scholarly journals Cardiovascular Pathology in Patients With COVID-19

Kardiologiia ◽  
2020 ◽  
Vol 60 (8) ◽  
pp. 23-26
Author(s):  
E. K. Serezhina ◽  
A. G. Obrezan
Keyword(s):  
Heart Failure ◽  
Chest Pain ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Myocardial Injury ◽  
Heart Rhythm ◽  
Hospitalized Patients ◽  
Cardiovascular Pathology ◽  
Heart Rhythm Disorders ◽  
Coronavirus Infection

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.

Abstract 395: A Synonymous Coding SNP Alters SCN5A Regulation by miR-24 and Associates With Non-Arrhythmic Death in Heart Failure

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Xiaoming Zhang ◽  
Jin-Young Yoon ◽  
Michael Morley ◽  
Patrick Breheny ◽  
Heather Bloom ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Clinical Signs ◽  
Heart Rhythm ◽  
Coding Sequence ◽  
Reduced Ejection Fraction ◽  
Arrhythmic Death ◽  
And Function ◽  
Myocardial Gene Expression

Mutations disrupting SCN5A coding sequence cause inherited arrhythmias and cardiomyopathy, and SNPs linked to SCN5A splicing, localization and function associate with heart failure-related sudden cardiac death. However, the clinical relevance of SNPs that modulate SCN5A expression levels remains understudied. Recently, we generated a transcriptome-wide map of microRNA (miR) binding sites in human heart and evaluated their interface with polymorphisms. Among >500 common SNPs residing within miR target regions, we identified a synonymous SNP (rs1805126) adjacent to a miR-24 site within SCN5A coding sequence. This SNP is known to reproducibly associate with heart rhythm measurements, but is not considered to be “causal”. Here, we show that miR-24 potently suppresses SCN5A and that rs1805126 modulates this regulation. In further exploring the clinical significance of this, we found that rs1805126 minor allele homozygosity associates with decreased cardiac SCN5A expression and increased mortality in heart failure patients. Unexpectedly, this risk was not linked with arrhythmic sudden cardiac death, but rather, with clinical signs of worsening heart failure (e.g. reduced ejection fraction) and myocardial gene expression changes related to bioenergetics, inflammation and extracellular remodeling. Together, these data attribute a molecular mechanism to this firmly-established GWAS SNP and highlight a novel and surprising link between common variations in SCN5A expression and non-arrhythmic death in heart failure.

THE NEW GENETIC ASPECTS OF ATRIAL FIBRILLATION IN PERSONS OF THE RUSSIAN POPULATION

2020 ◽  
pp. 27-33
Author(s):  
Aksyutina N.V. ◽  
Shulman V.A. ◽  
Aldanova E.E. ◽  
Nikulina S.Yu. ◽  
Mordovskii V.S. ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Chronic Heart Failure ◽  
Molecular Genetic ◽  
Genetic Research ◽  
Heart Rhythm ◽  
Control Group ◽  
Atrial Remodeling ◽  
Cardiovascular Pathology ◽  
Heart Rhythm Disorders

Atrial fibrillation (AF) is one of the most common and dangerous heart rhythm disorders. Lone AF is due to a genetic predisposition. Foreign studies have proven the association of rs2200733 polymorphism of chromosome 4q25 with AF. No such studies have been conducted in the Russian Federation. Purpose of the study: to determine the association of the rs2200733 polymorphism of chromosome 4q25 with the development of AF, and to exclude the possible connection of the studied polymorphic marker with concomitant cardiovascular pathology. A total of 247 patients with AF were examined (113 from lone AF, 134 from secondary). Control group - 182 healthy people. Behavior: ECG, EchoCG, Holter ECG monitoring, blood test for thyroid hormones, VEM, CAG, molecular genetic research. In the group of patients with AF, the TT genotype was detected in 12.95%, which is statistically significant more often than in the control group (4.94%), p<0.05. In the presence of a genotype with a rare T allele, the risk of developing AF increases by 1.5 times. The TT genotype was statistically significant more often in the subgroup of patients with isolated AF (17.70%) in comparison with the control group (4.94%), p<0.05. The risk of developing isolated AF in the presence of a genotype with a rare allele T is 1.8 times increased. Chronic heart failure, no statistically significant differences were found (p>0.05). In patients with the TT genotype, the mean LA size was 3.738 ± 0.494 cm, it was statistically significantly smaller than in patients with the CC genotype, which corresponded to 3.925 ± 0.629 cm, p<0.05; and than in individuals with a heterozygous CT genotype, its value in this subgroup is 4.018 ± 0.639 cm, p<0.05. Conclusions: Homozygous genotype for the rare TT allele and the T allele of the rs2200733 polymorphism of chromosome 4q25 are predictors of lone AF. The rs2200733 polymorphism has no association with any cardiovascular pathology, such as hypertension, ischemic heart disease and chronic heart failure. The TT genotype and the T allele of the rs2200733 polymorphism do not affect left atrial remodeling in patients with AF.

Prevention of sudden cardiac death in primary electrical disorders

ESC CardioMed ◽  
2018 ◽  
pp. 2363-2369
Author(s):  
Elena Arbelo ◽  
Josep Brugada
Keyword(s):  
Heart Disease ◽  
Sudden Cardiac Death ◽  
Risk Stratification ◽  
Cardiac Death ◽  
Heart Rhythm ◽  
Structural Heart Disease ◽  
Cardioverter Defibrillator ◽  
Active Population ◽  
Heart Rhythm Disorders ◽  
Genetically Determined

Cardiac channelopathies are genetically determined heart rhythm disorders affecting young individuals without structural heart disease, predisposing them to ventricular arrhythmias. Apart from avoiding triggers such as drugs, exercise, or fever, in most primary arrhythmia syndromes the only effective therapy for preventing sudden cardiac death is an implantable cardioverter defibrillator (ICD). However, in this group of a young, active population, ICD may cause a significant rate of device-related complications. Therefore, appropriate risk stratification and selective ICD indications are of utmost importance.

scholarly journals Management of asymptomatic arrhythmias: a European Heart Rhythm Association (EHRA) consensus document, endorsed by the Heart Failure Association (HFA), Heart Rhythm Society (HRS), Asia Pacific Heart Rhythm Society (APHRS), Cardiac Arrhythmia Society of Southern Africa (CASSA), and Latin America Heart Rhythm Society (LAHRS)

EP Europace ◽  
2019 ◽  
Author(s):  
David O Arnar ◽  
Georges H Mairesse ◽  
Giuseppe Boriani ◽  
Hugh Calkins ◽  
Ashley Chin ◽  
...  
Keyword(s):  
Heart Failure ◽  
Latin America ◽  
Clinical Practice ◽  
Sudden Cardiac Death ◽  
Southern Africa ◽  
Cardiac Death ◽  
Heart Rhythm ◽  
Asia Pacific ◽  
Prognostic Evaluation ◽  
Consensus Document

AbstractAsymptomatic arrhythmias are frequently encountered in clinical practice. Although studies specifically dedicated to these asymptomatic arrhythmias are lacking, many arrhythmias still require proper diagnostic and prognostic evaluation and treatment to avoid severe consequences, such as stroke or systemic emboli, heart failure, or sudden cardiac death. The present document reviews the evidence, where available, and attempts to reach a consensus, where evidence is insufficient or conflicting.

scholarly journals Diagnosis and management of hypertrophic cardiomyopathy

2015 ◽  
Vol 2 (1) ◽  
pp. R45-R53 ◽  
Author(s):  
Antonis Pantazis ◽  
Annina S Vischer ◽  
Maria Carrillo Perez-Tome ◽  
Silvia Castelletti
Keyword(s):  
Heart Failure ◽  
Chest Pain ◽  
Hypertrophic Cardiomyopathy ◽  
Sudden Cardiac Death ◽  
Disease Progression ◽  
Cardiac Death ◽  
Significant Proportion ◽  
Cardiovascular Complications ◽  
Diagnosis And Management ◽  
Different Types

The clinical spectrum of hypertrophic cardiomyopathy (HCM) is complex and includes a variety of phenotypes, which leads to different types of manifestations. Although most of the patients are asymptomatic, a significant proportion of them will develop symptoms or risk of arrhythmias and sudden cardiac death (SCD). Therefore, the objectives of HCM diagnosis and management are to relieve the patients' symptoms (chest pain, heart failure, syncope, palpitations, etc.), prevent disease progression and major cardiovascular complications and SCD. The heterogeneity of HCM patterns, their symptoms and assessment is a challenge for the cardiologist.

scholarly journals Anomalous origin of coronary arteries from pulmonary artery in adults: a case series

2020 ◽  
Vol 4 (2) ◽  
pp. 1-5
Author(s):  
Carlos Eduardo Vergara-Uzcategui ◽  
Barbara das Neves ◽  
Pablo Salinas ◽  
Antonio Fernández-Ortiz ◽  
Iván J Núñez-Gil
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Ventricular Tachycardia ◽  
Chest Pain ◽  
Sudden Cardiac Death ◽  
Coronary Arteries ◽  
Cardiac Death ◽  
Case Series ◽  
Sustained Ventricular Tachycardia ◽  
Anomalous Origin

Abstract Background Anomalous origin of a coronary artery from the pulmonary trunk is a small group of rare congenital anomalies present in up to 1% of the population. These patients, in absence of an adequate collateral supply, may present with congestive heart failure secondary to ischaemia, arrhythmia, or sudden cardiac death in up to 90% of cases within the first months of life. Case summary We present four cases diagnosed in adulthood over 10 years in two high-volume centres. The first patient presented with dyspnoea and orthopnoea. The second with chest pain and episodes of non-sustained ventricular tachycardia. The third patient presented during her third pregnancy with chest pain, palpitations, and arrhythmia (non-sustained ventricular tachycardia). The fourth patient presented with sudden cardiac death. Discussion In all cases with anomalous origin of coronary arteries, it is recommendable to consider surgical correction to avoid the progression of ischaemia, congestive heart failure, arrhythmia, and sudden death.

scholarly journals Prognostic implications of troponin T variations in inherited cardiomyopathies using systems biology

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Rameen Shakur ◽  
Juan Pablo Ochoa ◽  
Alan J. Robinson ◽  
Abhishek Niroula ◽  
Aneesh Chandran ◽  
...  
Keyword(s):  
Heart Failure ◽  
Systems Biology ◽  
Sudden Cardiac Death ◽  
Risk Stratification ◽  
Clinical Data ◽  
Cardiac Death ◽  
Troponin T ◽  
Management Options ◽  
Familial Cardiomyopathy ◽  
The Impact

AbstractThe cardiac troponin T variations have often been used as an example of the application of clinical genotyping for prognostication and risk stratification measures for the management of patients with a family history of sudden cardiac death or familial cardiomyopathy. Given the disparity in patient outcomes and therapy options, we investigated the impact of variations on the intermolecular interactions across the thin filament complex as an example of an unbiased systems biology method to better define clinical prognosis to aid future management options. We present a novel unbiased dynamic model to define and analyse the functional, structural and physico-chemical consequences of genetic variations among the troponins. This was subsequently integrated with clinical data from accessible global multi-centre systematic reviews of familial cardiomyopathy cases from 106 articles of the literature: 136 disease-causing variations pertaining to 981 global clinical cases. Troponin T variations showed distinct pathogenic hotspots for dilated and hypertrophic cardiomyopathies; considering the causes of cardiovascular death separately, there was a worse survival in terms of sudden cardiac death for patients with a variation at regions 90–129 and 130–179 when compared to amino acids 1–89 and 200–288. Our data support variations among 90–130 as being a hotspot for sudden cardiac death and the region 131–179 for heart failure death/transplantation outcomes wherein the most common phenotype was dilated cardiomyopathy. Survival analysis into regions of high risk (regions 90–129 and 130–180) and low risk (regions 1–89 and 200–288) was significant for sudden cardiac death (p = 0.011) and for heart failure death/transplant (p = 0.028). Our integrative genomic, structural, model from genotype to clinical data integration has implications for enhancing clinical genomics methodologies to improve risk stratification.

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