Cases Of Ventricular Arrhythmias Research Articles

The Influence of Arrhythmia on the Outcomes of Pediatric Patients with Idiopathic Dilated Cardiomyopathy.

Children diagnosed with dilated cardiomyopathy (DCM) are at an increased risk of developing arrhythmias, which can significantly affect their overall prognosis. However, the implantation and effectiveness of implantable cardioverter-defibrillators (ICDs) pose challenges in the pediatric population. Therefore, it is crucial to determine the prevalence of arrhythmia-related death in pediatric patients with DCM. This study investigated the correlation between arrhythmias and mortality in pediatric patients with DCM. This retrospective cohort study examined children with idiopathic DCM referred to Rajaie Cardiovascular, Medical, and Research Institute in Tehran, Iran, from 2017 to 2023. All patients underwent a standard 12-lead electrocardiogram, 24-h Holter monitoring, cardiac magnetic resonance imaging, and echocardiography. Patient outcomes, including death, heart transplantation, and survival, were evaluated within one year of Holter monitoring. A total of 178 children (79 males) with a mean age of 83.06 ± 56.41months were included in the study. Overall, 72 deaths (40.4%) and 46 heart transplants (25.8%) were recorded and 60 patients (33.7%) survived. There was no significant association between patients' outcomes with ventricular arrhythmias, late gadolinium enhancement, corrected QT interval, and QRS interval prolongation; however, a significantly higher proportion of dead patients had abnormal heart rate variability (P = 0.034). Heart failure was the leading cause of death, with ventricular arrhythmia accounting for two out of 72 deaths. Both cases of ventricular arrhythmia were associated with severe cardiac dysfunction. Arrhythmia-related mortality is rare in children with idiopathic DCM, with severe heart failure being the primary cause of death in this population. Life-threatening arrhythmias primarily occur in DCM children with more compromised cardiac function.

P3 EXERTIONAL SYNCOPE AND VENTRICULAR ARRHYTHMIA IN A PATIENT WITH CARDIAC AMYLOIDOSIS

Abstract Systemic amyloidosis is a multisystem disorder caused by the misfolding, aggregation, and deposition of certain proteins in various organs and tissues. Cardiac involvement is common and worsens the prognosis. Atrial fibrillation is the most frequent arrhythmia in cardiac amiloidosis (CA), but many cases of ventricular arrhythmias (VA) and sudden cardiac death (SCD) have been described. We present a case of a 64–year–old man admitted following exertional syncope occurred after climbing a flight of stairs. His medical history included left gonarthrosis and surgery for right carpal tunnel syndrome one year before. Physical examination did not revealed signs of heart failure. A 12–lead electrocardiogram (ECG) showed a pseudoinfarction pattern with QS waves in V2 and V3 leads and low voltage in all limb leads. Routine blood tests revealed NT–pro–BNP 3436 pg/ml(n.v.0–125) and high–sensitive troponin T 67 pg/ml(n.v.< 58). A trans–thoracic echocardiogram showed left ventricle (LV) concentric thickening wall with granular and sparkling pat[1]tern, mild reduced ejection fraction, reduced global longitudinal strain with apical sparing, grade 3 diastolic disfunction, biatrial enlargement, mild mitral regurgitation, right ventricle free wall thickening (8 mm), mild reduced TAPSE, and mild pericardial effusion. Cardiac magnetic resonance (CMR) confirmed ventricular wall thickening with evidence at T1 mapping of interstitial infiltration more evident in the septum and inferior–lateral wall with apical savings. A total body 99mTc–HDP scintigraphy showed cardiac uptake with intensity similar to bone signal (Perugini Score 2) suggesting ATTR cardiac amyloidosis. Both kappa and lambda concentrations were normal. The genetic testing did not reveled mutations in the TTR gene. We concluded for a diagnosis of ATTR wild–type CA. The Holter ECG monitoring registered numerous ventricular ectopic beats and an episode of non–sustained ventricular tachycardia. A coronary angiography ruled out coronary artery disease. In consideration of the clinical–instrumental picture an ICD was implanted. Conclusions CA is still underdiagnosed. VA and SCD may further complicate the prognosis. Early diagnosis and adequate stratification of the arrhythmic risk are essential to ensure patients the best therapeutic strategies.

Abstract 15827: A Case of Ventricular Arrhythmia as Presentation for Cardiac Involvement of Polymyositis

Introduction: Polymyositis is an autoimmune systemic disease which is characterized by chronic weakness and inflammation in skeletal muscle predominantly. Cardiac involvement has been reported and is a poor prognostic factor. Clinical course 61-year-old male with biopsy proven polymyositis with history of cardiac arrest secondary to ventricular fibrillation and dual chamber automatic implantable cardioverter defibrillator (AICD) implanted for secondary prevention. He had recurrent PVC-induced ventricular fibrillation causing AICD shocks. Eventually, he underwent electrophysiology study and successful ablation of PVC targeted to the basal lateral left ventricle.Transthoracic echocardiogram showed unremarkable systolic and akinetic basal inferolateral wall segment.He underwent PET-CT of myocardium which showed focal FDG uptake of the lateral basal left ventricular could indicate focal myocarditis.Endomyocardial biopsy did not show any evidence of myocarditis.Eventually he had recurrent rapid monomorphic ventricular tachycardia and was briefly placed on amiodarone. He was placed on immunosuppressive therapy managed by Rheumatology with etanercept, rituximab and IVIG. No recurrence of ventricular arrythmia has occurred since. Amiodarone has been discontinued. Discussion: Myocardial involvement of polymyositis is not uncommon and has been noted to increase morbidity and mortality.The most common reported manifestations include congestive heart failure, conduction abnormalities which can range from ventricular arrhythmia to complete heart block and coronary artery disease. ConclusionIt is very important to recognize polymyositis as a cause for ventricular arrhythmias in the right clinical setting as management with immunosuppressive therapy can decrease the burden in ventricular arrhythmias.

515 Exertional syncope and ventricular arrhythmia in a patient with cardiac amyloidosis

Abstract Aims Systemic amyloidosis is a multisystem disorder caused by the misfolding, aggregation, and deposition of certain proteins in various organs and tissues. Cardiac involvement is common and worsens the prognosis. Atrial fibrillation is the most frequent arrhythmia in cardiac amiloidosis (CA), but many cases of ventricular arrhythmias (VA) and sudden cardiac death (SCD) have been described. Methods and results We present a case of a 64-year-old man admitted following exertional syncope occurred after climbing a flight of stairs. In the previous 2 weeks he had experienced fatigue and poor tolerance to exertion; moreover, 2 days before he had another episode of transient loss of consciousness after exertion. His medical history included left gonarthrosis and surgery for right carpal tunnel syndrome one year before. Physical examination did not revealed signs of heart failure. A 12-lead electrocardiogram (ECG) showed a pseudoinfarction pattern with QS waves in V2 and V3 leads and low voltage in all limb leads (Figure 1). Routine blood tests revealed N-terminal pro-bran natriuretic peptide (NT-ProBNP) of 3436 pg/ml (n.v. 0–125) and high-sensitive troponin T of 67 pg/ml (n.v. < 58). A trans-thoracic echocardiogram showed left ventricle (LV) concentric thickening wall with granular and sparkling pattern, mild reduced ejection fraction, reduced global longitudinal strain with apical sparing, grade 3 diastolic disfunction, biatrial enlargement, mild mitral regurgitation, right ventricle free wall thickening (8 mm), mild reduced TAPSE, and mild pericardial effusion. Cardiac magnetic resonance (CMR) confirmed ventricular wall thickening with evidence at T1 mapping of interstitial infiltration more evident in the septum and inferior-lateral wall with apical savings (Figure 2). A total body 99mTc-HDP scintigraphy showed cardiac uptake with intensity similar to bone signal (Perugini Score 2) suggesting ATTR cardiac amyloidosis (Figure 3). Both kappa and lambda concentrations were normal. The genetic testing did not reveled mutations in the TTR gene. We concluded for a diagnosis of ATTR wild-type CA. The Holter ECG monitoring registered numerous ventricular ectopic beats and an episode of non-sustained ventricular tachycardia. A coronary angiography ruled out coronary artery disease. In consideration of the clinical-instrumental picture an ICD was implanted. Conclusions In conclusion, CA is still underdiagnosed. VA and SCD may further complicate the prognosis. Early diagnosis and adequate stratification of the arrhythmic risk are essential to ensure patients the best therapeutic strategies.

Pheochromocytoma in a patient presenting with ventricular fibrillation and carotid dissection: a case report.

BackgroundPheochromocytoma is an endocrine tumour secreting catecholamines, most often revealed by clinical symptoms (headache, palpitations, diaphoresis, or resistant hypertension). Some cases of ventricular arrhythmias were described in the literature, without any formal link between arrhythmia and pheochromocytoma.Case summaryWe report a case of pheochromocytoma discovered after cardiac arrest due to ventricular fibrillation in a 46-year-old patient. The diagnosis was suggested by clinical symptoms (headache, palpitation, and diaphoresis) and suspected on the abdominal computed tomography scan. The diagnosis was corroborated by metaiodobenzylguanidine scintigraphy and finally confirmed by anatomopathological analysis of the operative specimen. The cerebral imaging showed a dissection of the left internal carotid artery and an intraparenchymal haematoma that might be secondary to a catecholaminergic discharge of phaeochromocytoma and severe hypertension.DiscussionSince pheochromocytoma is accessible to curative treatment, its detection in case of cardiac arrest is essential to decrease the risk of arrhythmic recurrence.

Infusion therapy in treatment of patients with acute coronary syndrome

Objective. Introduction to the basic therapy of patients with acute coronary syndrome (ACS) without ST-segment elevation cardioprotective drug Tivorel (“Yuria-Pharm”) based on L-arginine and L-carnitine.
 Materials and methods. The present study was carried out in accordance with the requirements for clinical trials of drugs in the Department of Emergency Cardiology of the RSCEMPSF. Patients were admitted to the intensive care unit with a diagnosis of ACS without ST-segment elevation in the first 12 h after the onset of the disease. The study was carried out in two groups and included the following stages: screening and treatment period (10 days). The study involved 90 patients with ACS without ST segment elevation, who were allocated for treatment in the study and control groups in a 1:1 ratio. Patients of the study group, except for basic therapy (sublingual nitroglycerin, acetylsalicylic acid or clopidogrel, analgesics, β-adrenergic blockers or angiotensin-converting enzyme inhibitors), received the drug Tivorel 100 ml intravenously at a rate of 10 drops per minute for the first 10-15 min (then the rate of administration could be increased to 30 drops per minute) 1 time per day within 10 days. Control group patients were prescribed only basic therapy. Determination of markers of myocardial necrosis (troponin T), electrocardiography (ECG), echocardiography. Compulsory calculation of end-diastolic and end-systolic indices, left ventricular ejection fraction were performed.
 Results and discussion. It was found that the drug Tivorel, prescribed as part of complex therapy immediately after admission of patients to the hospital, improves the electrophysiological properties of the myocardium and prevents the appearance of temporary ECG disturbances, stabilizes the condition of patients. In patients of the main group, already in the first day after the development of acute myocardial infarction (AMI), late ventricular potentials were less often recorded, markers of the so-called arrhythmogenic substrate – 9.5 % compared to 18.7 % in patients in the control group. In the course of further observation, the prostate gland in the control group disappeared, and during treatment with Tivorel, it did not appear anymore. This suggests the presence of a pronounced anti-ischemic effect of the drug, which is also confirmed by clinical data. We have noted a reliably expressed positive dynamics of changes in the end part of the ventricular complex under the influence of therapy with Tivorel. Analysis of standard ECG and 24-hour monitoring data in a number of patients revealed rhythm disturbances. There were no significant differences between the groups in the frequency of occurrence of all manifestations of arrhythmic syndrome, both initially and after therapy, however, in the main group, during treatment, the number of cases of ventricular arrhythmias in the form of group ventricular extrasystole and ventricular tachycardia bursts significantly decreased. During the period of inpatient treatment, all patients showed positive clinical dynamics: a decrease in the frequency and severity of angina attacks, a decrease and stabilization of blood pressure, an increase in exercise tolerance. Already on the third day of treatment with the use of the study drug Tivorel, relapses of anginal pain occurred less frequently (21.9 % of cases in the main group and 33.0 % in the control group). At the same time, there was a decrease in the need for the use of nitroglycerin and narcotic analgesics in order to relieve recurrent pain syndrome (23.1 % and 35.3 % of cases, respectively). In addition, on the third day after the development of AMI in patients of the main compared with the control, a lower incidence of atrioventricular blockade was recorded (4.3 % and 13.6 %, respectively). In the course of the analysis of the entire hospital period, it was found that in patients receiving Tivorel, atrioventricular blockades occurred almost 3 times less often than in the control group. The frequency of registration of ventricular extrasystole decreased on the 7th (34.1 %) and 10th days (45.7 %) of the disease.
 Conclusions. The use of the drug Tivorel (“Yuria-Pharm”) in addition to basic therapy helps to optimize the management of ACS patients without ST-segment elevation. With complex treatment with the use of the drug Tivorel, a faster regression of clinical manifestations of ACS is observed. The use of Tivorel in ACS therapy without ST-segment elevation stabilizes the patient’s condition and reduces the incidence of complications.

Low prevalence of arrhythmias in clinically stable COVID-19 patients.

BackgroundNo studies investigated the prevalence of arrhythmias among clinically‐stable patients affected by COVID‐19 infection.MethodsWe assessed prevalence, type, and burden of arrhythmias, by a single‐day snapshot in seven non‐intensive COVID Units at a third‐level center.ResultsWe enrolled 132 inhospital patients (mean age 65±14y; 66% males) newly diagnosed with COVID‐19 infection. Arrhythmic episodes were detected in 12 patients (9%). In detail, 8 had atrial fibrillation, and 4 self‐limiting supraventricular tachyarrhythmias. There were no cases of ventricular arrhythmias or new‐onset atrioventricular blocks. In addition, we report no patients with QTc interval >450 ms.ConclusionsOur single‐day snapshot survey suggests that the prevalence of arrhythmias among clinically stable COVID‐19 patients is low. In particular, no life‐threatening arrhythmic events occurred.

Niepożądane efekty interakcji leków psychotropowych z produktami leczniczymi i suplementami diety zawierającymi wyciągi roślinne.

Assessment of adverse drug interactions with herbal preparations (HP), i.e., plant medicines and nutritional supplements which contain plant extracts. Analysis of 147 cases of adverse events with clinical picture indicating probability or certainty of resulting from inclusion of HP into the applied pharmacotherapy (mostly psychotropic drugs). The most common effect of interactions between SSRI or SNRI antidepressants and HP were hemorrhagic complications associated with Japanese ginkgo biloba (27.45% of complications in this subgroup). Another common complication was serotonin syndrome (SS) (11.8%) occurring during the use of ginseng (one case of SS after the addition of bacopa). In the group of antipsychotic drugs, the highest number of interactions was observed in the case of haloperidol, and the highest number of complications (29.8%) was associated with ginseng (including 6 cases of ventricular arrhythmias in combination with haloperidol), milk thistle (including 7 cases of pancreatitis in combination with haloperidol or risperidone, 1 case of hepatotoxicity after adding aripiprazole) and rhodiola rosea. As for hypnotics and sedatives - interactions with ginseng were most frequently reported, mainly intensified sedative effects, cognitive disorders and disturbances in consciousness. In 132 cases, withdrawal of the plant preparation resulted in a decrease in the severity of the reported adverse reactions or a complete resolution of the described symptoms. HP (especially ginseng, rhadiola rosea, ginkgo biloba, milk thistle) are associated with a significant risk of pharmacokinetic and pharmacodynamic interactions with psychotropic drugs. Because of the resulting complications and side effects, any decision to include a herbal supplement should be preceded by a detailed safety analysis with benefit and risk assessment.

Ventricular Arrhythmic Storm after Initiating Sacubitril/Valsartan

Objectives: Sacubitril/valsartan was approved recently for the treatment of patients with heart failure and reduced ejection fraction. We present 6 cases of ventricular arrhythmia, that occurred shortly after sacubitril/valsartan initiation, that required drug withdrawal. Other potential triggering factors of electrical storm were ruled out and, from the arrhythmic perspective, all of the patients were stable in the previous year. Our aim is to describe the possible association of sacubitril/valsartan with arrhythmic storm. Methods: This was an observational monocentric study performed in the first 7 months of sacubitril/valsartan commercialization in Spain (October 2016). All patients were included in the SUMA (Sacubitril/Varsartan Usado Ambulatoriamente en Madrid [Sacubitril/Valsartan Used in Outpatients in Madrid]) registry. Patients were consecutively enrolled on the day they started the drug. Ventricular arrhythmic storm was defined as ≥2 episodes of sustained ventricular arrhythmia or defibrillator therapy application in 24 h. Results: From 108 patients who received the drug, 6 presented with ventricular arrhythmic storm (5.6%). Baseline characteristics were similar in the patients with and without ventricular arrhythmic storm. The total number of days that sacubitril/valsartan was administered to each patient was 5, 6, 44 (8 since titration), 84, 93, and 136 (105 since titration), respectively. Conclusions: Our data are not enough to infer a cause-and-effect relationship. Further investigations regarding a potential proarrhythmic effect of sacubitril/valsartan are probably needed.

Final Analysis of the Australasian Leukaemia and Lymphoma Group (ALLG) APML4 Trial: All-Trans Retinoic Acid (ATRA), Intravenous Arsenic Trioxide (ATO) and Idarubicin (IDA) As Initial Therapy for Acute Promyelocytic Leukemia (APL)

▪BACKGROUNDThe combination of ATRA and anthracycline-based chemotherapy has traditionally been regarded as the gold standard for induction and consolidation in previously untreated APL patients (pts), with ATO usually reserved for relapse. Recent data in Sanz low-risk (LR) and intermediate-risk (IR) APL indicate ATRA + ATO is superior to ATRA + chemotherapy (N Engl J Med 2013), but the optimal therapy for high-risk (HiR) pts remains unclear. In an attempt to improve anti-leukemic efficacy whilst limiting reliance on anthracyclines for all risk categories of APL, the ALLG incorporated ATO into an ATRA + reduced chemotherapy backbone, and the results of an interim analysis with a median follow-up of 2 years (yr) have been published (Blood 120:1570, 2012). Herein, we report results of the protocol-specified final analysis, conducted when all surviving pts had been followed for at least 2 yr after completion of consolidation.METHODS As published, APML4 protocol treatment comprised: (i) induction with ATRA (45 mg/m2 d1-36), IDA (12 mg/m2 d2,4,6,8), ATO (0.15 mg/kg d9-36), prophylactic prednisone (1 mg/kg d1-10) and aggressive hemostatic support; (ii) consolidation with ATRA and ATO (continuous in cycle 1, intermittent in cycle 2); (iii) 2 yr oral maintenance with ATRA, 6-mercaptopurine and methotrexate. Between 2004-2009, 124 evaluable pts were accrued, and median follow-up by the censor-reversing Kaplan-Meier method in this final analysis is 4.2 yr.RESULTS Median age was 44 (3-78) yr, median white cell count was 2.4 x 109/L (0.1-85.8), and median platelet count 22 x 109/L (2-173). Risk groups were 33 LR, 67 IR, 23 HiR, 1 unknown. FLT3 mutations were present in 44%, and 11% had ≥ 2 additional cytogenetic abnormalities (2+ACA). There were 4 (3.2%) deaths during induction (myocardial infarction d1, cerebral hemorrhage d3 and d7, cerebral edema and seizures d30). Grade 3-4 non-hematological adverse events included differentiation syndrome in 14%, and frequent but reversible biochemical hepatic and gastrointestinal toxicity. Q-Tc prolongation > 500 msec occurred in 14%, but there were no cases of ventricular arrhythmias or torsades de pointe. Significant neurological and cutaneous toxicity were infrequent.After induction, 118 pts (95%) achieved hematological complete remission; 112 commenced consolidation, and all were in molecular remission after cycle 2. A total of 5 relapses and 3 deaths have occurred post-induction, but none of the deaths were attributable to protocol therapy. Severe adverse events were less common during the chemotherapy-free consolidation cycles, especially cycle 2. The frequency of grade 3-4 neutropenia was 62% in cycle 1 and 27% in cycle 2, but there was no grade 3-4 thrombocytopenia.The following table lists event-free survival (EFS), disease-free survival (DFS), overall survival (OS) and cumulative incidence of relapse (CIR):TableAll ptsLRIRHiR2 yr5 yr2 yr5 yr2 yr5 yr2 yr5 yrEFS92%90%97%97%93%89%83%83%DFS97%95%100%100%97%93%95%95%OS94%94%97%97%96%96%87%87%CIR3%5%0%0%3%7%5%5%In univariate analysis, 2+ACA predicted for inferior DFS (P = .04), whereas age > 70 was associated with increased risk of early death (ED, P = .02), inferior EFS (P = .0002), and inferior OS (P = .001). Neither Sanz risk category nor FLT3 mutation status was significantly correlated with these outcome endpoints (all P > .05). In multivariate analysis, the significant associations of 2+ACA (P = .04 for DFS) and age > 70 (P = .0002 for EFS, P = .005 for OS) were retained. In addition, Sanz risk category was correlated with EFS (P[trend] = .003) and OS (P[trend] = .02).When compared with our previous ALLG APML3 trial (ATRA + IDA for induction and consolidation without ATO; Haematologica 2012), treatment with APML4 was associated with substantial and statistically significant improvements (see Figure) in EFS (P = .002), DFS (P = .001) and OS (P = .02). The significance of trial assignment was retained in multivariate analysis when APML3 and APML4 data were combined.CONCLUSIONS APML4 is a potent anti-leukemic regimen with manageable toxicity and a low ED rate. EFS and OS remain impressive with mature follow-up, and were influenced primarily by advanced age and Sanz risk category. The CIR was 5%, and was only associated with 2+ACA. Our results support the inclusion of ATO in induction and consolidation as front-line therapy for APL whilst simultaneously limiting cumulative anthracycline exposure. [Display omitted] DisclosuresOff Label Use: Arsenic trioxide is currently only registered in the US, Europe and Australia for the treatment of relapsed APL. This report includes its use in the initial treatment of APL.

Trends in Reporting Methadone-Associated Cardiac Arrhythmia, 1997–2011

Long-acting opioids are a leading cause of accidental death in the United States, and methadone is associated with greater mortality rates. Whether this increase is related to the proarrhythmic properties of methadone is unclear. To describe methadone-associated arrhythmia events reported in the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS). Description of national adverse event registry data before and after publication of a 2002 report describing an association between methadone and arrhythmia. FAERS, November 1997 and June 2011. Adults with QTc prolongation or torsade de pointes and ventricular arrhythmia or cardiac arrest. FAERS reports before and after the 2002 report. 1646 cases of ventricular arrhythmia or cardiac arrest and 379 cases of QTc prolongation or torsade de pointes were associated with methadone. Monthly reports of QTc prolongation or torsade de pointes increased from a mean of 0.3 (95% CI, 0.1 to 0.5) before the 2002 publication to a mean of 3.5 (CI, 2.5 to 4.8) after it. After 2000, methadone was the second-most common primary suspect in cases of QTc prolongation or torsade de pointes after dofetilide (a known proarrhythmic drug) and was associated with disproportionate reporting similar to that of antiarrhythmic agents known to promote torsade de pointes. Antiretroviral drugs for HIV were the most common coadministered drugs. Reports to FAERs are voluntary and selective, and incidence rates cannot be determined from spontaneously reported data. Since 2002, reports to FAERS of methadone-associated arrhythmia have increased substantially and are disproportionately represented relative to other events with the drug. Coadministration of methadone with antiretrovirals in patients with HIV may pose particular risk. Colorado Clinical and Translational Sciences Institute, National Institutes of Health, and Agency for Healthcare Research and Quality.

A Clinical Approach to Inherited Arrhythmias

In the past decade, the discovery that cases of ventricular arrhythmias and sudden cardiac death (SCD) in young individuals potentially could be caused by an unrecognized genetic substrate has defined a new subset of cardiac conditions: inherited arrhythmogenic diseases (IADs).1 Although rare in clinical practice, these diseases are more common than previously thought. They represent a challenge for the arrhythmia specialist in terms of diagnosis and clinical management. The correct diagnosis of IADs, as well as the use and interpretation of the results of genetic testing, are not straightforward and require a specific expertise such as that provided by specialized and dedicated centers. Here we will review the general issues arising from the correct interpretation of genetic testing and its indications. We also will focus on the clinical management and use of genetic information in different inherited arrhythmias. The term “channelopathies” defines a group of inherited arrhythmic syndromes caused by mutations on genes encoding for ion channel proteins and proteins that regulate ion channels.1 These mutations disrupt the balance of currents in the cardiac action potential, favoring the onset of life-threatening arrhythmias in the absence of structural heart defects. The long QT syndrome (LQTS) is a heritable channelopathy characterized by an exceedingly prolonged cardiac repolarization that may trigger ventricular arrhythmias and SCD.2 LQTS is one of the first channelopathies in which clinical and genetic features have been discovered, and a large series of patients have been collected and followed over the years.2–4 Thanks to these studies, LQTS management takes into account a patient’s genetic background and has become a paradigm for the use of genetic information applied to the clinical practice.3,4 Long QT syndrome can manifest with syncope and cardiac arrest. These commonly are triggered by adrenergic stress; however, roughly 10% …

Radiofrequency Catheter Ablation from the Epicardial Sites for Ventricular Arrhythmias Originating from the Left Ventricular Summit—Two Case-Reports—

Introduction: We report 2 cases of ventricular arrhythmias (VAs) originating from the left ventricular summit (LVS) which required radiofrequency energy (RF) application in the great cardiac vein (GCV) and/or the epicardium for treating VAs. Case 1: Sixty-five year-old female with idiopathic VAs underwent RF-catheter ablation (CA). The earliest activation site of VAs was observed in GCV, to which left descending coronary artery (LAD) run close. Sufficient RF delivery could not be performed due to the concerns about the injury to LAD, and the procedure resulted in a transient therapeutic effect. Case 2: Fifty-one year-old male suffering from VAs associated with non-ischemic cardiomyopathy underwent RF-CA. In 1st session, the earliest activation site of VAs was recognized in GCV, however, RF-CA application in GCV failed to abolish VAs. In 2nd session with the subxiphoidal pericardial approach, the earliest site was located at LVS extremely close to LAD. Despite the multiple RF applications in the vicinity sites of that portion, we were unable to abolish VAs. Conclusion: In sporadic cases, epicardial approach is required to eliminate VAs. However, the discretion and attention have to be paid in order to avoid the serious complications for treating VAs originating from LVS.

The use of disopyramide in resistant cardiac arrhythmias due to acute ischaemic heart disease.

Disopyramide, a new anti-arrhythmic drug, has been assessed in twenty-one episodes of cardiac arrhythmia secondary to acute ischaemic heart disease which failed to respond to more conventional suppressive therapy with lignocaine and other standard drugs. The intravenous administration of 100 mg of disopyramide resulted in suppression of two out of seven episodes of supraventricular arrhythmia, and eleven out of fourteen episodes of ventricular arrhythmias. Successful suppression correlated with blood levels of disopyramide in most cases of ventricular arrhythmias but not in the supraventricular arrhythmias. There were no adverse effects on blood pressure or cardiac function. There were minimal effects on conduction in the electrocardiogram. It is concluded that disopyramide, which probably acts by direct depression of myocardial irritability, is a useful new anti-arrhythmic drug in acute myocardial infarction, especially in those patients with ventricular arrhythmias resistant to more conventional anti-arrhythmic therapy.