scholarly journals Electrically-Induced Ventricular Fibrillation Alters Cardiovascular Function and Expression of Apoptotic and Autophagic Proteins in Rat Hearts

2019 ◽  
Vol 20 (7) ◽  
pp. 1628 ◽  
Author(s):  
Andras Czegledi ◽  
Agnes Tosaki ◽  
Alexandra Gyongyosi ◽  
Rita Zilinyi ◽  
Arpad Tosaki ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Ventricular Fibrillation ◽  
Cardiac Death ◽  
Caspase 3 ◽  
Recovery Period ◽  
Heart Rhythm ◽  
Heart Tissue ◽  
Altered Expression ◽  
Cardiac Functions ◽  
Rat Hearts

Background: The pathological heart contractions, called arrhythmias, especially ventricular fibrillation (VF), are a prominent feature of many cardiovascular diseases leading to sudden cardiac death. The present investigation evaluates the effect of electrically stimulated VF on cardiac functions related to autophagy and apoptotic mechanisms in isolated working rat hearts. Methods: Each group of hearts was subjected to 0 (Control), 1, 3, or 10 min of spacing-induced VF, followed by 120 min of recovery period and evaluated for cardiac functions, including aortic flow (AF), coronary flow (CF), cardiac output (CO), stroke volume (SV), and heart rate (HR). Hearts were also evaluated for VF effects on infarcted zone magnitude and Western blot analysis was conducted on heart tissue for expression of the apoptotic biomarker cleaved-caspase-3 and the autophagy proteins: p62, P-mTOR/mTOR, LC3BII/LC3BI ratio, and Atg5-12 complexes. Results: Data revealed that VF induced degradation in AF, CF, CO, and SV, which prominently included-variable post-VF capacity for recovery of normal heart rhythm; increased extent of infarcted heart tissue; altered expression of cleaved-caspase-3 suggesting potential for VF-mediated amplification of apoptosis. VF influence on expression of p62, LC3BII/LC3BI, and Atg5-12 proteins was complex, possibly due to differential effects of VF-induced expression on proteins comprising the autophagic program. Conclusions: VF was observed to cause time-dependent changes in autophagy processes, which with additional analysis under ongoing investigations, likely to yield novel therapeutic targets for the prevention of VF and sudden cardiac death.

Monogenec Arrhythmic Syndromes: From Molecular and Genetic Aspects to Bedside

Acta Naturae ◽  
2016 ◽  
Vol 8 (2) ◽  
pp. 62-74 ◽  
Author(s):  
E. Z. Golukhova ◽  
O. I. Gromova ◽  
R. A. Shomahov ◽  
N. I. Bulaeva ◽  
L. A. Bockeria
Keyword(s):  
Ventricular Tachycardia ◽  
Sudden Cardiac Death ◽  
Ventricular Fibrillation ◽  
Long Qt Syndrome ◽  
Cardiac Death ◽  
Heart Rhythm ◽  
The United States ◽  
Polymorphic Ventricular Tachycardia ◽  
Long Qt ◽  
Qt Syndrome

The abrupt cessation of effective cardiac function that is generally due to heart rhythm disorders can cause sudden and unexpected death at any age and is referred to as a syndrome called sudden cardiac death (SCD). Annually, about 400,000 cases of SCD occur in the United States alone. Less than 5% of the resuscitation techniques are effective. The prevalence of SCD in a population rises with age according to the prevalence of coronary artery disease, which is the most common cause of sudden cardiac arrest. However, there is a peak in SCD incidence for the age below 5 years, which is equal to 17 cases per 100,000 of the population. This peak is due to congenital monogenic arrhythmic canalopathies. Despite their relative rarity, these cases are obviously the most tragic. The immediate causes, or mechanisms, of SCD are comprehensive. Generally, it is arrhythmic death due to ventricular tachyarrythmias - sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Bradyarrhythmias and pulseless electrical activity account for no more than 40% of all registered cardiac arrests, and they are more often the outcome of the abovementioned arrhythmias. Our current understanding of the mechanisms responsible for SCD has emerged from decades of basic science investigation into the normal electrophysiology of the heart, the molecular physiology of cardiac ion channels, the fundamental cellular and tissue events associated with cardiac arrhythmias, and the molecular genetics of monogenic disorders of the heart rhythm (for example, the long QT syndrome). This review presents an overview of the molecular and genetic basis of SCD in the long QT syndrome, Brugada syndrome, short QT syndrome, catecholaminergic polymorphic ventricular tachycardia and idiopathic ventricular fibrillation, and arrhythmogenic right ventricular dysplasia, and sudden cardiac death prevention strategies by modern techniques (including implantable cardioverter-defibrillator).

scholarly journals Screening and risk evaluation for sudden cardiac death in ischaemic and non-ischaemic cardiomyopathy: results of the European Heart Rhythm Association survey

EP Europace ◽  
2013 ◽  
Vol 15 (7) ◽  
pp. 1059-1062 ◽  
Author(s):  
A. Proclemer ◽  
T. Lewalter ◽  
M. G. Bongiorni ◽  
J. H. Nielsen ◽  
L. Pison ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Risk Evaluation ◽  
Heart Rhythm ◽  
Ischaemic Cardiomyopathy

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.

scholarly journals Early repolarisation among athletes

2020 ◽  
Vol 6 (1) ◽  
pp. e000694
Author(s):  
Femke M A P Claessen ◽  
Heidi A P Peeters ◽  
Bastiaan J Sorgdrager ◽  
Peter L J van Veldhoven
Keyword(s):  
Logistic Regression ◽  
Regression Analysis ◽  
Sudden Cardiac Death ◽  
Ventricular Fibrillation ◽  
Outpatient Clinic ◽  
Cardiac Death ◽  
Multivariable Analysis ◽  
Control Group ◽  
Multivariable Logistic Regression Analysis ◽  
Athlete Group

ObjectivesTraditionally, early repolarisation (ER) is considered a benign ECG variant, predominantly found in youths and athletes. However, a limited number of studies have reported an association between ER and the incidental occurrence of ventricular fibrillation or sudden cardiac death. Yet definite, direct comparisons of the incidence of ER in unselected, contemporary populations in athletes as compared with non-athletes and across different sports are lacking. This study therefore aimed to investigate whether ER is more common among athletes as compared with non-athletes, and if ER patterns differ between sport disciplines based on static and dynamic intensity.MethodsTo assess ER we retrospectively analysed ECGs of 2241 adult subjects (2090 athletes, 151 non-athletes), who had a sports medical screening between 2010 and 2014 in an outpatient clinic. The outcome was tested for confounders in a multivariable logistic regression analysis.ResultsER was found in 502 athletes (24%). We found a 50% higher prevalence of ER in the athlete group compared with the control group (OR 1.5 (SE 0.34), adjusted 95% CI 1.0 to 2.4) in multivariable analysis. A 30% higher prevalence of ER in the inferior leads only (OR 1.3 (SE 0.38), adjusted 95% CI 0.74 to 2.3), a 120% higher prevalence of ER in the lateral leads only (OR 2.2 (SE 1.0), adjusted 95% CI 0.87 to 5.4), and a 20% higher prevalence of ER in the inferior and lateral leads (OR 1.2 (SE 0.49), adjusted 95% CI 0.55 to 2.7) was found in athletes.ConclusionAthletes had a 50% higher prevalence of ER and a 30% higher prevalence of ER in the inferior leads specifically. There was no association between training duration or sports discipline and ER.

Impact of Acute Coronary Syndrome Complicated by Ventricular Fibrillation on Long-term Incidence of Sudden Cardiac Death

2015 ◽  
Vol 68 (10) ◽  
pp. 878-884
Author(s):  
Belén Álvarez-Álvarez ◽  
Noelia Bouzas-Cruz ◽  
Emad Abu-Assi ◽  
Sergio Raposeiras-Roubin ◽  
Andrea López-López ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Sudden Cardiac Death ◽  
Ventricular Fibrillation ◽  
Cardiac Death ◽  
Coronary Syndrome

Sudden cardiac death secondary to demonstrated reperfusion ventricular fibrillation in a woman with Takotsubo cardiomyopathy

2011 ◽  
Vol 20 (4) ◽  
pp. 254-257 ◽  
Author(s):  
Martino Pepe ◽  
Domenico Zanna ◽  
Donato Quagliara ◽  
Carlo Caiati ◽  
Andrea Marzullo ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Ventricular Fibrillation ◽  
Takotsubo Cardiomyopathy ◽  
Cardiac Death

scholarly journals Non-invasive detection of exercise-induced cardiac conduction abnormalities in sudden cardiac death survivors in the inherited cardiac conditions

EP Europace ◽  
2020 ◽  
Author(s):  
Kevin Ming Wei Leong ◽  
Fu Siong Ng ◽  
Matthew J Shun-Shin ◽  
Michael Koa-Wing ◽  
Norman Qureshi ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Recovery Period ◽  
Lower Score ◽  
Cardiac Conduction ◽  
Protective Mechanism ◽  
Significant Difference ◽  
Exercise Treadmill ◽  
Inherited Cardiac Conditions ◽  
Exercise Induced

Abstract Aims  Rate adaptation of the action potential ensures spatial heterogeneities in conduction across the myocardium are minimized at different heart rates providing a protective mechanism against ventricular fibrillation (VF) and sudden cardiac death (SCD), which can be quantified by the ventricular conduction stability (V-CoS) test previously described. We tested the hypothesis that patients with a history of aborted SCD due to an underlying channelopathy or cardiomyopathy have a reduced capacity to maintain uniform activation following exercise. Methods and results  Sixty individuals, with (n = 28) and without (n = 32) previous aborted-SCD event underwent electro-cardiographic imaging recordings following exercise treadmill test. These included 25 Brugada syndrome, 13 hypertrophic cardiomyopathy, 12 idiopathic VF, and 10 healthy controls. Data were inputted into the V-CoS programme to calculate a V-CoS score that indicate the percentage of ventricle that showed no significant change in ventricular activation, with a lower score indicating the development of greater conduction heterogeneity. The SCD group, compared to those without, had a lower median (interquartile range) V-CoS score at peak exertion [92.8% (89.8–96.3%) vs. 97.3% (94.9–99.1%); P < 0.01] and 2 min into recovery [95.2% (91.1–97.2%) vs. 98.9% (96.9–99.5%); P < 0.01]. No significant difference was observable later into recovery at 5 or 10 min. Using the lowest median V-CoS scores obtained during the entire recovery period post-exertion, SCD survivors had a significantly lower score than those without for each of the different underlying aetiologies. Conclusion  Data from this pilot study demonstrate the potential use of this technique in risk stratification for the inherited cardiac conditions.

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