Sudden Cardiac Death Syndrome Research Articles

Principal components analysis to evaluate complex association of polymorphisms in ACE and ACTN3 genes and the extent of cardiovascular adaptive changes in elite athletes.

Present article aims at clarifying the association of ACE and ACTN3 polymorphisms with adaptive heart changes in elite athletes from power, endurance and mixed sport disciplines using the principal component analysis (PCA). Overall, 281 elite male athletes are divided into three groups: strength-type sports, endurance and mixed sports. After anthropometric measurements, physical and ultrasound examination of the heart, the athletes were exposed to a physical load test. All groups were analyzed for functional ACE and ACTN3 polymorphisms. In order to convert a set of examined, possibly correlated adaptive cardiovascular changes into a set of values of linearly uncorrelated variables we used principal component analysis (PCA). The type of sport significantly affects not only the athlete's anthropometric characteristics, but also on the scope and specificity of the investigated adaptive cardiovascular changes. Athletes from the mixed group of sports showed the best working efficiency of the heart. PCA showed that the type of sport, but not genetic predisposition affects the co-adaptation of complex traits. Effect of genotype, type of sport and their interaction on observed variability in morpho-functional cardiovascular adaptive changes in elite athletes can be used for a better understanding of the clinical phenomenon of athlete's heart and sudden cardiac death syndrome.

Spontaneous coronary artery dissection: an unpredictable event.

Spontaneous coronary artery dissection (SCAD) is an under-recognized cause of acute coronary syndrome that predominantly affects women in adulthood and is the leading cause of acute myocardial infarction in pregnancy. The most common clinical presentation is ST-segment elevation myocardial infarction (STEMI) or non-STEMI, followed by cardiogenic shock (∼2%), sudden cardiac death (0.8% in autopsy series), cardiac arrest, ventricular arrhythmias (∼5%), and Takotsubo syndrome. The prevalence of SCAD in the general population is largely uncertain due to underdiagnosis. Oral contraceptives, post-menopausal therapy, and infertility treatments are recognized associated factors. The pathological substrates (fibromuscular dysplasia) and triggers (especially emotional stress) are commonly present in affected women. The few cases with a precise genetic aetiology occur in the context of syndromic and non-syndromic connective tissue diseases. The only true certainty in SCAD is the overwhelming prevalence in women. The first event as well as the recurrence (up to 30%, which varies depending on the definition) is largely unpredictable. The treatment strategy is highly individualized and requires extensive additional study in order to optimize outcomes and prevent major adverse cardiovascular events in affected individuals. We have known about SCAD for nearly a century, but we still do not know how best to prevent, diagnose, and treat it, making SCAD a highly important and unmet clinical need.

Out-of-Hospital Cardiac Arrest during the COVID-19 Pandemic: A Systematic Review.

Objective: Out-of-hospital cardiac arrest (OHCA) is a prominent cause of death worldwide. As indicated by the high proportion of COVID-19 suspicion or diagnosis among patients who had OHCA, this issue could have resulted in multiple fatalities from coronavirus disease 2019 (COVID-19) occurring at home and being counted as OHCA. Methods: We used the MeSH term "heart arrest" as well as non-MeSH terms "out-of-hospital cardiac arrest, sudden cardiac death, OHCA, cardiac arrest, coronavirus pandemic, COVID-19, and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)." We conducted a literature search using these search keywords in the Science Direct and PubMed databases and Google Scholar until 25 April 2022. Results: A systematic review of observational studies revealed OHCA and mortality rates increased considerably during the COVID-19 pandemic compared to the same period of the previous year. A temporary two-fold rise in OHCA incidence was detected along with a drop in survival. During the pandemic, the community's response to OHCA changed, with fewer bystander cardiopulmonary resuscitations (CPRs), longer emergency medical service (EMS) response times, and worse OHCA survival rates. Conclusions: This study's limitations include a lack of a centralised data-gathering method and OHCA registry system. If the chain of survival is maintained and effective emergency ambulance services with a qualified emergency medical team are given, the outcome for OHCA survivors can be improved even more.

A Novel Module Based Method of Teaching Electrocardiogram Interpretation for Emergency Medicine Residents.

A Novel Module Based Method of Teaching Electrocardiogram Interpretation for Emergency Medicine Residents.

КЛИНИЧЕСКИЕ И МОЛЕКУЛЯРНО-ГЕНЕТИЧЕСКИЕ ОСНОВЫ ВНЕЗАПНОЙ СЕРДЕЧНОЙ СМЕРТИ ПРИ ПЕРВИЧНЫХ ЭЛЕКТРИЧЕСКИХ ЗАБОЛЕВАНИЯХ СЕРДЦА У ДЕТЕЙ

Primary electrical heart diseases (PEHDs) are hereditary orphan life-threatening conditions leading to a sudden cardiac death in young adults in the absence of structural heart disease. Among the most common and studied diseases of this group are: long QT syndrome (LQTS), catecholaminergic ventricular tachycardia, Brugada syndrome, short QT syndrome, early ventricular repolarization syndrome. Also, this group of diseases includes congenital sick sinus syndrome, progressive cardiac conduction defect, idiopathic ventricular fibrillation, familial atrial fibrillation and a number of cases (from 5 to 10%) of the sudden cardiac death syndrome in infants. The total prevalence of PEHDs in the pediatric population is quite high and is about 1:2000, mainly due to long QT syndrome. PEHDs are poorly identified by the standard clinical approach, at the same time a delay in diagnosing and prescribing specific therapy may lead to fatal consequences and sudden cardiac death of the child at the first-ever syncope. The vast majority of PEHDs genes identified to date encode subunits of cardiac ion channels or proteins, which interact with ion channels and regulate their functions. The advent of the next generation sequencing led to a shift in most DNA diagnostics laboratories from screening single genes or small gene panels to examining of whole exome or whole genome data. These diseases, especially LQTS, have become unique cardiological models for clinical and genetic studies, analysis of genotype-phenotype correlations and the development of a modern strategy of multi-level hybrid therapy and the prevention of sudden cardiac death (SCD) in people of young age. The most PEHDs can and should be diagnosed in childhood, which now makes it possible to effectively prevent life-threatening arrhythmias. More and more patients are surviving into adulthood, as yet, and patients are interacting with traditional risk factors and obviously should have higher cardiovascular risks. Due to the high prevalence in the population, the association with the SCD, the polymorphism of clinical and genetic manifestations, high technology medicine, the research of PEHDs has become one of the priority places in both pediatric and adult cardiology, and the diseases have now become models for development of gene therapies. The paper outlines the clinical and genetic characteristics, the basics of diagnostics and up-to-date therapeutic, interventional and surgical technologies for the treatment of the most common PEHDs in childhood.

P377 CHALLENGING RISK STRATIFICATION IN BRUGADA SYNDROME: A CASE OF VENTRICULAR TACHYCARDIA IN A LOW–RISK PATIENT

Abstract A 22–year–old healthy athlete was referred to our hospital for electrocardiographic findings consistent with intermittent type–1 Brugada pattern. A routine electrocardiogram (ECG) performed during a check–up showed sinus rhythm, normal PR interval and QRS duration, rSR’ with a coved type ST–segment elevation in V2 lead (Figure 1).The patients denied history of syncope or palpitations and his family history did not show sudden cardiac death or Brugada syndrome (BrS). Transthoracic echocardiography was normal and a 12–lead Holter monitoring revealed the intermittence of the type–1 Brugada pattern. The patient was hospitalized for further investigation. On admission, ECG showed a type–2 Brugada pattern; therefore, Ajmaline challenge test (1 mg/kg injection in 10 minutes) was performed and resulted positive. Subsequently, the patient underwent an electrophysiological study (EPS) which was negative for induction of sustained arrhythmias. The protocol adopted consisted of double extrastimuli programmed electrical stimulation until refractoriness (drive 600/220 ms and 400/210 ms), at double sites (right ventricle apex and right ventricular outflow tract). Furthermore a genetic test was performed using next–generation sequencing, showing a heterozygous mutation in the SCN5A gene, encoding for sodium channel alpha subunit (variant c.5363delA), not previously described in the literature. Since the low arrhythmic risk, the patient was implanted with a loop recorder (ILR, Medtronic Reveal LINQ), entering a program of home monitoring. After a 15–months follow–up, an episode of ventricular polymorphic tachycardia lasting 2 minutes and 11 seconds, associated with lightheadedness and palpitations, was detected by the remote monitoring (Figure 2). The patient was therefore hospitalized. During the in–hospital stay a cardiac magnetic resonance was performed to exclude other underlying diseases, identifying an enlarged right ventricle (EDVi 114 ml/m2) and abnormal free wall motion (Figure 3), thus reaching one major criteria of arrhythmogenic cardiomyopathy (however not sufficient for the diagnosis). The patient was then implanted with a subcutaneous implantable cardiac defibrillator (Boston Scientific EMBLEM MRI S–ICD). We presented a case of complex arrhythmic risk stratification in a possible overlap of an arrhythmogenic cardiomyopathy and a Brugada Syndrome in a young athlete who experienced a sustained ventricular tachycardia during loop–recorder monitoring.

Metabolic Syndrome, Gamma-Glutamyl Transferase, and Risk of Sudden Cardiac Death.

Background: Metabolic syndrome is associated with a significantly increased risk of sudden cardiac death (SCD). However, whether temporal changes in the metabolic syndrome status are associated with SCD is unknown. We aimed to determine whether metabolic syndrome and gamma-glutamyl transferase (ɣ-GTP), including their temporal changes, are associated with the risk of SCD. Methods: We performed a nationwide population-based analysis using the Korean National Health Insurance Service. People who underwent a national health check-up in 2009 and 2011 were enrolled. The influence of metabolic syndrome and ɣ-GTP on SCD risk was evaluated. Results: In 2009, 4,056,423 (848,498 with metabolic syndrome) people underwent health screenings, 2,706,788 of whom underwent follow-up health screenings in 2011. Metabolic syndrome was associated with a 50.7% increased SCD risk (adjusted hazard ratio (aHR) = 1.507; p < 0.001). The SCD risk increased linearly as the metabolic syndrome diagnostic criteria increased. The ɣ-GTP significantly impacted the SCD risk; the highest quartile had a 51.9% increased risk versus the lowest quartile (aHR = 1.519; p < 0.001). A temporal change in the metabolic syndrome status and ɣ-GTP between 2009 and 2011 was significantly correlated with the SCD risk. Having metabolic syndrome in 2009 or 2011 indicated a lower SCD risk than having metabolic syndrome in 2009 and 2011 but a higher risk than having no metabolic syndrome. People with a ≥20-unit increase in ɣ-GTP between 2009 and 2011 had an 81.0% increased SCD risk versus those with a change ≤5 units (aHR = 1.810; p < 0.001). Conclusions: Metabolic syndrome and ɣ-GTP significantly correlated with an increased SCD risk. SCD was also influenced by temporal changes in the metabolic syndrome status and ɣ-GTP, suggesting that appropriate medical treatment and lifestyle modifications may reduce future SCD risk.

КОРОНАРНО-ПУЛЬМОНАЛЬНАЯ ФИСТУЛА

Coronary arteriovenous fistula (CAF) is a rare form of congenital heart disease. However, it is the most common type of congenital anomaly of the coronary arteries. [1] When there is the connection between the coronary artery and the chambers of the heart, it is called a coronary chamber fistula. The fistula may also be between a coronary artery and another adjacent vessel from the pulmonary or systemic circulation. An open fistula provides low-resistance flow by directing blood from an artery into a vein, heart chamber, or other low-pressure vessel such as the pulmonary artery. Patients with CAF may develop symptoms at birth or later in life, depending on the type of fistula and the presence of collateral circulation. Studies have reported an association between ventricular arrhythmias and sudden cardiac death syndromes in young adults and athletes with certain types of coronary anomalies, such as anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) [2-5]. The most common symptom is a myocardial ischemia. The purpose of this article is to present a clinical case of endovascular treatment of coronary pulmonary fistula. As a result of a modern diagnostic methods, such as CT angiography with three-dimensional reconstruction, it is not difficult to assess the degree and nature of the pathology. Having assessed the tactics, modern doctors are able to cope with coronary arteriovenous fistulas with great success using minimally invasive X-ray endovascular technologies.

Medikal Tedavi ile İyileşen Yaygın, İdiyopatik, Tekrarlayan Spontan Koroner Arter Diseksiyonu

Spontaneous coronary artery dissection is a rare cause of sudden cardiac death and acute coronary syndrome, and mainly affects young female. Treatment of this condition depends on the clinical features, hemodynamic and angiographic findings of the patient, but due to the rarity of the disease, guideline support was insufficient until the last period. Depending on the condition of the patient and the coronary blood flow, medical observation, percutaneous coronary intervention or coronary artery bypass graft surgery are used in the treatment. We present a young female patient who underwent emergency coronary artery bypass graft surgery after spontaneous left main coronary artery dissection four years ago and was recently diagnosed with extensive spontaneous coronary artery dissection in her right coronary artery. After the diagnosis, the patient was given medical treatment and recovered completely.

Innovative Approaches to Assess Intermediate Cardiovascular Risk Subjects: A Review From Clinical to Metabolomics Strategies.

Current risk stratification strategies for coronary artery disease (CAD) have low predictive value in asymptomatic subjects classified as intermediate cardiovascular risk. This is relevant because not all coronary events occur in individuals with traditional multiple risk factors. Most importantly, the first manifestation of the disease may be either sudden cardiac death or acute coronary syndrome, after rupture and thrombosis of an unstable non-obstructive atherosclerotic plaque, which was previously silent. The inaccurate stratification using the current models may ultimately subject the individual to excessive or insufficient preventive therapies. A breakthrough in the comprehension of the molecular mechanisms governing the atherosclerosis pathology has driven many researches toward the necessity for a better risk stratification. In this Review, we discuss how metabolomics screening integrated with traditional risk assessments becomes a powerful approach to improve non-invasive CAD subclinical diagnostics. In addition, this Review highlights the findings of metabolomics studies performed by two relevant analytical platforms in current use–mass spectrometry (MS) hyphenated to separation techniques and nuclear magnetic resonance spectroscopy (NMR) –and evaluates critically the challenges for further clinical implementation of metabolomics data. We also discuss the modern understanding of the pathophysiology of atherosclerosis and the limitations of traditional analytical methods. Our aim is to show how discriminant metabolites originated from metabolomics approaches may become promising candidate molecules to aid intermediate risk patient stratification for cardiovascular events and how these tools could successfully meet the demands to translate cardiovascular metabolic biomarkers into clinical settings.

Abstract 12296: Clinical and Functional Genetic Characterization of the Role of Cardiac Calcium Channel Variants in the Early Repolarization Syndrome

Introduction: Early repolarization syndrome (ERS) is an inherited sudden cardiac death syndrome. Hypothesis: In this study we test the role of genetic variants in cardiac calcium channel genes in the pathogenesis of ERS and probes the underlying mechanisms. Methods: PCR-based next-generation sequencing was carried out using a targeted gene approach. Unrelated ERS probands carrying calcium channel variants were evaluated clinically and compared with matched healthy controls. Wild type (WT) and mutant CACNA1C genes were co-expressed with CACNB2b and CACNA2D1 in HEK293 cells and studied using whole-cell patch-clamp and confocal fluorescence microscope . Results: Among 104 ERS probands, 16 carried pathogenic variants in calcium channel genes (32.2±14.6 years old, 87.5% male). The symptoms at diagnosis included syncope (56.3%), ventricular tachycardia/fibrillation (VT/VF, 62.5%), sudden cardiac death (SCD, 56.3%). Three cases (18.8%) had a family history of SCD or syncope. Eight patients (50.0%) had a single calcium gene rare variant. The other half carried rare variants in other ERS susceptible genes. Compared with controls, the heart rate was slower (72.7±8.9 vs. 65.6±16.1 bpm), QTc interval was shorter (408.2±21.4 vs. 386.8±16.9 ms) and Tp-e/QT was longer (0.22±0.05 vs.0.28±0.04) in calcium mutation carriers. Electrophysiological analysis of one mutation, CACNA1C -P817S revealed that the density of I Ca was reduced by approximately 84.6% compared to WT (-3.1±2.5 vs. -20.5±3.6 pA/pF, n=11 and 15, respectively). Heterozygous expression of mutant channels was associated with a 51.3% reduction of I Ca . Steady-state inactivation was shifted to more negative potentials and significantly accelerated. Confocal microscopy revealed trafficking impairment of CACNA1C -P817S (peripheral/central intensity: 0.94±0.1 in WT vs. 0.33±0.1 in P817S, n=10 and 9, respectively). Conclusions: ERS associated with loss of function (LOF) genetic defects in genes encoding the cardiac calcium channel represents a unique clinical entity characterized by decreased heart rate and QTc, as well as increased transmural dispersion of repolarization. In the case of CACNA1C -P817S impaired trafficking of the channel to the membrane contributes to the LOF.

Clinical and Functional Genetic Characterization of the Role of Cardiac Calcium Channel Variants in the Early Repolarization Syndrome.

Background: Early repolarization syndrome (ERS) is an inherited sudden cardiac death (SCD) syndrome. The present study investigates the role of genetic variants in cardiac calcium-channel genes in the pathogenesis of ERS and probes the underlying mechanisms.Methods: Polymerase chain reaction–based next-generation sequencing was carried out using a targeted gene approach. Unrelated ERS probands carrying calcium-channel variants were evaluated clinically and compared with matched healthy controls. Wild-type (WT) and mutant CACNA1C genes were coexpressed with CACNB2b and CACNA2D1 in HEK293 cells and studied using whole-cell patch-clamp techniques and confocal fluorescence microscope.Results: Among 104 ERS probands, 16 carried pathogenic variants in calcium-channel genes (32.2 ± 14.6 years old, 87.5% male). The symptoms at diagnosis included syncope (56.3%), ventricular tachycardia/fibrillation (62.5%), and SCD (56.3%). Three cases (18.8%) had a family history of SCD or syncope. Eight patients (50.0%) had a single calcium gene rare variant. The other half carried rare variants in other ERS-susceptible genes. Compared with controls, the heart rate was slower (72.7 ± 8.9 vs. 65.6 ± 16.1 beats/min, *p < 0.05), QTc interval was shorter (408.2 ± 21.4 vs. 386.8 ± 16.9 ms, **p < 0.01), and Tp-e/QT was longer (0.22 ± 0.05 vs. 0.28 ± 0.04, ***p < 0.001) in single calcium mutation carriers. Electrophysiological analysis of one mutation, CACNA1C-P817S (c.2449C>T), revealed that the density of whole-cell calcium current (ICa) was reduced by ~84.61% compared to WT (−3.17 ± 2.53 vs. −20.59 ± 3.60 pA/pF, n = 11 and 15, respectively, **p < 0.01). Heterozygous expression of mutant channels was associated with a 51.35% reduction of ICa. Steady-state inactivation was shifted to more negative potentials and significantly accelerated as well. Confocal microscopy revealed trafficking impairment of CACNA1C-P817S (peripheral/central intensity: 0.94 ± 0.10 in WT vs. 0.33 ± 0.12 in P817S, n = 10 and 9, respectively, **p < 0.01).Conclusions: ERS associated with loss-of-function (LOF) genetic defects in genes encoding the cardiac calcium channel represents a unique clinical entity characterized by decreased heart rate and QTc, as well as increased transmural dispersion of repolarization. In the case of CACNA1C-P817S, impaired trafficking of the channel to the membrane contributes to the LOF.

Cardiac potassium inward rectifier Kir2: Review of structure, regulation, pharmacology, and arrhythmogenesis

Potassium inward rectifier channel Kir2 is an important component of terminal cardiac repolarization and resting membrane stability. This functionality is part of balanced cardiac excitability and is a defining feature of excitable cardiac membranes. “Gain-of-function” or “loss-of-function” mutations in KCNJ2, the gene encoding Kir2.1, cause genetic sudden cardiac death syndromes, and loss of the Kir2 current IK1 is a major contributing factor to arrhythmogenesis in failing human hearts. Here we provide a contemporary review of the functional structure, physiology, and pharmacology of Kir2 channels. Beyond the structure and functional relationships, we will focus on the elements of clinically used drugs that block the channel and the implications for treatment of atrial fibrillation with IK1-blocking agents. We will also review the clinical disease entities associated with KCNJ2 mutations and the growing area of research into associated arrhythmia mechanisms. Lastly, the presence of Kir2 channels has become a tipping point for electrical maturity in induced pluripotent stem cell-derived cardiomyocytes (iPS-CMs) and highlights the significance of understanding why Kir2 in iPS-CMs is important to consider for Comprehensive In Vitro Proarrhythmia Assay and drug safety testing.

Sudden cardiac death during nighttime hours

In the absence of apparent triggers, sudden cardiac death (SCD) during nighttime hours is a perplexing and devastating phenomenon. There are few published reports in the general population, with insufficient numbers to perform sex-specific analyses. Smaller studies of rare nocturnal SCD syndromes suggest a male predominance and implicate sleep-disordered breathing. The purpose of this study was to identify mechanisms of nighttime SCD in the general population. From the population-based Oregon Sudden Unexpected Death Study, we evaluated SCD cases that occurred in the community between 10 PM and 6 AM (nighttime) and compared them with daytime cases. Univariate comparisons were evaluated using Pearson χ2 tests and independent samples t tests. Logistic regression was used to further assess independent SCD risk. A total of 4126 SCD cases (66.2% male, 33.8% female) met criteria for analysis and 22.3% (n = 918) occurred during nighttime hours. Women were more likely to present with nighttime SCD than men (25.4% vs 20.6%; P < .001). In a multivariate regression model, female sex (odds ratio [OR] 1.3 [confidence interval (CI) 1.1-1.5]; P=.001), medications associated with somnolence/respiratory depression (OR 1.2 [CI 1.1-1.4]; P = .008) and chronic obstructive pulmonary disease/asthma (OR 1.4 [CI 1.1-1.6]; P < .001) were independently associated with nighttime SCD. Women were taking more central nervous system-affecting medications than men (1.9 ± 1.7 vs 1.4 ± 1.4; P = .001). In the general population, women were more likely than men to suffer SCD during nighttime hours and female sex was an independent predictor of nighttime events. Respiratory suppression is a concern, and caution is advisable when prescribing central nervous system-affecting medications to patients at an increased risk of SCD, especially women.

A case of anomalous aortic origin of coronary artery associated with a coved‐type electrocardiogram

Brugada syndrome (BrS) is a sudden cardiac death syndrome characterized by a coved-type electrocardiogram (ECG). Different disorders, such as ischemia, can emulate a Brugada-pattern ECG (Brugada phenocopy). We report herein, the first case of surgical epicardial electrophysiological mapping in a successfully resuscitated patient with an anomalous aortic origin of the coronary artery (AAOCA) associated with a coved-type ECG. It was debatable whether the coved-type ECG and the abnormal arrhythmogenic substrate in the epicardial right ventricular outflow tract were derived from BrS or from repetitive ischemia due to AAOCA; however, the epicardial electrophysiological mapping helped in deciding the treatment strategy.

Overt long QT syndrome in children presenting with seizure disorders in Pakistan

Background and Objective:The long QT syndrome (LQTS) is a repolarization defect of heart involving potassium linked channels and it usually manifests clinically as seizures, syncope, or sudden cardiac death syndrome in children secondary to its characteristic ventricular tachy-arrhythmia like torsades de pointes. The reason behind epilepsy or seizures like activity in this disease is the sequelae of prolonged cerebral hypoperfusion secondary to the cardiac dysrhythmia. The aim of study is to look for clinical spectrum and risk factors associated with LQTS among children presenting with epilepsy, which can predict the early diagnosis of LQTS.Materials and Methods:For this observational study, 422 patients having epilepsy presenting for the first time in a 3-year period were enrolled. Demographical profile, LQTS measures, and various factors under observation were recorded.Results:Among the 422 enrolled children (M: F 1.8:1) with age ranging from 4 to 87 months (median 23 months), 8 (1.9%) children who presented with epilepsy had LQTS. Among those, mean QTc on electrocardiogram was 454 ± 31 msec and mean Schwartz score >3. Half of the patients with LQTS had deafness (P = 0.002) and 37.5% had a positive family history (P = 0.0045). Nearly a third (37.5%) presented with syncope and 87.5% patients with LQTS had no postictal drowsiness or sleep (P ≤ 0.004).Conclusions:LQTS is underestimated in children presenting with epilepsy and LQTS should be considered as an alternate diagnosis in children with recurrent seizures or syncopal attacks. The brief period of seizures with no postictal drowsiness, syncope, and strong family history are the features which may help in segregating LQTS from epilepsy.

Comparative characteristics of polymorphic allele propagation in the hemostasis system genes PAI-1 (-675 5G/4G) and FGB (-455 G/A) in sudden cardiac death and acute coronary syndrome in patients undergoing coronary artery stenting

Aim.To give comparative characteristics of the prevalence of polymorphic alleles in the genes of the hemostatic system PAI-1 (-675 5G/4G) and FGB (-455 G/A) in patients with sudden cardiac death and those with acute coronary syndrome undergoing coronary artery stenting.Material and methods.Genetic typing of biological material (BM) was performed for the prevalence of polymorphic alleles in two genes of the hemostasis system. BM was selected from people with a diagnosis of coronary artery disease, divided into three comparison groups: I-suddenly deceased citizens with a diagnosis of coronary artery disease, II-patients with ACS who underwent urgent coronary artery stenting, and III-patients with a chronic form of coronary artery disease in whom endovascular surgery was performed as planned.Results.The calculated criterion 2of the prevalence of polymorphisms in the FGB (-455 G/A) and PAI-1 (-675 5G/4G) genes turned out to be more than the critical (tabular) value, which indicates an existing relationship between the presence of IHD and the carriage of one of the polymorphic alleles. Based on the same data, the 2criterion was calculated without taking into account data for a group of healthy citizens. For carriers of the polymorphic allele of the FGB gene (-455 G/A), no statistically significant differences were found. For carriers of the PAI-1 gene polymorphic allele (-675 5G/4G), statistically significant differences were found.Conclusions.ACS with a favorable outcome (subject to emergency surgical intervention) occurs at an earlier age than in patients diagnosed with coronary artery disease who die suddenly. The presence of a mutant allele in the PAI-1 gene (-675 5G/4G) requires further studies in order to expertly assess the death rate in patients after surgery with coronary stenting.

Cardiovascular Pathology in Patients With COVID-19

In the recent months of the COVID-19 pandemics, the cardiological society has faced a new challenge, myocardial injury by the coronavirus infection. According to statistics, 20-40% of hospitalized patients have chest pain, heart rhythm disorders, heart failure, and sudden cardiac death syndrome. This review focuses on recent studies and clinical cases related with this issue.

Pharmacological spasm provocation testing in 2500 patients: provoked spasm incidence, complications and cardiac events

Pharmacological spasm provocation tests such as acetylcholine (ACh) and ergonovine (ER) had been performed in the clinic. We retrospectively analyzed the incidence of provoked spasm, complications during testing and the cardiac events after these tests. From January 1991 and October 2018, we performed pharmacological spasm provocation tests in 2500 patients: 1810 ACh tests, 1232 ER tests, 542 both tests, and 310 ACh added after ER tests. ACh was injected in incremental doses of 20/50/100/200μg into the LCA and 20/50/80μg into the RCA. ER was administered as a total dose of 64μg into the LCA and 40μg into the RCA. When adding ACh after ER, the total dose was 50/80μg into the RCA and 100/200μg into the LCA. Positive spasm was defined as ≥ 90% stenosis and usual chest pain or ischemic ECG changes. Mean follow-up duration was 47.5 ± 29.9months. Overall, provoked positive spasm was found in 1095 patients (43.8%). The incidence of positive provoked spasm during ACh testing was significantly higher than that during other tests (ACh: 48.7% vs. ER: 28.9%, Both: 24%, ACh added after ER: 33.5%, p < 0.001). Multiple spasms were remarkably more frequent during ACh testing compared with the other 3 types of testing (ACh: 28.2% vs. ER: 7.4%, Both: 4.1%, ACh added after ER: 13.2%, p < 0.001). No death or acute myocardial infarction was observed, while major complications during ACh testing were significantly more frequent than during ER testing. Readmission due to recurrent angina pectoris in spasm-positive patients was remarkably more frequent than in spasm-negative patients. The incidence of sudden cardiac death, ventricular fibrillation, and acute coronary syndrome were not different between the spasm-positive and spasm-negative groups during the follow-up periods. We could perform all spasm provocation tests without any irreversible complications. All sequential spasm provocation tests were useful for documenting coronary spasm.

Brugada phenocopy following coronary artery bypass graft surgery

A 71-year old male with a history of inferior myocardial infarction and hypertension underwent coronary artery bypass graft (CABG) surgery. He had no family or personal history of syncope, sudden cardiac death or Brugada syndrome. A series of twelve-lead electrocardiograms showed type 1 and type 2 Brugada ECG patterns after procedure, but resolution of ST segment changes to five days later. The electrophysiological mechanisms underlying these changes will be discussed.