scholarly journals Arrhythmogenic Remodeling in the Failing Heart

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3203
Author(s):  
Zoltán Husti ◽  
András Varró ◽  
István Baczkó
Keyword(s):  
Heart Failure ◽  
Cardiac Death ◽  
Myocardial Hypertrophy ◽  
Clinical Syndrome ◽  
Calcium Handling ◽  
Electrical Remodeling ◽  
Patients With Heart Failure ◽  
And Function ◽  
Transporter Expression ◽  
Arrhythmia Management

Chronic heart failure is a clinical syndrome with multiple etiologies, associated with significant morbidity and mortality. Cardiac arrhythmias, including ventricular tachyarrhythmias and atrial fibrillation, are common in heart failure. A number of cardiac diseases including heart failure alter the expression and regulation of ion channels and transporters leading to arrhythmogenic electrical remodeling. Myocardial hypertrophy, fibrosis and scar formation are key elements of arrhythmogenic structural remodeling in heart failure. In this article, the mechanisms responsible for increased arrhythmia susceptibility as well as the underlying changes in ion channel, transporter expression and function as well as alterations in calcium handling in heart failure are discussed. Understanding the mechanisms of arrhythmogenic remodeling is key to improving arrhythmia management and the prevention of sudden cardiac death in patients with heart failure.

scholarly journals Risk Stratification of Sudden Cardiac Death in Patients with Heart Failure: An update

2018 ◽  
Vol 7 (11) ◽  
pp. 436 ◽  
Author(s):  
Daniele Masarone ◽  
Giuseppe Limongelli ◽  
Ernesto Ammendola ◽  
Marina Verrengia ◽  
Rita Gravino ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sudden Cardiac Death ◽  
Risk Stratification ◽  
Cardiac Death ◽  
Clinical Syndrome ◽  
Pump Failure ◽  
Reduced Ejection Fraction ◽  
Clinical Challenge ◽  
Patients With Heart Failure ◽  
Symptoms And Signs

Heart failure (HF) is a complex clinical syndrome in which structural/functional myocardial abnormalities result in symptoms and signs of hypoperfusion and/or pulmonary or systemic congestion at rest or during exercise. More than 80% of deaths in patients with HF recognize a cardiovascular cause, with most being either sudden cardiac death (SCD) or death caused by progressive pump failure. Risk stratification of SCD in patients with HF and preserved (HFpEF) or reduced ejection fraction (HFrEF) represents a clinical challenge. This review will give an update of current strategies for SCD risk stratification in both HFrEF and HFpEF.

Electrophysiologic changes in heart failure: focus on pacemaker channelsThis article is one of a selection of papers from the NATO Advanced Research Workshop on Translational Knowledge for Heart Health (published in part 1 of a 2-part Special Issue).

2009 ◽  
Vol 87 (2) ◽  
pp. 84-90 ◽  
Author(s):  
Laura Sartiani ◽  
Francesca Stillitano ◽  
Elisabetta Cerbai ◽  
Alessandro Mugelli
Keyword(s):  
Heart Failure ◽  
Cardiac Myocytes ◽  
Ventricular Tachyarrhythmia ◽  
Rapid Onset ◽  
Clinical Syndrome ◽  
Electrical Remodeling ◽  
Hemodynamic Compromise ◽  
Research Workshop ◽  
Channel Expression ◽  
And Function

Heart failure is a common clinical syndrome occurring as a result of cardiac overload, injury, and a complex interplay among genetic, neurohormonal, inflammatory, and biochemical factors. Occurrence of arrhythmias in heart failure is largely a consequence of disease-induced electrical remodeling of cardiac myocytes, a phenomenon consisting of alterations of ion channels and the ion-transport function that predispose patients to develop lethal arrhythmias. In most cases, the mechanism is the rapid onset of a ventricular tachyarrhythmia progressing to ventricular fibrillation and hemodynamic compromise. This paper highlights some of the important changes in ion channel expression and function that underlie electrical remodeling of the failing heart. Particular attention will be focused on the presence, features, and pharmacologic modulation of f channels expressed in ventricular cardiac myocytes.

Abstract 13304: Liver Dispersion Predicts Adverse Outcomes in Patients With Heart Failure

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Yu Hotsuki ◽  
Akiomi Yoshihisa ◽  
Koichiro Watanabe ◽  
Yu Sato ◽  
Yusuke Kimishima ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Death ◽  
Cardiac Event ◽  
Liver Stiffness ◽  
Adverse Outcomes ◽  
Right Atrial ◽  
Gamma Glutamyl Transferase ◽  
Abdominal Ultrasonography ◽  
Patients With Heart Failure ◽  
Glutamyl Transferase

Background: It has been recently reported that liver stiffness assessed by transient elastography reflects right atrial pressure (RAP), and is associated with worse outcome in patients with heart failure (HF). However, the relationship between liver dispersion (LD, a novel indicator of liver viscosity) determined by abdominal ultrasonography and RAP, and prognostic impacts of LD on HF patients have not been fully examined. We aimed to clarify associations of LD with parameters of liver functional test (LFT) and right-heart catheterization (RHC), and cardiac event such as cardiac death and worsening HF in patients with HF. Methods and Results: We performed abdominal ultrasonography, LFT, RHC, and followed up cardiac events including cardiac death and unplanned hospitalization due to HF in patients with HF (n=157). We examined associations of LD with parameters of LFT and RHC. There were significant correlations between LD and circulating levels of gamma-glutamyl transferase (R=0.197, P=0.018), cholinesterase (R=-0.301, P=0.001), and 7S domain of collagen type IV (P4NP 7S, a marker of fibrosis, R=0.334, P<0.001), but not with RAP (R=0.067, P=0.514) or cardiac index (R=-0.038, P=0.667). During the follow up period (median 305 days), 6 cardiac deaths and 18 unplanned hospitalization due to HF occurred. In the Kaplan-Meier analysis ( Figure ), cardiac event rate was significantly higher in the high LD group (LD ≥10.0 (m/s)/kHz, n=79) than in the low LD group (LD < 10.0 (m/s)/kHz, n=78; log-rank, P=0.007). In the multivariable Cox proportional hazard analysis, high LD was found to be an independent predictor of cardiac event (hazard ratio 3.274, 95% confidence interval 1.203-8.912, P=0.020). Conclusions: LD assessed by abdominal ultrasonography reflects liver fibrosis rather than liver congestion, and is associated with adverse prognosis in HF patients.

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 Addressing Social Determinants of Health in the Care of Patients With Heart Failure: A Scientific Statement From the American Heart Association

Circulation ◽  
2020 ◽  
Vol 141 (22) ◽  
Author(s):  
Connie White-Williams ◽  
Laura P. Rossi ◽  
Vera A. Bittner ◽  
Andrea Driscoll ◽  
Raegan W. Durant ◽  
...  
Keyword(s):  
Heart Failure ◽  
Social Determinants Of Health ◽  
Social Determinants ◽  
Healthcare Providers ◽  
Clinical Syndrome ◽  
Assessment Tools ◽  
Determinants Of Health ◽  
Number Of Patients ◽  
Patients With Heart Failure ◽  
Scientific Statement

Heart failure is a clinical syndrome that affects >6.5 million Americans, with an estimated 550 000 new cases diagnosed each year. The complexity of heart failure management is compounded by the number of patients who experience adverse downstream effects of the social determinants of health (SDOH). These patients are less able to access care and more likely to experience poor heart failure outcomes over time. Many patients face additional challenges associated with the cost of complex, chronic illness management and must make difficult decisions about their own health, particularly when the costs of medications and healthcare appointments are at odds with basic food and housing needs. This scientific statement summarizes the SDOH and the current state of knowledge important to understanding their impact on patients with heart failure. Specifically, this document includes a definition of SDOH, provider competencies, and SDOH assessment tools and addresses the following questions: (1) What models or frameworks guide healthcare providers to address SDOH? (2) What are the SDOH affecting the delivery of care and the interventions addressing them that affect the care and outcomes of patients with heart failure? (3) What are the opportunities for healthcare providers to address the SDOH affecting the care of patients with heart failure? We also include a case study ( Data Supplement ) that highlights an interprofessional team effort to address and mitigate the effects of SDOH in an underserved patient with heart failure.

scholarly journals Atrial Electrophysiological Remodeling and Fibrillation in Heart Failure

2016 ◽  
Vol 10s1 ◽  
pp. CMC.S39713 ◽  
Author(s):  
Sandeep V. Pandit ◽  
Antony J. Workman
Keyword(s):  
Heart Failure ◽  
Molecular Mechanisms ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Calcium Handling ◽  
Ion Currents ◽  
Multiple Variables ◽  
The Individual ◽  
And Function

Heart failure (HF) causes complex, chronic changes in atrial structure and function, which can cause substantial electrophysiological remodeling and predispose the individual to atrial fibrillation (AF). Pharmacological treatments for preventing AF in patients with HF are limited. Improved understanding of the atrial electrical and ionic/molecular mechanisms that promote AF in these patients could lead to the identification of novel therapeutic targets. Animal models of HF have identified numerous changes in atrial ion currents, intracellular calcium handling, action potential waveform and conduction, as well as expression and signaling of associated proteins. These studies have shown that the pattern of electrophysiological remodeling likely depends on the duration of HF, the underlying cardiac pathology, and the species studied. In atrial myocytes and tissues obtained from patients with HF or left ventricular systolic dysfunction, the data on changes in ion currents and action potentials are largely equivocal, probably owing mainly to difficulties in controlling for the confounding influences of multiple variables, such as patient's age, sex, disease history, and drug treatments, as well as the technical challenges in obtaining such data. In this review, we provide a summary and comparison of the main animal and human electrophysiological studies to date, with the aim of highlighting the consistencies in some of the remodeling patterns, as well as identifying areas of contention and gaps in the knowledge, which warrant further investigation.

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