Abstract
Diabetes is a common endocrine disorder with an ever increasing prevalence globally, placing significant burdens on our healthcare systems. It is associated with significant cardiovascular morbidities. One of the mechanisms by which it causes death is increasing the risk of cardiac arrhythmias. The aim of this article is to review the cardiac (ion channel abnormalities, electrophysiological and structural remodelling) and extracardiac factors (neural pathway remodelling) responsible for cardiac arrhythmogenesis in diabetes. It is concluded by an outline of molecular targets for future antiarrhythmic therapy for the diabetic population.
Highlights
Cardiometabolic disorders place significant burdens on the healthcare system worldwide [1]
Diabetes mellitus is an endocrine disorder characterized by reduced insulin production or increased insulin resistance, leading to hyperglycaemia
The pathophysiology underlying cardiac arrhythmias in diabetes mellitus is explored in detail, followed by an outline of potential therapeutic targets for reducing arrhythmic risk and sudden death in diabetic patients
Summary
Cardiometabolic disorders place significant burdens on the healthcare system worldwide [1]. There is increasing evidence that diabetes increases the risk of cardiac arrhythmias This involves abnormalities in action potential conduction or repolarization (Figures 1 and 2), due to a complex interplay of ion channel abnormalities and electrophysiological remodelling superimposed upon a cardiomyopathic process together with autonomic dysregulation (Figure 3). Some of these findings are derived from experiments performed in animal models, which have been proven extremely useful for dissecting the molecular mechanisms responsible for arrhythmic phenotypes [4]. The pathophysiology underlying cardiac arrhythmias in diabetes mellitus is explored in detail, followed by an outline of potential therapeutic targets for reducing arrhythmic risk and sudden death in diabetic patients
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