DC Shock Research Articles

Abstract Su304: The Effect of Time to DC Shock on Return of Spontaneous Circulation in Out-of-Hospital Cardiac Arrest with Recurrent Shockable Rhythm

Objective: The optimal timing for defibrillation attempts in out-of-hospital cardiac arrest (OHCA) patients with recurrent shockable rhythms [ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT)] is uncertain. This study examined the association between "time to DC shock" and the return of spontaneous circulation (ROSC) in OHCA patients with recurrent shockable rhythms. Methods: This was a retrospective analysis of data from the Salt Lake City Fire Department (SLCFD) from 2012 to 2023. Rhythm-filtering technology, used since 2012, enabled real-time and accurate interpretation of cardiac rhythms during CPR, with local protocols allowing early defibrillation for recurrent VF/ pulseless VT cases. Patients who experienced four or five episodes of shockable rhythms and received defibrillation were included. Generalized estimating equation (GEE) analysis was used to evaluate the association between time to shock preceding recurrent defibrillation and ROSC. Results: A total of 142 patients were included, with a mean age of 59.7 ± 15 years; 105 (73.9%) were male, 63 (44.4%) arrested in public locations, and 101 (71.1%) had witnessed arrests. Adjusted GEE analysis revealed that longer time to shock was associated with lower odds of achieving ROSC (OR: 0.81, 95% CI: 0.72–0.93, p = 0.005). Every one-minute delay in defibrillation is predicted to decrease the likelihood of achieving ROSC by 19%. Conclusion: In patients with recurrent shockable rhythms, every one-minute delay in delivering a shock was associated with a statistically significant 19% reduction in the chance of achieving ROSC. This finding highlights the importance of reducing the time to defibrillation in managing recurrent shockable rhythms and suggests reevaluating the current recommendation of two-minute intervals for rhythm check and shock delivery.

Clinical outcomes of patients with in-hospital witnessed cardiac arrest: effect of co-morbidities

IntroductionCardiopulmonary resuscitation (CPR) is frequently performed in hospitalized patients after in-hospital cardiac arrest (IHCA), especially in the intensive care unit (ICU) (J Crit Care 24:408-414, 2009). Despite the fact that nearly half of the in-hospital cardiac arrests (IHCA) actually happen in intensive care units (ICUs) (N Engl J Med 367:1912-1920, 2012), intensive care unit cardiac arrest (ICU-CA) compared to IHCA or out-of-hospital cardiac arrests (OHCA) has received little attention, and data on ICU-CA remains scanty (Intensive Care Med 40:1853-1916, 2014).AimWe aimed to evaluate the clinical status and factors associated with the survival of patients subjected to cardiopulmonary resuscitation (CPR) after a witnessed cardiac arrest (CA) inside the medical intensive care unit (MICU).PatientsThe study included 110 patients, mean age of 60 ± 18 years, 69 (63%) males, and 41 (37%) females. Co-morbidities included diabetes mellitus was present in 46 (42%), hypertension 57 (52%), central nervous system (CNS) disease 31 (29%), cardiovascular (CVS) 76 (69%), respiratory 63 (57%), hepatic 16 (15%), shock 35 (32%), and renal 44 (40%). Mechanical ventilation was present in 97 (88%) of patients. SOFA score < 9 was present in 38%, MPM III score < 10 in 37%, and GCS > 7 in 66% of patients. Non-shockable rhythm occurred in 95 (86%) while shockable rhythm in 15 (14%) of patients.MethodsData were collected prospectively at the medical ICU of Cairo University from Jan. 2013 to Feb 2013. A resuscitation protocol was done according to the latest recommendation of the European Society of Cardiology at the time of patient inclusion. Clinical data were recorded and surviving patients were clinically followed daily until hospital discharge.ResultsOut of 110 witnessed cardiac arrests, CPR was initially successfully manifested by return of spontaneous circulation (ROSC) in 60 patients (55%), of whom 22 (20%) survived hospital discharge and only 9 patients (8%) were functionally independent. Compared to non-survivors, 60 patients (55%) with ROSC had a MPM III < 10 (p 0.015), EF ≥ 50% (p 0.001), and non-shocked patients (p 0.008). Other factors such as DC shocks < 3 (p 0.02), CPR cycles < 2 (p < 0.001), resuscitation duration < 10 min (p 0.03), time to start CPR < 1 min (p 0.001), maintained HCO3 (p 0.03), and PaCO2 (p 0.002) were found to improve ROSC. Mortality before discharge decreased with asystole (p < 0.01). Mortality before discharge increased with CNS (p < 0.02) and respiratory comorbidities (p 0.02), shock (p < 0.001) and mechanical ventilation (p < 0.0001), SOFA > 9 (p 0.001), MPM III > 10 (0.018), and time to start CPR > 1 min (p 0.001).ConclusionNot all ROSC reached long-term survival and hospital discharge. Several co-morbidities affect ROSC and short-term and long-term patient survival after witnessed MICU cardiac arrest.

CARDIOPULMONARY SUPPORT WITH EXTRACORPOREAL MEMBRANE OXYGENATION (ECMO) DURING CATHETER ABLATION OF VENTRICULAR FIBRILLATION: A CASE REPORT

Abstract The clinical case deals with a 46–year–old man, severely obese and suffering from type II diabetes mellitus and arterial hypertension, a smoker. He was admitted to our department for iterative ventricular fibrillation (VF) following a recent acute myocardial infarction with ST–segment elevation treated with percutaneous coronary angioplasty (PTCA) and implantation of drug–eluting stents on the anterior interventricular. Control coronary angiography showed good results of previous PTCA. On the echocardiogram, left ventricular pump function moderately reduced (EF 45%) with district alterations of the kinetics and aneurysmal dilatation of the ascending aorta. During hospitalization, iterative episodes of VF despite maximal antiarrhythmic therapy, promptly treated with DC shock. Continuous telemetry monitoring showed frequent early premature ventricular complex (PVC) triggering VF episodes. A 12–lead Holter ECG was performed to better identify the morphology of these PVC, documenting PVC of morphology compatible with origin from Purkinjie fibres. An electrophysiological study and mapping of the left ventricle were performed with extracorporeal membrane oxygenation (ECMO) support. During mapping of the middle left interventricular septum, VF occurred several times and was promptly treated with DC shock. In this area have been documented Purkinje fibers and low voltage and multifragmented areas; ablation was then performed by delivering radiofrequency in this area until the all potentials were completely eliminated. After ablation, no more ventricular arrhythmias were induced. Cardiac magnetic resonance imaging was performed which showed large areas of late gadolinium enhancement. The patient underwent automatic defibrillator implantation. Ventricular arrhythmias were no longer documented during telemetric monitoring. In this complex case of significant arrhythmic instability in ischemic heart disease with moderate left ventricular pump dysfunction, ECMO assistance allowed us to effectively and safely perform the ablation of the arrhythmic substrate triggering the iterative episodes of VF.

PERCUTANEOUS LEFT STELLATE GANGLION BLOCK TO INCREASE VENTRICULAR FIBRILLATION THRESHOLD AND DEFIBRILLATION SUCCESS RATE IN ACUTE FULMINANT MYOCARDITIS WITH ELECTRICAL STORM

Abstract Introduction Acute fulminant myocarditis represents a predisposing substrate for life–threatening ventricular arrhythmias (VAs). Percutaneous left stellate ganglion block (PLSGB) usage has been reported for the prevention of recurrent VAs, but clinical data on its acute effect on ongoing ventricular fibrillation (VF) are missing. Case A 57–years–old man suffering gastroenteritis and fever in the past week presented in the ED with typical chest pain. ECG depicted infero–lateral ST–segment elevation, cardiac ultrasound showed a mildly reduced LVEF and coronary angiography ruled out coronary lesions. In the following hours the patient developed frequent premature ventricular complexes with R on T phenomenon triggering short coupled torsade de pointes with rapid degeneration into VF. VAs episodes, initially responsive to single DC shock, kept recurring despite intravenous (iv) amiodarone, iv lidocaine and iv correction of potassium and magnesium. The patient was therefore treated with deep sedation, intubation and ECMO VA placement; still, he reached a status of persistently ongoing VF, refractory even to DC shocks (n=20). Therefore, ultrasound–guided PLSGB using a local bolus of lidocaine 150 mg + ropivacaine 50 mg was performed. After 5 minutes, a single DC shock was delivered, effective in achieving a stable sinus rhythm at 35 bpm with no more recurrences. Despite electrical stabilization, the patient developed a severe cardiogenic shock due to bradycardia and severe biventricular disfunction, treated with vasopressin and dobutamine. In the next 48 hours we observed a significant improvement, resumption of biventricular contractility and absence of VAs recurrences, so the patient was slowly weaned off ECMO and vasopressors. Immunological tests showed Enterovirus IgM positivity, while endomyocardial biopsy was negative for inflammatory infiltrates in the analyzed sections. Cardiac MRI (performed 10 days after onset) showed edema and non–ischemic LGE in the antero–lateral and infero–lateral basal subepicardial regions of the left ventricle, LVEF was 55%. After 15 days from admission, despite ongoing amiodarone and bisoprolol, the patient developed a run of monomorphic VA of 30 beats at 170 bpm, therefore he underwent sICD implantation. Conclusion PLSGB played a key role for the acute management of refractory VF unresponsive to DC shocks, allowing for acute stabilization. More clinical data are needed on acute neuromodulation for electrical storm.

PROSTHETIC GRAFT INFECTION: WHEN ECHOCARDIOGRAPHY IS NOT ENOUGH!

Abstract A 68–year–old Caucasian male, post–Bentall procedure with a bioprosthetic valve following extensive aortic dissection involving the ascending aorta and aortic arch, presented to the Emergency Department with persistent fever for over a month. During his hospitalization, he experienced ventricular fibrillation in the setting of hypokalemia, successfully managed with Advanced Cardiovascular Life Support (ACLS) and DC shock, leading to the restoration of sinus rhythm. Subsequently, he was admitted to the Cardiovascular Intensive Care Unite. Blood tests revealed neutrophilic leukocytosis with elevated inflammatory markers, anemia, and a troponin curve consistent with myocardial injury in the context of sepsis and anemia. Echocardiography demonstrated a left ventricle of normal dimensions with globally depressed function (EF 45%), attributed to apical akinesia. The prosthetic valve was functioning normally, and there were no signs of endocarditic vegetations or pericardial involvement. A transesophageal echocardiogram confirmed the absence of vegetations. Given echocardiographic signs of myocardial ischemia, coronary angiography was performed, revealing a coronary circulation free from significant stenosis. Cultural exams showed positivity for Enterococcus faecalis. A PET–CT revealed the presence of radioisotope uptake around the vascular prosthesis situated in the aortic arch. An Infectious Disease specialist recommended antibiotic therapy with Piperacillin/Tazobactam and Teicoplanin. At the one–month follow–up, the patient remained asymptomatic, free from new febrile episodes. The follow–up echocardiogram indicated improved global systolic function, and inflammatory markers remained consistently negative. Repeat blood cultures were negative. This case illustrates a suspected endocarditis on a prosthetic valve where both transthoraci and transesophageal echocardiography yielded negative results. The use of PET–CT, on the other hand, revealed the presence of vascular graft infection, proving to be a valuable method in this clinical setting.

A PARTICULAR CASE OF CARDIAC ARREST

Abstract 88–year–old man with arterial hypertension, cognitive impairment, carrier of dual–chamber PM due to sinus node disease. Diagnosis of congenital long QT syndrome (LQT1) approximately 20 years ago during family screening (syncopal episodes in his son positive for LQT1), no history of syncope or major arrhythmias. In home therapy with mirtazapine and norvasc. He arrived in our cardiac intensive care unit for ACC on torsade de pointes trated with two cycles of CPR and 1 DC shock at 200 Joules with ROSC. On arrival ECG evidence of electrically induced ventricular rhythm, QTc 850 msec. On echocardiogram akinesia of the mid–basal segments of all the LV walls (takotsubo–like) with EF 25–30%. On coronary angiography non critical multivessel coronary disease. At laboratory tests increase of WBC, PCR and PCT, slight plateau movement of troponin, normal electrolytes. The patient underwent a chest CT scan with evidence of an inflammatory focus for which antibiotic therapy was started. Congenital long QT syndrome (LQTS) is an inherited condition characterized by prolongation of the QT interval (more than 450 ms in men and 460 ms in women), associated with repolarization abnormalities. There are three main forms transmitted via AD: LQT1, LQT2 and LQT3. The most common variant is LQT1 caused by a loss of function mutation in the KCNQ1 gene which causes a reduction in the outgoing potassium current during phase 3 of the action potential. In these patients, episodes of syncope caused by torsade de pointes, major arrhythmias and sudden cardiac death are frequent. Patients with LQTS should avoid taking drugs that can prolong the QT interval such as some antipsychotics, antidepressants (like mirtazapina that can cause QT prolongation, torsade de pointes, ventricular tachycardia and sudden cardiac death if administered at high doses or in patients with predisposing factors), antibiotics. Furthermore, there are various factors that can influence the QT prolongation: electrolyte alterations, physical stress, cerebrovascular events. The use of mirtazapine for a long period in association with takotsubo syndrome (probably triggered by underlying pneumonia) in a patient with LQTS, may have resulted in massive lengthening of the QT interval causing torsade de pointes and therefore ACC. During the hospitalization, mirtazapine was suspended and nadolol was introduced with a progressive reduction of the QT segment. No new arrhythmic events were recorded.

A VENTRICULAR TACHYCARDIA CASE NOT TREATABLE WITH TRANSCATHETER ABLATION DUE TO APICAL THROMBOSIS OF THE LEFT VENTRICLE RESOLVED WITH RADIOTHERAPY BASED ON THE NON–INVASIVE MAPPING SYSTE

Abstract The clinical case focuses on a 52–year–old man smoker, heavy alcohol consumer. In 2017 he began with sustained ventricular tachycardia (VT) effectively treated with DC–shock. The following ECG showed signs of anterior necrosis. Severe left ventricular (LV) dilatation, apical thrombosis and severe impairment of LV function were found on echocardiogram. Angiography was performed and LAD occlusion was found. Since of 68% necrosis of the LV at myocardial scintigraphy, no revascularization was performed. He underwent to a dual chamber ICD implantation and started oral anticoagulation therapy. In the following years recurrence of arrhythmic episodes, despite the optimization of antiarrhythmic therapy, led the patient to numerous hospitalizations. Unfortunately the persistence of the apical thrombosis, made transcatheter ablation NOT possible. The only chance for the patient remained stereotactic arrhythmia radioablation. But which area of the LV to highlight as responsible for the arrhythmia and how to program the radiotherapy treatment plan was a challenging problem. We proposed in March 2023 non–invasive mapping of arrhythmia using Cardioinsight. The patient performed heart high–resolution computed tomography (CT) for the anatomical reconstruction with precise spatial resolution of all LV aereas and surrounding structures. A 252–electrode vest is applied to the patient’s torso and connected to the system Cardioinsight. A programmed ventricular stimulation was performed using ICD inducing two VT morphologies. Through electroanatomical mapping we identified the mid LV antero–septal and infero–septal sites as target areas. Thanks to multidisciplinary team a personalized treatment plan was created to deliver an effective lesion in the target area and minimize exposure to nearby organs at risk. The treatment was generated, optimized and delivered by TrueBeam, lasted 3 minutes and no complications arose. The patient was quickly discharged in good clinical condition. After 3 months of clinical well–being he was hospitalized for a single episode of VT. Up to now no hospitalizations occurred. This treatment may represent a "bail–out" choice in patients with advanced heart failure with arrhythmic storm who have exhausted all other therapeutic options.

THE CONUNDRUM OF DRUG INTERACTIONS AND HOLTER MONITORING: LAMIN GENE MUTATION DISCOVERED BY A TORSADE DE POINTES EPISODE FOLLOWED BY OUT–OF–THE–HOSPITAL RESUSCITATION

Abstract The prolongation of the QTc interval on the electrocardiogram is known to be associated with an increased risk of developing life–threatening ventricular arrhythmias such as torsades de pointes (TdP). QTc values exceeding 500 ms can double or even triple the risk of TdP. Many drugs, including amiodarone and some SSRI antidepressants like paroxetine, can prolong the QTc interval. A 57–year–old patient experienced cardiac arrest during an overnight Holter recording prescribed to exclude brady–tachy syndrome in the presence of persistent atrial fibrillation. ECG ambulatory monitoring revealed significant bradycardia with the onset of idioventricular rhythm, followed by TdP triggered by premature ventricular contractions, subsequently degenerating into ventricular fibrillation. The patient was resuscitated by family members and later by emergency medical personnel using 3 DC shocks, leading to the restoration of spontaneous circulation. The patient was transferred to the cardiology intensive care unit where a coronary angiography showed normal results. Blood tests indicated low potassium levels (3.3 mEq/L), with a moderately reduced left ventricular ejection fraction at 45%. The patient was discharged after ICD implantation and during the diagnostic follow–up the genetic testings for long QT syndrome were negative, but showed a mutation of the LMNA lamin A/C gene. During the two months previous to hospital admission, the patient had complained of fatigue in the presence of atrial fibrillation with a low ventricular response. Nonetheless, she had been prescribed oral amiodarone to optimize the chances of successful electrical cardioversion, in combination with paroxetine that the patient was already taking at home. The combination of these two drugs and the patient‘s idiopathic bradycardia contributed to a marked prolongation of the QT interval, leading to TdP degenerated into ventricular fibrillation. This case, notable for the prolonged recording of ventricular fibrillation and subsequent resuscitation chest compressions during a Holter monitoring, suggests caution in the use of antiarrhythmic drugs unless strongly indicated in the presence of potentially ominous drug interactions. It is encouraging to note how the widespread adoption of cardiopulmonary resuscitation culture has enabled individuals who might not have otherwise received medical attention to be effectively resuscitated.

A COMPLEX POST CARDIAC–ARREST SYNDROME: FROM UNCERTAIN NEUROLOGICAL OUTCOME TO HEMORRHAGIC COMPLICATION

Abstract A 49–years–old woman with type II diabetes mellitus, hypothyroidism and Churg–Strauss syndrome experienced chest pain with loss of consciousness. Emergency service was called and CPR promptly started. Cardiac arrest with shockable rhythm was documented, DC–shock performed with sign of anterior STEMI after ROSC, then refractory cardiac arrest appeared. The patient was centralized in our hospital and VA–ECMO was positioned through a percutaneous femoral access in cath–lab. Coronary angiography showed acute occlusion of the mid–proximal LAD and subocclusive stenosis of the dominant Cx for which PCI with DES was performed, then intra–aortic balloon pump (IABP) was implanted. At ICCU admission the patient was supported by ECMO and IABP with MAP 65 mmHg and lactates 3.5 mmol/L. Echocardiography and chest X–ray showed severe biventricular dysfunction and pulmonary overload (Fig 1). She was ventilated via ECMO circuit and mechanical ventilation setting protective TV values of 6 ml/kg. Diuresis was good with low dose of furosemide, lactates progressively decreased. Temperature control was set within 36°C with the cooling system of the ECMO circuit. Cardioaspirin, ticagrelor and bivalirudin were administered. At early neurological stratification EEG documented absence of epileptiform anomalies, responsiveness to painful stimuli, SSPE showed normal and symmetrical morphology, NSE at 48 h was 59 ng/mL, she opened eyes and performed simple orders. Levosimendan was administered with partial recovery of the right ventricular dysfunction leading to ECMO removal on 5th day. Due to poor consciousness recovery despite sedation reduction, percutaneous tracheostomy was performed on 8th day, IABP removed and the following day all vasopressors suspended. Neurological improvement allowed transition to spontaneous breathing and weaning from mechanical ventilation; on 19th day tracheostomy was removed. Massive enterorrhagia appeared after ECMO removal (figure 2). The colonoscopy showed ischemic pancolitis, therefore ticagrelor was suspended. On 18th day clopidogrel was reintroduced based on hemoglobin stability and endoscopic improvement. She was discharged from the cardiology department after a total length of stay of thirty days, with normal neurological status, no motor deficits, recovery of left and right ventricular function, stable hemoglobin levels.

A CATASTROPHIC COMPLICATION OF A CHEST TRAUMA: A CASE REPORT

Abstract A 43 year old patient came to the Emergency Department of our hospital for a cardiology visit. The EKG revealed polymorfic ventricular tachycardia with a heart rate of 160 bpm so that he was admitted to the Intensive Care Unit. In 2005, he had a post traumatic myocardial infarction after a car accident treated with the implantation of one drug eluted stent on the descending artery. Three years later, a single–chamber ICD was placed. On admission in Intensive Care Unit, cardiac auscultation revealed normal heart sounds without murmurs. No lower extremity edema was observed. A transthoracic echocardiogram showed general hypokinesis with reduced global left ventricle systolic function and no pericardial effusion (EF=20%). The patient was haemodynamically stable, the blood pressure was of 130/80 mmHg. The device was also interrogated and it showed six ineffective attempts of antitachycardia pacing. After that, the patient was given an effective intracavitary shock. Moreover, the patient underwent coronary angiography which showed no disease progression and patency of the stent previously implanted on the proximal descending artery. The electrophysiological study was performed and subsequently 3 ventricular ectopic focuses were effectively ablated. Multiple DC shocks were delivered during the procedure and the atrioventricular bundle was damaged. In consideration of the clinical features and the left ventricular reduced ejection fraction, an indication to the implantation of CRT–D was given. Conclusions This case report describes a rare complication of a blunt chest trauma. A young patient with no significant past medical history suffered a dissection of the coronary descending artery resulting in ST–elevation myocardial infarction. The mechanism of coronary occlusion following blunt chest injury may be due to: shear force applied to the coronary arteries leading to intraluminal thrombosis; vascular rupture; embolism to the coronary arteries; fissuring of an atherosclerotic plaque with dislodgment of plaque material; vascular spasm at the site of the injury. Anyway, severe left ventricular dysfunction caused the developing of polymorfic ventricular tachycardia which was unresponsive to medical treatment and was treated with ablation.

The significance of early-onset malignant arrhythmias in ST-elevation myocardial infarction patients treated with primary percutaneous coronary intervention and their relationship with biomarkers

Background/Aim. Patients who were treated with primary percutaneous coronary intervention (pPCI) and survived ventricular tachycardia (VT) and ventricular fibrillation (VF) in the first 48 hrs after ST-elevation myocardial infarction (STEMI) had, in most investigations, a similar long-term prognosis of the outcome, compared to those patients who did not have VT and VF during the first 48 hrs after STEMI. The aim of the study was to determine the association of myocardial infarction markers: creatine kinase-MB fraction (CK-MB), heart failure marker ? B-type natriuretic peptide (BNP), and systemic inflammation factor ? C-reactive protein (CRP) with early VT and VF onset, in relation to patient mortality during the first six months after STEMI. Methods. The retrospective study included 971 patients with STEMI treated with pPCI for ten years. VF and sustained VT (sVT) were detected outside of the hospital and during the first 48 hrs of hospitalization. Results. During the first 4 8 hrs from admission, 1 08 ( 11.1%) patients had life-threatening arrhythmias, of which 75 (69.4%) had VF, and 33 (30.6%) had sVT and were treated with direct current ? DC shock and intravenous amiodarone. Intrahospital mortality was significantly higher in patients with VF/sVT in the first 48 hrs compared to patients without VF/sVT (14.8% vs. 5.7%, p = 0.001). BNP level had higher accuracy in the prediction of six-month death than the maximum blood level of CRP in patients without VF/sVT after 48 hrs. However, in patients with early-onset malignant arrhythmias, BNP showed a lower level of accuracy in predicting the six-month mortality, a s did the CRP values, which had almost the same level of accuracy. Admission glycemia had a much lower predictive value in both groups of patients compared to BNP and C RP [ 0.705 ( 0.628? 0.781), p &lt; 0.001 and 0.662 (0.521?0.803), p = 0.046, respectively]. In either of the groups, maximum CK-MB levels were not significant in predicting the six-month all-cause mortality. Conclusion. Our study indicates that STEMI patients with early onset of VF and sVT, treated with pPCI, with a high BNP level, have a statistically significantly higher mortality rate compared to patients with a lower BNP level.

Abstract 15009: Extra-Low Energy Defibrillation With Epicardial Implantable Cardioverter Defibrillator Networks With Electrically Conductive Fibers in Disease Models

Introduction: We previously reported that extra-low energy (&lt;0.6J) defibrillation is possible with the epicardial ICD net lead system (Ep-ICD) in normal canine hearts. Hypothesis: The aim of this study was to test whether the Ep-ICD can terminate ventricular fibrillation (Vf) with the same energy in two disease models (heart failure and long QT syndrome (LQT)). Methods: 1. Ep-ICD was constructed by fine tungsten fibers at the top and bottom of the cardiac mesh (Figure 1), connected to the RV and SVC coils of the DF-1 lead, respectively. 2. Heart failure was induced by rapid right ventricular pacing (170 bpm, 8 weeks). 3. Vf was induced by placing a 9V battery on the surface of the heart. DC shock was delivered with a minimum energy of 0.4J (Medtronic Viva XT). 4. Defibrillation threshold (DFT) was defined as 75% of defibrillation success. 5. LQT was simulated by reducing the conductance (Gk) of the IKS current by (x 1.0(CTL) or 0.8(LQT)) by computer simulation. Results: 1. DFT(J) of Ep-ICD in the canine HF model: 0.8, 1.2, 1.2. 3, Minimum DF energy(J): 0.6, 0.6, 0.8, 2. Maximum DF energy(J): 1.2, 1.6, 5, 52. Immediate return to sinus rhythm (SR) was achieved in most cases after DC delivery. In a small number of cases, brief periods of VT occurred, with rapid return to SR. No tachycardic arrhythmias occurred after return to SR. 3. The DFT was 0.39 for LQT and 0.52 for CTL. Conclusions: 1. DFT of Ep-ICD increased from 0.6 J in normal canine heart to 1.2 J in canine HF model, but still much lower energy used in current ICD system (36 J). 2. The Ep-ICD lead system is the least traumatic and still within the acceptable range while conscious. 3. DFT of LQT with Ep-ICD is 25% lower than normal heart. 4. Ultra-low energy DC can avoid conduction abnormalities or malignant arrhythmias after shock. Hearts return to SR immediately. 5. Ep-ICD can deliver the DC shock before loss of consciousness, improving quality of life and safety of ICD therapy.

Abstract 14930: A Case of Flecainide Toxicity Causing Wide Complex Tachycardia, Unresponsiveness, Hemodynamic Instability and Pacemaker Under-Sensing

Introduction: Flecainide toxicity (FT) is an uncommon yet potentially lethal complication. We report a case of FT precipitated by acute kidney injury (AKI) in a patient with paroxysmal atrial fibrillation (AF) and a permanent pacemaker (PPM), who presented with wide complex tachycardia (WCT) and PPM under-sensing. Case presentation: An above 85-year-old female with paroxysmal AF and a PPM presented with an episode of unresponsiveness. While en route to the ED via ambulance, she had another episode associated with hemodynamic instability precipitated by a WCT. She regained consciousness after 1 biphasic DC shock. An EKG in the ED revealed sinus rhythm with atrial under-sensing and pacing spikes during ventricular refractory period (see picture). Laboratory data were consistent with AKI and normal electrolytes levels. PPM interrogation showed atrial under-sensing. Flecainide was discontinued and following drug washout the EKG changes resolved and the QRS normalized. She was discharged on amiodarone with no recurrence of arrhythmias on follow up. Discussion: Flecainide is Class 1C Antiarrhythmic drug that blocks fast the sodium channels. Prolongation of PR interval and QRS duration, in addition to supraventricular and ventricular arrhythmias, may occur with FT. Left ventricular dysfunction, myocardial scar, and high serum levels are considered risk factors for proarrhythmia. The drug half-life is prolonged in patients with renal disease/AKI. There are limited data on PPM malfunction due to FT, but it may cause increased pacing thresholds and failure to capture. Sodium bicarbonate, lidocaine, and ECMO have been used in treatment. Conclusion: FT can lead to lethal arrhythmias and PPM malfunction. Since flecainide serum levels are not always readily available, its diagnosis can be challenging. Therefore, physicians should be aware of the clinical presentation and EKG changes that accompany FT.

C71 EFFICACY AND SAFETY OF PERCUTANEOUS LEFT STELLATE GANGLION BLOCK IN PATIENTS WITH REFRACTORY ELECTRICAL STORM

Abstract Background Neuromodulation by percutaneous stellate ganglion block (PSGB) with local anaesthetic has proved its antiarrhythmic effect suitable for an emergency setting. Purpose To assess the efficacy and safety of PSGB performed with an anterior anatomical approach in patients with refractory electrical storm refractory. Methods Patients with electrical storm at the Policlinico S.Matteo of Pavia were enrolled from November 2017 to January 2022. Left PSGB (PLSGB) was performed after failure of at least one intravenous antiarrhythmic drug. Its repetition or a continuous infusion of the local anaesthetic were considered in selected cases. Clinical data, characteristics of the block and complications were collected. The efficacy was evaluated by comparing the number of arrhythmias treated with ATP or DC–shocks by external or internal defibrillator 1 hour before the block with 1 hour after the block. Per–patient efficacy was assessed by comparing the number of ATP/shocks in the 12 hours before the first procedure with that in the 12 hours after the last one. Results 37 patients were enrolled: 76% male, mean age 65 years; 11 with dilated cardiomyopathy, 18 with chronic ischemic heart disease, 11 with STEMI, 3 with NSTEMI, 1 with ARVC and 1 with drug intoxication. A total of 62 PLSGBs were performed: 19 for VT, 26 for VF and 17 for both VT and VF episodes; 15 on intubated patients, 4 in extracorporeal circulation, 7 in cardiogenic/septic shock, 28 on patients on single antiplatelet therapy, 11 on dual antiplatelet therapy, 33 on anticoagulant therapy. PLSGBs were performed during intravenous infusion of antiarrhythmics (amiodarone in 30, lidocaine in 37 procedures). The local anaesthetic used was lidocaine in 27/62 PLSGB, bupivacaine in 6/62 and both in 29/62. The per–procedure analysis showed a significant reduction of the number of ATP/shocks in the hour after PLSGB compared with the hour before [0 (0–0) vs 5 (1–8) p&amp;lt;0.001]. Similarly, in the per–patient analysis, the number of ATP/shocks significantly decreased in the 12 hours after the PLSGB compared with that in the 12 hours before [0 (0–1.3) vs 7 (4.8–12.5) p&amp;lt;0.001]. No complications occurred. Conclusions This is the case series with the highest number of PLSGB for antiarrhythmic purposes in literature and it confirms its efficacy and safety in refractory electrical storm. The exiguity of the equipment required makes the anatomical approach suitable to be easily performed by cardiologists.

P136 “THERE’S NO TWO WITHOUT THREE”: A STRANGE CASE OF RECURRENT CORONARY EMBOLISM

Abstract Background A 68 year–old woman with rheumatic heart disease underwent surgery replacement of aortic and mitral valves with mechanical prostheses 20 years ago, and since then has been in VKAs therapy. One year after the operation, she was hospitalized for ischemic stroke without relics. For detection of 2:1 block on the ECG Holter/24h a PM was implanted. After 4 years, she had an acute coronary syndrome (ACS) with VF (treated with DC–Shock). Coronary angiography (CA) showed no coronary stenosis. It was replaced PM to ICD. In 2017, she had a TIA and a mitral prosthesis dysfunction was detected from EET with hemidisk thrombosis. After CA, mitral valve replacement was performed but on the 2nd day after surgery she had an anterior STEMI caused by the occlusion of LAD. PTCA and stenting were performed. In October u.s. the patient was referred to the Emergency room for typical angina. An inferior–posterior STEMI was revealed to ECG. CA highlighted embolic occlusion of Cx and good result of prior LAD’s stenting. After multiple and ineffective attempts, invasive recanalization’s procedure was interrupted considering both patient’s high bleeding risk and embolic aetiology. Excluded prosthetic thrombosis and thrombophilic anomalies, patient was discharged in clinical stability with SAPT+ VKAs therapies. Discussion Coronary embolism (CE) represents 3% of ACS because the coronary arteries are protected from embolism thanks to their acute’s angle origin from the aorta. Embolism origin is various and it can originate from left (LAA, LVx, valvular, prosthetic structures) or right heart sections (paradoxical embolism in the case of PFO),generally during AF. In our case, prosthetic origin is the most probable embolic source as demonstrated by cerebral ischemic (TIA/stroke) and coronary events (first anterior then inferior–posterior STEMI) after valves surgery. Treatment consists of restoring antegrade flow without DES implantation, using if possible intracoronary thrombolysis or thromboaspiration. In secondary prevention, embolism sources removal and anticoagulant therapy are mandatory. In our case we recommended SAPT+VKAs with strict INR’s control (range 3.5–4). Conclusions Although CE is a rare and potentially fatal phenomenon it should be suspected in the absence of coronary atherosclerosis and in the presence of predisposing conditions such as those mentioned above. This case demonstrates that CE can occur in absence of prosthetic thrombosis with suboptimal INR control.

P162 ARRHYTHMIC MITRAL VALVE PROLAPSE OCCURRING AS ABORTED SUDDEN CARDIAC DEATH

Abstract Mitral valve prolapse (MVP) is the common valvular heart disease, with a prevalence about 1–3% in the population. MVP is characterized on echocardiography by an abnormal systolic displacement of mitral valve leaflets into left atrium (LA) ≥ 2 mm above the mitral annulus. We described a clinical case of a 15 years–old boy with a first clinical presentation of out–of–hospital cardiac arrest related to ventricular fibrillation (VF) with a successful resuscitation after 2 DC shocks. Retrospectively, an episode of loss of awareness reported as post–minational. No familiar history of sudden cardiac death (SCD) or MVP was noticed. In the emergency room, the patient was hemodynamically unstable and was sedated and intubated. The surface electrocardiogram (ECG) showed sinus rhythm, QRS with fragmentation, and frequent monomorphic isolated premature ventricular contractions (PVCs) with RBBB/LAFB configuration.Frequent monomorphic PVCs with bigeminy was observed during continuous ECG monitoring, so the patient was treated with magnesium sulphate and metoprolol. The patient was subsequently weaned from ventilation support, presenting good gas exchange and without neurological sequalae. The 24h Holter monitoring showed an average of 53 bpm, extremely rare supraventricular extrasystoles, high incidence of monomorphic PVCs (23% of the total beats) with 4 couplets. Transthoracic echocardiography documented normal size and thickness with systolic function (GLS –21%, mild asynchrony of posterior basal segments), bi–leaflet prolapse associated to mild–moderate mitral regurgitation, and mitral annular disjunction (MAD) of 6.2 mm. The late gadolinium enhancement cardiac magnetic resonance showed bi–leaflet prolapse with mild insufficiency and maximum MAD 9 mm, mild LA dilatation, and slightly dilated both ventricles, without regional wall motion abnormalities; no scar or fibrosis at the late gadolinium enhancement was observed. According to guidelines, the patient received a subcutaneous implantable cardiac defibrillator for the secondary prevention of SCD and maintained under betablockers in order to control the arrhythmic burden. The genetic sampling did not show any pathogenetic mutation potentially related to cardiomyopathies or channelopathies. This case show an arrhythmic MVP complex with probably posterior papillary muscle source. The early PVCs with R/T constituted a possible trigger of VF. The betablocker therapy exhibited a full suppression of extrasystolic burden.

P88 CARDIAC INVOLVEMENT IN FOUR NOVEL NESPRIN–1 GENETIC VARIANTS

Abstract Background Nesprins are proteins encoded by synaptic nuclear envelope (SYNE)–1 and –2 genes, that concur, together with lamin A/C and emerin, to nuclear envelope function. Almost 140 disease–related variants were identified, mostly resulting in central nervous system and skeletal muscle disorders; only a few were associated with cardiomyopathy, mostly with relatively late onset and no specific arrhythmic profile. Purpose To describe cardiac involvement in 4 novel SYNE1 variants. Methods 189 patients underwent genetic analysis in our center (2019–2022) for suspected genetic cardiomyopathy (TruSight Cardio panel, Illumina); 72% had a positive genetic report, including pathogenic/likely pathogenic or variants of undetermined significance (VUS). Among them, 4 (2%) males presented with a sole SYNE1 heterozygous VUS (figure). Results None had muscle or neurological involvement. Patients 1 and 2 had negative family history (FH) and underwent pacemaker implantation under 50 years old for high–grade atrioventricular block (AVB). Transthoracic echocardiography (TTE) and cardiac magnetic resonance (CMR) showed a mildly impaired left ventricular ejection fraction (LVEF) without oedema or fibrosis. During 3 and 6 years of follow–up (FU), several non–sustained episodes of fast ventricular tachycardia (VT) and of atrial tachycardia occurred. Patient 3 is a 55–year–old man with negative FH and a left bundle branch block (LBBB) known since the age of 45.In 2021, while playing football, he suffered a cardiac arrest due to ventricular fibrillation treated with two DC shocks; ECG showed first–degree AVB and LBBB; TTE and CMR revealed a mildly impaired LVEF without oedema or fibrosis. A subcutaneous ICD was implanted, which recorded 3 atrial fibrillation episodes in a 1–year FU. Patient 4 is a 49–year–old man, with FH of sudden death (mother’s brothers at 40 and 50 years) and of polycystic kidney, who underwent renal transplant. He had left anterior fascicular block and suffered 2 episodes of sustained monomorphic VT from the right ventricle treated with ablation. TTE and CMR showed mild LV concentric hypertrophy with normal LVEF, segmental abnormalities in right and LV strain, no fibrosis. Conclusions SYNE1 genetic variants were found to be associated with a complex cardiac phenotype, including early onset conduction disease, atrial and ventricular arrhythmias, and cardiomyopathy. Further studies are needed to determine the functional significance of the variants.

P325 CARDIAC SARCOIDOSIS PRESENTING WITH ATRIOVENTRICULAR BLOCK AND SUBSEQUENT CARDIAC ARREST: A CASE REPORT

Abstract A 53–year–old male patient with no significant past medical history and no familiar history for cardiac diseases presented to the emergency department for asymptomatic bradycardia. The ECG showed complete atrioventricular block in the absence of pathological findings on the echocardiogram and no coronary lesions were found on coronary angiography. The patient underwent pacemaker (PM) implantation. A few months later the patient suffered from cardiac arrest in sustained ventricular tachycardia, effectively treated with DC shock. The echocardiogram showed mild right ventricular dilation and dysfunction with regional wall motion abnormalities, especially in the subtricuspid site. Cardiac magnetic resonance imaging (MRI) showed focal areas of delayed enhancement with a non–ischaemic pattern and distribution with a hook sign, highly suggestive of cardiac sarcoidosis. FDG PET showed cardiac, hepatic, splenic, and lymph nodal uptake. In the suspicion of systemic sarcoidosis, an hepatic biopsy was performed, being the liver the most accessible site. The histological examination showed the presence of non–caseating granulomas. Therefore, a diagnosis of Systemic Sarcoidosis (SS) with Cardiac involvement was made and the PM was upgraded to CRT–D in secondary prevention. The patient was discharged with cortisone therapy. Three months after discharge, a new total body PET–CT scan was performed and showed, in comparison to the previous one, the absence of areas of significant hypermetabolism in the cardiac, hepatic and bone fields. Cardiac sarcoidosis (CS) is a rare inflammatory granulomatous myocardial disease of unknown etiology that should be suspected in young patients with atrioventricular conduction disturbances and complex ventricular arrhythmias. The diagnostic approach is challenging: imaging techniques (MRI, PET) can be suggestive of CS but biopsy with histological demonstration of the non–caseous granuloma is mandatory. Endomyocardial biopsy (which has suboptimal sensitivity due to focal lesion) could be avoided if there is a more accessible and less invasive extracardiac site for biopsy. Early diagnosis relies on multidisciplinary collaboration and is essential for staging and long–term management of the disease and prevention of sudden cardiac death. Cortisone therapy remains the mainstay of treatment.

P318 A LETHAL SPASM

Abstract S.F.E.G., a 52–year–old woman of Filipino origin, with no previous cardiology except arterial hypertension under therapy, came to our attention for a witnessed episode of cardiac arrest at home. Rescued by the emergency medical team, who found ventricular fibrillation at presentation, and performed ACLS with ROSC obtained after 3 DC shocks. The first ECG was unremarkable (sinus rhythm, diffuse ST depression). Total body CT was negative. Admitted to the Coronary Unit, the echocardiogram was normal for cavity dimensions and kinetics, as well was coronary angiography except for “short intramyocardial course in the second segment of LAD with slight systolic "milking". In the following days, however, there was a significant rise in HsTnI (1,000 → 47,000 ng/L), with concomitant sudden ventricular bigeminy and negative anterior T waves, akinesia of the anterior apical segments of the LV at cardiac ultrasound (not present at admission), in a patient still intubated and therefore with a non–evaluable clinic. Coronary angiography was repeated, which highlighted this time significant vasospasm affecting the middle segment of the LAD, that regressed after intracoronary nitrates. She was extubated without neurological sequelae, and subjected to ICD implantation by secondary prevention. To treat the vasospastic angina she was discharged with calcium channel blockers at the maximum tolerated dosage, as per guidelines (diltiazem 120mg TID + nifedipine 60mg BID). One month later the patient returned to our attention due to worsening dyspnoea, abdominal pain and anasarca (ascites, bilateral pleural effusion, peripheral oedemas). Hospitalized in a medical setting and treated with diuretics for suspected heart failure, despite the echocardiogram showing preserved biventricular systolic function, normal diastolic function, no valve disease, no pericardial effusion. BNP was 359 pg/mL, subsequently decreasing to 148 pg/mL. After excluding every other possible causes even with total body CT, our hypothesis was that of calcium channel blocker collateral effect (vasodilatory edema). We tapered the dosage until only diltiazem 60mg TID was mainteined, obtaining a significant clinical improvement (weight loss by 10 kg), without further recurrence of coronary vasospasm. This clinical case demonstrates the potential lethality of coronary vasospasm, and a rare complication during therapy with high doses of calcium channel blockers, with very few cases described in the literature.

C34 AN UNUSUAL CASE OF CARDIAC ARREST DUE TO TRAUMA–INDUCED QT PROLONGATION

Abstract Background QT prolongation is a well–known cause of sudden cardiac death due to polymorphic ventricular tachycardia triggered by early afterdepolarizations. Acquired long QT is a common finding in several clinical scenarios and invariably represents a high risk feature. Case Report An 84 years–old woman presented to our emergency department (ED) after experiencing a blunt chest trauma due to a car accident. She reported mild dyspnea and chest pain exacerbated by breathing and movement while denied palpitations and loss of consciousness. Baseline ECG showed atrial fibrillation with normal ventricular rate and a prolonged QT interval (QTc 640, Fig 1A) not present at previous ECGs. She did not assume any QT–prolonging drug and laboratory tests at admittance revealed troponin I values slightly elevated (29,6 ng/ml; n.v.: &amp;lt;11,6 ng/l) and no other significant abnormalities. A CT scan demonstrated a displaced fracture of the sternal body. Due to the QT prolongation, the patient was admitted for ECG monitoring.. During the stay in our ED the patient suffered a cardiac arrest. A torsade des pointes triggered by a late–coupled premature ventricular complex (PVC) was documented (Fig 1B). The arrhythmia was interrupted with external DC shock and magnesium solfate infusion was started. The coronary angiography demonstrated normal coronary arteries. The patient underwent cardiac magnetic resonance (CMR) four days later which showed transmural necrosis of the middle third of the lateral wall of the left ventricle at the insertion of the anterolateral papillary muscle (Fig 2). No further ventricular arrhythmias were observed and the patient was discharged after QTc normalization. Cardiac arrhythmias are a rare complication of cardiac contusion ranging from isolated PVCs to atrial or ventricular fibrillation. However, the role of the ECG in this peculiar subset is unclear. The most common ECG abnormalities are non specific ST–T wave changes, whereas in our case the marked QTc prolongation resulted in a closer monitoring of the patient allowing a prompt recognition of cardiac arrest. On the other hand CMR proved to be an effective method to identify a cardiac injury showing the typical pattern of myocardial damage associated with cardiac contusion (stress–induced lesions at the insertions of papillary muscles due to sudden increase of left ventricular pressure) and, thus, could be adopted as a useful tool to identify patients at higher risk for arrhythmic complications.