Episodes Of Ventricular Tachycardia Research Articles

Catastrophic implantable cardioverter-defibrillator misclassification of ventricular tachycardia

Inappropriate therapy is a frequent adverse consequence of implantable cardioverter-defibrillator. Inappropriate therapy often occurs due to the misinterpretation of sinus tachycardia or atrial fibrillation/flutter with rapid atrioventricular conduction by the device. Current implantable cardioverter-defibrillator (ICD) mechanisms integrate various discriminators into algorithms to differentiate supraventricular tachycardia (SVT) from ventricular tachycardia (VT), to prevent such occurrences. A 40-year-old man suffered seizures and cardiac arrest abruptly, without prior complaints of chest pain. Without delay, he initiated cardiopulmonary resuscitation (CPR), resulting in the regaining of spontaneous circulation. The patient had previously received a single-chamber ICD due to recurring VT and a prior episode of cardiac arrest. The patient had a medical background of coronary artery disease with complete revascularisation and no previous occurrence of SVT. Interrogating the ICD revealed captured non-sustained ventricular tachycardia (NSVT) and SVT events but no VT episode or shock therapy. During the specified time period, the patient underwent an electrophysiological study, and no SVT was induced with the normal function of the atrioventricular and sinoatrial nodes. Various causes can lead to errors in morphology discrimination criteria in single-chamber ICDs. Extending the detection interval is highly recommended to avoid misclassification of ICDs.

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.

Stratification of arrhythmic risk in patients admitted for acute coronary syndrome: the role of the machine learning-derived PRAISE score

Abstract Funding Acknowledgements None. Background Patients with acute coronary syndrome (ACS) have a high arrhythmic burden, and either ventricular and supraventricular arrhythmias are very common during hospitalization[1]. Patients who develop arrhythmias show higher mortality and worse prognosis. The PRAISE (Prediction of Adverse Events Following an Acute Coronary Syndrome) score is a machine-learning based model for predicting 1-year all cause death, recurrent acute myocardial infarction and major bleedings in patients after ACS[2]. To date, its role to predict arrhythmic complications in ACS remains unknown. Purpose We hypothesized that patients with higher PRAISE score have a higher arrhythmic burden. Aim was to evaluate in a prospective protocol the PRAISE score capability for identifying patients with ACS at higher risk of arrhythmic complications during in-hospital stay. Methods A total of 365 consecutive patients admitted to our cardiac intensive care unit for ACS and undergoing percutaneous coronary intervention were enrolled. All patient was monitored by continuous electrocardiogram during hospitalization. The PRAISE score was obtained for each patient <24 hours from admission. Patients were divided into 2 groups based on the results of the PRAISE score for all-cause of death as patients without high PRAISE score (e.g. with low to intermediate risk, n=350) and patients with high PRAISE score (e.g. with high risk, n=15). The occurrence of atrial fibrillation (AF) and ventricular arrhythmias (VAs) up to discharge was recorded. AF was defined by detection of at least one episode of uncoordinated atrial electrical activation and irregular R-R intervals, in absence of distinct repeating P waves and with irregular atrial activations lasting at least 5 minutes. We considered as VAs all episodes of ventricular non-sustained tachycardia, sustained ventricular tachycardia and ventricular fibrillation. Results ROC curve analysis indicated a significant relationship between high PRAISE score and risk of both in-hospital AF (AUC 0.89, 95%CI 0.82-0.94, p=0.0001) and VAs (AUC 0.69, 95%CI 0.64-0.75, p=0.0001). A high PRAISE score had a specificity of 99% for AF and 92% for VAs. By Kaplan-Meier analysis, patients with high PRAISE score more frequently developed AF (30% vs 4% in those without high score; log rank p=0.00001) and VAs (77% vs 35%; log rank p=0.00001). Multivariate analysis showed that a high PRAISE score was an independent predictor of both AF (HR 4.08, 95%CI 1.14-14.58, p=0.030) and VAs (HR 2.36, 95%CI 1.08-5.14, p=0.030). Conclusions In patients hospitalized for ACS, the PRAISE score has a comprehensive capability to identify with high specificity those patients prone to develop arrhythmic events during hospitalization. This may be important in order to stratify patients with higher arrhythmic risk in whom individualized strategies may improve the clinical outcome.Baseline features of the populationKaplan-Meier anaysis

Takotsubo cardiomyopathy following pacemaker insertion complicated with polymorphic ventricular tachycardia: a case report

BackgroundTakotsubo cardiomyopathy is a novel form of rapidly reversible heart failure occurring secondary to a stressor that mimics an acute coronary event. The underlying etiology of the stressor is highly variable and can include medical procedures. Pacemaker insertion is an infrequent cause of Takotsubo cardiomyopathy.Case presentationAn 86-year-old Caucasian woman underwent an uncomplicated pacemaker insertion for symptomatic complete heart block in the background of slow atrial fibrillation. A transient episode of polymorphic ventricular tachycardia was noted on day 1 following the procedure; however, her pacemaker was checked and, as she remained stable, she was discharged home. She presented again 5 days later with symptomatic heart failure. Chest X-ray confirmed pulmonary edema. Echocardiography confirmed new onset severe left ventricle dysfunction. Pacemaker checks were normal and lead placement was confirmed. Though her troponin I was elevated, her coronary angiogram was normal. Contrast enhanced echocardiography suggested apical ballooning favoring Takotsubo cardiomyopathy. She was treated for heart failure and made a good recovery. Her follow-up echocardiography a month later showed significant improvement in left ventricle function.ConclusionsTakotsubo cardiomyopathy is mediated by a neuro-cardiogenic mechanism due to hypothalamic–pituitary–adrenal axis activation. It generally has a good prognosis. Complications though uncommon, can occur and include arrhythmias. Pacemaker insertion as a precipitant stressor is an infrequent cause of Takotsubo cardiomyopathy. As pacemaker insertions are more frequent in the elderly age group, this phenomenon should be recognized as a potential complication.

Automatic implantable cardioverter defibrillator (AICD) implantation as secondary prevention of cardiac sarcoidosis-associated ventricular tachycardia

Background: Cardiac sarcoidosis can cause a wide range of symptoms, including shortness of breath, chest pain, oedema, and fatal arrhythmias such as ventricular tachycardia (VT). Because the symptoms can be nonspecific, diagnosing cardiac sarcoidosis can be challenging. Treatment options may include corticosteroids to reduce inflammation, immunosuppressive drugs to prevent further damage, medications to control symptoms, ablation procedures, and defibrillators to prevent cardiac arrest. Case: A 60-year-old woman who has sarcoidosis affecting multiple organs including cardiac sarcoidosis, non-ischemic cardiomyopathy with reduced ejection fraction, and hypertension, was admitted with tachycardia, shortness of breath, and a recently fired automatic implantable cardioverter defibrillator (AICD). Three months prior, the patient was admitted for a syncopal episode and diagnosed with cardiac sarcoidosis through cardiac magnetic resonance imaging (MRI) and positron emission tomography (PET), which demonstrated active inflammation, and an AICD was implanted. During this admission, the patient had an episode of ventricular tachycardia and was treated with amiodarone and lidocaine. The patient received steroids, sacubitril/valsartan, and methotrexate. After 48 hours of observation, the patient was discharged without further events. Conclusion: Cardiac sarcoidosis is a rare but serious disease that can lead to life-threatening cardiac complications such as ventricular tachycardia. Early diagnosis and aggressive management are crucial for improving outcomes and preventing sudden cardiac death. AICD implantation as a secondary prevention in cardiac sarcoidosis might prevent cardiac arrest.

SYMPATHETIC DENERVATION OF STELLATE GANGLION FOR MANAGEMENT OF PERSISTENT VENTRICULAR TACHYCARDIA: A CASE REPORT

SYMPATHETIC DENERVATION OF STELLATE GANGLION FOR MANAGEMENT OF PERSISTENT VENTRICULAR TACHYCARDIA: A CASE REPORT

Carnitine palmitoyltransferase II (CPT II) deficiency responsible for refractory cardiac arrhythmias, acute multiorgan failure and early fatal outcome

BackgroundCarnitine palmitoyltransferase II (CPT II) deficiency is a rare inborn error of mitochondrial fatty acid metabolism with autosomal recessive pattern of inheritance. Its phenotype is highly variable (neonatal, infantile, and adult onset) on the base of mutations of the CPT II gene. In affected subjects, long-chain acylcarnitines cannot be subdivided into carnitine and acyl-CoA, leading to their toxic accumulation in different organs. Neonatal form is the most severe, and all the reported patients died within a few days to 6 months after birth. Hereby, we report on a male late-preterm newborn who presented refractory cardiac arrhythmias and acute multiorgan (hepatic, renal, muscular) injury, leading to cerebral hemorrhage, hydrocephalus, cardiovascular failure and early (day 5 of life) to death. Subsequently, extended metabolic screening and target next generation sequencing (NGS) analysis allowed the CPT II deficiency diagnosis.Case presentationThe male proband was born at 36+ 4 weeks of gestation by spontaneous vaginal delivery. Parents were healthy and nonconsanguineous, although both coming from Nigeria. Family history was unremarkable. Apgar score was 9/9. At birth, anthropometric measures were as follows: weight 2850 g (47th centile, -0.07 standard deviations, SD), length 50 cm (81st centile, + 0.89 SD) and occipitofrontal circumference (OFC) 35 cm (87th centile, + 1.14 SD). On day 2 of life our newborn showed bradycardia (heart rate around 80 bpm) and hypotonia, and was then transferred to the Neonatal Intensive Care Unit (NICU). There, he subsequently manifested many episodes of ventricular tachycardia, which were treated with pharmacological (magnesium sulfate) and electrical cardioversion. Due to the critical conditions of the baby (hepatic, renal and cardiac dysfunctions) and to guarantee optimal management of the arrythmias, he was transferred to the Pediatric Cardiology Reference Center of our region (Sicily, Italy), where he died 2 days later. Thereafter, the carnitines profile evidenced by the extended metabolic screening resulted compatible with a fatty acid oxidation defect (increased levels of acylcarnitines C16 and C18, and low of C2); afterwards, the targeted next generation sequencing (NGS) analysis revealed the known c.680 C > T p. (Pro227Leu) homozygous missense mutation of the CPTII gene, for diagnosis of CPT II deficiency. Genetic investigations have been, then, extended to the baby’s parents, who were identified as heterozygous carriers of the same variant. When we meet again the parents for genetic counseling, the mother was within the first trimester of her second pregnancy. Therefore, we offered to the couple and performed the prenatal target NGS analysis on chorionic villi sample, which did not detect any alterations, excluding thus the CPT II deficiency in their second child.ConclusionsCPTII deficiency may be suspected in newborns showing cardiac arrhythmias, associated or not with hypertrophic cardiomyopathy, polycystic kidneys, brain malformations, hepatomegaly. Its diagnosis should be even more suspected and investigated in cases of increased plasmatic levels of creatine phosphokinase and acylcarnitines in addition to kidney, heart and liver dysfunctions, as occurred in the present patient. Accurate family history, extended metabolic screening, and multidisciplinary approach are necessary for diagnosis and adequate management of affected subjects. Next generation sequencing (NGS) techniques allow the identification of the CPTII gene mutation, essential to confirm the diagnosis before or after birth, as well as to calculate the recurrence risk for family members. Our report broads the knowledge of the genetic and molecular bases of such rare disease, improving its clinical characterization, and provides useful indications for the treatment of patients.

Effects of ranolazine on the arrhythmic substrate in hypertrophic cardiomyopathy.

Introduction: Hypertrophic cardiomyopathy (HCM) is a leading cause of lethal arrhythmias in the young. Although the arrhythmic substrate has been hypothesised to be amenable to late Na+ block with ranolazine, the specific mechanisms are not fully understood. Therefore, this study aimed to investigate the substrate mechanisms of safety and antiarrhythmic efficacy of ranolazine in HCM. Methods: Computational models of human tissue and ventricles were used to simulate the electrophysiological behaviour of diseased HCM myocardium for variable degrees of repolarisation impairment, validated against in vitro and clinical recordings. S1-S2 pacing protocols were used to quantify arrhythmic risk in scenarios of (i) untreated HCM-remodelled myocardium and (ii) myocardium treated with 3µM, 6µM and 10µM ranolazine, for variable repolarisation heterogeneity sizes and pacing rates. ECGs were derived from biventricular simulations to identify ECG biomarkers linked to antiarrhythmic effects. Results: 10µM ranolazine given to models manifesting ventricular tachycardia (VT) at baseline led to a 40% reduction in number of VT episodes on pooled analysis of >40,000 re-entry inducibility simulations. Antiarrhythmic efficacy and safety were dependent on the degree of repolarisation impairment, with optimal benefit in models with maximum JTc interval <370ms. Ranolazine increased risk of VT only in models with severe-extreme repolarisation impairment. Conclusion: Ranolazine efficacy and safety may be critically dependent upon the degree of repolarisation impairment in HCM. For moderate repolarisation impairment, reductions in refractoriness heterogeneity by ranolazine may prevent conduction blocks and re-entry. With severe-extreme disease substrates, reductions of the refractory period can increase re-entry sustainability.

Electrical storm after left ventricular assist device (LVAD) implantation.

Ventricular tachycardia storm or electrical storm (ES) is a common complication following left ventricular assist device (LVAD) implantation. The factors contributing to ES and outcomes are less studied. The study aimed to determine the factors associated with ES and the probability of survival in patients undergoing LVAD in three tertiary centers over a span of 15 years. We performed a retrospective cohort study on all patients who underwent LVAD implantation at the Mayo Clinic (Rochester, Phoenix, and Jacksonville) from January 1, 2006to December 31, 2020. ES was defined as ≥3 episodes of sustained ventricular tachycardia over a period of 24 h with no identifiable reversible cause. Detailed chart reviews of the electronic health records within the Mayo Clinic and outside medical records were performed. A total of 883 patients who underwent LVAD implantation were included in our study. ES occurred in 7% (n = 61) of patients with a median of 13 days (interquartile range [IQR]: 5-297 days) following surgery. We found 57% of patients (n = 35) developed ES within 30 days, while 43% (n = 26) patients developed ES at a median of 545 (IQR 152-1032) days after surgery. Following ES, 26% of patients died within 1 year. Patients with ES had a significant association with a history of ventricular arrhythmias and implantable cardioverter defibrillator(ICD) shocks before the procedure. ES was significantly associated with reduced survival compared to patients without ES(hazards ratio [HR]: 1.92, 95% CI: 1.39-2.64, p < .001). Following LVAD implantation, the rate of ES was 7% with majority of ES occurring within 30 days of LVAD. Risk factors for ES included pre-implant history of ventricular arrhythmias and ICD shock. ES was significantly associated with reduced survival compared to patients without ES.

Electrical Storm/Refractory Ventricular Tachycardia.

This simulation case was created for emergency medicine (EM) residents at all levels of training. Cardiac electrical storm (ES) is commonly defined as three or more episodes of sustained ventricular tachycardia, ventricular fibrillation, or three shocks from an implantable defibrillator within a 24 hour period.1 This can occur in up to 30-40% of patients with implantable defibrillators; however, it may also present in a wide variety of patients, including those with structural heart disease, myocardial infarction, electrolyte disturbances, and channelopathies.2,3 With each subsequent episode of ventricular arrhythmia, the arrhythmogenic potential of the heart may increase secondary to increased intracellular calcium dysregulation, myocardial injury, and increased endogenous release of catecholamines. The increased pain and catecholamine release from cardioversion/defibrillation and exogenous epinephrine during cardiac arrest further exacerbates ES.2 This carries a significant mortality risk of up to 12% in the first 48 hours.3This case involves a basic knowledge of the Advanced Cardiac Life Support (ACLS) for ventricular tachycardia, both with and without a pulse, and the application of Sgarbossa criteria in a patient with an ST elevation myocardial infarction (STEMI) which makes it ideal for the PGY-1. However, the case quickly becomes refractory to the basic management prescribed in ACLS, requiring trouble shooting and quick thinking about deeper pathophysiology, a skill that is crucial for all emergency medicine physicians. There are multiple ways to troubleshoot this case, making for a good variety of discussion and recent literature review on the complexities of a relatively common arrhythmia, ventricular tachycardia. By the end of this simulation, learners should be able to: 1) recognize unstable ventricular tachycardia and initiate ACLS protocol, 2) practice dynamic decision making by switching between various ACLS algorithms, 3) create a thoughtful approach for further management of refractory ventricular tachycardia, 4) interpret electrocardiogram (ECG) with ST-segment elevation (STE) and left bundle branch block (LBBB), 5) appropriately disposition the patient and provide care after return of spontaneous circulation (ROSC), 6) navigate a difficult conversation with the patient's husband when she reveals that the patient's wishes were to not be resuscitated. This simulation was performed using high-fidelity simulation followed by an immediate debriefing with nine learners who directly participated in the SIM and twenty-three residents, who were online observers via Zoom. This case was done during our conference day, and there were a total of approximately forty total learners comprised of medical students, PGY-1, PGY-2 and PGY-3 residents. There were several medical students who also observed via Zoom but were not surveyed, and the survey was sent to 32 learners. The case was run three separate times with each session consisting of three-four learners at the same level of training, with other learners in the same level of training observing via Zoom™ video platform. Since we can only have a team of three-four learners participate per group during simulation, the rest of the learners were observing the case and the debrief. There was one simulation instructor and one technician. We sent an online survey to all the participants and the observers after the debrief via surveymonkey.com. The survey collected responses to the following statements: (1) the case was believable, (2) the case had right amount of complexity, (3) the case helped in improving medical knowledge and patient care, (4) the simulation environment gave me a real-life experience and, (5) the debriefing session after simulation helped improve my knowledge. Likert scale was used to collect the responses. A total of thirteen participants responded to the survey. One hundred percent of them either strongly agreed or agreed that the case was believable and that it helped in improving medical knowledge and patient care. Fifty-four percent strongly agreed, 38 percent agreed, and eight percent were neutral about the case having the right amount of complexity. Thirty one percent strongly agreed, 61 percent agreed, and eight percent were neutral about the case giving them real-life experience. All of them agreed that the debriefing session helped them improve their knowledge. The high-fidelity simulation case was helpful with educating learners with ventricular tachycardia and fibrillation. Learners learned how to switch between various ACLS algorithms and how to manage a patient with refractory ventricular fibrillation. Learners enforced their knowledge in how to communicate with patient's family members when the patient does not want resuscitation. Stable ventricular tachycardia, unstable ventricular tachycardia, refractory ventricular tachycardia, electrical storm, STEMI equivalents, medical simulation.

Premature ventricular complexes: Assessing burden density in a large national cohort to better define optimal ECG monitoring duration

BackgroundPremature ventricular contraction (PVC) burden is a risk factor for heart failure and cardiovascular death in patients with structural heart disease. Long-term electrocardiographic monitoring can have a significant impact on PVC burden evaluation by further defining PVC distribution patterns. ObjectiveThis study aimed to ascertain the optimal duration of electrocardiographic monitoring to characterize PVC burden and to understand clinical characteristics associated with frequent PVCs and nonsustained ventricular tachycardia in a large US cohort. MethodsCommercial data (iRhythm’s Zio patch) from June 2011 to April 2022 were analyzed. Inclusion criteria were age >18 years, PVC burden ≥5%, and wear period ≥13 days. PVC burden cutoffs were determined on the basis of AHA/ACC/HRS guidelines for very frequent PVCs (10,000–20,000 during 24 hours). Patients were assigned to categories by PVC densities: low, <10%; moderate, 10% to <20%; and high, ≥20%. Mean measured error was assessed at baseline and daily until the wear period’s end for overall PVC burden and different PVC densities. ResultsAnalysis of 106,705 patch monitors revealed a study population with mean age of 70.6 ± 14.6 years (33.6% female). PVC burden was higher in male patients and those >65 years of age. PVC burden mean error decreased from 2.9% at 24 hours to 1.3% at 7 days and 0.7% at 10 days. Number of ventricular tachycardia episodes per patient increased with increasing PVC burden (P < .0001). ConclusionExtending ambulatory monitoring beyond 24 hours to 7 days or more improves accuracy of assessing PVC burden. Ventricular tachycardia frequency and duration vary by initial PVC density, highlighting the need for prolonged cardiac monitoring.

Safety and efficacy of levosimendan in patients with cardiac amyloidosis

BackgroundPatients with cardiac amyloidosis (CA) often experience heart failure (HF) episodes. No evidence is available on inotropic therapy. This study aims to fill this gap by examining the safety and efficacy of levosimendan. MethodsWe retrieved all HF patients receiving ≥1 levosimendan infusion from 2013 to 2023. CA patients were matched with HF patients without CA (controls) based on sex, age, and left ventricular ejection fraction (LVEF). The response to levosimendan was measured as changes in daily urinary output, body weight, N-terminal pro-B-type natriuretic peptide (NT-proBNP), and estimated glomerular filtration rate (eGFR). ResultsCA patients (median age 77 years, 73% men, 59% with ATTR-CA) and controls were compared. Levosimendan infusion was stopped because of hypotension in 2 cases with CA and (in 1 case) worsening renal function, and in 2 controls because of ventricular tachycardia episodes and (in 1 case) hypotension. CA patients showed a trend toward increased daily urinary output (p = 0.078) and a significant decrease in body weight (p < 0.001), without significant changes in NT-proBNP (p = 0.497) and eGFR (p = 0.732). Both CA patients and controls displayed similar changes in urinary output, weight, and eGFR, but NT-proBNP decreased more significantly among controls (p < 0.001). No differences were noted in rehospitalization rates, but CA patients experienced higher mortality at 6 and 12 months (p = 0.003 and p = 0.001, respectively). ConclusionsLevosimendan appears safe for CA patients needing inotropic support. The diuretic response and weight decrease during hospitalization were comparable between CA patients and matched HF patients, despite the greater mortality of CA patients after discharge.

Delineating postinfarct ventricular tachycardia substrate with dynamic voltage mapping in areas of omnipolar vector disarray

BackgroundDefining post-infarct ventricular arrhythmic substrate is challenging with voltage mapping alone, though may be improved in combination with an activation map. Omnipolar Technology on the EnSite X system displays activation as vectors that can be superimposed onto a voltage map. ObjectiveTo optimise voltage map settings during ventricular tachycardia (VT) ablation, adjusting them dynamically using Omnipolar vectors. MethodsConsecutive patients undergoing substrate mapping were retrospectively studied. We categorised Omni-vectors as “uniform” when pointing in one direction, or in “disarray” when pointing in multiple directions. We superimposed vectors onto voltage maps coloured purple in tissue >1.5mV, and the voltage settings were adjusted so uniform vectors appeared within purple voltages, a process termed “Dynamic Voltage Mapping” (DVM). Vectors in disarray appeared within red-blue lower voltages. Results17 substrate maps were studied in 14 patients (mean age 63±13 years; mean LVEF 35±6%, median 4 (IQR 2-8.5) recent VT episodes). The DVM mean voltage threshold that differentiated tissue supporting uniform vectors from disarray was 0.27mV, ranging between patients from 0.18-0.50mV, with good inter-observer agreement (median difference: 0.00mV). We found that VT isthmus components, as well as sites of latest activation, isochronal crowding, and excellent pace-maps co-located with tissue along the DVM borderzone surrounding areas of disarray. ConclusionDynamic Voltage Mapping, guided by areas of Omnipolar vector disarray, allows for individualised post-infarct ventricular substrate characterisation. Tissue bordering areas of disarray may harbour greater arrhythmogenic potential.

Acute myocardial infarction-like event in a young patient with biventricular arrhythmogenic cardiomyopathy

The article describes a clinical case of biventricular arrhythmogenic cardiomyopathy (ACM) presented with myocardial infarction (MI) — like event in a young patient. The patient was hospitalized with suspected acute coronary syndrome and an episode of ventricular tachycardia (VT). Based on increased cardiac troponin, left ventricular systolic dysfunction with wall motion abnormalities, and nonobstructive coronary arteries the initial diagnosis of type 2 MI was made. To verify the etiology behind VT and ventricular structural abnormalities cardiac magnetic resonance imaging (MRI) was performed. Abnormalities of both right and left ventricles demonstrated by MRI and supported by the genetic testing established the diagnosis of biventricular ACM. Since the diagnosis was made, initially diagnosed MI was reassessed in favor of acute myocardial injury as a characteristic of ACM course. ACM should be included into differential diagnosis with MI and acute myocarditis in patients with elevated troponin and nonobstructive coronary arteries.

Sex- and age-dependent susceptibility to ventricular arrhythmias in the rat heart ex vivo

The incidence of life-threatening ventricular arrhythmias, the most common cause of sudden cardiac death (SCD), depends largely on the arrhythmic substrate that develops in the myocardium during the aging process. There is a large deficit of comparative studies on the development of this substrate in both sexes, with a particular paucity of studies in females. To identify the substrates of arrhythmia, fibrosis, cardiomyocyte hypertrophy, mitochondrial density, oxidative stress, antioxidant defense and intracellular Ca2+ signaling in isolated cardiomyocytes were measured in the hearts of 3- and 24-month-old female and male rats. Arrhythmia susceptibility was assessed in ex vivo perfused hearts after exposure to isoproterenol (ISO) and hydrogen peroxide (H2O2). The number of ventricular premature beats (PVBs), ventricular tachycardia (VT) and ventricular fibrillation (VF) episodes, as well as intrinsic heart rate, QRS and QT duration, were measured in ECG signals recorded from the surfaces of the beating hearts. After ISO administration, VT/VFs were formed only in the hearts of males, mainly older ones. In contrast, H2O2 led to VT/VF formation in the hearts of rats of both sexes but much more frequently in older males. We identified several components of the arrhythmia substrate that develop in the myocardium during the aging process, including high spontaneous ryanodine receptor activity in cardiomyocytes, fibrosis of varying severity in different layers of the myocardium (nonheterogenic fibrosis), and high levels of oxidative stress as measured by nitrated tyrosine levels. All of these elements appeared at a much greater intensity in male individuals during the aging process. On the other hand, in aging females, antioxidant defense at the level of H2O2 detoxification, measured as glutathione peroxidase expression, was weaker than that in males of the same age. We showed that sex has a significant effect on the development of an arrhythmic substrate during aging. This substrate determines the incidence of life-threatening ventricular arrhythmias in the presence of additional stimuli with proarrhythmic potential, such as catecholamine stimulation or oxidative stress, which are constant elements in the pathomechanism of most cardiovascular diseases.

Spontaneous Coronary Artery Dissection Presenting as Electrical Storm: A Case Report.

Spontaneous coronary artery dissection (SCAD) is an important cause of myocardial infarction in patients of younger age without typical atherosclerotic risk factors and can present with ventricular arrhythmia such as ventricular tachycardia (VT) or ventricular fibrillation (VF). Electrical storm (ES) is defined as greater than or equal to 3 episodes of VT or VF occurring within 24 hours. A healthy 38-year-old-male developed chest pain while exercising at the gym and presented to the emergency department unresponsive in a ventricular arrhythmia defined as ES. The patient's cardiac arrest was initially refractory to standard defibrillation and Advanced Cardiac Life Support medications. He was ultimately diagnosed with SCAD of the left anterior descending artery, which was stented. The patient survived neurologically intact after a 13-day hospital stay. Spontaneous coronary artery dissection is a significant cause of acute coronary syndrome and occurs in healthier patients without cardiac risk factors. Electrical storm represents a unique manifestation of SCAD. Emergency physicians should maintain a heightened suspicion for SCAD for accurate diagnosis and treatment.

Complex Substrate Leading to PVC-Mediated Systolic Dysfunction in addition to Sustained Monomorphic VT in Repaired Tetralogy of Fallot.

Frequent premature ventricular complexes (PVCs) are associated with deleterious effects on left ventricular (LV) function in various clinical scenarios. Repaired tetralogy of Fallot (rTOF) is frequently affected by sustained ventricular arrhythmias dependent on complex post-surgical substrates. However, there is limited data regarding the potential of arrhythmogenic isthmuses to generate frequent PVCs and PVC-mediated LV systolic dysfunction development in rTOF. We present a case of rTOF experiencing relatively infrequent episodes of internal shocks for episodes of sustained monomorphic ventricular tachycardia and a high burden of PVCs associated with left ventricular systolic function deterioration, in which the successful substrate ablation of the anatomical VT isthmuses also led to PVC abolition and consequently to LV systolic function normalization. In such cases, understanding the pathogenic mechanisms that lead to LV dysfunction is only possible by rigorous clinical reasoning, which leads to a tailored specific treatment.

Arrhythmias in patients with acute ST-elevation myocardial infarction induced by various risk factors during the first day after myocardial reperfusion by primary percutaneous coronary intervention

Introduction. Acute coronary syndrome, in particular acute ST-elevation myocardial infarction (STEMI), is often accompanied by complex hemodynamically significant arrhythmias and conduction disorders. Such patients have a worse prognosis compared to patients with sinus rhythm. Arrhythmias in patients with STEMI are facilitated by the presence of comorbidities such as arterial hypertension, diabetes mellitus, obesity, and post-COVID-19 syndrome. The aim of the study. To elucidate the nature of arrhythmias in patients with acute STEMI induced by various risk factors during the first day after myocardial reperfusion by primary percutaneous coronary intervention. Materials and methods. The study involved 50 patients aged 45 to 83 years (average age – 63,4 ± 9,6 years; men – 70,97 %, women – 29,03 %), who were treated during 2021-2023 at the cardiology and reperfusion therapy department of Cardio-vascular center of ʺSaint Panteleimon Hospital in Lvivʺ and the infarction department of ʺLviv Regional Clinical Cardiological Centerʺ. The patients under investigation were subjected to daily electrocardiogram (ECG) monitoring for 24 hours after stenting of the infarct-related coronary artery, using a 7-channel ECG recorder Solvaig 06000.7 with computer processing of the recording using the DiaCard2 software. The obtained material was further subjected to software packages Microsoft Excel 2022, Statistica 10. Results. It was established that among supraventricular rhythm disturbances the most common were premature contractions, the average number of which per patient was significantly higher in the presence of obesity. Similarly high it was in post COVID-19 patients, as well as in those with hypertension. In post-coronavirus infection and in hypertension cases, extrasystoles were often in the form of pairs, triplets, bigemia, and trigemia; paroxysms of supraventricular tachycardia were also recorded in these patients. Among the ventricular arrhythmias also the most frequent were premature cardiac contractions, significantly more oftenly recorded in patients with hypertension and those experienced COVID-19; only in these patients were documented extrasystoles in the form of pairs, triplets, bigeminy, trigeminy, runs of ʺR to Tʺ, which are currently considered as harbingers of life-threatening ventricular arrhythmias. In the presence of hypertension and post-COVID-19, episodes of unstable ventricular tachycardia were also observed. Conclusions. In patients with STEMI, both supraventricular and ventricular premature contractions and episodes of supraventricular and unstable ventricular tachycardia are quite common during the first day after primary percutaneous coronary intervention with infarct-related coronary artery stenting, which is evidence of myocardial electrical instability. The nature of rhythm disturbances in the presence of hypertension and post-COVID-19 is prognostically unfavorable and indicates a higher risk of lifethreatening arrhythmias in these patients. Myocardial revascularization should be supplemented with optimal medical treatment in order to prevent the adverse cardiovascular events in post-STEMI patients. Further research should be directed toward elucidation of predictive value of detected arrhythmias with respect to the occurrence of unfavorable cardiovascular events in the early and long-term post-infarction period.

Neonatal Near Fatal Flecainide Toxicity

Background: Flecainide is an anti-arrhythmic medication with a narrow therapeutic index and a high mortality rate, when overdosed. Few cases of flecainide toxicity in neonates and children due to medication error have been reported in the literature. A case of an accidental flecainide overdose in a neonate in Oman was presented. Case Presentation: A 19-day-old newborn girl developed persistent supra ventricular tachycardia (SVT) after receiving nebulized albuterol for acute bronchitis. After unsuccessful treatment with adenosine, she was given flecainide 5.6 mg orally every 24 hours for resolution of the SVT. On day four of admission, the child inadvertently received 100 mg of flecainide orally due to a dose calculation error. The child developed wide complex tachyarrhythmia followed by pulseless ventricular tachycardia (VT) requiring cardiopulmonary resuscitation. Sodium bicarbonate IV bolus followed by an infusion was administered. The patient developed two additional episodes of pulseless VT that coincided temporally with two interruptions of the sodium bicarbonate infusion, and required high dose of inotropic support. The patient developed convulsions but her brain ultrasound was normal. Her condition stabilized on day three after the toxicity occurred. Repeated echo showed a normal EF. The patient was discharged on propranolol and levetiracetam and was doing well on outpatient follow up. Conclusion: Flecainide is a potentially lethal medication in overdose due to its sodium channel blocking properties. Sodium bicarbonate remains an essential component of treatment.

Cardiac radiotherapy transiently alters left ventricular electrical properties and induces cardiomyocyte-specific ventricular substrate changes in heart failure.

Ongoing clinical trials investigate the therapeutic value of stereotactic cardiac radioablation (cRA) in heart failure patients with ventricular tachycardia. Animal data indicate an effect on local cardiac conduction properties. However, the exact mechanism of cRA in patients remains elusive. Aim of the current study was to investigate in vivo and in vitro myocardial properties in heart failure and ventricular tachycardia upon cRA. High-density 3D electroanatomic mapping in sinus rhythm was performed in a patient with a left ventricular assist device and repeated ventricular tachycardia episodes upon several catheter-based endocardial radio-frequency ablation attempts. Subsequent to electroanatomic mapping and cRA of the left ventricular septum, two additional high-density electroanatomic maps were obtained at 2- and 4-month post-cRA. Myocardial tissue samples were collected from the left ventricular septum during 4-month post-cRA from the irradiated and borderzone regions. In addition, we performed molecular biology and mitochondrial density measurements of tissue and isolated cardiomyocytes. Local voltage was altered in the irradiated region of the left ventricular septum during follow-up. No change of local voltage was observed in the control (i.e. borderzone) region upon irradiation. Interestingly, local activation time was significantly shortened upon irradiation (2-month post-cRA), a process that was reversible (4-month post-cRA). Molecular biology unveiled an increased expression of voltage-dependent sodium channels in the irradiated region as compared with the borderzone, while Connexin43 and transforming growth factor beta were unchanged (4-month post-cRA). Moreover, mitochondrial density was decreased in the irradiated region as compared with the borderzone. Our study supports the notion of transiently altered cardiac conduction potentially related to structural and functional cellular changes as an underlying mechanism of cRA in patients with ventricular tachycardia.