-operative fluoroscopy, a further verify of leads position was observed (the ventricular one into left ventricle through PFO and mitral valve, the atrial one mildly displaced upwards) and the leads repositioning was performed. After positioning of temporary stimulator lead in right ventricle, the ventricular lead has been withdrawn from left-side chambers and positioned into septal-apical right ventricle; furthermore, the position of right atrial lead has been optimized (because of frequent spontaneous passage to the left atrium through the PFO, during manual maneuvers). Finally, the optimal stability of the device was obtained, as well as the optimal atrial and ventricular capture during stimulation test. During the observation in Cardiology Unit in following days, the telemetry monitoring and ECG showed a PM-induced rhythm, without capture nor sensing failure. The chest Radiography confirmed the correct position of atrial and ventricular leads. Finally, the pre-discharge transthoracic Echocardiography showed a LVEF 57% with no valvular pathology nor pericardial effusion, and with atrial and ventricular leads into right-side chambers.

565 UNUSUAL LIFE-THREATENING FLECAINIDE TOXICITY: A CASE REPORT

Abstract Background Anti-arrhythmic drug therapy has often a narrow therapeutic index and could be responsible of toxic side effects including malignant arrhythmias and life-threatening hemodynamic deterioration. Flecainide toxicity can occur even at normal serum levels in the setting of electrolyte disturbances such as hyponatremia. We report a case of flecainide toxicity, likely due to dual mechanism: reduced excretion and potentiation of the toxic effects due to concomitant hyponatremia. Case description A 82-year-old woman was admitted to our hospital for syncope. The ECG at admission showed atrial fibrillation, complete atrio-ventricular (AV) block and a wide QRS escape rhythm. She has a history of hypertension, COPD and atrial fibrillation. She was currently taking flecainide at a dosage of 150 mg per die. Laboratory tests reported an elevated lactate concentration (4.6 mmol/L), hyponatremia (128 mmol/L), severe reduction of renal function (eGFR 19 ml/min), and NT-proB-type Natriuretic Peptide 17563 pg/ml, (ULN&amp;lt;450). Echocardiography showed a reduced left ventricular ejection fraction (EF=35%). Suspecting flecainide poisoning, we started intravenous sodium bicarbonate and temporary pacing for severe bradycardia and pauses. However, despite numerous attempts of lead reposition and the use of maximum output, we failed to document ventricular capture in the immediate post-operative. Half hour later, dopamine infusion was started for sustained severe hypotension. The day after we were able to obtain ventricular capture. At serial ECG examination, she also developed progressive QRS narrowing with concomitant clinical improvement. Discussion Flecainide toxicity is a rare but potentially life-threatening condition. The excess of sodium channel blockade causes in fact delayed conduction through the AV node, His-Purkinje system, and ventricles with possible AV block, ventricular tachycardia, ventricular fibrillation, and asystole. In addition, hemodynamic instability can develop rapidly in flecainide intoxication due to chronotropic and inotropic incompetence. The majority of flecainide intoxication reported cases are due to a drug overdose. However, flecainide toxicity can occur with serum levels within the range of normality. Particularly, this can occur in the setting of hyponatremia. The observed pacemaker malfunction was also due to flecainide intoxication. In our case, the patient was taking therapeutic doses of this drug. The toxic effect was probably due to the reduced excretion (secondary to kidney failure) and the simultaneous presence of hyponatremia. The main treatment for flecainide intoxication is sodium bicarbonate and supportive care. However, there is currently no recommended standardized protocol for flecainide toxicity. The inotropic agents could be helpful in case of cardiogenic shock, but their use may be limited by the rate-dependent effect of flecainide and the increased risk ventricular arrhythmias. Left ventricular assist devices have been also used to support hemodynamic through flecainide-induced cardiogenic shock.

An unusual cause of pacemaker malfunction: A case report of an association of twiddler and reel syndrome

Lead dislodgement syndromes (Twiddler, Ratchet or Reel syndromes) are rare causes of cardiac stimulation device malfunction that can occur most commonly early after device implantation. Each one of them associated with a unique pattern of lead coiling and dysfunction. Our clinical case reports an unusual association and shed the light on the available diagnostic modalities. A 62-year-old woman who was referred to our hospital for a symptomatic high degree AV block, she underwent dual chamber pacemaker implantation. She experienced 3 weeks following implantation a rhythmic twitching of the right arm without syncope. The device interrogation revealed an increase in both leads pacing impedance and chest X-ray showed leads had pulled out of the heart and were tangling and wrapped repeatedly around the pulse generator. Revision procedure was performed to reposition the leads. Recognizing this complication early can prevent life threatening complication and is then of the utmost importance. Twiddler's syndrome is due to rotation of the device along its long axis. Reel syndrome is produced by device rotation along the transverse axis. In most cases, lead replacement or reposition is needed. Preventive measures such as patient education and use of a smaller pocket will reduce the risk of developing the syndrome. Our case highlights the available diagnostic modalities for early detection of twiddler's syndrome. The unique nature of this case increases the importance of considering device lead dislodgement as the cause for patients presenting with extra-cardiac symptoms.

IN-HOSPITAL OUTCOME OF PATIENTS REQUIRING TEMPORARY TRANSVENOUS PACEMAKER AFTER ST ELEVATION MYOCARDIAL INFARCTION

Objectives: Bradyarrhythmias and Electrical conduction defects are common sequelae of acute myocardial ischemia (AMI). Many of these arrhythmias are symptomless and do not require urgent intervention while others are life threatening. Of all other potential causes myocardial ischemia is the commonest and important causative agent of acute and potentially dangerous conduction defect. This study will upgrade various aspects of patients’ care with Acute MI who need TPM which will improve outcome and make the cause of death along with long term sequelae clear in such patients in our local population. To determine the in hospital outcomes of patients requiring temporary transvenous pacemaker after ST elevation MI.&#x0D; Methodology: This cross-sectional descriptive study was conducted at cardiology Department, MTI-KTH, Peshawar from 25 Jan, 2020 to 25 Jun, 2020. All temporary pacemakers were implanted in our Coronary Care Unit procedures and were done in an exploration room. All procedures performed by consultant cardiologists and trainee registrars. Pacemaker malfunction was described as capture failure, failure to sense, or both. Death secondary to cardiac tamponade, a systole or ventricular arrhythmias as well as improvement and need for permanent pacing was also be documented as mentioned above in operational definitions. Data was obtained after performing the procedure and during stay of patient in the coronary care unit, as determined by set protocol. The electrocatheter used was 110 cm bipolardevices of caliber 6F. Cardiac catheterization was generally via the right subclavian or internal jugular by the Seldinger’s wire technique, with insertion in the apical region of the right ventricle under aseptic measures. A sensing threshold values for pacing of 0.5=2 mV were set. Pacing was initially deployed at values double the threshold voltages, using the TPM in WI mode.&#x0D; Results: As per in-hospital outcomes, death occurred in 14 (9.7%) died, 49 (34.0%) patients had malfunction, 10 (6.9%) patients had hematoma, 26 (18.1%) patients had fever, 27 (18.8%) patients experienced improvement while 18 (12.5%) required permanent pacing.&#x0D; Conclusion: In-hospital adverse outcomes were observed in a significant number of patients.

Pacemaker-Mediated Tachycardia Interpolated Into Ventricular Tachycardia

In a 77-year-old patient with a history of inferior myocardial infarction and dual-chamber pacemaker (Effecta DR, Biotronik) implanted for carotid sinus syndrome, a routine Holter electrocardiogram recorded 3 consecutive tachycardias: irregular monomorphic ventricular tachycardia (VT), pacemaker-mediated tachycardia (PMT), and reoccurred VT (re-VT) of the same morphology as the initial one, but regular and faster than the PMT (Fig. 1).The pacemaker settings were as follows: DDD mode; pacing rate, 50 to 130 bpm; programmed atrioventricular delay, paced 145 ms and sensed 105 ms; and postventricular atrial refractory period (PVARP), 250 ms and 400 ms following premature ventricular contraction.What was the most likely mechanism of this arrhythmia?B) PMT was triggered by atrial premature beat and terminated by the re-VT (Fig. 2) Concerning the mode of the PMT initiation, the VT could not trigger PMT because its retrograde P wave (in Fig. 2, stars denote retrograde P waves; those of the VT and re-VT are marked below and those of the PMT above the middle electrocardiographic channel) occurred during the PVARP (gray horizontal marks in the ladder diagram). Given that the interrogation showed no pacemaker malfunctions and that the electrocardiogram showed no artifacts, an atrial ectopic beat (with isoelectric P wave) is the only likely trigger for PMT.Concerning the mode of PMT termination, the episode was too short to activate the device's PMT termination algorithm. Furthermore, the retrograde P wave from the last PMT beat, which appeared after 344 ms, indicates that retrograde conduction has been prolonged, but without occurrence of a block that would have stopped the PMT. Thus, the re-VT is what terminated the PMT by the first impulse following fusion (f2 in Fig. 2), which depolarized ventricles before the possible onset of the next paced beat. Retrograde conduction prolongation (by 24 ms) and programmed atrioventricular delay prolongation (by 50 ms, for Biotronik's PMT status confirmation) during the last PMT cycle provided a time for the onset of the re-VT and thus indirectly participated in the PMT termination.Based on the constant cycle length (382 ms) of the re-VT during the prolongation of ventriculoatrial conduction (from 170 to 240 ms), the re-VT was most probably microreentrant. Different retrograde conduction times of the VT (160 ms) and PMT (315 ms) might suggest the existence of a dual retrograde conduction with separate pathways for each of the 2 tachycardias, but any evidence for such speculation is lacking. In any case, this case illustrates the complexity of possible interactions between spontaneous and device-mediated arrhythmias.

PO-632-06 REAL-TIME EX-VIVO RADIOTHERAPY IMPACTS ON PACEMAKER FUNCTION ARE MINIMAL

There is a paucity of data regarding the safety of radiotherapy in patients with pacemakers and the impact of linear accelerator parameters is unclear. To assess the function of pacemakers when exposed to different linear accelerator parameters. Pacemakers (2 single, 1 dual chamber) were exposed to radiation at dose rates 0.2-11.8Gy/min. Dose rate was modulated by adjusting the distance from the beam edge, linear accelerator pulse repetition rate (rep rate) and distance from source. Noise amplitude, pacemaker output, and device behavior during irradiation were assessed in VVI or DDD modes. Each device was irradiated 28 times for 10 seconds. Noise amplitude on bipolar (Bi) channel increased with dose rate (r2=0.3611, p<0.0001, B) and on unipolar (Uni) channel decreased with rep rate (r2 = 0.09, p<0.01; C). On both channels noise amplitude decreased with distance from field edge (Bi r2 = 0.53, p<0.01; Uni r2 = 0.42, p<0.01; D). No over-sensed events occurred in response to radiation induced background noise. Low frequency signals on the Uni and Bi channels were observed with beam on and off (E), resulting in over-sensed events only when directly in the radiation beam and sensing Uni. When directly in the beam, oversensing of A pacing on the V sensing Uni channel was observed leading to pacing inhibition (F). Post-radiation exposure interrogation was unremarkable revealing no evidence of device malfunction. Pacemaker malfunctions when directly in photon radiation beam are related to oversensing and crosstalk phenomena preferentially affecting the unipolar sensing channel. There was no evidence of long-term device malfunction upon repeated interrogations despite multiple exposures.

In-vitro investigation of cardiac implantable electronic device malfunction during and after direct photon exposure: A three-centres experience.

Radiotherapy may cause malfunction of implantable cardioverter-defibrillators (ICDs) and pacemakers (PMs). We carried-out a multicentre randomized in-vitro study on 65 ICDs and 145 PMs to evaluate malfunctions during and after direct irradiation to doses up to 10Gy. Three centres equipped with different linear accelerator and treatment-planning systems participated in the study. Computed Tomography (CT) acquisitions were performed to build the treatment plans. All devices were exposed to dose of 2, 5, or 10Gy (6 MV). All devices underwent a baseline examination and 64 wireless real-time telemetry-transmissions (47 ICDs and 17 PMs) were monitored during photon exposures. All devices were interrogated after exposure and once monthly for six subsequent months. Fifty-four of the 64 wireless-enabled CIEDs (84.4%) recorded noise-related interferences during exposure. In detail, 40/47 ICDs (85.1%) reported interference, of which 16 ICDs (34%) reported potentially clinically relevant pacing inhibition and inappropriate detections. Following exposure, a soft reset occurred in 1/145 PM (0.7%) while 7/145 PMs (4.8%) reported battery issues. During the six-month follow-up, 1/145 PM (0.7%) reported a soft reset, while 12/145 more PMs (8.3%) and 1/64 ICD (1.5%) showed abnormal battery depletion. All reported issues occurred independently of exposure dose. Finally, irreversible effects on software and battery life occurred in only non-MRI-compatible devices. ICDs mostly featured real-time transient sensing issues, while PMs mostly experienced long-term battery or software issues that were observed immediately following radiation exposure and during follow-up. Irreversible effects on battery life and software occurred in only non-MRI-compatible devices.

Abstract 6945: A Pacemaker Red Herring and a Hypertrophic Cardiomyopathy Copycat

A 53-year old man with a history of hypertension, atrial flutter, and complete heart block with a dual chamber pacemaker presented to the hospital due to concern for pacemaker malfunction. Remote pacemaker monitoring found over-sensing events. He works in an automobile repair shop and his family history is notable for a son with Wolf Parkinson White syndrome treated with ablation. On presentation to the emergency department, he had normal vital signs and no lab abnormalities. His electrocardiogram showed sequential atrioventricular pacing at 60 beats per minute. He underwent an echocardiogram which showed a newly reduced left ventricular ejection fraction of 40-45% with global left ventricular hypokinesis, and left ventricular hypertrophy. The patient’s over-sensing events were initially concerning for pacemaker malfunction, particularly because he is known to be pacemaker-dependent. The differential diagnosis for the over-sensing events included battery depletion, insulation failure, insufficient programmed sensitivity value, and electromagnetic interference. An electrogram of one of the over-sensing events revealed simultaneous over-sensing of the both the atrial and right ventricular leads and otherwise stable lead parameters, which was consistent with electromagnetic interreference during arc-welding. The differential diagnosis for the left ventricular hypertrophy included sarcomeric hypertrophic cardiomyopathy, left ventricular hypertrophy secondary to hypertension, and hypertrophic cardiomyopathy phenocopies including Danon disease, Fabry Disease, Pompe disease, and PRKAG2 syndrome. Due to his family history of pre-excitation, genetic testing was conducted and demonstrated a pathogenic variant in the PRKAG2 gene. Shared decision-making with the patient informed his choice to upgrade his pacemaker to an implantable cardioverter defibrillator for primary cardiovascular prevention. The diagnosis of PRKAG2 syndrome served as the catalyst for his family members to undergo genetic testing. This case highlights the need for a high index of suspicion for hypertrophic cardiomyopathy phenocopies when pre-excitation and ventricular hypertrophy collocate to the same patient or family.

Efficacy of left bundle branch area pacing in patients with indication for cardiac resynchronization therapy

Abstract Background Cardiac resynchronization therapy (CRT) with biventricular pacing has demonstrated clinical benefits in heart failure patients with left bundle branch block (LBBB) and ventricular dysfunction. Left bundle branch area pacing (LBBAP) results in a relatively short QRS duration (QRSd) with fast left ventricular activation and could be considered as an alternative to conventional CRT. Purpose The aim of the present study was to evaluate the feasibility and outcomes of LBBAP in patients with indications for CRT. Methods Consecutive patients with indications for CRT were included. LBBAP was performed via transventricular septal approach (1–3). We aimed to achieve a paced QRS with right bundle branch conduction delay morphology, a stimulus to peak left ventricular activation time (S-LVAT) &amp;lt;100ms and/or a QRSd ≤130ms. AV delay programming was individualized in patients in sinus rhythm, taking consideration of the AV conduction, programming the one that generated the shortest QRSd at rest. Rate adaptive AV was also activated in these patients. Pacing electrical and echocardiographic parameters were recorded at baseline and during follow-up. Results LBBAP was achieved in 19 of 21 (90.5%) patients with indication for CRT. Indications were heart failure with LBBB and left ventricular ejection fraction (LVEF) ≤35% in 8 (42%), AV node ablation or AV block with LVEF &amp;lt;50% and high expected RV pacing burden in 9 (47%), 1 pacing-induced cardiomyopathy and 1 patient with biventricular pacemaker malfunction (high LV capture threshold). The mean follow-up was 4.6±1.7 months and the percentage of ventricular pacing was 93.4±13.9%. There were no device-related complications during this period. LBBA capture threshold was 0.6±0.3V at 0.4ms at the implantation, and remained stable (0.7±0.1 V, p=0.17). The lead impedance and R-wave amplitude at implantation were 636±106 ohms and 13.4±6.8 mV, and 541±88 ohms and 13.0±5.1 mV during the follow-up (p&amp;lt;0.001 and p=0.27, respectively). Mean S-LVAT was 85.5±13.9 ms, and mean QRSd was 122±9 ms, that remained stable during follow-up (122 vs 124 ms, p=0.21). In patients with LBBB, a significant narrowing of paced QRSd was achieved (160.9±16.7 vs. 123.9±9.7 ms, p&amp;lt;0.001). Mean LVEF increased by 15.9%, from 35.4±8.9% at baseline to 51.3±9.8% at follow-up (p&amp;lt;0.001) in the overall population, and 14.5% (from 32.7±4.8% to 47.2±10.7%, p=0.001) in patients with LBBB. After one month, estimated time for elective replacement was 11.9±0.4 years. Conclusions LBBPA was successfully achieved in 90.5% of the patients with indication for CRT, with good and stable pacing electrical parameters, long estimated battery longevity and relatively narrow QRS, and was associated with improvement in cardiac function. LBBAP may be considered as a first-line option for patients with indications for CRT. Funding Acknowledgement Type of funding sources: None.

Pacemaker malfunction? What is the mechanism?

Pacing artifacts on ECG are commonly encountered in clinical practice. We present a case of an external interference from a chronic retained abdominal generator leading to an ECG manifestation of atria lead malfunction. Careful attention to history and physical examination can identify sources of external pacemaker artifact.

Conformal Radiation Therapy in Patients With Cardiovascular Implantable Electronic Devices: Proposed Practical Implementation of the 2019 American Association of Physicists in Medicine Task Group No. 203 Risk-Stratified Interrogation Schedule

PurposeRadiation therapy (RT) in patients with cardiac implantable electronic devices (CIED) carries a risk of device malfunction from radiation exposure. We sought to evaluate the incidence of CIED malfunction in a cohort of patients treated with modern RT techniques. Methods and MaterialsA retrospective analysis of 193 CIED patients treated with RT between 2000 and 2018 was conducted. All patients underwent pre-, intra-, and post-RT CIED interrogations. Patient demographics, CIED details, RT details, including total dose, modality, treatment site, CIED distance from RT field, treatment planning system maximum dose and in vivo dose estimates, and CIED malfunction data were analyzed. ResultsCIEDs in use were mainly pacemakers (single-chamber 10%, dual-chamber 49%) and defibrillators (35%). Patients received a median RT dose of 50 Gy (range, 7-80 Gy), treated with 3-dimensional CRT (47%), intensity modulated RT/volumetric modulated arc therapy (38%), and stereotactic body radiation therapy (10%). Neutron producing energies were used in 13% of the treatments. A strong correlation was noted between treatment planning system estimated maximum dose and in vivo estimated CIED dose when the CIED distance from the treatment field was >3 cm. However, in vivo measurements provide a lower estimated absorbed dose for CIED devices <3 cm from the RT field. During a median follow-up of 24 months (range, 7-64 months), 2 adverse CIED-related events were recorded: a spontaneous defibrillator discharge and a pacemaker malfunction subsequently causing ventricular tachycardia. Both patients received stereotactic body radiation therapy to the thorax, with CIED dose of 5 and 19.2 cGy, respectively. Both events occurred 2 years posttreatment without any intra- or post-RT CIED interrogations changes noted. ConclusionsIn this series of patients treated with modern RT techniques, we observed a CIED malfunction rate of 1.04%. These low event rates establish the safety of delivering modern RT in CIED patients with the possibility of reducing the burden of intra- and posttreatment CIED monitoring.

In‐Body Electromagnetic Sensor Combined with AI‐Enhanced Electrocardiography for Pacemaker Working Status Telemonitoring

This paper describes the design and implementation of an in‐body electromagnetic sensor for patients with implanted pacemakers. The sensor can either be mounted on myocardial tissue and monitor the electrocardiography (ECG) with contact electrodes or implanted under the skin and monitor the ECG with coaxial leads. A 16‐bit high‐resolution analog front‐end (AFE) and an energy‐efficient 32‐bit CPU are used for instantaneous ECG recording. Wireless data transmission between the sensor and clinician’s computer is achieved by an embedded low‐power Bluetooth transmitter. In order to automatically recognize the working status of the pacemaker and alarm the episodes of arrhythmias caused by pacemaker malfunctions, pacing mode classification and fault diagnosis on the recorded ECG were achieved based on an AI algorithm, i.e., a resource allocation network (RAN). A prototype of the sensor was implemented on a human torso, and the in vitro test results prove that the sensor can work properly for the 1‐4‐meter transmission range.

Abstract 15480: Twiddler’s Syndrome in a Subcutaneous Implantable Cardioverter-Defibrillator

Introduction: Twiddler’s syndrome refers to deliberate or unintentional twisting of pulse generator in device pocket resulting in lead migration, which can present as malfunction of pacemaker or implantable cardioverter-defibrillator (ICD). In the past 50 years, twiddler’s syndrome with transvenous ICD and pacemaker has been well-described and thoroughly studied. However, there are very little data on twiddler’s syndrome with subcutaneous ICD (S-ICD). Case presentation: The patient is a 50-year-old male with a past medical history of hypertrophic cardiomyopathy, cardiac MRI showing left ventricular hypertrophy with a wall thickness of 24 mm, non-sustained ventricular tachycardia and evidence of late gadolinium enhancement scar, who underwent implantation of S-ICD for primary prevention. First follow-up 2 weeks post-implant showed appropriate device function. Two weeks later, remote monitor documented atrial fibrillation and ICD shocks. Surface ECG showed reduced R wave and delivered shock impedance was 7 ohms. Patient reported no symptoms and was clapping hands to music when it occurred. Chest X-Ray revealed S-ICD lead dislodged and retracted with coiling around the generator in the left lateral chest wall (Figure 1). Subsequently patient underwent lead revision and device replacement. To reduce the risk of future dislodgement, during re-implantation, the tip of the ICD lead was secured with 0-Silk. Conclusion: Twiddler’s syndrome is a rare complication after ICD implantation, not only with transvenous-ICDs but also involving S-ICDs. Risk factors include advanced and younger ages, redundant skin, obesity, oversized pocket, and psychiatric disorder. It can be a potentially dangerous and even fatal due to undetected or unsuccessful therapy for ventricular tachyarrythmias. Therefore, it is of paramount importance to diagnose and intervene early to avoid morbidity and mortality in these patients.