Search Results for: Antiaritmici (Amiodarone)

Introduction
New-onset supraventricular arrhythmia (NOSVA) is the most common arrhythmia in patients with septic shock and is associated with haemodynamic alterations and increased mortality rates. With no data available from randomised trials, clinical practice for patient management varies widely. In this setting, rate control or rhythm control could be beneficial in limiting the duration of shock and preventing evolution to multiorgan dysfunction.

Methods and analysis
The Control Atrial Fibrillation in Septic shock (CAFS) study is a binational (French and Belgium), multicentre, parallel-group, open-label, randomised controlled superiority trial to compare the efficacy and safety of three management strategies in patients with NOSVA during septic shock. The expected duration of patient enrolment is 42 months, starting from November 2021. Patients will be randomised to receive either risk control (magnesium and control of risk factors for NOSVA), rate control (risk control and low dose of amiodarone) or rhythm control (risk control and cardioversion using high dose of amiodarone with external electrical shock if NOSVA persists) for 7 days. Patients with a history of SVA, NOSVA lasting more than 48 hours, recent cardiac surgery or a contraindication to amiodarone will not be included. We plan to recruit 240 patients. Patients will be randomised on a 1:1:1 basis and stratified by centre. The primary endpoint is a hierarchical criterion at day 28 including all-cause mortality and the duration of septic shock defined as time from randomisation to successful weaning of vasopressors. Secondary outcomes include: individual components of the primary endpoint; arterial lactate clearance at day 3; efficacy at controlling cardiac rhythm at day 7; proportion of patients free from organ dysfunction at day 7; ventricular arrhythmia, conduction disorders, thrombotic events, major bleeding events and acute hepatitis related to amiodarone at day 28; intensive care unit and hospital lengths of stay at day 28.

Ethics and dissemination
The study has been approved by the French (Comité Sud-Ouest et Outre-Mer II, France, registration number 2019-A02624-53) and Belgian (Comité éthique de l’hôpital Erasme, Belgium, registration number CCB B4062023000179) ethics committees. Patients will be included after obtaining signed informed consent. The results will be submitted for publication in peer-reviewed journals.

Trial registration number
NCT04844801.

Circulation, Volume 150, Issue Suppl_1, Page A4143264-A4143264, November 12, 2024. Background:R-on-T phenomenon occurs when an electrical stimulus is delivered at a critical point during ventricular repolarization. This can initiate ventricular arrhythmias like polymorphic ventricular tachycardia (PMVT). We describe a case of ventricular pacemaker spikes delivered on the T wave causing PMVT.Case:A 53-year-old female with CAD s/p stent, postpartum cardiomyopathy s/p Bi-V CRT-D (Boston Scientific G124), and paroxysmal atrial fibrillation presented for elective endoscopy and colonoscopy to evaluate her dysphagia and abdominal pain. Her CRT-D was reprogrammed from DDD pacing with lower rate limit (LRL) 50 bpm to an asynchronous Bi-V DOO mode at 50 bpm (‘electrocautery mode’) for the procedure (tachy therapy disabled). Her LV-RV offset was 40 msec. Prior to receiving sedation or medications, she was found unresponsive. Telemetry showed Spike-on-T phenomenon which initiated PMVT. She was externally defibrillated with 200J and received magnesium and an IV amiodarone bolus. She returned to sinus rhythm, but one minute later had another Spike-on-T event initiating PMVT. She was successfully defibrillated with 360J. Post-shock EKG showed an asynchronous Bi-V paced rhythm at 50 bpm.Decision Making:The patient was admitted to the CCU for post-resuscitation care. Her electrolytes and cardiac enzymes were unremarkable. Her CRT-D was reprogrammed to DDD 80-140 bpm. Transthoracic echocardiogram showed normal biventricular systolic function. Cardiac catheterization did not show obstructive CAD. After reprogramming of her device, she had no further events. After initial treatment with IV amiodarone load, she was discharged home on oral magnesium gluconate.Discussion:The only intervention prior to her procedure was device reprogramming (DDD 50 bpm to DOO 50 bpm). Telemetry showed pacer spikes initiating PMVT. Given the LV-RV offset of 40 msec, she would have received these two tightly coupled pacemaker spikes in an asynchronous mode, in this unfortunate instance during her T wave. While her bowel preparation may have led to electrolytes abnormalities, post-resuscitation electrolytes were normal. Fortunately, she received prompt therapy and was reprogrammed with increased LRL.Conclusion:We described a case of Spike-on-T PMVT prior to colonoscopy without obvious provocation other than asynchronous pacemaker spikes. Reprogramming devices in DOO mode with increased LRL may prevent PVCs and asynchronous pacemaker spikes from triggering PMVT.

Circulation, Volume 150, Issue Suppl_1, Page A4145899-A4145899, November 12, 2024. Introduction:Premature Ventricular Contractions (PVCs) are often a benign arrhythmia. However, those originating from the Purkinje system can result in fatal arrhythmias. One example is PVCs originating from the moderator band (MB) within the right ventricle (RV) of the heart. We present a case of PVCs originating from the MB triggering idiopathic ventricular fibrillation (VF) and electrical storm.Case:A previously healthy 49-year-old woman was admitted following a witnessed VF cardiac arrest. She had recurrent episodes of VF, initially treated with Amiodarone and Procainamide which failed to suppress the recurrent VF. She received 54 external defibrillations before a transvenous pacer (TVP) was placed to override the PVCs at a pacing rate of 110 bpm. Post-resuscitation ECGs revealed frequent PVCs originating from the RV free wall, potentially from the lateral part of MB (Figure 1). Quinidine was added to suppress the PVCs ultimately allowing removal of the TVP. Transthoracic Echocardiogram revealed normal cardiac function and a prominent MB. A cardiac MRI was performed showing no infiltrative disease or any other abnormalities. The patient underwent sympathectomy and defibrillator placement. Despite recurrent cardiac arrest, she had excellent neurologic recovery and was subsequently discharged on Quinidine.Discussion:MB extends from the septal wall to the base of the anterior papillary muscle in the RV, carrying Purkinje fibers(PF) from the right bundle branch as it exits the septum. Purkinje fibers have been shown to initiate arrhythmias by several mechanisms including enhanced automaticity, triggered activity and re-entry. In the genesis of PVCs, triggered activity is the likely mechanism. This can degenerate into VF in a structurally normal heart, hence the term “idiopathic VF”. Familiarity with this entity and ECG features of MB ectopy leads to timely management and may potentially prevent lethal arrhythmias in symptomatic patients with such PVCs. Further studies are required to fully understand the arrhythmogenic mechanisms and the optimal management approach for MB ectopy.

Circulation, Volume 150, Issue Suppl_1, Page ASa307-ASa307, November 12, 2024. Background:Elevation of the head and thorax (HUP) in combination with active compression decompression (ACD) cardiopulmonary resuscitation (CPR) and an impedance threshold device (ITD) is starting to be used clinically by first responders. Extracorporeal membrane oxygenation in cardiac arrest (ECPR) for refractory cardiac arrest is also increasingly used and evolving. The potential benefit of ACD+ITD HUP CPR with ECPR is unclear.Aim:Demonstrate superior incidence of survival with ACD+ITD HUP CPR versus ACD+ITD CPR flat in an animal model that includes salvage with ECPR.Methods:Female and male Yorkshire-hybrid swine (~40 kg) were sedated and anesthetized. After intubation, bilateral percutaneous venous and arterial access were obtained. High fidelity micromanometer pressure transducers were used to measure arterial and venous pressures. Regional cerebral tissue oxygenation (rSO2) was also continuously monitored. Ventricular fibrillation was induced and left untreated for 15 minutes. During this time, animals were randomized to 1) HUP CPR or 2) flat CPR, and ACD+ITD CPR in both groups was then performed for 45 minutes. At 44 minutes, epinephrine and amiodarone were given and defibrillation attempted up to 3 times. If return of spontaneous circulation (ROSC) was not obtained, ECPR was then performed and continued for up to 6 hours. Neurological assessment was performed at 24 hours post arrest by a veterinarian blinded to the intervention. A Fisher’s exact test was used to compare outcomes between groups and an unpaired t-test for continuous data.Results:In this ongoing study (n=17), 8 animals were randomized to HUP and 9 to flat. After 44 minutes of CPR, mean ± SD rSO2 (%) was 63 ± 7.7 for the HUP group and 54.7 ± 6.6 for the flat group (p = 0.04). ROSC was achieved in 4/8 (50%) in the HUP group and 4/9 (44%) in the flat group (p = 1.0). ECPR was performed in 3/8 (37.5%) in the HUP group and 5/9 (56%) in the flat group (p = 0.64). Most animals (7/8, 88%) had ECPR performed successfully. ROSC was not obtained and ECPR deemed futile in one HUP animal. At 24 hours, 3/8 (37.5%) of the HUP animals and 0/9 (0%) of the flat animals survived (p= 0.08). One HUP animal (12.5%) survived without any neurologic deficit. None of the animals that required ECPR survived to 24 hours.Conclusions:In this severe model of cardiac arrest, a small number of animals survived, all of them receiving ACD+ITD HUP CPR and did not require ECPR.

Circulation, Volume 150, Issue Suppl_1, Page A4144539-A4144539, November 12, 2024. Introduction:Pregnancy-induced cardiomyopathy is typically idiopathic, with no predisposing condition identified. In some cases, women with pre-existing genetic mutations may initially present with cardiomyopathy in pregnancy.Case:A 30-year-old G2P1001 woman presented to Labor&Delivery with frequent palpitations, dyspnea on exertion, and reduced exercise tolerance in the third trimester. Her previous pregnancy was complicated by frequent premature ventricular contractions (PVCs) but otherwise unremarkable. She had a family history of early-onset atrial fibrillation in her mother and a maternal cousin with pregnancy-induced arrhythmias. ECGs and telemetry demonstrated significant ectopy (bigeminy, non-sustained ventricular tachycardia) and atrial arrhythmias including supraventricular tachycardia, atrial tachycardia, and atrial fibrillation (Figure 1). Transthoracic echocardiogram (TTE) showed an ejection fraction (EF) of 20-25%, reduced from 50% 2 weeks prior. Ectopy was associated with reduced fetal heart rate variability suggestive of fetal malperfusion, for which an urgent C-section was performed at 38 weeks and 6 days. Following delivery, she was started on amiodarone, metoprolol, and spironolactone, as part of guideline-directed medical therapy. Subsequent TTEs showed improvement in EF to 30-35% at 2 days and 45-50% at 4 weeks postpartum. Cardiac MRI showed no evidence of fibrosis or inflammation. Given her maternal family history of arrhythmic events, genetic testing was pursued. Genetic testing revealed a pathogenic SCN5A variant (c.638G >A (p.Gly213Asp)).Discussion:SCN5A variants are associated with dilated cardiomyopathy, conduction disorder, and arrhythmias. It is a rare variant of pregnancy-induced cardiomyopathy. This case highlights the value of genetic testing in patients with significant arrhythmia burden and cardiomyopathy in pregnancy and a family history of cardiomyopathy and arrhythmias. For pregnant women with genetic variants predisposing to arrhythmias and cardiomyopathy, comprehensive longitudinal, multidisciplinary care is essential at a referral center with Cardio-Obstetrics expertise and an Inherited Heart Disease Clinic.

Circulation, Volume 150, Issue Suppl_1, Page A4139982-A4139982, November 12, 2024. INTRODUCTION:Asynchronous ventricular pre-excitation over an accessory pathway (AP) in the absence of tachyarrhythmia is sometimes reported to cause left ventricular dysfunction (LVD).AIMS:To analyze the pathophysiological mechanism, role of AP location, evaluation modalities, and management of pre-excitation-related LVD.Methods:PubMed and Google Scholar databases were searched for reports on pre-excitation-induced LVD regardless of patient’s age, and publication date.Results:Out of 11,775 citations retrieved, 53 met inclusion criteria, including 41 case reports and 12 observational studies with 611 total participants, age range of 1.14-60.8 years, and M: F of 325:265 (Table). At initial presentation, acute HF was common in pediatric patients, with poor response to medical therapy; while adults were more often asymptomatic. Right septal and right free wall were the commonest APs location associated with LVD. Amiodarone and propafenone achieved improvement in HF status by causing AP block and restoring ventricular synchrony in pediatric patients deemed unfit for catheter ablation (CA). Septal dyskinesia (SD) and intra-LV dyssynchrony (ILVD) were the key pathophysiological mechanisms causing LVD, leading to regional myocardial wall thinning and hypotrophy. Two-dimensional strain echocardiography (2D-STE) was used in quantifying regional myocardial strain, noninvasive localization of APs, and assessing therapeutic response to CA. Systolic intervals ratio [(pre-ejection period (PEP)/LV ejection time (LVET)] assessed via continuous Doppler detected derangement in LVEF with high accuracy. Preexcitation-induced myocardial changes were usually reversible after CA of APs with recovery of LV function. However, irreversible myocardial tissue damage even after CA was reported, especially in adults. Resolution of ILVD and SD in the immediate post-CA period was predictive of response to CA.Conclusions:We report the largest aggregation of data regarding preexcitation-induced LV dysfunction. Long-term asynchronous activation of the LV via an AP, even without tachyarrhythmias, can causes adverse myocardial changes leading to cardiac dysfunction, especially in children with right-sided APs. 2D-STE and systolic intervals (PEP/LVET) are efficient tools for evaluation. Ablation of APs usually restores cardiac function largely; however, irreversible myocardial fibrosis can ensue. Based on these data, early CA of the APs associated with LV dysfunction is, therefore, recommended.

Circulation, Volume 150, Issue Suppl_1, Page A4144537-A4144537, November 12, 2024. Introduction:Vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor (TKI) therapy has been associated with cardiotoxicity, particularly hypertension. Cardiomyopathy and ventricular arrhythmias (VA) have rarely been reported.Case Report:A 51-year-old male with metastatic sarcoma on pazopanib, a VEGFR-TKI, for the past 4 years presented with 1 month of increasing palpitations and lightheadedness leading to a fall. On arrival, telemetry showed paroxysmal AF with RVR rates to 120 bpm followed by incessant runs of NSVT with rates 200-240 bpm. Initial labs included BNP 191 pg/mL and HS troponin-I 6 ng/L (8000 NSVT episodes.Discussion:This patient had an unusual, delayed presentation of VEGFR-TKI induced myocarditis presenting with significant VA. Although TKI induced myocarditis is rare and the mechanism is not well understood, recurrence of myocarditis in this case with an alternative agent indicates a possible medication-class effect.

Circulation, Volume 150, Issue Suppl_1, Page A4124354-A4124354, November 12, 2024. Background:To realize efficient regenerative medicine using human iPS cell (hiPSC)-derived cardiac tissue, it is necessary to achieve electrical synchronization between the graft and the host heart and to improve conduction disturbances in the impaired heart. In this study, we aimed to demonstrate that the transplantation of hiPSC-derived vascularized cardiac tissue can improve these conduction disturbances using a porcine myocardial injury model.Methods:We prepared cell sheet-shaped vascularized cardiac microtissue (VCM) by seeding cardiomyocytes, endothelial cells, and vascular mural cells differentiated from hiPSCs onto temperature-responsive culture plates and thickening them using dynamic rocking culture. We induced myocardial injury (MI) via epicardial cryoablation in immunosuppressed crown minipigs and transplanted the VCMs immediately after MI induction, covering the cryoinjury-induced MI area. The pigs underwent epicardial electroanatomic mapping under sinus rhythm and epicardial pacing, both immediately before and one week after MI induction, while using amiodarone. Differences in myocardial voltages and conduction velocities were assessed between VCM and sham groups (N=3 in each group). After electroanatomic analysis, the hearts were harvested and subjected to histological examination.Results:One week after MI induction, mean voltages at the MI site decreased in both groups during sinus rhythm, remote site pacing, and combined remote and MI site pacing (11.05 to 1.74 mV, 14.26 to 3.44 mV, and 15.61 to 3.67 mV, respectively, in the VCM group; and 8.72 to 2.70 mV, 19.64 to 3.64 mV, and 14.66 to 1.96 mV, respectively, in the Sham group). Mean voltages at the remote site also decreased in both groups during the same conditions (12.57 to 4.53 mV, 10.61 to 3.38 mV, and 19.56 to 5.85 mV, respectively, in the VCM group; and 8.75 to 6.03 mV, 14.15 to 5.79 mV, and 13.67 to 6.23 mV, respectively, in the Sham group). The mean conduction velocity between the remote and MI sites was numerically higher in the VCM group compared to the Sham group (2.84 m/s vs. 1.74 m/s, respectively). Histological examination confirmed that in the VCM transplantation group, the VCM remained intact, completely covering the MI area.Conclusions:The transplantation of VCM showed a tendency to improve conduction disturbances in the porcine MI model. This suggests that the graft may synchronize with the host and function mechanically after cell transplantation.

Circulation, Volume 150, Issue Suppl_1, Page A4120434-A4120434, November 12, 2024. Introduction:Mitral annular disjunction (MAD) is an abnormality of the mitral valve where a portion of the mitral annulus and valve leaflets insert into the left atrium away from the fibrous annulus. Since its identification in 1981 its diagnosis has increased due to the advancements in cardiac imaging. It’s association with ventricular arrythmia (VA) and sudden cardiac death (SCD) underscores the importance of its identification. We present a case of ventricular tachycardia (VT) that is attributed to MAD with associated sub-mitral valve left ventricular aneurysm (SMA) formation.Case:A 51-year-old African American male with history of posterior papillary muscle premature ventricular contractions (PVC), PVC induced cardiomyopathy, and family history of sudden cardiac death in his mother who presented to the emergency department due to palpitations. Electrocardiogram (ECG) showed sustained monomorphic VT at a rate of 160 bpm. This converted to normal sinus rhythm with intravenous amiodarone and metoprolol. Further work up included cardiac magnetic resonance which identified a 4 x 1.8 x 1.4 cm SMA on the basal inferior and inferolateral walls. There was near transmural late gadolinium enhancement (LGE) of the aneurysm and an associated 7 mm of MAD with posterior mitral valve prolapse (MVP). He underwent left heart catheterization which was normal. ECG showed a superior right axis with associated right bundle branch block which correlated to a basal inferolateral exit and to the location of the SMA. Ultimately the patient underwent implantation of secondary prevention implantable cardioverter-defibrillator and initiation of sotalol.Discussion:The prevalence of MAD is approximately 30% in those with MVP and 8% in the general population. Those patients with MAD and MVP appear to be at higher risk for VA and SCD. The most likely mechanism for this association is the fibrotic changes that occur in the basal inferolateral left ventricle because of mechanical stretch on the papillary muscles by the prolapsing leaflets. The scar and aneurysm that develop can serve as substrate for reentrant VA. Treatment for this involves surgical repair of the mitral valve annulus and correction of the MAD distance which has been shown to improve arrythmia.Conclusion:This case illustrates an important but poorly understood arrhythmogenic entity that will increase in incidence as cardiac imaging advances. Its implications in VA and SCD warrant further research.

Circulation, Volume 150, Issue Suppl_1, Page ASu906-ASu906, November 12, 2024. Background:Cardiac rearrest post-return of spontaneous circulation (ROSC) is a critical concern in emergency care, as it is associated with worse outcomes. Patient characteristics and arrest factors associated with rearrest remain poorly understood, making predicting rearrest after out of hospital cardiac arrest (OHCA) challenging.Aim:To examine rearrest patterns, identify patient-specific risk factors for rearrest, and assess the impact of rearrest on patient outcomes.Hypothesis:Patients that experience rearrest after OHCA will have greater cardiac comorbidities, unfavorable arrest characteristics, and greater mortality.Methods:We performed an observational single-site clinical trial of consecutive adult EMS OHCA patients with ROSC (1/01/2018 to 3/31/24). EMS reports, continuous EMS ECG recordings, and electronic health records were analyzed to determine rearrest occurrence at any time during EMS and ED care. Patient demographics, comorbidities, and arrest/rearrest characteristics were determined. The primary outcome was survival at 6 months. Statistical significance was determined using Chi-square and logistic regression (LR) analyses.Results:We examined 344 patients with OHCA and ROSC, of whom 173 patients rearrested and 171 did not. Patients experiencing rearrest were older (p

Circulation, Volume 150, Issue Suppl_1, Page A4140664-A4140664, November 12, 2024. Introduction:Birt-Hogg-Dubé syndrome (BHDS) is a rare autosomal-dominant disorder due to mutations in the FLCN gene. As an AMPK-mTOR interacting molecule, this loss-of-function mutation impacts energy homeostasis leading to uninhibited cell growth. While studies have linked this genetic mutation to severe cardiac hypertrophy, a connection to persistent atrial fibrillation (AF) is unestablished. We present a case in which an individual’s initial symptoms of AF ultimately led to a diagnosis of BHDS.Case Summary:A 56-year-old male with a history of “holiday heart syndrome” presented for an AF consultation. Despite alcohol cessation, he continued to have paroxysmal AF with severe fatigue and palpitations. After three unsuccessful cardioversions and refractory episodes despite Dronedarone therapy, he was scheduled for an ablation. A pre-procedural transesophageal echocardiogram showed a left ventricular (LV) ejection fraction of 55%, mild concentric LV hypertrophy, and mild left atrial enlargement. These enlargements were new compared with imaging one year prior. A cardiac gated CT detailed the pulmonary vein structure and incidentally revealed bilateral cystic lung changes, leading to a pulmonology referral. Despite an initial successful ablation targeting the pulmonary vein, his symptoms returned within days. He was loaded with amiodarone. Monitoring on his apple watch showed a high burden of AF. He underwent a repeat ablation to achieve complete pulmonary vein isolation with improvement in his symptoms. Further pulmonary evaluation highlighted a family history of spontaneous pneumothorax and a dermatology consultation then confirmed BHDS via fibrofolliculoma biopsy.Discussion:This case underscores the importance of comprehensive evaluations, revealing a rare genetic disorder from an initial AF assessment. While no definitive link exists between BHDS and cardiomyopathy, we aim to understand possible connections between this rare condition and its systemic cardiovascular impacts. We propose that upregulation of mTORC1 activity and attenuation of AMPK from the loss of function of FLCN lead to uncontrolled cell division and left ventricular hypertrophy. This hypertrophy then results in left atrial dilation, contributing to the development and persistence of AF. Given the rarity of this condition, more research is needed on symptom onset and systemic linkages. Swift diagnosis from incidental findings are crucial for managing symptoms and the underlying disease.

Circulation, Volume 150, Issue Suppl_1, Page A4147152-A4147152, November 12, 2024. Introduction:Patients with Fontan circulation are at an increased risk of sinus node dysfunction and atrial tachyarrhythmias. These are associated with significant morbidity and mortality, and management constitutes a significant clinical challenge.Case Description:A 44-year-old male with right ventricular hypoplasia, tricuspid and pulmonic valve atresia and a ventricular septal defect, corrected with a modified Blalock-Taussig Shunt, bidirectional Glenn Shunt and atrio-pulmonary Fontan, was admitted with a supraventricular tachycardia (SVT) and heart failure. His electrocardiogram showed a narrow complex mid-RP tachycardia consistent with atypical atrial flutter or atrial tachycardia. His echocardiogram showed an LVEF of 21%. He was started on a beta-blocker and loaded with dofetilide, resulting in bradycardia, QT interval prolongation and Torsades de Pointes. Amiodarone was substituted, but he had incessant SVTs. He was taken for an electrophysiology study and radiofrequency ablation of a right-sided re-entrant flutter around an area of block in the anterior septum. Four additional unstable atrial tachycardias were induced but not ablated. He was discharged, then readmitted within hours for SVT. Due to insurance status, the patient was not a candidate for transplant or Fontan revision. To enable treatment with a beta-blocker, an Abbott leadless atrial pacemaker (AVEIR AR) was implanted in the high lateral Fontan, in an area of normal voltage (Figure 1). Post-implant interrogation showed stable device parameters (capture 0.25 V @ 0.4 ms, sensing 7.6 mV, impedance: 380 Ω).Conclusions:This is the first case of an AVEIR AR implanted within an atrio-pulmonary Fontan circulation. Access to atriopulmonary Fontan circulation for endovascular device therapy is feasible, but requires careful pre-procedural planning to ensure vascular patency, and anatomic and physiologic feasibility. Leadless pacing mitigates complications from endocardial and epicardial pacing systems, but long-term safety and efficacy are unknown.

Circulation, Volume 150, Issue Suppl_1, Page A4135425-A4135425, November 12, 2024. Background:Aberrant diastolic Ca2+leak through the cardiac ryanodine receptor (RyR2) is an important cause of heart failure (HF) and lethal arrhythmia. Dantrolene (DAN) specifically binds to the Leu601-Cys620of N terminal domain in RyR2 and stabilizes the tetrameric structure of RyR2, preventing the Ca2+leak through RyR2. Our previous study as a proof-of-concept showed that intravenous injection (i.v.) of DAN was effective in termination and prevention of refractory ventricular tachycardia (VT) storm in HF.Research Question:How much is loading dose of DAN i.v. to terminate VT storm in HF? We hypothesized that the optimal dose was within 3mg/kg from our previous study.Aim:This study aimed to verify that 3mg/kg DAN i.v. was optimal for the termination of amiodarone-resistant VT storm in HF.Methods:This was an open-label, uncontrolled, single-center study. The detail in the study design and methods is shown inFig.1. We studied patients with episodes of VT storm regardless of medications, such as amiodarone and beta-blockers, recommended by HF guidelines. DAN(3mg/kg) was intravenously added on the above guideline treatment. The acute anti-arrhythmic efficacy of DAN was assessed as follows: 1) proportion of patients whose VT storm was terminated by 3mg/kg DAN i.v., 2) incidence rate of VT storm within 24 hours before and after DAN i.v..Results:The consecutive 7 patients with refractory VT storm were enrolled in this study (median age:72 years old, male/female: 4/3, median LVEF29%). Underlying heart disease included 3 ischemic cardiomyopathy, 3 acute myocardial infarction after successful percutaneous coronary intervention and 1 tachycardia-induced cardiomyopathy. 2 of 7 patients underwent mechanical circulatory support before DAN i.v. because of pulseless VT. All patients were classified as NYHA class III/IV. 3 mg/kg of DAN i.v. ceased VT storm within 60 min in 7/7 (100%)(Fig.2, left).The number of sustained VT within 24 h after DAN i.v. were significantly lower than those within 24 h prior to DAN administration(Fig 2, right). A representative case is shown inFig.3The VT storms refractory to amiodarone and landiolol (beta-blocker) as well as sedation showed complete response to 3mg/kg DAN i.v..Conclusions:DAN, a RyR2 stabilizer, was effective in the termination of VT storm in HF resistant to guideline directed medical treatment. This is the first study to evaluate the optimal dose of DAN i.v. against the refractory VT storm in HF.

Circulation, Volume 150, Issue Suppl_1, Page A4139536-A4139536, November 12, 2024. Background:Limited data exist on the incidence of severe QT prolongation (SQTP) in patients using antipsychotics or antidepressants and the associated risk of ventricular arrhythmias (VA) and sudden cardiac death (SCD).Aims:This study aimed to investigate the incidence, risk factors, and outcomes of SQTP in patients using antipsychotics or antidepressants.Methods:Electronic medical records from a multicenter healthcare system in Taiwan were analyzed to identify patients using antipsychotics or antidepressants with baseline and follow-up electrocardiograms. SQTP was defined as a corrected QT interval exceeding 500 ms post-treatment or an increase of >60 ms compared to baseline. Risk factors for SQTP development and associated risks of VA and SCD were assessed using multivariate logistic regression.Results:Following antipsychotic use (n = 28,892) and antidepressant use (n = 14,634), mean corrected QT interval increases were +7.7 ± 39.0 ms and +6.7 ± 36.1 ms, respectively. Over 10% of patients using haloperidol, amisulpride, olanzapine, quetiapine, or risperidone experienced SQTP. Antipsychotics with a known or conditional risk of torsades de pointes and antidepressants with a known risk of torsades de pointes had a higher likelihood of SQTP compared to alprazolam control. Risk factors for SQTP included age >65 years, electrolyte imbalances, renal insufficiency, amiodarone use, left ventricular ejection fraction

Circulation, Volume 150, Issue Suppl_1, Page A4129440-A4129440, November 12, 2024. Background:Ventricular stunning refers to a transient mechanical dysfunction of the myocardium, typically manifesting in response to ischemic insults, reperfusion injury, inflammatory states, or neurohormonal overload. Here, we present an unusual case of ventricular stunning precipitated by direct current electrical cardioversion (DEC).Case Report:A 73-year-old man with a history of heart failure with reduced ejection fraction, paroxysmal atrial fibrillation (AF), coronary artery disease, and chronic kidney disease was admitted to a Veterans Affairs hospital for heart failure exacerbation. His hospitalization was complicated by recurrent episodes of symptomatic AF with ventricular rates in the 120-150’s. This was initially managed with intravenous amiodarone and eventually DEC. He continued to experience symptomatic episodes of AF. Later in the hospitalization a repeat DEC with a single 200 joule shock was performed with restoration of sinus rhythm. Several hours afterwards he was found to be unresponsive and hypotensive. Cool extremities and rising serum lactate raised suspicion for cardiogenic shock resulting in transfer to the intensive care unit where vasopressor and inotropic support were initiated. Echocardiogram revealed a precipitous decrease in left ventricular ejection fraction from 25% to 5%. Serum troponin concentrations were unchanged from prior and ECGs demonstrated rate-controlled AF.Clinical Decision Making:This case highlights an episode of unexpected decrease in cardiac output following an otherwise routine repeat DEC for recurrent AF requiring escalation to mechanical circulatory support. His decompensation worsened, necessitating transfer to the local university center for placement of catheter-based miniaturized ventricular assist device (Impella 5’5). Over the subsequent days, with supportive care, his left ventricular ejection fraction recovered to baseline, and mechanical and inotropic support were withdrawn.Conclusion:Ventricular stunning, leading to cardiogenic shock, is a rare and incompletely understood complication of DEC. It warrants consideration when monitoring patients after cardioversion. Implementing vigilant observation protocols post-DEC to detect ventricular stunning and predisposing risk factors could significantly enhance clinical management strategies.

Circulation, Volume 150, Issue Suppl_1, Page A4143538-A4143538, November 12, 2024. Introduction:Transthyretin amyloid cardiomyopathy (ATTR-CM) is an underdiagnosed disease that may result in heart failure (HF), arrhythmias, and valvular disease. Our aim was to develop (1) screening criteria to identify high-risk patients for ATTR-CM and (2) our own predictive tool of ATTR-CM.Methods:This was a prospective observational registry at 2 academic sites in Canada. We designed screening criteria to identify high-risk patients in HF, atrial fibrillation, transcatheter valve clinics, and in cardiologist’s offices from January 2019-December 2022. Patients >60 years were included if one of several screening criteria was met and they were referred for pyrophosphate scan by the cardiologist. Univariate and multivariate logistic regression were used to identify predictive clinical, imaging, and biochemical characteristics.Results:In total, 2500 patients were screened, and 200 patients were enrolled with a follow-up duration of 3 years. The mean age was 78 years and 65% were male. Forty-six (23%) had a diagnosis of ATTR-CM and 7 (4%) were diagnosed with AL-amyloidosis. ATTR-CM patients were older (83±7 vs. 77±8; p