Abstract

Patients with heart failure often develop cardiac arrhythmias. The mechanisms and interrelations linking heart failure and arrhythmias are not fully understood. Historically, research into arrhythmias has been performed on affected individuals or in vivo (animal) models. The latter however is constrained by interspecies variation, demands to reduce animal experiments and cost. Recent developments in in vitro induced pluripotent stem cell technology and in silico modelling have expanded the number of models available for the evaluation of heart failure and arrhythmia. An agnostic approach, combining the modalities discussed here, has the potential to improve our understanding for appraising the pathology and interactions between heart failure and arrhythmia and can provide robust and validated outcomes in a variety of research settings. This review discusses the state of the art models, methodologies and techniques used in the evaluation of heart failure and arrhythmia and will highlight the benefits of using them in combination. Special consideration is paid to assessing the pivotal role calcium handling has in the development of heart failure and arrhythmia.

Highlights

  • Heart failure and cardiac arrhythmias are intrinsically linked in a complex interplay of cause and effect

  • Many of the methods and systems used to Approaches to Evaluate Cardiac Arrhythmias evaluate the electrophysiological changes that occur in cardiac arrhythmias are common to those used in heart failure research

  • Another study has employed machine learning techniques to classify different phenotypes of hypertrophic cardiomyopathy, the mechanisms behind their heterogeneities and differences in arrhythmic risks (Lyon et al, 2019). These studies highlight the exciting development in applying ML techniques to experimental data and could facilitate significant change in the ways we currently evaluate genetic variants and the increased risk they confer on arrhythmogenesis

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Summary

Introduction

Heart failure and cardiac arrhythmias are intrinsically linked in a complex interplay of cause and effect. Heart failure and arrhythmias have shared physiological and genetic causes. Advancements in medical therapies have led to the survival of patients with heart failure and arrhythmias for longer, increasing the prevalence of both conditions (Schmitt et al, 2009). In patients with inherited cardiac conditions, arrhythmias are common and represent a significant financial and clinical burden (Verheugt et al, 2010). An increased prevalence of atrial fibrillation (AF; 3.29% in 2016) in the United Kingdom over the past decade has compounded the issue, as it predisposes many to the development of heart failure and ischaemic stroke (Pozzoli et al, 1998; Eckardt et al, 2016; Adderley et al, 2019)

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