Prediabetes and diabetes increase the prevalence of atrial fibrillation through structural, electrical, and neural remodeling driven by oxidative stress, inflammation, and endoplasmic reticulum stress.
This review highlights the molecular mechanisms by which prediabetes and diabetes contribute to atrial fibrillation, emphasizing the need for individualized glycemic and AF management.
Based on glucose levels, people fall into three groups, normal individuals, prediabetic patients, and diabetic mellitus (DM) patients. Prediabetes (pre-DM) is an intermediate condition that exists between normal glucose levels and DM. Atrial fibrillation (AF), one of the most prevalent cardiac arrhythmias in medical practice, contributes to a considerable morbidity and mortality rate. In this review, we looked at the clinical symptoms, pathological alterations, molecular mechanisms, and associated risk factors of pre-DM, type 2 DM (T2DM), and AF. In clinical practice, pre-DM can increase the prevalence of AF. In the hyperglycemic state, oxidative stress, inflammation, and endoplasmic reticulum stress can cause alterations in atrial cell or cardiac fibroblast function through tumor necrosis factor-α/nuclear factor-κB (NF-κB)/transforming growth factor-β, mitogen-activated protein kinase-matrix metalloproteinase-9 and PARP-1 is poly (ADP-ribose) polymerase 1. IκB kinase-α/NF-κB pathways, and further cause atria undergo structural, electrical, and neural remodeling which lead to the occurrence and persistence of AF. In addition, pre-DM and T2DM may worsen as a result of obesity, obstructive sleep apnea, and arterial hypertension. Furthermore, clinical researches have demonstrated that lifestyle interventions and/or pharmacotherapy in pre-DM patients can effectively delay the progresssion of pre-DM to T2DM. Individualized glycemic management and AF management should be provided to AF patients with pre-DM or DM.
Han et al. (Sun,) conducted a review in Prediabetes, diabetes, and atrial fibrillation. Prediabetes and diabetes increase the prevalence of atrial fibrillation through structural, electrical, and neural remodeling driven by oxidative stress, inflammation, and endoplasmic reticulum stress.