Atrial remodeling and atrial fibrillation in acquired forms of cardiovascular disease

Abstract

Atrial fibrillation (AF) is prevalent in common conditions and acquired forms of heart disease, including diabetes mellitus (DM), hypertension, cardiac hypertrophy, and heart failure. AF is also prevalent in aging. Although acquired heart disease is common in aging individuals, age is also an independent risk factor for AF. Importantly, not all individuals age at the same rate. Rather, individuals of the same chronological age can vary in health status from fit to frail. Frailty can be quantified using a frailty index, which can be used to assess heterogeneity in individuals of the same chronological age. AF is thought to occur in association with electrical remodeling due to changes in ion channel expression or function as well as structural remodeling due to fibrosis, myocyte hypertrophy, or adiposity. These forms of remodeling can lead to triggered activity and electrical re-entry, which are fundamental mechanisms of AF initiation and maintenance. Nevertheless, the underlying determinants of electrical and structural remodeling are distinct in different conditions and disease states. In this focused review, we consider the factors leading to atrial electrical and structural remodeling in human patients and animal models of acquired cardiovascular disease or associated risk factors. Our goal is to identify similarities and differences in the cellular and molecular bases for atrial electrical and structural remodeling in conditions including DM, hypertension, hypertrophy, heart failure, aging, and frailty.

Higher long-term visit-to-visit glycemic variability predicts new-onset atrial fibrillation in patients with diabetes mellitus

“…Decreased sodium ion channel, intracellular calcium dysregulation, and abnormal expression of connexins from connexin-40 to connexin-43, can change atrial refractoriness, resulting in electrical remodeling. Autonomic imbalance, sympathetic overactivation, and heterogeneous distribution of sympathetic nerves lead to autonomic remodeling [ 3 , 4 ].…”

New aspects of endocrine control of atrial fibrillation and possibilities for clinical translation

“…LA I Na is reduced by approximately 50% in angiotensin-II infused mice, apparently via enhanced PKCα activity as dialysis with BIM1 (a PKC inhibitor) normalized I Na density and activation kinetics. 69 , 71 APD-prolongation occurred in conjunction with decreased outward K + -current (I K ), attributed to reductions in I to and I Kur independently of a change in K v 4.2, K V 4.3, KChIP2, and K v 1.5 protein levels.…”

“…AF is prevalent in both T1DM and T2DM. 69 , 71 , 105 T1DM is associated with atrial electrical and structural remodelling. 69 Experimental studies have evaluated atrial effects in genetic (Akita mice) or chemically induced [streptozotocin (STZ) or alloxan] animal models, of T1DM 106 that are characterized by substantial increases in AF susceptibility and duration.…”

Higher Long-term Visit-to-Visit Glycemic Variability Predicts New-Onset Atrial Fibrillation in Patients with Diabetes Mellitus

“…[1,2] In molecular perspective, hyperglycemia has been proved to increase interstitial brosis of atrial tissue and intracellular calcium dysregulation, both of which contribute to the impairment of atrial tissue relaxation, atrial electrical and structural remodeling and nally leads to atrial brillation. [3] Apart from focusing primarily on measurement of fasting plasma glucose (FG), hemoglobin A1c (HbA1c), advanced glycation end products (AGEs), glucagon-like peptide 1 (GLP-1), short-term glycemic variability within-days or months or even years have been considered as important risk factors for cardiovascular disease. [4] Glycemic uctuation has been shown to over-activate oxidative stress and in ammation system, aggravating greater vascular damage and cardiomyopathy than that in chronic stable hyperglycemia.…”