@article{3077136,
    title = "Atrial fibrillation risk in patients suffering from type I diabetes mellitus. A review of clinical and experimental evidence",
    author = "Vrachatis, D.A. and Papathanasiou, K.A. and Kossyvakis, C. and Giotaki, S.G. and Raisakis, K. and Iliodromitis, K.E. and Reimers, B. and Stefanini, G.G. and Cleman, M. and Sianos, G. and Lansky, A. and Deftereos, S.G. and Giannopoulos, G.",
    journal = "Diabetes Research and Clinical Practice",
    year = "2021",
    volume = "174",
    publisher = "Elsevier Ireland Ltd",
    issn = "0168-8227",
    doi = "10.1016/j.diabres.2021.108724",
    keywords = "glucose, atrial fibrillation;  cardiovascular risk;  disease association;  disease course;  evidence based medicine;  exocytosis;  heart arrhythmia;  heart atrium;  heart muscle fibrosis;  human;  insulin dependent diabetes mellitus;  muscle cell;  oxidative stress;  pathophysiology;  Review;  risk factor;  signal transduction;  systematic review;  thromboembolism;  aged;  atrial fibrillation;  complication;  female;  insulin dependent diabetes mellitus;  male;  middle aged;  pathology, Aged;  Atrial Fibrillation;  Diabetes Mellitus, Type 1;  Female;  Humans;  Male;  Middle Aged",
    abstract = "Atrial fibrillation (AF) and diabetes mellitus (DM) are commonly encountered in clinical practice. Although, the long term macrovascular and microvascular sequela of DM are well validated, the association between the less prevalent type 1 DM (T1DM) and atrial arrhythmogenesis is poorly understood. In the present review we highlight the current experimental and clinical data addressing this complex interaction. Animal studies support that T1DM, characterized by insulin deficiency and glycemic variability, impairs phosphatidylinositol 3‑kinase (PI3K)/protein kinase B signaling pathway. This pathway holds a central role in atrial electrical and structural remodeling responsible for arrhythmia initiation and maintenance. The molecular ‘’footprint’’ of T1DM in atrial myocytes seems to involve a state of increased oxidative stress, impaired glucose transportation, ionic channel dysregulation and eventually fibrosis. On the contrary only a few clinical studies have examined the role of T1DM as an independent risk factor for AF development, and are discussed here. Further research is needed to solidify the real magnitude of this association and to investigate the clinical implications of PI3K molecular signaling pathway in atrial fibrillation management. © 2021 Elsevier B.V."
}