Atrial fibrillation and type 2 diabetes: Prevalence, etiology, pathophysiology and effect of anti‐diabetic therapies

• Published in: Diabetes, obesity & metabolism Vol. 21; no. 2; pp. 210 - 217
• Main Authors: Bell, David S. H., Goncalves, Edison
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.02.2019; Wiley Subscription Services, Inc
• Subjects: Antidiabetics; atrial fibrillation; Atrial Fibrillation - drug therapy; Atrial Fibrillation - epidemiology; Atrial Fibrillation - etiology; Cardiac arrhythmia; Diabetes; Diabetes mellitus; Diabetes mellitus (non-insulin dependent); Diabetes Mellitus, Type 2 - complications; Diabetes Mellitus, Type 2 - drug therapy; Diabetes Mellitus, Type 2 - epidemiology; Diabetes Mellitus, Type 2 - physiopathology; Diabetic Angiopathies - drug therapy; Diabetic Angiopathies - epidemiology; DPP‐4 inhibitors; Drug development; Drug resistance; Etiology; Fibrillation; Fibrosis; GLP‐1 agonists; Humans; Hypoglycemia; Hypoglycemic Agents - therapeutic use; Insulin; Metabolic syndrome; metformin; NAF; Pioglitazone; Prevalence; SGLT2 inhibitors; Steatosis; sulfonylureas; sympathetic activity; Sympathetic nervous system; thiazolidinediones; Treatment Outcome; type 2 diabetes; metabolic syndrome; thiazolidinediones; NAF; atrial fibrillation; type 2 diabetes; insulin; DPP-4 inhibitors; GLP-1 agonists; sulfonylureas; metformin; sympathetic activity; SGLT2 inhibitors
• ISSN: 1462-8902; 1463-1326
• DOI: 10.1111/dom.13512

New‐onset atrial fibrillation (NAF) is increased in the type 2 diabetic patient because of the presence of the metaboli syndrome and increased sympathetic activity. This results in inflammation, endothelial dysfunction and myocardial steatosis which, in turn, lead to atrial fibrosis and dilatation. The end result is the development of structural and electrical atrial remodeling. Drugs that lower insulin resistance, particularly pioglitazone, decrease the incidence of NAF while drugs that, through hypoglycaemia, stimulate the sympathetic nervous system, insulin and secretagogues, increase the incidence of NAF. Currently there is no evidence that GLP‐1 agonists, SGLT2 inhibitors and DPP‐4 inhibitors either accelerate or decelerate the development of NAF.