Heart failure as a substrate and trigger for ventricular tachycardia

Alvarez, Chikezie; Cronin, Edmond M.; Baker, William L.; Kluger, Jeffrey

doi:10.1007/s10840-019-00623-x

Cited by 45 publications

(40 citation statements)

References 186 publications

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“…The tool used for the detection and diagnosis of cardiac arrhythmias is the ECG, thus, the aim of antiarrhythmic therapy could be considered for acute termination or long-term treatment to prevent recurrence of various types of arrhythmias. However, antiarrhythmic drugs have multiple effects on the generation of AP and the waves of ECG, and their mechanisms are very complex (Alvarez et al, 2019;Paar et al, 2019). In addition, an antiarrhythmic agent could modulate other targets and tissues in the different parts of the myocardium in comparison with its primary site of action.…”

Section: The Heart and Arrhythmiasmentioning

confidence: 99%

ArrhythmoGenoPharmacoTherapy

Tósaki

2020

Front. Pharmacol.

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This review is focusing on the understanding of various factors and components governing and controlling the occurrence of ventricular arrhythmias including (i) the role of various ion channel-related changes in the action potential (AP), (ii) electrocardiograms (ECGs), (iii) some important arrhythmogenic mediators of reperfusion, and pharmacological approaches to their attenuation. The transmembrane potential in myocardial cells is depending on the cellular concentrations of several ions including sodium, calcium, and potassium on both sides of the cell membrane and active or inactive stages of ion channels. The movements of Na + , K + , and Ca 2+ via cell membranes produce various currents that provoke AP, determining the cardiac cycle and heart function. A specific channel has its own type of gate, and it is opening and closing under specific transmembrane voltage, ionic, or metabolic conditions. APs of sinoatrial (SA) node, atrioventricular (AV) node, and Purkinje cells determine the pacemaker activity (depolarization phase 4) of the heart, leading to the surface manifestation, registration, and evaluation of ECG waves in both animal models and humans. AP and ECG changes are key factors in arrhythmogenesis, and the analysis of these changes serve for the clarification of the mechanisms of antiarrhythmic drugs. The classification of antiarrhythmic drugs may be based on their electrophysiological properties emphasizing the connection between basic electrophysiological activities and antiarrhythmic properties. The review also summarizes some important mechanisms of ventricular arrhythmias in the ischemic/ reperfused myocardium and permits an assessment of antiarrhythmic potential of drugs used for pharmacotherapy under experimental and clinical conditions.

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Section: The Heart and Arrhythmiasmentioning

confidence: 99%

ArrhythmoGenoPharmacoTherapy

Tósaki

2020

Front. Pharmacol.

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“…Neprilysin plays a role as its mechanism, degrading the gross excess of circulating NPs in HF patients[ 7 ]. Compared to enalapril, SAC/VAL leads to reductions in symptoms of HF, cardiovascular death or HF hospitalization, sudden cardiac death, and disease progression, and improved QOL, in patients undergoing evidence-based contemporary medical therapy for HFrEF, and the NP assays for B-type NP (BNP) and N-terminal-proBNP (NT-proBNP) assays have been shown to have similar diagnostic accuracy for the differentiation of HF from other etiologies of shortness of breath[ 11 , 17 , 32 , 34 - 36 ]. In real-world settings, SAC/VAL was found to be associated with improved survival and reduced HF-related hospitalization compared to enalapril in Asian HF patients, with consistent effectiveness even in older populations[ 37 ].…”

Section: Effects Of Arni On Chfmentioning

confidence: 99%

Angiotensin receptor blocker neprilysin inhibitors

Usuda

Higashikawa

Hotchi

et al. 2021

WJC

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Heart failure (HF) is a clinical syndrome that results from a structural or functional cardiac disorder that reduces the ability of the ventricle of the heart to fill with, or eject, blood. It is a multifaceted clinical condition that affects up to 2% of the population in the developed world, and is linked to significant morbidity and mortality; it is therefore considered a major concern for public health. Regarding the mechanism of HF, three neurohumoral factors - the renin-angiotensin-aldosterone system, the sympathetic nervous system, and natriuretic peptides — are related to the pathology of chronic HF (CHF), and the targets of treatment. Angiotensin receptor blocker and neprilysin inhibitor (angiotensin-receptor neprilysin inhibitor), namely sacubitril/valsartan (SAC/VAL), has been introduced as a treatment for CHF. SAC/VAL is an efficacious, safe, and cost-effective therapy that improves quality of life and longevity in patients with HF with reduced ejection fraction (HFrEF), and reduces hospital admissions. An in-hospital initiation strategy offers a potential new avenue to improve the clinical uptake of SAC/VAL. In the last five years, SAC/VAL has been established as a cornerstone component of comprehensive disease-modifying medical therapy in the management of chronic HFrEF. On the other hand, further work, with carefully designed and controlled preclinical studies, is necessary for understanding the molecular mechanisms, effects, and confirmation of issues such as long-term safety in both human and animal models.

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“…Heart failure (HF) remains an egregious disease with poor prognosis that is estimated to afflict ~64 million people worldwide 1 . Patients with HF are predisposed to developing cardiac arrhythmias including complex ventricular arrhythmias, ventricular tachycardia and atrial fibrillation 2,3 .…”

Section: Introductionmentioning

confidence: 99%

Phytosterol Accumulation Results in Ventricular Arrhythmia, Impaired Cardiac Function and Death

Liu

Yamawaki

et al. 2021

Preprint

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Heart failure (HF) and cardiac arrhythmias share overlapping pathological mechanisms that act cooperatively to accelerate disease pathogenesis. Cardiac fibrosis is associated with both pathological conditions. Our previous work identified a link between phytosterol accumulation and cardiac injury in a mouse model of phytosterolemia, a rare disorder characterized by elevated circulating phytosterols and increased cardiovascular disease risk. Here, we uncover a previously unknown pathological link between phytosterols and cardiac arrhythmias in the same animal model. Phytosterolemia resulted in inflammatory pathway induction, premature ventricular contractions (PVC) and ventricular tachycardia (VT). Both pharmacological and genetic inhibition of phytosterol absorption prevented the induction of both pathways. Inhibition of phytosterol absorption reduced inflammation and cardiac fibrosis, improved cardiac function, reduced the incidence of arrhythmias and increased survival in a mouse model of phytosterolemia. Collectively, this work identified a pathological mechanism whereby elevated phytosterols result in inflammation and cardiac fibrosis leading to impaired cardiac function, arrhythmias and sudden death. These phytosterolemia-associated comorbidities provide novel insight into the underlying pathophysiological mechanism that predispose these patients to increased risk of sudden cardiac death.

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Heart failure as a substrate and trigger for ventricular tachycardia

Cited by 45 publications

References 186 publications

ArrhythmoGenoPharmacoTherapy

ArrhythmoGenoPharmacoTherapy

Angiotensin receptor blocker neprilysin inhibitors

Phytosterol Accumulation Results in Ventricular Arrhythmia, Impaired Cardiac Function and Death

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