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.

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.

Assessing Acute Decompensated Heart Failure – Strategies and Tools

2012 ◽  
Vol 8 (2) ◽  
pp. 128
Author(s):  
Ali Vazir ◽  
Martin R Cowie ◽  
◽  
Keyword(s):  
Heart Failure ◽  
Acute Decompensated Heart Failure ◽  
Pulse Contour Analysis ◽  
Decompensated Heart Failure ◽  
Rapid Onset ◽  
Clinical Syndrome ◽  
Response To Therapy ◽  
Contour Analysis ◽  
Physiological Variables ◽  
Co Morbidity

Acute heart failure – the rapid onset of, or change in, signs and/or symptoms of heart failure requiring urgent treatment – is a serious clinical syndrome, associated with high mortality and healthcare costs. History, physical examination and early 2D and Doppler echocardiography are crucial to the proper assessment of patients, and will help determine the appropriate monitoring and management strategy. Most patients are elderly and have considerable co-morbidity. Clinical assessment is key to monitoring progress, but a number of clinical techniques – including simple Doppler and echocardiographic tools, pulse contour analysis and impedance cardiography – can help assess the response to therapy. A pulmonary artery catheter is not a routine monitoring tool, but can be very useful in patients with complex physiology, in those who fail to respond to therapy as would be anticipated, or in those being considered for mechanical intervention. As yet, the serial measurement of plasma natriuretic peptides is of limited value, but it does have a role in diagnosis and prognostication. Increasingly, the remote monitoring of physiological variables by completely implanted devices is possible, but the place of such technology in clinical practice is yet to be clearly established.

scholarly journals The right-sided heart failure

2019 ◽  
Vol 29 (2) ◽  
pp. 135-147
Author(s):  
A. G. Chuchalin
Keyword(s):  
Heart Failure ◽  
Clinical Manifestations ◽  
Clinical Syndrome ◽  
Lv Function ◽  
Right Heart ◽  
Heart Abnormalities ◽  
Lv Volume ◽  
The Right ◽  
And Function ◽  
Heart Physiology

The right-sided heart failure (RSHF) is a complex clinical syndrome including different pathogenic mechanisms and processes resulted from the right ventricle (RV) dysfunction and manifested with signs of heart failure (HF). Recently, there is a growing scientific interest in the right-sided acute and chronic heart abnormalities; this is due to growing knowledge in this field and development of novel diagnostic, therapeutic and pharmacological approaches to treatment of pulmonary hypertension that is a common cause of RSHF. Cardiac embryogenesis, anatomic particularities, difference and interdependence of RV and the left ventricle (LV) are described in the article in order to improve the knowledge on structure and function of both the right heart and the left heart. Discussion on pathophysiology, causes and clinical manifestations of acute RSHF (aRSHF) and chronic RSHF (cRSHF) should consider the right heart physiology. Pharmacological treatment should be targeted to ventricle pre-load, myocardial contractility and RV post-load, correction of pulmonary circulation and LV volume resulting in post-load reduction and improvement in the LV function. Patients with biventricular dysfunction should be treated according to current clinical guidelines on therapy of chronic HF. Vasoactive agents and diuretics have an important role for the treatment of RSHF as this is the basic therapy of pulmonary congestion both in aRSHF and cRSHF. Step-by-step therapeutic algorithm is given in the article.

scholarly journals Role of the cardiac extracellular matrix in the onset and progression of heart failure

2021 ◽  
Vol 26 (2S) ◽  
pp. 4362
Author(s):  
N. N. Ilov ◽  
K. Sh. Arnaudova ◽  
A. A. Nechepurenko ◽  
A. L. Yasenyavskaya ◽  
O. A. Bashkina ◽  
...  
Keyword(s):  
Heart Failure ◽  
Extracellular Matrix ◽  
Ventricular Arrhythmias ◽  
Additional Data ◽  
Clinical Syndrome ◽  
Electrical Remodeling ◽  
Cardiovascular Patients ◽  
The Individual ◽  
Diastolic Functions

Any cardiovascular disease leads to heart failure (HF) — a complex clinical syndrome, the course of which is probably specified by the influence of cardiovascular factors on cardiac extracellular matrix (ECM).The presented literature data indicate that the cardiac ECM is an important pathophysiological link in the onset and progression of HF. The morphological and electrical remodeling negatively affects the systolic and diastolic functions of the heart. Impaired myocardial blood delivery, cellular maladaptation, atrial and ventricular arrhythmias are additional mechanisms of the influence of myocardial fibrosis on HF course.Understanding this role of ECM and the development of algorithms for verifying the individual status of ECM in cardiovascular patients can provide additional data on the course of HF, help to assess the risk of adverse cardiovascular events and effectively control the ongoing pharmacological and non-drug therapy.

Electrical remodeling in a transgenic mouse model of α1B-adrenergic receptor overexpression

2009 ◽  
Vol 296 (3) ◽  
pp. H704-H718 ◽  
Author(s):  
Katy Rivard ◽  
Véronique Trépanier-Boulay ◽  
Hansjorg Rindt ◽  
Céline Fiset
Keyword(s):  
Heart Failure ◽  
Ventricular Arrhythmias ◽  
Transgenic Animals ◽  
Delayed Rectifier ◽  
Electrical Remodeling ◽  
Adrenergic Stimulation ◽  
Channel Expression ◽  
End Stage ◽  
Electrocardiogram Ecg

Cardiac-specific overexpression of wild-type α1B-adrenergic receptors (α1B-AR) in mice predisposes to dilated cardiomyopathy and sudden death. Although α-adrenergic stimulation is thought to contribute to induction of arrhythmias in heart failure, the electrophysiological consequences of chronic α1-adrenergic activation have not been clearly defined. Thus we characterized ventricular repolarization and monitored incidence of spontaneous arrhythmias in end-stage heart failure α1B-AR mice (9–12 mo) and younger α1B-AR mice (2–3 mo) that do not present signs of heart failure. Compared with aged-matched controls, the corrected QT interval was 34% longer in the 9- to 12-mo α1B-AR mice, and the action potential durations were also significantly prolonged in these mice. These changes were associated with a decrease in the density of the outward K+ currents, Ca2+-independent transient, ultrarapid delayed rectifier, and steady state (at +30 mV, reduction of 68, 64, and 41%, respectively), and underlying K+ channel expression. Electrocardiogram (ECG) recordings revealed that older α1B-AR mice exhibited spontaneous ventricular arrhythmias. The alterations in repolarization can contribute to these rhythm abnormalities and are likely caused by chronic α1B-AR activity. Additional data obtained in 2- to 3-mo α1B-AR mice clearly showed that electrical remodeling was already observed in younger transgenic animals. However, it appeared to be slightly less pronounced than in older mice. These results suggest that there are two waves of remodeling: one due to chronic α1B-AR activity, and a second due to heart failure. Taken together, these data provide strong evidence for a pathological role of chronic α1B-AR activity in the development of repolarization defects and ventricular arrhythmias.

Pharmacology of Ivabradine and the Effect on Chronic Heart Failure

2019 ◽  
Vol 19 (21) ◽  
pp. 1878-1901 ◽  
Author(s):  
Yue Zhou ◽  
Jian Wang ◽  
Zhuo Meng ◽  
Shuang Zhou ◽  
Jiayu Peng ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Chronic Heart Failure ◽  
Underlying Mechanism ◽  
Clinical Syndrome ◽  
Hcn Channels ◽  
Therapeutic Effects ◽  
Diastolic Depolarization ◽  
High Incidence ◽  
Spontaneous Phase

Chronic Heart Failure (CHF) is a complex clinical syndrome with a high incidence worldwide. Although various types of pharmacological and device therapies are available for CHF, the prognosis is not ideal, for which, the control of increased Heart Rate (HR) is critical. Recently, a bradycardic agent, ivabradine, is found to reduce HR by inhibiting the funny current (If). The underlying mechanism states that ivabradine can enter the Hyperpolarization-activated Cyclic Nucleotide-gated (HCN) channels and bind to the intracellular side, subsequently inhibiting the If. This phenomenon can prolong the slow spontaneous phase in the diastolic depolarization, and thus, reduce HR. The clinical trials demonstrated the significant effects of the drug on reducing HR and improving the symptoms of CHF with fewer adverse effects. This review primarily introduces the chemical features and pharmacological characteristics of ivabradine and the mechanism of treating CHF. Also, some expected therapeutic effects on different diseases were also concluded. However, ivabradine, as a typical If channel inhibitor, necessitates additional research to verify its pharmacological functions.

scholarly journals Long-term outcomes in young patients with atrioventricular block of unknown aetiology

2021 ◽  
Author(s):  
Johnni Resdal Dideriksen ◽  
Morten K Christiansen ◽  
Jens B Johansen ◽  
Jens C Nielsen ◽  
Henning Bundgaard ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrioventricular Block ◽  
Ventricular Tachyarrhythmia ◽  
Pacemaker Implantation ◽  
Young Patients ◽  
Composite Endpoint ◽  
Unknown Aetiology ◽  
Successful Resuscitation

Abstract Aims Atrioventricular block (AVB) of unknown aetiology is rare in the young, and outcome in these patients is unknown. We aimed to assess long-term morbidity and mortality in young patients with AVB of unknown aetiology. Methods and results We identified all Danish patients younger than 50 years receiving a first pacemaker due to AVB between January 1996 and December 2015. By reviewing medical records, we included patients with AVB of unknown aetiology. A matched control cohort was established. Follow-up was performed using national registries. The primary outcome was a composite endpoint consisting of death, heart failure hospitalization, ventricular tachyarrhythmia, and cardiac arrest with successful resuscitation. We included 517 patients, and 5170 controls. Median age at first pacemaker implantation was 41.3 years [interquartile range (IQR) 32.7–46.2 years]. After a median follow-up of 9.8 years (IQR 5.7–14.5 years), the primary endpoint had occurred in 14.9% of patients and 3.2% of controls [hazard ratio (HR) 3.8; 95% confidence interval (CI) 2.9–5.1; P < 0.001]. Patients with persistent AVB at time of diagnosis had a higher risk of the primary endpoint (HR 10.6; 95% CI 5.7–20.0; P < 0.001), and risk was highest early in the follow-up period (HR 6.8; 95% CI 4.6–10.0; P < 0.001, during 0–5 years of follow-up). Conclusion Atrioventricular block of unknown aetiology presenting before the age of 50 years and treated with pacemaker implantation was associated with a three- to four-fold higher rate of the composite endpoint of death or hospitalization for heart failure, ventricular tachyarrhythmia, or cardiac arrest with successful resuscitation. Patients with persistent AVB were at higher risk. These findings warrant improved follow-up strategies for young patients with AVB of unknown aetiology.

scholarly journals The Role of Serum Chloride in Acute and Chronic Heart Failure: A Narrative Review

2021 ◽  
Vol 11 (2) ◽  
pp. 87-98
Author(s):  
Frederick Berro Rivera ◽  
Pia Alfonso ◽  
Jem Marie Golbin ◽  
Kevin Lo ◽  
Edgar Lerma ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chloride Channel ◽  
Chloride Channels ◽  
Prognostic Value ◽  
Diuretic Therapy ◽  
Juxtaglomerular Apparatus ◽  
Sodium Chloride Cotransporter ◽  
Serum Chloride ◽  
And Function

Clinical guidelines include diuretics for the treatment of heart failure (HF), not to decrease mortality but to decrease symptoms and hospitalizations. More attention has been paid to the worse outcomes, including mortality, associated with continual diuretic therapy due to hypochloremia. Studies have revealed a pivotal role for serum chloride in the pathophysiology of HF and is now a target of treatment to decrease mortality. The prognostic value of serum chloride in HF has been the subject of much attention. Mechanistically, the macula densa, a region in the renal juxtaglomerular apparatus, relies on chloride levels to sense salt and volume status. The recent discovery of with-no-lysine (K) (WNK) protein kinase as an intracellular chloride sensor sheds light on the possible reason of diuretic resistance in HF. The action of chloride on WNKs results in the upregulation of the sodium-potassium-chloride cotransporter and sodium-chloride cotransporter receptors, which could lead to increased electrolyte and fluid reabsorption. Genetic studies have revealed that a variant of a voltage-sensitive chloride channel (CLCNKA) gene leads to almost a 50% decrease in current amplitude and function of the renal chloride channel. This variant increases the risk of HF. Several trials exploring the prognostic value of chloride in both acute and chronic HF have shown mostly positive results, some even suggesting a stronger role than sodium. However, so far, interventional trials exploring serum chloride as a therapeutic target have been largely inconclusive. This study is a review of the pathophysiologic effects of hypochloremia in HF, the genetics of chloride channels, and clinical trials that are underway to investigate novel approaches to HF management.

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