Onset Of Ventricular Tachycardia Research Articles

Ventricular tachycardia initiation patterns on electrograms of implantable defibrillator devices

Abstract Introduction Sudden cardiac death is an unexpected death from a cardiac origin attributed by arrhythmias such as ventricular fibrillation (VF) and ventricular tachycardia (VT). The predominant treatment to terminate VT and VF is the implantation of an implantable cardioverter defibrillator (ICD). Currently, VT initiation in specific and small cohorts such as structural heart disease and reduced left ventricular ejection fraction patients have been explored. However, there is limited literature comparing the association between VT initiation patterns and defibrillators therapy outcome. This study aimed to investigate the most prevalent type of VT initiation from stored electrograms on ICDs and to explore the association between VT initiation pattern and therapy outcome (i.e., the ability to terminate VT). Method 344 stored electrograms amongst 65 patients from an existing database were visually inspected to classify VT initiation pattern as sudden onset (not preceded by premature ventricular complexes), non-sudden onset (preceded by premature ventricular complexes) and pacing-induced (device induced). Wilcoxon rank sum and Fisher’s Exact tests were used to assess differences between these groups. Mixed-effect logistic regression models accounting for multiple events occurring in individual patients were used to investigate association between the VT initiation pattern and therapy outcome. Results The mean age for the study group was 53±20 years and 54 (83%) subjects were males. Aetiology includes: 29 ischemic heart disease (45%), 10 hypertrophic cardiomyopathy (15%), 8 dilated cardiomyopathy (12%) and 18 other conditions (28%). Non-sudden onset VT (51%) was the most prevalent type of VT initiation pattern on defibrillators followed by sudden onset (44%) and pacing induced (5%). Non-sudden onset was 3 times more likely than the other 2 groups combined to be associated with unsuccessful therapies with an OR: 3.05 (95% confidence interval: 1.14, 8.15); p =0.03. There was no association between pacing-induced onset and unsuccessful therapies with an OR: 0.33 (95% confidence interval: 0.03, 3.33); p = 0.35. No association was identified for any of the three initiation patterns versus the other two combined and unsuccessful therapies when mixed-effect models were constructed. Discussion/ Conclusion: This study is consistent with other findings showing that non-sudden onset (51%) is the most prevalent VT onset. Pacing-induced VT accounted for 5% of VT with the predominant reason for initiation being undersensing of R-waves leading to pacing on the T-wave. This study reiterates the importance of programming strategies to prevent pacing induced VT. No associations were found with VT initiation and therapy outcome with mixed-effect models, possibly due to pseudo-replication being a limitation of this study. Prospective studies should be carried out in future to attempt to maximise success rate and establish the most effective treatment in ICDs.

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

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

Abstract 18088: Survival After Ventricular Tachycardia Onset in Left Ventricular Assist Device Recipients

Introduction: Left Ventricular Assist Devices (LVADs) revolutionized the care of patients with heart failure. However, the burden of ventricular tachycardia (VT) increases after LVAD insertion. The role of ablation in treating VT in LVAD recipients is unclear. Hypothesis: The incidence of VT following LVAD insertion is associated with worse survival, but this association is ameliorated by VT ablation. Methods: This is a single-center retrospective review of 549 LVAD recipients. LVADs implanted elsewhere, LVADs prior to 2011, and patients with inadequate follow up were excluded. Endpoints were transplantation, explantation, and last date of follow up. Event failure was defined as patient death. Cox and Kaplan-Meier survival analysis was performed with STATA and reported as hazard ratio with 95% confidence interval (HR [95% CI]). Results: Pre-LVAD VT was seen in 52% of patients: 33% had a prior ICD shock and 12% had a prior VT ablation. At study conclusion, 57% had died, 22% were transplanted, 9% were explanted, and 12% remained alive. Regardless of VT incidence, worse survival was seen in ischemic cardiomyopathy (HR 2.0 [1.5-2.7]), RV failure necessitating RVAD (HR 2.6 [1.9-3.6]), and pre-LVAD ICD shocks (HR 1.3 [1.0-1.7]). While post-LVAD VT overall was not associated with worse survival (HR 1.1 [0.8-1.3]), VT within 1 year of LVAD insertion demonstrated worse survival (HR 1.9 [1.3-2.6]; Figure 1). Incremental years between LVAD insertion and VT onset improved survival (HR 0.8 [0.7-0.9]). Among those with post-LVAD VT, ablation was not associated with a survival difference (IRR 0.9 [0.6-1.4]) regardless of the timing of ablation or VT onset. Conclusions: The incidence of VT within 1 year of LVAD insertion is associated with worse survival. However, mortality was not improved by VT ablation. This study is limited by its retrospective design, and further prospective studies would better determine the impact of VT ablation on survival in LVAD recipients.

Anesthesia in patients with Brugada syndrome: two case reports

BackgroundBrugada syndrome is a rare disease. It causes sudden cardiac arrest, which is a serious life-threatening event. Sudden cardiac death mostly results from coronary artery disease. However, patients with Brugada syndrome show normal cardiac anatomy and no evidence of ischemia or electrolyte imbalance. Anesthesia in patients with Brugada syndrome is challenging due to its unpredictable nature, and is worth our attention.Case presentationWe report two cases of Brugada syndrome during anesthesia. In case one, a 31-year-old Filipino laborer was scheduled for laparoscopic appendectomy. The patient denied any preexisting cardiac disease. The preoperative vital signs were stable, with mild fever of 37.9 °C. The operation was smooth. During the emergence period, the patient suffered from sudden onset of ventricular tachycardia. After resuscitation, the cardiac rhythm returned to normal. Later, he was confirmed to have a genetic trait of Brugada syndrome. In case two, a young Taiwanese patient with pre-diagnosed Brugada syndrome underwent an operation. The perioperative precautions were taken to prevent the occurrence of ventricular arrhythmia. The surgery was uneventful.ConclusionsBrugada syndrome, although rare, has the highest incidence in South East Asian healthy young males. It brings attention to possible fatal cardiac arrhythmia in this population. Careful preoperative evaluation and perioperative management can help reduce the harmful outcome of the disease and prevent any untoward events.

Lateral Boundaries of the Ventricular Tachycardia Circuit Align With Sinus Rhythm Discontinuities

BackgroundSinus rhythm electrical activation mapping can provide information regarding the ischemic re-entrant ventricular tachycardia (VT) circuit. The information gleaned may include the localization of sinus rhythm electrical discontinuities, which can be defined as arcs of disrupted electrical conduction with large activation time differences across the arc. ObjectivesThis study sought to detect and localize sinus rhythm electrical discontinuities that might be present in activation maps constructed from infarct border zone electrograms. MethodsMonomorphic re-entrant VT with a double-loop circuit and central isthmus was repeatedly inducible by programmed electrical stimulation in the epicardial border zone of 23 postinfarction canine hearts. Sinus rhythm and VT activation maps were constructed from 196 to 312 bipolar electrograms acquired surgically at the epicardial surface and analyzed computationally. A complete re-entrant circuit was mappable from the epicardial electrograms of VT, and isthmus lateral boundary (ILB) locations were ascertained. The difference in sinus rhythm activation time across ILB locations, vs the central isthmus and vs the circuit periphery, was determined. ResultsSinus rhythm activation time differences averaged 14.4 milliseconds across the ILB vs 6.5 milliseconds at the central isthmus and 6.4 milliseconds at the periphery (ie, the outer circuit loop) (P ≤ 0.001). Locations with large sinus rhythm activation difference tended to overlap ILB (60.3% ± 23.2%) compared with their overlap with the entire grid (27.5% ± 18.5%) (P < 0.001). ConclusionsDisrupted electrical conduction is evident as discontinuity in sinus rhythm activation maps, particularly at ILB locations. These areas may represent permanent fixtures relating to spatial differences in border zone electrical properties, caused in part by alterations in underlying infarct depth. The tissue properties producing sinus rhythm discontinuity at ILB may contribute to functional conduction block formation at VT onset.

PO-05-063 MORTALITY IN LEFT VENTRICULAR ASSIST DEVICE RECIPIENTS WITH VT REQUIRING ABLATION

Left Ventricular Assist Devices (LVADs) improve survival in patients with heart failure. However, an increased burden of ventricular tachycardia (VT) can occur following LVAD implantation. The role of ablation in the treatment of VT for LVAD recipients and the timing of when ablation should occur is unclear. To determine mortality in LVAD recipients with VT who required an ablation We retrospectively reviewed all patients who received a ventricular ablation from January 2014 to February 2021 and included those who underwent VT ablation after LVAD placement. The composite endpoints included transplant, lost to follow up, or last date of data collection. Event failure was defined as patient death. Survival rates were calculated with Kaplan-Meier analysis. Rate of event failure was calculated as per patient-year incident death rate (IR) and was compared between treatment groups by incident rate ratio with 95% confidence intervals (IRR [95% CI]). Survival analysis was performed using STATA. 36 patients underwent VT ablation after LVAD placement. Of those, 21 (58%) had documented VT prior to LVAD placement and 14 (42%) had de novo VT after LVAD placement. Within 30 days, one patient died (IR 0.339 over 2.95 patient-years); within one year, four patients died (IR 0.128 over 31.1 patient-years); within two years, ten patients died (IR 0.183 over 54.5 patient-years); and within eight years, twenty patients died (IR 0.217 over 92.2 patient-years). At a study endpoint of 2 years (the time interval between the most recent LVAD placement and the last date of data collection), a significantly higher death rate per patient-year was found in patients with VT onset within 7 days of LVAD placement (IRR 5.19 [1.08-21.87]), with a trend towards significantly higher death rate seen in patients with ischemic cardiomyopathy (ICM) (IRR 4.12 [0.82-39.9]) (Table 1). All patients who died underwent a VT ablation within 90 days of VT onset (Figure 1). Mortality in LVAD recipients was highest in the immediate post-operative period, especially when VT occurred within 7 days of LVAD placement. A higher death rate was also seen when ablation was performed within 90 days of VT onset. Further comparison to matched LVAD recipients without VT requiring ablation is needed to better understand the impact of VT on mortality in LVAD recipients.Tabled 1Table 1. IRRs of Patient Mortality Stratified by Presence or Absence of Specific Risk FactorsAbsentPresentIRR95% CIp-valueIschemic Cardiomyopathy0.0720.2984.12[0.82-39.9]0.059LVAD as Destination Therapy0.1100.2572.32[0.53-13.93]0.223HeartWare LVAD Placed0.1450.2241.55[0.37-7.47]0.516VT Prior to LVAD Placement0.1150.2462.14[0.49-12.80]0.283VT Ablation Prior to LVAD Placement0.2020.1680.83[0.14-3.64]0.825VT Within 7 Days of LVAD Placement0.1240.6455.19[1.08-21.87]0.023Ablation of VT Within 90 Days of VT Onset00.260------0.031Multiple Ablations Performed for Recurrent VT0.2180.0760.35[0.08-2.50]0.322 Open table in a new tab

Pneumologie meets Kardiologie: Kardiale Sarkoidose

Cardiac sarcoidosis is variable in its clinical manifestations and is characterized by challenges in the diagnostics, treatment and prognosis assessment. Due to increased awareness and advances in diagnostic tools, a rising incidence of the disease has been observed. This article presents the developments and necessary background knowledge based on the current guidelines. A case report of a 50-year-old male patient with sudden onset of ventricular tachycardia serves as an illustrative case.

Abstract 10554: Major Cardiac Side Effects of BTK and BCR-ABL Kinase Inhibitor Therapy in Cancer Patients: A Global WHO Database Analysis

Introduction: Bruton’s tyrosine kinase (BTK) and BCR-ABL kinase inhibitors have transformed the treatment for hematological cancers, such as mantle cell lymphoma and chronic myelogenous leukemia. However, these therapies present unique cardiac events that remain underexplored. Hypothesis: We hypothesize that the two groups of targeted therapies commonly used to treat hematological cancers will differ in cardiac side-effect profiles. Methods: The World Health Organization database, VigiBase ®, contains over 20 million Individual Case Safety Reports and is maintained by the Uppsala Monitoring Centre. Reports for unique cardiac events associated with the use of BTK and BCR-ABL kinase inhibitors were analyzed. Reporting odds ratios (ROR), 95% confidence intervals (CI) and chi-squared tests were used to compare differences in cardiac side-effect profiles between the two groups of therapies. Results: A total of 24,385 adverse cardiac events from the use of BTK inhibitors (ibrutinib, acalabrutinib, zanubrutinib, tirabrutinib) and BCR-ABL kinase inhibitors (imatinib, dasatinib, nilotinib, bosutinib, ponatinib) have been observed based on records obtained to-date. Compared to BCR-ABL kinase inhibitors, BTK inhibitors have significantly increased reporting for atrial fibrillation (ROR: 6.995; 95% CI: 6.493-7.537; P &lt; 0.001) and ventricular tachycardia (ROR: 1.829; 95% CI: 1.342-2.493; P &lt; 0.001). However, BCR-ABL inhibitors have significantly increased reporting for myocardial infarction (ROR: 2.077; 95% CI: 1.863-2.316; P &lt; 0.001) but similar reporting for congestive cardiac failure (ROR: 0.949; 95% CI: 0.852-1.058; P = 0.343). The median onset of ventricular tachycardia from the use of BTK inhibitors is 176 days (interquartile range: 48-636 days). For BCR-ABL kinase inhibitors, the median onset of ventricular tachycardia is similar at 137 days (interquartile range: 92-396 days), P = 0.741 from nonparametric tests. Conclusion: We conclude that BTK inhibitors are associated with arrhythmic events, while BCR-ABL kinase inhibitors are associated with myocardial infarction. Both groups have similar reporting for congestive cardiac failure. Research is underway to study the mechanisms behind these novel side-effect profiles.

A FEBRILE CRISIS: MONOMORPHIC VENTRICULAR TACHYCARDIA IN A STRUCTURALLY INTACT HEART

A FEBRILE CRISIS: MONOMORPHIC VENTRICULAR TACHYCARDIA IN A STRUCTURALLY INTACT HEART

Cardio-protective effect of Cocculus hirsutus in experimental hypertension in rats

BackgroundAyurdvedic derived medicines are most promising and effective in the treatment of several cardiovascular diseases. Cocculus hirsutus (CH) has been reported for broad spectrum of activities like anticancer, antidiabetic, antioxidant, cardiotonic and hypotensive etc. ObjectivesThe present study aimed to find the cardio-protective effect of CH in experimental hypertension in rats. Materials and methodsFor acute renal hypertension, CH animals were pre-treated with CH-1 (250 mg/kg) and CH-2 (500 mg/kg) p. o. for 14 days. On the 15th day, hypertension was induced by renal occlusion and the mean arterial blood pressure (MABP) was recorded. For CAL pretreatment of CH-1 and CH-2 was given for 7 days on the 8th day animals were operated on for ligation. The MABP and the time of onset of ventricular tachycardia (VT), premature ventricular systole (PVS) were recorded. For induction of hypercholesterolemia, animals were fed with a high cholesterol diet (CD) with CH-1 and CH-2 for 21 days. The antioxidant potential of CH was done using the assay of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx). ResultsCH treatment significantly decreases the MABP, the onset of VT and PVS. The histology show intact cardiac muscle with minimum necrosis and inflammation. CH treatment shows significant decrease in cholesterol, triglycerides, and glucose while HDL levels are significantly increased. The aortic section of CH-treated animals shows the intact layers of the artery, normal thickness and restoration of antioxidant enzymatic activity. ConclusionThe study shows significant cardio protective effect of CH in experimental animals.

Abstract 12116: Sex Differences in Arrhythmia Prevalence in a Large Patient Cohort Examined With Mobile Cardiac Telemetry

Introduction: The frequency of clinically relevant arrhythmia on long-term ambulatory ECG recordings is not sufficiently well described. We aimed to address this in a large patient cohort monitored with mobile cardiac telemetry. Methods: All patients 18-100 years who were monitored in the USA in 2017 (n=27.203, 58% female) with the PocketECG device (MediLynx), which registers and transmits a full-disclosure ECG for ≤30 days with beat-to-beat analysis, were included. Frequent premature ventricular complexes (PVCs) and frequent premature atrial complexes (PACs) were defined as ≥200 PVCs or ≥500 PACs in any recording day. Supraventricular tachycardia (SVT) episodes were defined as both any SVT &gt;3 beats, and SVT ≥30 seconds. AV-blocks II and III were not differentiated. Results: In the 18-40-year age group the overall prevalence of any arrhythmia was low (Figure 1 a-f). Frequent PACs, atrial fibrillation, AV-blocks and ventricular arrhythmias were more common in men than women (all p&lt;0.0001), and SVTs, both &gt;3 beats and &gt;30 seconds, were more common in women (p&lt;0.001 and p&lt;0.004, respectively). The overall prevalence of any VT event was 22.9% in women and 40.8% in men (p&lt;0.0001) and the mean age at onset of VT was lower in women (71.9 vs 72.6 years, 95%CI for difference (-1.3; -0.3). Conclusions: Most arrhythmias are more prevalent among men of all ages, but SVTs are more prevalent among women. VT events are common in a patient population, and the age at onset of ventricular tachycardia is lower among women.

VENTRICULAR TACHYCARDIA IN FETUS AND NEONATE: A SINGLE CENTRE EXPERIENCE

<h3>BACKGROUND</h3> Ventricular tachycardia (VT) is a very rare condition in the fetus and neonate, which can occur in the presence of structurally normal hearts, congenital heart disease (CHD), cardiomyopathy, or channelopathy. Overall there is a paucity of information about its management and outcomes in the literature <h3>METHODS AND RESULTS</h3> A single center retrospective study was performed. All fetuses and neonates with VT managed at the Stollery Children's Hospital between 2005-2020 were included. We recorded the age at diagnosis, presenting symptoms/features, associated syndromes, presence of CHD, presence of other medical diseases, diagnostic investigations, family history, management strategies, and length of stay in hospital. A total of 5 fetal and 8 neonatal cases were diagnosed with VT from 2005-2020. Two (40%) fetal compared to 5(62%) neonatal cases had CHD(p=0.59). Only 1/13, a fetus, had a cardiomyopathy with findings suggesting restriction prior to onset of VT. Median age at VT presentation was 32(26-37) weeks for fetal and 11(1-27) days for neonatal cases. Two fetuses were treated transplacentally with propranolol and two needed amiodarone. One fetus had resolution before birth with no postnatal recurrence, 2 had supressed VT prenatally that recurred after birth necessitating propranolol therapy as neonates, and 1 (cardiomyopathy case) never achieved full control. The 5th fetal case had rare episodes of VT and was not treated. Of the neonatal cases, 5 received intravenous anti-arrhythmics on admission: 4 amiodarone and 1 esmolol. Of these, 2 were converted to propranolol, 2 sotalol and the last was discharged on no medication. Three of the other 8 neonates initially received propranolol, 2 discharged on propranolol and the last discharge on mexiletine after failed propranolol and sotalol treatment. VT was suppressed or resolved with pharmacologic treatment in 3/4(75%) fetal cases and in 6/8 (75%) neonates at < 1 month after birth. Postnatal VT treatment was for a median of 10 (8-12) and 7 (2-12)months for fetal and neonatal cases, respectively. Demise occurred in only 1 case, the fetus with cardiomyopathy who had progressive hydrops(fetal vs neonatal p=0.04). <h3>CONCLUSION</h3> The majority of fetal and neonatal VT is manageable with pharmacologic therapy. There may be a higher risk of demise in fetal versus neonatal VT. Given its rarity, a, multi-center studies are needed to identify optimal management strategies for this age group and further understand clinical outcomes.

Prevalence and clinical correlates of exercise-induced ventricular arrhythmias in arrhythmogenic right ventricular cardiomyopathy.

Exercise has a deleterious effect on the phenotypic expression of arrhythmogenic right ventricular cardiomyopathy (ARVC) and increases the risk of sudden death. The aim of the study was to determine the prevalence and correlates of exercise-induced arrhythmias during exercise tolerance test (ETT) in patients with ARVC. Between 2010 and 2019, 30 (47% males, mean age 42 ± 12years) consecutive patients with a definite diagnosis of ARVC underwent a full genotypic and phenotypic characterization at our center. Exercise-induced arrhythmic response (EIAR) was defined by the development of complex or repetitive ventricular arrhythmias after stage 2 of exercise. A heart rate ≥ 85% of predicted was achieved by 23 (77%) patients. In 16 (53%) cases, a desmosomal pathogenic variant was found [most commonly PKP2 (n = 7) and DSP (n = 3)]. In 12 (40%) cases, an EIAR was observed. In 2 (6%) patients, ETT was interrupted due to the onset of ventricular tachycardia (sustained with a LBBB/inferior axis pattern in one case, and non-sustained LBBB/superior axis pattern in the other). Mean body surface area (BSA)-indexed left ventricular (LV) end-diastolic volumes (EDV) were higher in the EIAR group (92 ± 12ml/m2 vs 80 ± 7ml/m2, p = 0.002), as well as right ventricular EDV/BSA (110 ± 18ml/m2 vs 91 ± 27ml/m2, p = 0.04). Subepicardial/mid-wall LV late gadolinium enhancement (LGE) was more common in the EIAR group (67% vs 22%, p = 0.01). ARVC patients commonly exhibit exercise-induced ventricular arrhythmias. Patients with more significant RV remodeling and LV involvement (based on the presence of LV dilatation and LGE) appear more susceptible to exercise-induced arrhythmias.

Arrhythmia Mechanism and Dynamics in a Humanized Mouse Model of Inherited Cardiomyopathy Caused by Phospholamban R14del Mutation.

Arginine (Arg) 14 deletion (R14del) in the calcium regulatory protein phospholamban (hPLNR14del) has been identified as a disease-causing mutation in patients with an inherited cardiomyopathy. Mechanisms underlying the early arrhythmogenic phenotype that predisposes carriers of this mutation to sudden death with no apparent structural remodeling remain unclear. To address this, we performed high spatiotemporal resolution optical mapping of intact hearts from adult knock-in mice harboring the human PLNWT (wildtype [WT], n=12) or the heterozygous human PLNR14del mutation (R14del, n=12) before and after ex vivo challenge with isoproterenol and rapid pacing. Adverse electrophysiological remodeling was evident in the absence of significant structural or hemodynamic changes. R14del hearts exhibited increased arrhythmia susceptibility compared with wildtype. Underlying this susceptibility was preferential right ventricular action potential prolongation that was unresponsive to β-adrenergic stimulation. A steep repolarization gradient at the left ventricular/right ventricular interface provided the substrate for interventricular activation delays and ultimately local conduction block during rapid pacing. This was followed by the initiation of macroreentrant circuits supporting the onset of ventricular tachycardia. Once sustained, these circuits evolved into high-frequency rotors, which in their majority were pinned to the right ventricle. These rotors exhibited unique spatiotemporal dynamics that promoted their increased stability in R14del compared with wildtype hearts. Our findings highlight the crucial role of primary electric remodeling caused by the hPLNR14del mutation. These inherently arrhythmogenic features form the substrate for adrenergic-mediated VT at early stages of PLNR14del induced cardiomyopathy.

Ventricular tachycardia in cardiolaminopathy: Characteristics and considerations for device programming

Mutations in LMNA cause an arrhythmogenic cardiomyopathy (cardiolaminopathy) with high risk of ventricular tachycardia (VT). The natural history of VT among patients with cardiolaminopathy is incompletely understood. The purpose of this study was to determine the longitudinal burden and progression of VT, including change in tachycardia cycle length (TCL), response to antitachycardia pacing (ATP), and prognostic significance of high-burden VT (>5 episodes of VT at any device interrogation) in cardiolaminopathy patients. Patients with cardiolaminopathy and an implantable cardioverter-defibrillator (ICD) were identified from a single-center database. Serial device interrogations and medical records were used to collect data on VT burden, TCL, and response to ATP. Cardiolaminopathy patients with primary (n = 27) or secondary prevention (n = 16) ICDs were followed for 2 years (interquartile range [IQR] 1-5). VT burden was substantially higher in patients receiving secondary prevention ICDs (28 ± 40.9 vs 3.6± 7.3 episodes per 100 patient-years; P <.001). ATP was highlyeffective (94%) at terminating VT except for short TCL (<250 ms), for which ATP failed in 60%. Among patients with recurrent VT, TCL increased by 112 ± 93.6 ms during follow-up. Inappropriate shocks were rare (0.4% of all therapies). Median time to transplantation, ventricular assist device, or death was 18 months (IQR 0.7-27.1) in patients with high-burden VT. In patients with cardiolaminopathy, VT is recurrent and highly responsive to ATP, which supports the use of transvenous ICDs iteratively programmed to manage VT of various TCLs. Onset of high-burden VT indicates poor prognosis and should warrant referral to a heart failure specialist.

Role of infarct scar dimensions, border zone repolarization properties and anisotropy in the origin and maintenance of cardiac reentry

Cardiac ventricular tachycardia (VT) is a life-threatening arrhythmia consisting of a well organized structure of reentrant electrical excitation pathways. Understanding the generation and maintenance of the reentrant mechanisms, which lead to the onset of VT induced by premature beats in presence of infarct scar, is one of the most important issues in current electrocardiology. We investigate, by means of numerical simulations, the role of infarct scar dimension, repolarization properties and anisotropic fiber structure of scar tissue border zone (BZ) in the genesis of VT. The simulations are based on the Bidomain model, a reaction-diffusion system of Partial Differential Equations, discretized by finite elements in space and implicit-explicit finite differences in time. The computational domain adopted is an idealized left ventricle affected by an infarct scar extending transmurally. We consider two different scenarios: i) the scar region extends along the entire transmural wall thickness, from endocardium to epicardium, with the exception of a BZ region shaped as a central sub-epicardial channel (CBZ); ii) the scar region extends transmurally along the ventricular wall, from endocardium to a sub-epicardial surface, and is surrounded by a BZ region (EBZ). In CBZ simulations, the results have shown that: i) the scar extent is a crucial element for the genesis of reentry; ii) the repolarization properties of the CBZ, in particular the reduction of IKs and IKr currents, play an important role in the genesis of reentrant VT. In EBZ simulations, since the possible reentrant pathway is not assigned a-priori, we investigate in depth where the entry and exit sites of the cycle of reentry are located and how the functional channel of reentry develops. The results have shown that: i) the interplay between the epicardial anisotropic fiber structure and the EBZ shape strongly affects the propensity that an endocardial premature stimulus generates a cycle of reentry; ii) reentrant pathways always develop along the epicardial fiber direction; iii) very thin EBZs rather than thick EBZs facilitate the onset of cycles of reentry; iv) the sustainability of cycles of reentry depends on the endocardial stimulation site and on the interplay between the epicardial breakthrough site, local fiber direction and BZ rim.

Catheter Ablation of Scar-mediated Ventricular Tachycardia: Are Substrate-based Approaches Replacing Mapping?

Scar-mediated ventricular tachycardia (VT) is a recognized cause of morbidity and mortality in patients with ischemic cardiomyopathy and other cardiomyopathies such as nonischemic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and cardiac sarcoidosis. Implantable cardioverter-defibrillator (ICD) therapy improves survival but does not prevent the onset of recurrent VT or associated morbidity from ICD shocks. While randomized controlled trials have demonstrated advantages of scar-mediated VT ablation in comparison with antiarrhythmic drugs, procedural success has remained overall modest at between 50% and 70%. Standard scar-mediated VT ablation has relied on the use of activation and entrainment mapping during sustained VT to identify critical isthmuses for ablation. Substrate-based approaches have emerged as options to address hemodynamically unstable VT and have focused on identifying electrograms characteristic of critical isthmuses (eg, late potentials, local abnormal ventricular activities, conducting channels) within dense scar during sinus rhythm. Scar homogenization, a more recent approach, relies minimally on mapping and focuses on complete substrate modification. Core isolation, on the other hand, another recent development, relies heavily on mapping to identify regions within scar that are “cores” for arrhythmogenicity and then concentrates ablation to these areas. At this time, scar-mediated VT ablation appears to be at a crossroads wherein evolving substrate-based approaches are exploring whether to rely less or increasingly more on mapping. This review will therefore discuss the evolution of substrate-based, scar-mediated VT ablation and in the process try to answer whether there is still a role for mapping.

‘Lest We Forget’: A Case Report of an Unusual Complication of Standard Treadmill Exercise Stress Test

Ventricular arrhythmia and cardiac arrest are unusual complications of electrocardiogram exercise stress test. This case report presents a 72-year-old gentleman who developed sustained ventricular tachycardia and subsequent cardiac arrest during a standard treadmill exercise stress test on the background of a 2-month history of intermittent atypical thoracic back pain. Interestingly, thoracic back pain recurred with the onset of ventricular tachycardia. Cardiovascular risk factors were significant for being a current smoker and reported ‘impaired glucose tolerance’. Transthoracic echocardiogram showed preserved left ventricular function and multiple regional wall motion abnormalities, which were consistent with multivessel coronary artery disease. Coronary angiography confirmed severe three-vessel disease. He subsequently underwent coronary artery bypass surgery with an uncomplicated recovery. A retrospective review of glucose tests performed 3 years prior was consistent with the diagnosis of diabetes mellitus.

Coexistence of tachyarrhythmias in patients with tetralogy of Fallot

The expanding population of adult patients with tetralogy of Fallot (ToF) requires knowledge of its long-term sequelae. The purpose of this study was to examine the coexistence and order of appearance of atrial fibrillation (AF), other supraventricular tachycardias (SVTs), ventricular tachycardia (VT), and ventricular fibrillation (VF), and their impact on survival during long-term follow-up. Adult, corrected ToF patients [N = 225; 128 male; mean ± SD (minimum-maximum) age 41 ± 12 (19-79) years] were included in the study. Medical correspondence, ECGs, and Holter recordings were reviewed for documented AF, other SVTs, VT, and VF. During follow-up of 35 ± 9 (16-64) years, sustained tachyarrhythmias, including SVT (n=50, 22%), AF (n=29, 13%), VT (n=20, 9%), and VF (n=9, 4%), were observed in 71 patients (32%), of whom 27 (38%) had coexistence of different tachyarrhythmias. In 18 patients with coexisting SVT and AF, SVT most often preceded AF in 13 (72%). Age at SVT onset was similar between those with and those without subsequent AF development (40 ± 17 years vs 35 ± 16 years; P = .283). However, age at SVT and AF onset were positively correlated (rho 0.585; P = .011). Prevalence of SVT/AF was associated with VT/VF prevalence (odds ratio [OR] 4.59; P < .001). Although 11% of patients with SVT/AF subsequently develop VT/VF, onset of SVT/AF could not predict future VT/VF development (OR 1.81; P = .233). Adult ToF patients are initially at risk for SVT development, followed by AF, VT, and VF at 46 (43-50), 56 (53-59), 57 (54-61), and 62 (61-63) years after ToF correction (P < .001), respectively. Survival time decreased when sustained tachyarrhythmias developed (P = .024). Age at onset of SVT, AF, and VT was positively correlated with age at death (SVT: rho 0.734; P = .004; AF: rho 0.783; P = .007, VT: rho 0.755; P= .050). Coexistence of different (supra)ventricular tachyarrhythmias is frequently observed in adult ToF patients. In these patients, a specific order of these tachyarrhythmias was observed. Tachyarrhythmias are associated with decreased survival time, and, more importantly, age at tachyarrhythmia development positively correlates with age at death.

Source-Sink Mismatch Causing FunctionalConduction Block in Re-Entrant VentricularTachycardia.

Ventricular tachycardia (VT) caused by a re-entrant circuit is a life-threatening arrhythmia that at present cannot always be treated adequately. A realistic model of re-entry would be helpful to accurately guide catheter ablation for interruption of the circuit. In this review, models of electrical activation wavefront propagation during onset and maintenance of re-entrant VT are discussed. In particular, the relationship between activation mapping and maps of transition in infarct border zone thickness, which results in source-sink mismatch, is considered in detail and supplemented with additional data. Based on source-sink mismatch, the re-entry isthmus can be modeled from its boundary properties. Isthmus boundary segments with large transitions in infarct border zone thickness have large source-sink mismatch, and functional block forms there during VT. These alternate with segments having lesser thickness change and therefore lesser source-sink mismatch, which act as gaps, or entrance and exit points, to the isthmus during VT. Besides post-infarction substrates, the source-sink model is likely applicable to other types of volumetric changes in the myocardial conducting medium, such as when there is presence of fibrosis or dissociation of muscle fibers.