Glycemic variability and diabetic cardiac autonomic neuropathy

Abstract

Cardiac autonomic neuropathy (CAN) is closely associated with an approximately five-fold increase in the risk of cardiovascular mortality in patients with diabetes mellitus (DM). Impaired autonomic function of the cardiovascular system in DM, which leads to the development of CAN, can be accompanied by coronary artery ischemia, heart rhythm disturbances, “silent” myocardial infarction, severe orthostatic hypotension, and sudden cardiac death syndrome. The article provides an analysis of literature data on the impact of glycemic variability (GV) on diabetic CAN development. This review analyzed the possible relationships between GV in people with diabetic CAN. In particular, the issues related to glycemic control and CAN, the link between GV and CAN in diabetes were analyzed. Unsatisfactory glycemic control and uncontrolled glycemic status are considered the main risk factors for chronic complications of DM, in particular CAN. An increase of GV is associated with a higher risk of chronic complications of DM, cardiovascular risk, all-cause mortality and morbidity. The clinical trial results demonstrated that time in range might be a promising metric for assessing glycemic control and prognosis of diabetic complications. This review is based on a search in PubMed and MEDLINE, Scopus, BIOSIS, EMBASE, Google Scholar and Springer Online Archives Collection. The following keywords were used: glycemic variability, cardiac autonomic neuropathy and diabetes mellitus. Research findings missed by the web search have been identified through a manual search of the bibliography of publications. CAN is one of the frequent long-term complications of DM, and reasonable control of GV may be necessary for its prevention. Determination of GV may have advantages for predicting future complications of DM in clinical trials and practice. The association of autonomic dysfunction and glucose levels, insulin resistance, and HbA1c variability suggest further research to reduce chronic complications development. Further investigation is needed to study the mechanisms of GV and evaluate them as therapeutic targets in the treatment of patients with T2DM.