Arrhythmia Disorders Research Articles

P378 CARDIAC DEATH AND NURSING CARING: A LITERATURE REVIEW

Abstract Background Brugada syndrome is a genetically determined disease that predisposes to the risk of malignant ventricular arrhythmias and can cause sudden death in young adults with structurally healthy hearts. Currently the main treatment consists in the implantation of the defibrillator (ICD) but new therapeutic profiles emerge from the literature. Objective To redefine the recommendations on early diagnosis and treatment of brs (Brugada syndrome). Provide an overview of the orientation and new clinical pathways emerging from scientific literature Materials and Methods A critical review of the literature was conducted, on the major MEDLINE data bases through PUB MED, CHINAL, COCHRANE LIBRARY and Google schoolar to narrow the search we used mesh terms from the thesaurus library. RCT, meta–analysis, systematic and scoping reviews in English published in the last 5 years for a total of 31 articles Results we estimated an average value of brs in young subjects (between 35 and 65 years) of about 9300 cases per year (∼ 17% of the total): the causes of the phenomenon vary greatly: in older subjects the pathology is more frequently associated with arrhythmic disorders. The review identified ICD implantation as a Class 1 indication in individuals who survived cardiac arrest and had ventricular tachycardia with or without syncope. The radiofrequency ablation technique, on the other hand, involves a preliminary electrophysiological study to identify the epicardial arrhythmogenic substrate. Therefore it seems that epicardial ablation will currently serve as an adjuvant rather than a real alternative to the ICD implant Conclusions Currently, no drug therapy can prevent sudden death in patients with brs some drugs are very effective in reducing symptoms or treating arrhythmias induced by ICD, therefore defibrillator implantation associated with different levels of therapeutic education is recommended, Early diagnosis with radiofrequency ablation technique that actually produces a realignment of the ST tract but in fact does not reduce arrhythmogenic events from the results there are no solving techniques other than the ICD impaction. Therapeutic education is an absolutely effective tool to improve the management of ICD–carrying patients with brs.

P170 VALUE OF ELECTROCARDIOGRAPHIC SCREENING FOR EARLY DETECTION OF ARRHYTHMIC AND MALIGNANT HEART DISEASE IN CHILDREN

Abstract Background Twelve–lead electrocardiography (ECG) is a tool that can identify cardiac conduction abnormalities that predispose to sudden cardiac death (SCD) in completely asymptomatic subjects. The rate of sudden cardiac death in childhood is estimated at 1–1.5 cases per 100,000 individuals and 10–15% of events occur during physical activity. We evaluated the importance of the electrocardiogram performed in childhood in the early diagnosis of asymptomatic electrocardiographic changes suggestive for electrical or structural heart disease potentially at risk of sudden death. Materials and Methods we analyzed 623 patients aged 0–16 years who were referred to the pediatric arrhythmology clinic in Padua Hospital between October 2013 and March 2020. Patients were referred to our second–level clinic after a first electrocardiographic alteration found out in ECG screening performed for sports activity. All patients were evaluated with clinical history and ECG. Then, depending on the suspected pathology, Holter ECG, ergometric test, echocardiogram, MRI were performed for adequate risk stratification. Results Of the 623 patients evaluated, 393 (63%) were referred by sports medicine, 179 (29%) by the hospital pediatric clinic or family pediatrician, and 51 patients (8%) were referred for familiarity. 45% of patients (280) were referred for suspected WPW; 124 patients (20%) for many BEV and suspected ARVD; 85 patients (14%) for suspected long QT, 31 patients (5%) for suspected Brugada pattern; 7 patients (1%) for suspected CPVT; 8 patients (1%) for electrocardiographic changes with suspected HCM; 1 patient (0.01%) for suspected short QT and 88 patients (14%) for other arrhythmic disorders not at risk of sudden death. The diagnosis of WPW was confirmed in 280 patients (100%), LQTS in 45 patients (52%), SQTS in 1 patient (100%), S. of Brugada in 8 patients (25%), CPVT in 5 patients (71%), HCM in 8 patients (100%) and ARVD in 6 patients (5%). Conclusions Our study demonstrates that electrocardiographic screening in childhood allows early diagnosis and treatment of life–threatening arrhythmic heart disease.

Generation of an induced pluripotent stem cell line from a long QT syndrome patient carrying KCNH2/1956C > A mutation

Long QT syndrome (LQT) is an inherited primary arrhythmic disorder characterized by prolonged QT interval on the surface electrocardiogram and life-threatening arrhythmia. In this study, a skin biopsy was obtained from an LQT type 2 (LQT2) patient, who carried a nonsense mutation (c.1956C > A; p.Y652X) in the potassium voltage-gated channel subfamily H member 2 (KCNH2) gene. The skin fibroblasts were reprogrammed by non-integrated Sendai viral method to generate a patient-specific induced pluripotent stem cell (iPSC) line. The generated iPSC line showed typical embryonic stem cell-like morphology, exhibited normal karyotype, expressed pluripotency markers, and was capable to differentiate into three germ layers.

Характеристики функціонального та структурно-функціонального стану серцево-судинної системи хворих при ішемічній хворобі серця та ожирінні

The purpose of the study was to determine the changes in the functional and structural-functional state of the cardiovascular system of individuals with ischemic heart disease against the background of obesity. Materials and methods. 105 people of the diagnostic group were examined: 70 people with ischemic heart disease and obesity (1st diagnostic group) and 35 patients with ischemic heart disease without obesity (2nd diagnostic group), who were treated in the municipal non-commercial enterprise «City Clinical Hospital No. 27» of Kharkiv Regional Council. In the 1st diagnostic group, the majority of patients with I (26 (37.1%) degree of obesity, unlike II (24 (34.3%) and III (20 (28.6%). The control group was formed by 35 healthy persons without any diseases of the cardiovascular system. In the 1st diagnostic group there were 51 (72.9%) ill female and 19 (27.1%) male, in the 2nd – 24 (68.6%) male and 11 (31.4%) female. Age of the 1st and 2nd diagnostic groups amounted to 63.6±8.8 and 69.7±7.9 years respectively, and the control group – 35.2±4.9 years. Body weight and body weight index (p < 0.001) was higher in the 1st diagnostic group (respectively 101.3±15.8 kg and 36.2±4.4 kg/m2) compared to the 2nd (respectively 71.9±8.8 kg and 24.2±1.4 kg/m2) and control (respectively 64.3±7.4 kg and 22.1±1.2 kg/m2). Results and discussion. The presence of arrhythmic disorders of cardiovascular system in coronary heart disease was noted, especially against the background of obesity. The predominance of the cardiovascular system characteristics of the functional state in coronary heart disease with obesity in comparison with the monocurrent coronary heart disease has been determined: accordingly, diastolic arterial pressure is 91.7±7.8 and 89.3±9.1 mmHg; heart frequency – 81.9±11.2 and 78.8±9.5 b/min and pulse 81.2±9.8 and 78.2±9.6 b/min. The advantage of cardiovascular system characteristics in obesity of the III degree in comparison with the II and I degrees is fixed: accordingly, systolic arterial pressure is 160.0±15.9, 158.8±16.1 and 152.7±11.8 mmHg; diastolic arterial pressure – 93.5±8.1, 91.9±8.8 and 90.19±6.6 mmHg; heart rate – 82.0±7.4, 81.4±10.6 and 82.3±14.2 b/min and pulse – 82.0±7.4, 81.0±10.3 and 80.8±11.2 b/min. Conclusion. A reliable possibility of provoking significant reductions in the characteristics of the heart functional state in patients with coronary heart disease and obesity compared with the control group was determined. There is a significant advantage of changes in the structural characteristics of the heart in coronary heart disease and obesity and monocurrent coronary heart disease in contrast to the control group. Significant (p < 0.001) increase in aortic diameter was determined in patients with single coronary heart disease (3.30±0.33 cm) and on the background of obesity (3.22±0.29 cm) compared with the control group (2.86±0.14) and intentionally comparable values of E and A and their ratios in the 1st and 2nd groups (respectively E 0.71±0.18 and 0.69±0.17 cm/s (p = 0.463); A – 0.81±0.19 and 0.85±0.24 cm/s (p = 0.342) and E/A – 0.90±0.27 and 0.82±0.27 (p = 0.102). The predominance of the structural and functional state of the heart values in III and II degrees of obesity compared to I degree was intentionally determined

PO-629-03 IN-DEPTH ANALYSIS OF THE SCN5A LOCUS HIGHLIGHTS DISTINCT GENETIC ARCHITECTURES FOR BRUGADA SYNDROME IN DIFFERENT ANCESTRIES AND IDENTIFIES A NOVEL RARE ENHANCER VARIANT ASSOCIATED WITH DISEASE IN SOUTHEAST ASIAN PATIENTS

Brugada syndrome (BrS) is a cardiac arrhythmia disorder that can cause sudden death in young adults. Genetic variation in the Nav1.5 cardiac sodium channel encoding SCN5A gene is robustly associated with BrS, across both rare coding and common non-coding variants. Despite a markedly higher prevalence of BrS, the diagnostic yield from SCN5A genetic testing in east and southeast Asia has been reported to be much lower than other regions. To compare the contribution of different classes of SCN5A variants (by variant type and rarity) to BrS between northwest European and Thai populations in order to investigate the apparent paradox between high disease prevalence and low diagnostic yield in southeast Asia. Genome sequencing data from European (412 cases, 769 controls) and Thai (202 cases, 410 controls) samples was analysed. SCN5A coding variants were binned by gnomAD exomes (v2.1) filtering allele frequency (FAF) and case-control odds ratios (OR) were calculated for each bin and ancestry. Rare non-coding variants in promoter and enhancer regions of SCN5A and SCN10A were assessed for enrichment or depletion in BrS cohorts. Ultra-rare (FAF<0.00001) SCN5A coding variants are more prevalent and enriched in European (22.6% of cases, OR=22.1, 11.4-43.0) compared to Thai (5.9% of cases, OR=4.3, 1.6-11.5) BrS patients. In contrast, low frequency variants (FAF 0.00005-0.001) that are expected to have intermediate effect sizes are uniquely enriched in Thai samples, occurring in 9.9% of patients. 3/6 of these variants (p.R965C, p.A1428S, p.V2016M) are known to affect Nav1.5 function. A rare non-coding variant in the SCN5A RE5 enhancer region (GRCh37:3-38621871-A-C), affecting a base conserved across species, was highly and uniquely enriched in Thai BrS cases (4.5% vs 0.2%, OR=19.1, p=3e-04). Distinct SCN5A genetic architectures are observed in European and southeast Asian BrS patients. The increased prevalence of BrS in southeast Asia is not due to an increased population burden of ultra-rare and highly deleterious SCN5A coding variants (which are relatively depleted in case cohorts). Our data suggest that other SCN5A variant classes, including coding variants of intermediate effect size and rare non-coding enhancer variants, are genetic risk factors in Thai BrS cases.

BS-513-02 GENOME-WIDE ASSOCIATION ANALYSES IDENTIFY NOVEL BRUGADA SYNDROME RISK LOCI AND HIGHLIGHT A NEW MECHANISM OF SODIUM CHANNEL REGULATION IN DISEASE SUSCEPTIBILITY

Brugada syndrome (BrS) is a cardiac arrhythmia disorder associated with sudden death in young adults. With the exception of SCN5A, encoding the cardiac sodium channel NaV1.5, susceptibility genes remain largely unknown.

PO-655-05 IS ANKYRIN-2 A POTENTIAL GENETIC MODIFIER IN PEDIATRIC CATECHOLAMINERGIC POLYMORPHIC VENTRICULAR TACHYCARDIA?

Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) is a rare inherited arrhythmia disorder with variable expressivity and penetrance. Most cases are attributed to variants in RYR2. The factors that affect disease expression and severity have not been fully elucidated. Variant burden and genetic modifiers are possible influencers of disease presentation and risk.

Atrial cardiomyopathy: Pathophysiology and clinical implications

The term atrial cardiomyopathy appears sporadically in the medical literature, and generally has been used in conjunction with atrial fibrillation (AF), or as “atrial fibrotic cardiomyopathy”, a pathological determinant of AF, caused by a primary cardiomyopathic process, independent of the arrhythmic disorder [1,2].

The Antiarrhythmic Mechanisms of Flecainide in Catecholaminergic Polymorphic Ventricular Tachycardia.

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a severe yet rare inherited arrhythmia disorder. The cornerstone of CPVT medical therapy is the use of β-blockers; 30% of patients with CPVT do not respond well to optimal β-blocker treatment. Studies have shown that flecainide effectively prevents life-threatening arrhythmias in CPVT. Flecainide is a class IC antiarrhythmic drug blocking cardiac sodium channels. RyR2 inhibition is proposed as the principal mechanism of antiarrhythmic action of flecainide in CPVT, while it is highly debated. In this article, we review the current progress of this issue.

OVERVIEW ON THALASSEMIA: A REVIEW ARTICLE

Thalassemia is a hereditary blood disorder which is passed down through families in which the body makes an abnormal form of hemoglobin. This disorder results in the destruction of red blood cell in large number, which leads to anemia. It is caused by mutation in the DNA of cells that make hemoglobin. Thalassemia should be prevented by premarital screening and prenatal diagnosis which is helpful in decreasing prevalence and future incidence of thalassemia. The most important problem in thalassemia patients are iron overload, cardiac arrhythmia, hepatitis, osteoporosis and endocrine disorder however there are typical signs and symptoms of anemia. People with thalassemia can get treatment as indicated by the degree of seriousness of their condition. Blood transfusion is the common treatment for thalassemia. This review presents the types, diagnosis, prevalence, complications and treatment of thalassemia. Thalassemias are a major public health issue in many populations which many health authorities fail to address. These requirements are notrecognized by measures such as the Global Burden of Disease project, which ranks thalassemia very low in terms of disability-adjusted life years (DALYs), and fails to consider that it ranks highly in the one to four-year-oldag egroup, making itanimportant contributor to under-5mortality. Thalassemia doesnot fulfil the criteria to be accepted as a target disease for neonatal screening. Nevertheless, dependingon the screening methodology, severe cases of thalassemia will be detected inmostneonatalscreening programs for sickle cell disease. This is very valuable because: (1) it helps to prepare the affected families for having asick childand (2) it is an important measure of secondary prevention.

Premature Ventricular Complexes: Diagnose, Evaluation, and Management

Premature ventricular complexes (PVCs) are arrhythmias due to abnormal impulse formation in the ventricles. The incidence is detected as much as 1% on standard electrocardiographic (ECG) examination. The aim of this literature review is to explain the diagnosis, evaluation, and management of PVC. The diagnosis of PVC is determined from the symptoms and evidence from the ECG recording. Symptoms may include a faster heartbeat sensation, chest discomfort, skipped beat, and intermittenly strong heartbeat. Evidence of PVC is established by regular ECG recordings or Holter. A 12-ECG can help determine the location of source. PVC evaluation includes determine the dangerousity, the next examination step, the treatment options, and whether ablation is needed. Managements include medical therapy and catheter ablation. Catheter ablation is performed where treatment is unsatisfactory or if the PVC causing life threathening arrhythmia or cardiomyopathy. PVC is considered dangerous if the underlying disease is found in the form of cardiac structural abnormalities, ischemic heart disease or other arrhythmic disorders, more than 2000 PVC is found in 24 hours, complex morphology, different morphology, increased with exercise, PVC with non-outflow tract form, with short coupling interval, and with a wider QRS duration The incidence of VVC that is considered to be able to induce cardiomyopathy is from 10-26%. PVC requires a structured and systematic diagnosis and evaluation step to determine the appropriate treatment.

Genome-wide association analyses identify new Brugada syndrome risk loci and highlight a new mechanism of sodium channel regulation in disease susceptibility.

Brugada syndrome (BrS) is a cardiac arrhythmia disorder associated with sudden death in young adults. With the exception of SCN5A, encoding the cardiac sodium channel NaV1.5, susceptibility genes remain largely unknown. Here we performed a genome-wide association meta-analysis comprising 2,820 unrelated cases with BrS and 10,001 controls, and identified 21 association signals at 12 loci (10 new). Single nucleotide polymorphism (SNP)-heritability estimates indicate a strong polygenic influence. Polygenic risk score analyses based on the 21 susceptibility variants demonstrate varying cumulative contribution of common risk alleles among different patient subgroups, as well as genetic associations with cardiac electrical traits and disorders in the general population. The predominance of cardiac transcription factor loci indicates that transcriptional regulation is a key feature of BrS pathogenesis. Furthermore, functional studies conducted on MAPRE2, encoding the microtubule plus-end binding protein EB2, point to microtubule-related trafficking effects on NaV1.5 expression as a new underlying molecular mechanism. Taken together, these findings broaden our understanding of the genetic architecture of BrS and provide new insights into its molecular underpinnings.

Genetic Diagnostics Contribute to the Risk Stratification for Major Arrhythmic Events in Pediatric Patients with Long QT Syndrome Type 1–3

Long QT syndrome (LQTS) is an inherited arrhythmic disorder associated with sudden cardiac death (SCD). This study aimed to identify the clinical and molecular genetic risk factors that contribute to major arrhythmic events (MAEs) in patients with genetically confirmed childhood onset LQTS 1–3. This study was a retrospective double-center study. An MAE was defined as the occurrence of SCD, aborted SCD, appropriate implantable cardioverter defibrillator discharge, or sustained ventricular tachycardia. During a median follow-up of 4.6 years (range 0.1–24.3 years), MAEs occurred in 18 (17.8%) of 101 patients diagnosed with LQTS at a median of 7.7 years (range 0.0–18.0 years) despite the use of beta-blockers in 91.6% of patients at the last follow-up. A multivariate analysis identified a genetic diagnosis of LQTS2 and LQTS3 and variants within the KCNH2 S5-loop-S6 pore region as independent risk factors for MAEs, independent of the QTc value or a history of syncope detected from a univariate analysis. MAEs occur frequently in childhood onset LQTS despite beta-blocker treatment. A detailed molecular genetic diagnosis can contribute to the arrhythmia risk stratification and optimize the use of preventive measures in this vulnerable patient population.

Predictor properties of indicators of undifferentiated connective tissue dysplasia in children with gastroesophageal reflux for prediction of the development of heart rhythm and conduction disorders

The aim: to improve the early diagnosis of cardiac arrhythmia and conduction disorders in children with gastroesophageal reflux by studying the predictor properties of indicators of undifferentiated connective tissue dysplasia in this category of patients.&#x0D; Materials and methods. We examined 56 children aged 8 to 18 years, with an average age of 14.93±2.62 years, of which 28 children with gastroesophageal reflux in combination with cardiac arrhythmias and conduction disorders were divided into group I, and 28 children with only gastroesophageal reflux without heart rhythm and conduction disturbances – into group II (control). All examined patients underwent clinical and instrumental studies (electrocardiography, 24-hour ECG Holter monitoring, esophagogastroduodenoscopy and PH-metry) and an assessment of the phenotypic signs of undifferentiated connective tissue dysplasia according to the criteria of T. Milkovskaya-Dimitrova and A. Karkashov.&#x0D; Results. When analyzing the predictor properties of indicators of undifferentiated connective tissue dysplasia for predicting the development of cardiac arrhythmias and conduction disorders in children with gastroesophageal reflux, it was found that scoliotic posture had very high predictor properties (I=5.99), а high growth (I=1.94) and a short upper lip (I=1.17) – high, dysplastic tooth growth (I=0 .6) – moderate, and an abnormal shape of the auricles – low ones (I=0.27).&#x0D; Other indicators of undifferentiated connective tissue dysplasia did not have predictive properties at all: joint hypermobility (I=0.22), total number of signs of undifferentiated connective tissue dysplasia (I=0.11), asthenic type of constitution (I=0.11), flat feet (I=0.08), refractive errors (I=0.05), deviated septum of nose (I=0.03), dilated bridge of the nose (I=0.01), short neck (I=0.01).&#x0D; The mean value of the prognostic significance of indicators of undifferentiated connective tissue dysplasia was high (І̅=1,99).&#x0D; Conclusions. It was found that the mean value of the prognostic significance of indicators of undifferentiated connective tissue dysplasia was high (І̅=1,99).&#x0D; It was determined that arrhythmias and cardiac conduction disturbances in children with gastroesophageal reflux are associated with the presence of a scoliotic posture (І=5,99), high growth (І=1,94), dysplastic growth of teeth (І=0,6); in the absence of a short upper lip (І=1,17) and an abnormal shape of the auricles (І=0,27)

An Adaptive Cognitive Sensor Node for ECG Monitoring in the Internet of Medical Things

The Internet of Medical Things (IoMT) paradigm is becoming mainstream in multiple clinical trials and healthcare procedures. Cardiovascular diseases monitoring, usually involving electrocardiogram (ECG) traces analysis, is one of the most promising and high-impact applications. Nevertheless, to fully exploit the potential of IoMT in this domain, some steps forward are needed. First, the edge-computing paradigm must be added to the picture. A certain level of near-sensor processing has to be enabled, to improve the scalability, portability, reliability and responsiveness of the IoMT nodes. Second, novel, increasingly accurate data analysis algorithms, such as those based on artificial intelligence and Deep Learning, must be exploited. To reach these objectives, designers, and programmers of IoMT nodes, have to face challenging optimization tasks, in order to execute fairly complex computing tasks on low-power wearable and portable processing systems, with tight power and battery lifetime budgets. In this work, we explore the implementation of a cognitive data analysis algorithm, based on a convolutional neural network trained to classify ECG waveforms, on a resource-constrained microcontroller-based computing platform. To minimize power consumption, we add an adaptivity layer that dynamically manages the hardware and software configuration of the device to adapt it at runtime to the required operating mode. Our experimental results show that adapting the node setup to the workload at runtime can save up to 50% power consumption. Our optimized and quantized neural network reaches an accuracy value higher than 97% for arrhythmia disorders detection on MIT-BIH Arrhythmia dataset.

Detection and classification of arrhythmia disorders using machine learning algorithm

Detection and classification of arrhythmia disorders using machine learning algorithm

The long COVID: Findings of 24 rhythmic Holter in patients suffering from palpitations

IntroductionMany patients showed long COVID syndrome after recovery from the CORONAVIRUS – SARS infection (40–50%). Many patients showed palpitations and we do not know the cause of these palpitations.Patients and methodsThis is an observational study including patients showing palpitations after recovery from the COVID-19. We analyzed the results of 24 hours recording as well as echocardiographic findings and we analysed the correlation between myocardial strain and rhythms disorders.ResultsAmong 2338 COVID-19 patients, 45% showed long COVID symptoms at 30 days, 7% patients suffered from palpitations. We noted an inappropriate sinusal tachycardia in 60% of cases, 3 cases of ventricle disorders arrhythmia disorders. Longitudinal strain was significantly lower in patients who showed arrhythmia in the 24 recordings than in patients with normal 24 hours rhythm recordings.ConclusionThere is correlation between rhythmic disorders and myocardial damages in patients who showed COVID-19.

Novel SCN5A and GPD1L Variants Identified in Two Unrelated Han-Chinese Patients With Clinically Suspected Brugada Syndrome.

Brugada syndrome (BrS) is a complexly genetically patterned, rare, malignant, life-threatening arrhythmia disorder. It is autosomal dominant in most cases and characterized by identifiable electrocardiographic patterns, recurrent syncope, nocturnal agonal respiration, and other symptoms, including sudden cardiac death. Over the last 2 decades, a great number of variants have been identified in more than 36 pathogenic or susceptibility genes associated with BrS. The present study used the combined method of whole exome sequencing and Sanger sequencing to identify pathogenic variants in two unrelated Han-Chinese patients with clinically suspected BrS. Minigene splicing assay was used to evaluate the effects of the splicing variant. A novel heterozygous splicing variant c.2437-2A>C in the sodium voltage-gated channel alpha subunit 5 gene (SCN5A) and a novel heterozygous missense variant c.161A>T [p.(Asp54Val)] in the glycerol-3-phosphate dehydrogenase 1 like gene (GPD1L) were identified in these two patients with BrS-1 and possible BrS-2, respectively. Minigene splicing assay indicated the deletion of 15 and 141 nucleotides in exon 16, resulting in critical amino acid deletions. These findings expand the variant spectrum of SCN5A and GPD1L, which can be beneficial to genetic counseling and prenatal diagnosis.

The impact of concomitant anemic syndrome on the clinical course of coronary artery disease

The presence of comorbid pathology negatively affects the prognosis of patients with coronary artery disease (CAD). Today it is important to clarify the features of CAD on the background of concomitant anemia and identify the main risk factors for complications to improve the tactics of this category of patients. The aim. To investigate the influence of concomitant anemic syndrome on the clinical course of coronary artery disease, frequency and features of the main cardiovascular events. Materials and methods. The study involved 91 patients with coronary artery disease (42 men and 49 women, age – 70 (49; 93)). All patients were divided into 2 groups: the main group (n = 46) consisted of patients with coronary artery disease with iron-deficiency anemia, the comparison group (n = 45) – patients with coronary artery disease without iron-deficiency anemia. The study of the main cardiovascular events took into account re-hospitalization due to arrhythmic disorders, progression of heart failure (HF), CAD destabilization within the observed period (1 year), as well as death from cardiovascular causes. The data analysis was performed using Statistica 13.0. Results. During the year, 42 non-fatal cardiovascular events were noted in patients of both groups, however in the main group their total number was 30 (67 %) versus 12 (27 %) in the comparison group (χ2 = 13.603; P &lt; 0.05). The presence of concomitant anemia in CAD patients significantly increased the relative risk of re-hospitalizations (RR = 1.9; 95 % CI 1.230–3.112; P &lt; 0.05). Among the reasons for hospitalization in the main group, HF decompensation prevailed – 17 (57 %) patients, unstable angina – 7 (23 %), arrhythmic disorders – 6 (20 %); in the comparison group, among the reasons for re-hospitalization, 7 (57 %) had HF decompensation, 3 (25 %) had unstable angina, and 2 (17 %) cases had arrhythmic disorders. In total, 9 (19.5 %) deaths were recorded in the main group, while in the comparison group 1 (2.2 %) death was recorded during the year (χ2 = 6.995; P &lt; 0.05). The presence of concomitant anemia in patients with CAD increases the risk of fatal outcome by 8.8 times (RR = 8.8; 95 % CI 1.162–66.685; P &lt; 0.05). The presence of moderate anemia in patients with CAD significantly increases the incidence of combined critical events by 39 % during the year of follow-up compared with mild anemia (χ2 = 12.843; P &lt; 0.05). Conclusions. The presence of concomitant anemia is associated with a worsened prognosis for patients having coronary artery disease due to an increased risk of non-fatal cardiovascular events that require re-hospitalization during the year of observation, and an increased incidence of death. Increasing severity of anemia is associated with an increase in the frequency of the combined critical event during 1 year of follow-up.

Abstract 9209: Type 1 Brugada Syndrome Diagnosed in a Patient With an Unaffected Identical Twin

Introduction: Brugada syndrome is a rare arrhythmia disorder due to a cardiac channelopathy with a predisposition to ventricular arrhythmias or SCD. It is characterized by an ECG pattern of complete or incomplete right bundle branch block and ST segment elevation in leads V1-V3. It is normally inherited in an autosomal dominant pattern however environmental factors such as viral infections and inflammation may create myocardial cell damage that may induce an ECG pattern consistent with the diagnosis of Brugada syndrome. Case: A 39-year-old male with no significant past medical history presented to the hospital for two weeks of intermittent dizziness and nocturnal symptoms of being “jolted” awake. ECG on admission was suggestive of a Type 2 Brugada pattern. He denied a family history of first-degree relatives with cardiac disease, SCD or unexplained syncope but did note that he had an identical twin brother. Given symptoms and ECG findings, he was given 400 mg of oral flecainide for a sodium blockade challenge. Four hours after administration of flecainide he developed an overt Type 1 Brugada pattern. Due to issues with the MRI, a cardiac CTA was performed to assess for ARVD. Cardiac CTA showed a mild amount of fat in the apex of the right ventricular wall but was otherwise unremarkable. He was discharged with a wearable external defibrillator and outpatient follow up with EP. During outpatient follow up he reported resolution of symptoms. Interrogation of the defibrillator did not reveal any arrhythmias. An ECG was done on his identical twin brother which did not show evidence of a Type 1 Brugada pattern. He completed a cardiac MRI that showed normal morphology and motion of the right ventricle without evidence of fat dysplasia or late gadolinium enhancement. Given resolution of his symptoms with a normal cardiac MRI and an unremarkable ECG from his identical twin, he was diagnosed with an acquired Brugada syndrome likely due to a viral myocarditis. Conclusion: While Brugada syndrome is normally an inherited genetic disorder, there are instances of acquiring the syndrome through environmental factors. As demonstrated by our case of identical twin brothers with the same genetic makeup, one was diagnosed with Brugada syndrome while the other had an unremarkable ECG.