**5. Conclusion**

**Figure 4** summarizes the various events leading to a decreased HR or bradyarrhythmia and subsequently, SCD. It is postulated that DM, via an elevation in HG, can initiate the production of ROS and RCS to induce cardiac muscle damage, apoptosis, fibrosis, and subsequently cardiac remodeling. These pathophysiological changes are associated with severe damage to nerves and β1-adrenergic receptors as well as electrical and mechanical dysfunction of the myocardium leading to a decrease in HR, cardiac arrhythmias, and subsequently SCD. Experiments with animal models have consistently shown that diabetes can alter the expression and regulation of cardiac ion channels and contractile proteins, which impair impulse generation, conduction,

#### **Figure 4.**

*A flow diagram summarizes the effects of DM on the myocardium starting with hyperglycemia to the generation of ROS and RCS followed by apoptosis, fibrosis, and subsequent damage to the cardiac conduction system and β2-adrenergic nerves and receptors leading to arrhythmias and sudden cardiac death (CCS = cardiac conduction system; ROS = reactive oxygen species; RCS = reactive carbonyl species; NF-M = neuro-filament M). Note that both ROS and RCS exert lethal damage to the different parts of the cardiac conduction system as well as cation and contractile proteins in the myocardium.*

ECC, and subsequently, myocyte contractility. Prolonged QTc intervals persist in many treated diabetic patients, suggesting that glycemic control has to be adequate to normalize electrophysiological and mechanical disorders in the myocardium. Available hypoglycemic agents that can improve cardiovascular prognosis are important for the management of patients with type 2 diabetes (T2DM) who have existing CVDs and high cardiovascular risk. More research is required to understand the exact pathophysiological mechanisms at subcellular, cellular, and molecular levels, which can lead to cardiac conduction disorders in DM patients. In turn, this will help in the development of novel hypoglycemic drugs to treat the condition.
