Effects of Diabetes Mellitus on the Conduction System of the Heart: Mini-Review

Abstract

Diabetes mellitus can induce substantial damage to the conduction system of the heart, especially the sinoatrial node. This is due to hyperglycemia leading to bradyarrhythmia. DM, via the elevation of HG, generates the production of a number of insulting agents in the myocardium known as reactive oxygen species and reactive carbonyl species, which elicit direct damage to neuro-filament-M and β2-adrenergic receptors in the conducting system as well as a number of cardiac contractile, cation transporting and channel proteins. One cation channel protein is the hyperpolarization-activated cyclic nucleotide-gated potassium channel. It encodes the protein responsible for the hyperpolarizing-activated current or the “funny current” that participates in spontaneous diastolic membrane depolarization in sinoatrial node cells. Gene expression of these proteins and their physiological functions are decreased in the diabetic heart, which affects the generation of electrical impulses or action potentials resulting in increases in RR and PR intervals and QRS complex duration of the electrocardiogram. The heart rate and force of contraction of the myocardium are decreased leading to bradyarrhythmia and sudden cardiac death. This review attempts to explain the cellular mechanism(s) involved in diabetes-induced bradyarrhythmia with emphasis on cation-transporting proteins, especially the hyperpolarization-activated cyclic nucleotide-gated channels pacemaker current channels.