**15. Conclusion**

**Figure 5** summarizes the major events leading to SCD during the development of DM as a result of the various risk factors. It is proposed that during elevated or uncontrolled level of blood glucose (hyperglycemia) due to DM, the body produces a number of endogenous pathological compounds called oxidants, which are classified either as reactive oxygen species (ROS such as 2O− , H2O2, and others) or RCS. One particular RCS is methylglyoxal (MGO), which is elevated to toxic levels.

#### **Figure 5.**

*A flow diagram illustrating the events, starting from the risk factors that lead to sudden cardiac death in diabetes mellitus. ROS, reactive oxygen species; MGO, methylglyoxal; TGF-beta, transforming growth factorbeta; SCD, sudden cardiac death.*

This is due to increased synthesis and a decrease in the activity of glyoxylase-1, the enzyme that metabolizes MGO in the different organs of the body [55]. In the heart, MGO exerts a deleterious effect resulting in death of some cells (apoptosis), enlargement and disarray of the structure of cardiac muscles and other tissues which are associated with an elevation of transforming growth factor beta-1 (TGF-beta-1), which in turn elicits hypertrophy of the heart and infiltration of fibrosis [86]. These processes lead to a derangement in cellular calcium homeostasis (elevated diastolic calcium) followed by DC. The resulting effect is remodeling of the heart so that it can maintain its function to pump blood around the body but not at physiological level [87]. Thus, the pathogenesis of diabetic cardiomyopathy in diabetic patients is multifactorial and complex, eventually leading to an energetically compromised heart with reduced working capacity or heart failure, arrhythmias, and SCD. Luckily, patients now have a number of therapies including non-pharmacological and pharmacological interventions to treat SCD.

**149**

**Author details**

Khemraj Rupee3

United Kingdom

Georgetown, Guyana

Centre, Omaha, NE, USA

Farah Ahmed Sleiman4

Manal M.A. Smail1,2, Frank C. Howarth1

Emirates University, United Arab Emirates

4 Corniche Hospital, United Arab Emirates

provided the original work is properly cited.

5 Fatima College for Health Science, United Arab Emirates

\*Address all correspondence to: kbidasee@unmc.edu

, Jaipaul Singh<sup>2</sup>

, Carlin Hanoman2,3, Abla Mohammed Ismail4

1 Department of Physiology, College of Medicine and Health Sciences, United Arab

2 School of Natural Sciences, University of Central Lancashire, Preston, England,

3 School of Medicine, Faculty of Health Sciences, University of Guyana, Turkeyen,

6 Department of Pharmacology and Neurosciences, University of Omaha Medical

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

, Samar Abdulkhalek<sup>5</sup>

, Sunil Rupee3

,

and Keshore Bidasee6

,

\*

*Mechanisms of Diabetes Mellitus-Induced Sudden Cardiac Death*

*DOI: http://dx.doi.org/10.5772/intechopen.93729*
