Monomorphic Ventricular Tachycardia Research Articles

The Impact of Coronary Ischemia Assessment on Outcomes in Those With Scar-Dependent Ventricular Tachycardia.

Guidance and outcomes of coronary ischemia assessment (IA) in those with structural heart disease (SHD), presenting with monomorphic ventricular tachycardia (MMVT) is unclear. To assess the impact of IA on arrhythmic and non-arrhythmic outcomes in those with SHD. Patients presenting with MMVT over a 6-year period to a tertiary center were retrospectively analyzed. Propensity score-matched analysis was performed comparing those undergoing IA to those who did not. The primary endpoint was a composite of VT recurrence, appropriate ICD therapy, heart failure hospitalization, and death. Secondary analysis of the individual components of the composite was performed. Kaplan-Meier, univariate and multivariate analysis was performed to compare the two groups and derive predictors of poor outcomes. Two hundred and seventeen patients (57.6% ICM) were analyzed. 55.8% underwent IA. Following propensity score-matching, 120 patients remained. At 12 months, freedom from the primary endpoint was 68.3% of those undergoing IA versus 43.3% who did not, p < 0.001, multivariate HR 0.56 (0.34-0.92). This was driven by a reduction in all-cause mortality, with a 12-month survival of 98.3% in those undergoing IA versus 86.5% in those not undergoing IA (p < 0.01). Coronary intervention was associated with a significantly higher event-free 12-month survival compared to those who did not undergo intervention (82.4% vs 51.5%, respectively, p = 0.01). Patients with SHD presenting MMVT who undergo an IA have significantly improved freedom from VT recurrence, appropriate ICD therapies, HF hospitalization, and death compared to those who do not, driven by a reduction in mortality.

Effect of Ischemia Testing and Coronary Revascularization on Mortality and Ventricular Tachycardia Recurrence in Patients With Monomorphic Ventricular Tachycardia Without Acute Coronary Syndrome: A Meta-Analysis and Systematic Review.

Studies show mixed results regarding the effect of coronary revascularization on mortality benefit and ventricular tachycardia (VT) recurrence in patients with monomorphic VT without acute coronary syndrome (ACS). This meta-analysis aimed to assess the effect of ischemia testing and/or coronary revascularization on mortality and VT recurrence in a pooled data set. Databases including PubMed, Google Scholar, and the Cochrane Library were searched from January 2000 to December 2023 for studies reporting event data on mortality and VT recurrence in patients without ACS who presented with monomorphic VT. Data were pooled and analyzed using random effects meta-analysis. The pooled sample consisted of a total of five studies, with 1062 patients, of whom 433 underwent ischemia testing and/or coronary revascularization and 629 did not. There was no statistically significant difference in the mortality and VT recurrence in the patients who underwent ischemia testing and/or revascularization versus those who did not (mortality odds ratio [OR]: 0.98; [95% confidence interval (CI): 0.62 to 1.53]; p = 0.92; VT recurrence OR: 1.07; [95% CI: 0.51 to 2.26]; p = 0.86). No publication bias was detected by examination of the funnel plot, Begg-Mazumdar's test (p = 0.80), and Egger's test (p = 0.91). In conclusion, in patients with sustained monomorphic VT in the absence of ACS, ischemia testing and/or revascularization does not lead to improved mortality or a decrease in the incidence of VT recurrence.

Abstract 4137919: Electrical Storm Caused by Chagasic Cardiomyopathy Successfully Treated with Ventricular Aneurysmectomy

Introduction: Chronic Chagasic cardiomyopathy (CCC) is a serious complication of Chagas disease that can manifest as LV dysfunction, ventricular aneurysms, and ventricular arrhythmias. Management of the electrical storm in CCC is challenging, especially when it is refractory to catheter ablation. Case Presentation: A 59-year-old woman from southern Peru presented to the ED with palpitations and dyspnea for 1 week. Physical exam was normal. ECG showed Q waves in III and AVF leads. TTE revealed an LVEF of 45% with an inferolateral LV aneurysm. Coronary angiography showed no lesions. CCC was suspected and serology was ordered, which was positive for T. cruzi . Cardiac MRI confirmed the presence of a 32x22mm basal inferolateral LV aneurysm. During hospitalization, she experienced 4 episodes of unstable monomorphic ventricular tachycardia (VT) within 24 hours, requiring defibrillation with 200J, vasopressor support, and invasive mechanical ventilation. The diagnosis of electrical storm secondary to CCC was proposed, for which amiodarone infusion was started until complete impregnation was achieved. Additionally, support was provided with IABP and specific antiparasitic treatment with benznidazole. Electrophysiology determined that the probable focus of the VT was situated at the level of the LV aneurysm. Therefore, ablation with endocardial-epicardial mapping was performed. However, the patient continued to experience recurrent episodes of VT. Consequently, in a multidisciplinary discussion, it was decided to perform a ventricular aneurysmectomy, which was successful. The patient's clinical progress was favorable, with initiation of GDMT and placement of a single-chamber ICD for secondary prevention. After one year of outpatient follow-up, the patient remains free of VT recurrences. Conclusion: Ventricular aneurysmectomy is a successful management approach for patients with CCC who present with electrical storm refractory to antiarrhythmic drugs and catheter ablation, and whose VT is believed to originate from the aneurysm. The diagnosis of CCC is highly arrhythmogenic and should be suspected at an early stage, given the patient's demographics and the presence of LV aneurysm in the absence of coronary artery disease.

Abstract 4148095: The Impact of Body-Mass Index on Ventricular Tachycardia Outcomes Post-Catheter Ablation

Background: In recent years, catheter ablation has emerged as a sustainable, first-line therapy for the management of ventricular tachycardia (VT). Given the rise of the “obesity paradox” theory in atrial ablation outcomes, we sought to study the effect of BMI on patients undergoing structural VT ablation. Purpose: To assess the outcomes of VT ablation, specifically VT recurrence, in patients with elevated vs. normal BMI. Methods: Clinical characteristics and demographic data were collected for VT patients who underwent ablation at Mayo Clinic Rochester from 2012-2022. Patient BMI was classified as non-obese (&lt;30 kg/m2), obese (30-40 kg/m2), and morbidly obese (≥40 kg/m2). The endpoint was a composite of initial monomorphic VT recurrence and repeat ablation after adjusting for age, sex, and comorbidities. Results: A total of 399 patients underwent 508 ablations. 51.4% of ablations had a BMI &lt;30, 39.2% were between 30-40, and 9.4% were ≥40. There was a greater prevalence of hypertension and type 2 diabetes mellitus in morbidly obese patients (p &lt;0.01). Morbidly obese individuals also had a significantly increased rate of general anesthesia during ablation and long VT cycle lengths. The Kaplan-Meier curve demonstrates no statistically significant differences in time to VT recurrence among the three BMI groups (p = 0.324). Neither morbid-obesity (aHR= 1.20; CI = 0.94-1.56, p = 0.14) nor nonmorbid-obesity (aHR = 0.92; CI = 0.76-1.10, p = 0.4), compared to non-obesity was a significant independent predictor of VT recurrence or repeat ablation on multivariate regression after adjusting for age, sex and comorbidities. Conclusion: There was no significant association between BMI groups and VT recurrence or repeat ablation, and no difference in complications. We did not find the obesity paradox to be relevant for VT ablation in our patient population. Further study would be needed with larger samples to corroborate these findings.

Abstract 4120434: A Rare Case Of Localized Ventricular Tachycardia Due To Mitral Annular Disjunction And a Subvalvular Aneurysm

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.

Prognosis of patients with wild-type transthyretin cardiac amyloidosis and non-sustained ventricular tachycardia.

Little is known regarding the prevalence and prognostic implications of non-sustained ventricular tachycardia (NSVT) in patients with wild-type transthyretin cardiac amyloidosis (ATTRwt-CA). We aimed to investigate the prevalence of NSVT in patients with ATTRwr-CA, and the association of NSVT with sustained ventricular arrhythmias (VA) and all-cause mortality. In a cohort of ATTRwt-CA patients from 2011 to 2022 without prior sustained VA, we ascertained the presence and characteristics of NSVT during clinically indicated ambulatory Holter monitoring. Patients were stratified based on the presence of NSVT at baseline. The primary and secondary endpoints of sustained VA and all-cause mortality, respectively, were assessed during follow-up. The cohort included 217 patients with ATTRwt-CA (95% males, median age 75 years; median NYHA class 2). Baseline Holter monitoring demonstrated NSVT in 116 (53%) patients. During a median follow-up of 27 months (IQR 16-45) after the index Holter monitor, 11 (5.1%) patients reached the primary endpoint of sustained VA (incidence 1.8 per 100 person-years, all monomorphic VT), and 46 (21%) patients died. In univariable Cox proportional hazard model, NYHA class 3 or 4 heart failure (p = .048), the presence of NSVT (p = .04), the duration of longest NSVT run (p = .029), and the percentage of ventricular ectopy (p < .001) were associated with the primary outcome. When adjusting for age and NYHA class 3 or 4 heart failure, the presence of NSVT remained associated with the primary outcome (p = .03). All-cause mortality was not significantly different between patients with and without NSVT. A cutoff for ventricular ectopy burden of 0.5%, the median for all patients in this study, was associated with increased risk in sustained VA (log-rank p = .004) and mortality (log-rank p = .02). NSVT is highly prevalent among ATTRwt-CA patients undergoing clinically indicated Holter monitoring and may confer an increased risk of incident sustained VA.

Yield of Coronary Assessment in Sustained Monomorphic Ventricular Tachycardia

Coronary assessment is frequently conducted in patients with sustained monomorphic ventricular tachycardia (SMVT); however, its yield and subsequent treatment implications remain unclear. This study aimed to determine the prevalence of coronary artery disease (CAD) in patients presenting with SMVT, factors influencing clinician referral for coronary assessment, and clinical outcomes based on revascularisation or medical management of CAD. Consecutive patients presenting with acute SMVT requiring inpatient admission between 2017 and 2022 were identified. A total of 249 individual patients with SMVT were identified, with 140 undergoing coronary assessment. Referral for coronary assessment was driven by chest pain (p<0.001) and increased troponin kinetics (p<0.001). No patient with SMVT had an acute coronary occlusion. Significant CAD was found in 48 (34%) patients, and traditional ischaemic features did not predict significant CAD. Nineteen (40%) patients with significant CAD underwent revascularisation (n=15 percutaneous coronary intervention, n=4 coronary artery bypass grafting). There was no significant difference in time to ventricular tachycardia (VT) recurrence between revascularised and medically managed CAD (hazard ratio 1.670; 95% confidence interval 0.756-3.687; p=0.199). A total of five of six patients who underwent a revascularisation-only strategy (no upfront antiarrhythmic therapy or ablation) had VT recurrence (median time to recurrence 8.9 months). Despite being frequently performed, coronary assessment in SMVT has only modest yield, with no patients having an acute coronary occlusion. Traditional clinical factors of ischaemia did not improve this yield. Revascularisation alone did not improve freedom from VT.

Atrial rates during treated ventricular tachycardia in patients with implantable cardioverter defibrillators: clinical implications of a vagal sinus node response

Abstract Introduction Autonomic tone plays an important role in the genesis and sustenance of ventricular tachycardia (VT). Whilst sympathetic hyperactivity is an established driver of ventricular arrhythmias, sinus node response during VT varies broadly between patients, and can be paradoxical. Purpose We hypothesized that device-detected changes in sinus node rate could be an important surrogate of the autonomic response to VT, and may exert significant – and potentially modifiable – haemodynamic consequences independent of ventricular activity. Methods Device electrograms were analysed from consecutive patients with dual chamber implantable cardioverter defibrillators (ICDs) requiring anti-tachycardia pacing (ATP) or defibrillation for sustained monomorphic VT. Atrial rates were measured before VT onset (‘baseline’) and again at the point of detection by the device. Sinus node response was characterized as ‘stable’ (atrial rate remained within 10% of baseline), ‘sympathetic’ (atrial rate increased &amp;gt;10%) or ‘vagal’ (atrial rate decreased &amp;gt;10%). Patients who did not maintain ventriculoatrial dissociation or who presented in atrial tachyarrhythmia were excluded. Symptoms and electrical response to ICD therapies were recorded. Results 172 treated episodes of VT were included from 97 patients (median age: 69 years, 65% male, 31% ischaemic cardiomyopathy, median ventricular rate: 205bpm, median ejection fraction: 30%). Sinus node response was stable in 55%, sympathetic in 24% and vagal in 21%. A vagal response was associated with ATP-refractory VT (OR: 2.2 (1.1-4.8) p=0.03) and, when adjusting for ventricular rate, was independently associated with symptoms of presyncope or syncope (adjusted OR: 6 (2.7-13.7), p&amp;lt;0.0001). Conclusions This preliminary analysis suggests that a vagal sinus node response during VT is associated with adverse outcomes in ICD patients. Vagolytic therapy has recently been demonstrated to improve haemodynamic tolerance during VT ablation; whether supportive atrial pacing during VT could mitigate symptoms and potentiate arrhythmia termination in ICD patients warrants further exploration. Figure 1: Change in sinus node rate during sustained monomorphic ventricular tachycardia in patients with dual chamber ICDs, stratified by the occurrence of presyncopal symptoms or syncopeFigure 1

Development and implementation of a guideline-based decision support system for etiological diagnosis of Sustained Monomorphic Ventricular Tachycardia (SMVT)

Abstract Background Guideline (GL)-based decision support systems (DSSs) play a significant role in supporting physicians in their decision-making processes by providing structured clinical guidance. While these systems have shown significant success in enhancing practitioner performance and patient outcomes in general practice, their application in the context of ventricular arrhythmias remains limited. Moreover, the clinical etiological diagnosis of ventricular arrhythmias presents various challenges for healthcare professionals, such as adherence to updated diagnostic criteria and understanding of complex arrhythmia mechanisms. Purpose In this study, we aim to design, implement, and evaluate a guideline-based decision support systems for etiological diagnosis of sustained monomorphic ventricular tachycardia (SMVT), which could potentially address critical challenges associated with the disease diagnosis and management. Methods To comprehensively capture the semantics embedded in clinical guidelines, we first developed a dedicated knowledge graph tailored to the clinical decision-making. This involved extracting entities and relationships pertinent to key decision procedures from ESC guidelines for ventricular arrhythmias, clinical textbooks or literatures. Subsequently, we translated instances within the knowledge graph into archetypes within openEHR, amplifying the interoperability of clinical information. To enhance the interpretability of the DSS, we established executable diagnostic and treatment processes to offer visual representation of clinical steps in diagnosis and treatment. Ultimately, we constructed a decision support engine to implement the GL-DSS, and its effectiveness was evaluated with anonymous real-world data. Results The proposed GL-DSS was found to be quite feasible and could provide etiological diagnosis for SMVT. The knowledge base for the constructed GL-DDS included more than 2000 entities and relations, which played a vital role in representing disease pathogenesis. The proposed system can map the clinical entities to a set of openEHR archetypes, thus mitigate the interoperability issues of the hospital information systems and CDSS data integration. Also, this module improved system usability and ensured that guidelines could be easily translated and updated into decision support tools. Real-word medical records from 20 patient were collected for model evaluation, the results showed that the GL-DSS covered most of the entities and relations between diseases and diagnostic evidence recorded in clinical texts and achieved a diagnosis accuracy of 80%. Conclusions The results demonstrated that our proposed GL-DSS could completely and accurately capture the diagnostic information under the concrete EHR data. Thus, the implement decision support system could have the potential to improve clinical decision-making, patient care, and outcomes in this specialized medical domain.

Expect the unexpected: fulminant myocardial cytotoxic Injury from Trabectedin

BackgroundTrabectedin (Tbt) is an alkylating agent prescribed for soft tissue sarcomas after treatment failure of first line agents. While cardiomyopathy can occur with Tbt treatment after anthracycline exposure, Tbt-induced fulminant myocardial cytotoxic injury in the setting of other systemic cytotoxicity associated with Tbt has not been reported.Case presentation51-year-old female with hypertension, hyperlipidemia, metastatic leiomyosarcoma with progression of disease despite several lines of chemotherapy including doxorubicin-based therapy was started on Trabectedin (Tbt) 5 days prior to presentation with symptoms of fever, myalgias, arthralgias, and palpitations. She was admitted for management of rhabdomyolysis, acute kidney and liver injuries which were reportedly known to be associated with Tbt treatment. A baseline electrocardiogram (ECG) revealed sinus tachycardia with non-specific T-wave changes, and a transthoracic echocardiogram (TTE) was unremarkable. However, on day 3 of hospitalization, an episode of asymptomatic sustained monomorphic ventricular tachycardia with a heart rate of 150 beats per minute was captured on telemetry. A 12-lead ECG revealed new septal T-wave inversions. Labs revealed rising hs-TnI levels (peak at 37,933ng/L) and serum markers suggested multi-organ failure. Steroids were initiated given its role in treating multi-organ Tbt-induced toxicity. A cardiac MRI to rule out myocarditis and left heart catheterization to rule out obstructive coronary artery disease were forgone due to acute renal failure. A right heart catheterization with an endomyocardial biopsy was performed revealing normal cardiac filling pressures and indices. Pathology showed cytoplasmic vacuoles indicating drug-induced myocardial cytotoxicity. Serial echocardiograms revealed preserved biventricular function. The patient’s clinical condition deteriorated with multi-organ failure despite maximal supportive care in the intensive care unit. She ultimately passed away, and an autopsy was declined.ConclusionThis is the first reported case of fulminant myocardial injury after initiation of Tbt with histologic evidence of drug-induced myocardial cytotoxicity. While it is unclear if anthracyclines potentiate Tbt cytotoxic injury as in this case, it is plausible; and that Tbt-induced cardiotoxicity ranges from subclinical to fulminant. Given increasing use of Tbt in refractory high-grade sarcomas, raising awareness of its toxicity profile will improve early detection and outcomes.

Effect of Spatial Resolution on Accurate Detection and Localization of Arrhythmia Rotors in Human Right Ventricular Tachycardia.

The goal of this study was to identify the spatial resolution requirements for accurate rotor detection and localization in human right ventricular tachyarrhythmias. Poor spatial resolution is often cited as a reason for the inaccuracy of cardiac mapping catheters in detecting and localizing arrhythmia rotors. High-resolution (0.7 mm) arrhythmia data from optical recordings obtained from human donor hearts (n = 12) were uniformly downsampled to lower resolutions (1.4-7 mm) to approximate the spatial resolution (4 mm) of clinical mapping catheters. Rotors were tracked at various subresolutions and compared to the rotors in the original data by computing F1-scores to create accuracy profiles for both rotor detection and localization. Further comparisons were made according to arrhythmia type, donor sex, anatomical region, and mapped surface: endocardium or epicardium. For a spatial resolution of 4.2 mm, the accuracies of rotor detection and localization were 57% ± 4% and 61% ± 7%, respectively. Arrhythmia type affected the accuracy of rotor detection (monomorphic ventricular tachycardia, 58% ± 4%; ventricular fibrillation, 56% ± 8%) and localization (monomorphic ventricular tachycardia, 70% ± 4%; ventricular fibrillation, 54% ± 13%). However, donor sex, anatomical region (right ventricular outflow tract, mid, and apical), and mapped surface (epicardium and endocardium) did not significantly affect rotor detection or localization accuracy. To achieve rotor detection accuracy of 80%, a spatial resolution of 1.4 mm or better is needed. The accuracy profiles provided here serve as a guideline for future mapping device development.

Dofetilide for the treatment of premature ventricular complexes and ventricular tachycardia in patients with structural heart disease.

Dofetilide is a class III antiarrhythmic agent approved for the treatment of atrial fibrillation and atrial flutter. Given the efficacy of other class III agents, it has been used off-label for the treatment of premature ventricular complexes (PVCs) and ventricular tachycardias (VTs). The purpose of this study was to determine the efficacy and safety of dofetilide for ventricular arrythmias (VAs). In this retrospective cohort study, 81 patients (59 men; age = 60 ± 14 years; LVEF = 0.34 ± 0.16) were admitted for dofetilide initiation to treat PVCs (29), VTs (42) or both (10). A ≥ 80% decrease in PVC burden was defined as a satisfactory response. An ICD was present in 72 patients (89%). Another antiarrhythmic was previously used in 50 patients (62%). Prior catheter ablation had been performed in 33 patients (41%). During intitiation, dofetilide was discontinued in 12 patients (15%) due to QT prolongation (8) and inefficacy to suppress VAs (4). Among the 32 patients with PVCs who successfully started dofetilide, the mean PVC burden decreased from 20 ± 10% to 8 ± 8% at a median follow-up of 2.6 months (p < .001). PVC burden was reduced by ≥80% in only 11/32 patients (34%). During 7 ± 1 years of follow-up, 41/69 patients (59%) continued to have VAs and received appropriate ICD therapies for monomorphic VTs (35) and polymorphic VT/VF (6) at a median of 8.0 (IQR 2.6-33.2) months. Dofetilide had to be discontinued in 50/69 patients (72%) due to inefficacy or intolerance. The composite outcome of VT/VF recurrence, heart transplantation, or death occurred in 6/12 patients (50%) without dofetilide and 49/69 patients (71%) with dofetilide. The event free survival was similar between patients treated with and without dofetilide (log-rank p = .55). Treatment with dofetilide was associated with a decrease in PVCs, however clinically significant suppression occurred in a minority of patients. Dofetilide failed to suppress the occurrence of VTs in a majority of patients.

Implementing stereotactic arrhythmia radioablation with STOPSTORM.eu consortium support: intermediate results of aprospective Israeli single-institutional trial.

Ventricular tachycardia (VT) is alife-threatening arrhythmia originating from the heart's ventricles. Traditional treatments include antiarrhythmic medications, implantable cardioverter-defibrillators (ICDs), and catheter ablation. Stereotactic body radiation therapy (SBRT) targeting the arrhythmogenic focus in the left ventricle-stereotactic arrhythmia radioablation (STAR)-is an emerging treatment and may offer apotential solution for patients with refractory VT. We designed an interventional prospective clinical trial in Israel aligned with the STOPSTORM.eu consortium's benchmarks, recommendations, and directives to assess the safety and efficacy of STAR in patients with refractory VT. Our phaseI/II single-institutional trial was approved by the Ministry of Health of Israel for 10patients, initially assessing safety in the first 3patients. We included patients with ICDs experiencing symptomatic monomorphic VT after an inadequate response to previous therapies. The primary endpoints were treatment-related serious adverse events and areduction in VT burden as assessed by ICD interrogation. Secondary outcomes included areduction in antiarrhythmic medications and changes in quality of life. From August 2023 to August 2024, 3patients underwent STAR treatment. The prescription dose was asingle fraction of 25 Gy. Planning target volumes were 47.8, 49.7, and 91.8 cc, and treatment was successfully delivered with no grade3 or higher adverse events reported. Over afollow-up period of 12months for the first patient and 8months for the second one, no VT events were recorded after treatment. The third patient died from progressive heart failure 3months after treatment. Left ventricular ejection fraction remained stable, and no significant radiation-induced inflammatory changes were noted. The initial results of this trial suggest that STAR can reduce VT episodes in patients with refractory VT without severe adverse effects. The study highlights the importance of international collaboration and standardization in pioneering new treatments. Further follow-up and additional patient data will be necessary to confirm these findings and evaluate long-term outcomes, including potential adjustments to antiarrhythmic medication regimens.

Enhancing risk assessment in Chagas cardiomyopathy: Electrophysiology study stratified by Rassi score

BackgroundChagas cardiomyopathy (CCM) is increasingly prevalent in developed countries due to migration from endemic areas. Accurate risk stratification is crucial due to the variable clinical course of CCM. ObjectiveTo analyze the association between Rassi score progression and electrophysiology study (EPS) changes in CCM patients. MethodsThis prospective, observational cohort study involved CCM patients from two tertiary hospitals. Patients were classified as low, intermediate, or high risk based on the Rassi score. Data collected included demographics, clinical history, and diagnostic tests. EPS assessed AH, HH, and HV intervals, and inducibility of ventricular arrhythmias. Follow-ups were at 30 days and six-month intervals, with individualized discussions for cardiac implantable electric devices (CIED) based on EPS results. ResultsOf 67 screened CCM patients, 59 underwent EPS. The mean Rassi score was 8.7 ± 4.5 points, with 33.8 % low, 38.9 % intermediate, and 27.1 % high risk. EPS abnormalities were found in 57.6 % of patients, mainly VT/VF (52.5 %). Most induced ventricular arrhythmias were monomorphic VT (80.7 %). A significant association was found between Rassi score risk classification and EPS changes (OR = 1.88 95 %CI: 1.15–3.06 p = 0.02). Higher Rassi scores correlated with VT presence on EPS (p = 0.0036). Syncope/pre-syncope had an OR 2.45 95 %CI:1.21–4.94; p = 0.012, independent of Rassi risk. Decreased ejection fraction was linked to EPS changes (p = 0.04). ConclusionEPS changes among CCM was associated with progression of the Rassi score, indicating its utility as a stratification tool. Factors such as the presence of syncope/pre-syncope, decreased LVEF and wall motion abnormalities emerged as independent predictors within Rassi scores for changes in EPS.

Abstract Tu060: Unveiling Arrhythmogenic Right Ventricular Dysplasia In Pregnancy

Introduction: Arrhythmogenic right ventricular dysplasia (ARVD) is a rare autosomal dominant disease, caused by desmosomal gene mutations, and characterized by fibrofatty replacement of right ventricular (RV) myocardium with left ventricular (LV) involvement in advanced stages. It is mostly diagnosed between the second and forth decades of life and can present with ventricular tachycardia and arrhythmic sudden death. Here we present a case of ARVD diagnosis in a female in her forth pregnancy. Case description: A 28-year-old female, on her 27 th week of gestation (G4P3) was admitted to the hospital with preterm premature rupture of membranes. She also endorsed intermittent chest pressure, palpitations and shortness of breath. Her vital signs were stable, and electrocardiogram (ECG) revealed normal sinus rhythm with frequent premature ventricular contractions (PVCs) and T wave inversions in leads V1- V3. Laboratory studies showed normal troponin and D-dimer levels, and slightly elevated brain natriuretic peptide 240 pg/mL. Patient notably had frequent runs of monomorphic non-sustained ventricular tachycardia (NSVT) arising from RV apical territory, with left bundle branch morphology on telemetry. An echocardiogram revealed a dilated right atrium and RV with hypokinesis of RV; LV size and function were normal. Overall, patient met the revised task force diagnostic criteria for ARVD based on PVC morphology, abnormal ECG and dilated and hypokinetic RV. She had no sustained or hemodynamically unstable VT, no history of syncope or family history of sudden cardiac death and did not meet class I indication for implantable cardioverter defibrillator. She was started on oral metoprolol succinate 25 mg daily with which her arrhythmias significantly improved. She was recommended a cardiac magnetic resonance imaging and genetic testing for confirmation and to assess familial implications. Conclusion: Recognition of ARVD during pregnancy is challenging given the overlapping symptoms of normal pregnancy-related changes. Hormonal surge and sympathetic drive may have driven the increased frequency of NSVT in our patient and beta blocker was effective in managing these. Early recognition and tailored management are crucial to ensure the well-being of both the mother and the fetus. A close follow-up is necessary to understand the long-term implications for the patient and potential genetic predisposition in the family.

Correlations of ventricular fibrillation and monomorphic ventricular tachycardia with SCN5A mutations and other clinical variables in Brugada syndrome

Correlations of ventricular fibrillation and monomorphic ventricular tachycardia with SCN5A mutations and other clinical variables in Brugada syndrome

Ventricular Angiography: A Forgotten Diagnostic Tool?

A 76-year-old male patient presented to the emergency room with acute decompensated right heart failure and presyncope episodes. Upon admission, his electrocardiogram (ECG) showed sustained monomorphic ventricular tachycardia at 180 bpm, which was electrically cardioverted, and the patient was subsequently admitted to the intensive care unit. The echocardiography showed a very dilated right ventricle (RV) with global systolic dysfunction and akinetic anterior and lateral walls. The coronary angiography was normal. The cardiac magnetic resonance showed signs of fibro-fatty replacement of the RV myocardium. Furthermore, the ECG after cardioversion showed inverted T waves and an epsilon wave in V1-V3 leads and late potentials by signal-averaged ECG. As such, a diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC) was suspected. However, he presented no familial history of ARVC, was 76 years of age at the time of diagnosis and was asymptomatic until now. Given these considerations, we performed a right ventricular angiography which showed dilatation of the RV with akinetic/dyskinetic bulging, creating the "pile d'assiettes" image suggestive of ARVC. In the case of this patient, the RV angiography contributed to establish a diagnosis of ARVC with a very late presentation, to our knowledge the latest presentation in terms of age described in the literature.

Aberrancy masquerading as ventricular tachycardia: Importance of invasive electrophysiology study for diagnosis of wide complex tachycardias

BackgroundDifferentiation between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrancy based on the 12‑lead ECG alone can be imprecise. Implantable cardiac defibrillators (ICD) may be inserted for presumed VT, particularly in patients with syncopal presentation or atypical aberrancy patterns. Accurate diagnosis of these patients facilitated by an electrophysiology study (EPS) may alter diagnosis and management. MethodsWe present a prospective collection of cases across 3 cardiac centers of consecutive patients with WCT presumed to be VT who were referred for consideration of an ICD, and in whom further evaluation including an EPS ultimately demonstrated SVT with aberrancy as the culprit arrhythmia. Results22 patients were identified (17 male, mean age 50±13 years. Available rhythm data at the time of referral was presumptively diagnosed as monomorphic VT in 16 patients and polymorphic VT in 6 patients. Underlying structural heart disease was present in 20 (91%). EPS resulted in a diagnosis of SVT with aberrancy in all cases: comprising AV nodal re-entry tachycardia (n=10), orthodromic reciprocating tachycardia (n=3), focal atrial tachycardia (n=3), AF/AFL (n=3) and 'double fire' tachycardia (n=2). 21 (95%) patients underwent successful ablation. All patients remained free of arrhythmia recurrence at a median of 3.4 years of follow-up. ICD insertion was obviated in 18 (82%) patients, with 1 patient proceeding to ICD extraction. ConclusionSVT with atypical aberrancy may mimic monomorphic or polymorphic VT. Careful examination of all available rhythm data and consideration of an EPS can confirm SVT and obviate the need for ICD therapy.

Tachyarrhythmias in congenital heart disease.

The prevalence of congenital heart disease (CHD) in adult patients has risen with advances in diagnostic and surgical techniques. Surgical modifications and hemodynamic changes increase the susceptibility to arrhythmias, impacting morbidity and mortality rates, with arrhythmias being the leading cause of hospitalizations and sudden deaths. Patients with CHD commonly experience both supraventricular and ventricular arrhythmias, with each CHD type associated with different arrhythmia patterns. Macroreentrant atrial tachycardias, particularly cavotricuspid isthmus-dependent flutter, are frequently reported. Ventricular arrhythmias, including monomorphic ventricular tachycardia, are prevalent, especially in patients with surgical scars. Pharmacological therapy involves antiarrhythmic and anticoagulant drugs, though data are limited with potential adverse effects. Catheter ablation is preferred, demanding meticulous procedural planning due to anatomical complexity and vascular access challenges. Combining imaging techniques with electroanatomic navigation enhances outcomes. However, risk stratification for sudden death remains challenging due to anatomical variability. This article practically reviews the most common tachyarrhythmias, treatment options, and clinical management strategies for these patients.

The influence of endurance exercise training on myocardial fibrosis and arrhythmogenesis in a coxsackievirus B3 myocarditis mouse model

Nonischaemic myocardial fibrosis is associated with cardiac dysfunction, malignant arrhythmias and sudden cardiac death. In the absence of a specific aetiology, its finding as late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging is often attributed to preceding viral myocarditis. Athletes presenting with ventricular arrhythmias often have nonischaemic LGE. Previous studies have demonstrated an adverse effect of exercise on the course of acute viral myocarditis. In this study, we have investigated, for the first time, the impact of endurance training on longer-term outcomes such as myocardial fibrosis and arrhythmogenicity in a murine coxsackievirus B3 (CVB)-induced myocarditis model. Male C57BL/6J mice (n = 72) were randomly assigned to 8 weeks of forced treadmill running (EEX) or no exercise (SED). Myocarditis was induced 2 weeks later by a single intraperitoneal injection with CVB, versus vehicle in the controls (PBS). In a separate study, mice (n = 30) were subjected to pretraining for 13 weeks (preEEX), without continuation of exercise during myocarditis. Overall, continuation of exercise resulted in a milder clinical course of viral disease, with less weight loss and better preserved running capacity. CVB-EEX and preEEX-CVB mice tended to have a lower mortality rate. At sacrifice (i.e. 6 weeks after inoculation), the majority of virus was cleared from the heart. Histological assessment demonstrated prominent myocardial inflammatory infiltration and cardiomyocyte loss in both CVB groups. Inflammatory lesions in the CVB-EEX group contained higher numbers of pro-inflammatory cells (iNOS-reactive macrophages and CD8+ T lymphocytes) compared to these in CVB-SED. Treadmill running during myocarditis increased interstitial fibrosis [82.4% (CVB-EEX) vs. 56.3% (CVB-SED); P = 0.049]. Additionally, perivascular and/or interstitial fibrosis with extensive distribution was more likely to occur with exercise [64.7% and 64.7% (CVB-EEX) vs. 50% and 31.3% (CVB-SED); P = 0.048]. There was a numerical, but not significant, increase in the number of scars per cross-section (1.9 vs. 1.2; P = 0.195), with similar scar distribution and histological appearance in CVB-EEX and CVB-SED. In vivo electrophysiology studies did not induce sustained monomorphic ventricular tachycardia, only nonsustained (usually polymorphic) runs. Their cumulative beat count and duration paralleled the increased fibrosis between CVB-EEX and CVB-SED, but the difference was not significant (P = 0.084 for each). Interestingly, in mice that were subjected to pretraining only without continuation of exercise during myocarditis, no differences between pretrained and sedentary mice were observed at sacrifice (i.e. 6 weeks after inoculation and training cessation) with regard to myocardial inflammation, fibrosis, and ventricular arrhythmogenicity. In conclusion, endurance exercise during viral myocarditis modulates the inflammatory process with more pro-inflammatory cells and enhances perivascular and interstitial fibrosis development. The impact on ventricular arrhythmogenesis requires further exploration.