Cardiovascular autonomic neuropathy affects over 50% of diabetic patients with peripheral neuropathy, with emerging treatments targeting inflammatory biomarkers and oxidative stress.
This review highlights the molecular mechanisms, diagnostic approaches, and potential therapeutic targets for diabetes-induced cardiovascular autonomic neuropathy.
Cardiovascular autonomic neuropathy (CAN) is a severe complication of the advance stage of diabetes. More than 50% of diabetic patients diagnosed with peripheral neuropathy will have CAN, with clinical manifestations including tachycardia, severe orthostatic hypotension, syncope, and physical exercise intolerance. Since the prevalence of diabetes is increasing, a concomitant increase in CAN is expected and will reduce quality of life and increase mortality. Autonomic dysfunction is associated with reduced baroreflex sensitivity and impairment of sympathetic and parasympathetic modulation. Various autonomic function tests are used to diagnose CAN, a condition without adequate treatment. It is important to consider the control of glucose level and blood pressure as key factors for preventing CAN progression. However, altered biomarkers of inflammatory and endothelial function, increased purinergic receptor expression, and exacerbated oxidative stress lead to possible targets for the treatment of CAN. The present review describes the molecular alterations seen in CAN, diagnosis, and possible alternative treatments.
Sudo et al. (Thu,) conducted a review in Cardiovascular autonomic neuropathy in diabetes. Cardiovascular autonomic neuropathy affects over 50% of diabetic patients with peripheral neuropathy, with emerging treatments targeting inflammatory biomarkers and oxidative stress.