The contribution of the perpetuation of atrial fibrillation is caused by electrical remodeling in which calcium, sodium and potassium channels could refer to changes in the ion channel protein expression, development of fibrosis, gene transcription and ion channel redistribution. Calcium and magnesium could influence the risk of atrial fibrillation which is the leading cause of cardiac death, heart failure and ischemic stroke. The elevated serum concentration of calcium had a higher range of in-patient’s mortality, increased total cost of hospitalization and increased length of hospital stay as compared to those without hypercalcemia in atrial fibrillation patients. Moreover, chloride channels could affect homeostasis, atrial myocardial metabolism which may participate in the development of atrial fibrillation. Up to a 50% risk of incidence of AF are higher in which left ventricular hypertrophy, sudden cardiovascular death and overall mortality relate to a low serum magnesium level. Additionally, magnesium prevents the occurrence of AF after cardiac surgery, whereas greater levels of serum phosphorus in the large population-based study and the related calcium–phosphorus products were linked with a greater incidence of AF. Numerous clinical studies had shown the high preoperative risk of AF that is linked with lower serum potassium levels. The conventional risk factor of increased risk of new onset of AF events could independently link with high dietary sodium intake which enhances the fibrosis and inflammation in the atrium but the mechanism remains unknown. Many drugs were used to maintain the electrolyte imbalance in AF patients.

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Background Insulin resistance is associated with metabolic disorders including diabetes, obesity, hypertension, and inflammation which are the risk factors for Atrial Fibrillation. Many studies have reported that type 2 diabetes and AF are related and also their prevalence is increasing globally. Moreover, insulin resistance begins the type 2 diabetes. Main body This review explains the pathophysiological aspects of insulin resistance in AF patients and discusses the drugs that are used to manage insulin resistance including Biguanides (metformin), thiazolidinediones (TZDs) [Pioglitazone, rosiglitazone], Sodium-glucose cotransporter 2 (SGLT2) inhibitors, Concentrated Insulin Products, Dipeptidyl peptidase-4 (DPP-4) Inhibitors, Glucagon-like peptide 1 (GLP-1) receptor Agonists, Pramlintide, Sulfonylureas, Meglitinides, α-Glucosidase Inhibitors, Colesevelam, Bromocriptine. This review will highlight a few major drugs that played a significant role in AF patients. For this purpose, many databases were used for reviewing the literature and keywords are used such as Insulin Resistance, Pathophysiology, Atrial Fibrillation, and Drugs. Conclusion This review article concludes that insulin resistance is related to AF. It also provides an outlook on the recent pathophysiological aspects of insulin resistance in AF; however, more studies are needed to clarify the management of insulin resistance in AF patients to prevent the development of type 2 diabetes.

Interleukins (IL) are a group of cytokines with complex immunomodulatory functions, whereas atrial fibrillation (AF) is the most common cardiac arrhythmia. This review article highlights the role of major IL in the pathogenesis of AF. IL-1 had elevated levels in permanent and persistent AF patients as compared to paroxysmal AF. A study had shown a straightforward connection between the development of postoperative atrial fibrillation and IL-2 sera levels shortly after cardiopulmonary bypass graft for the first time. IL-4 has been involved in anti-inflammatory response and played no role in the contribution of AF. The elevated level of IL-6 rapidly induces atrial electrical remodeling by downregulating cardiac connexins. This change could be significantly increased the risk of AF and related complications during active inflammatory processes. Moreover, a study has shown higher IL-8 levels in permanent AF patients as compared with paroxysmal AF patients. An association was found between IL-10 gene -592A/C polymorphism and AF in Han Chinese. Recombinant human IL-11 therapy shortened atrial refractoriness and also created favorable conditions for AF by an indirect mechanism involving volume expression, stretching of atrial myocardial tissue and sodium retention. An elevated IL-12 expression was observed in the left atrial tissues of AF patients. IL-17 signaling pathway has played a significant role, and some genes could be used as potential therapeutic targets for AF. An association between the risk of AF with single nucleotide polymorphism of IL-18 and also resulted in the increased left atrial diameter and decreased left ventricular ejection fraction in AF subjects as compared to control. IL-27 genetic variants had increased the occurrence of AF. AF patients had elevated levels of IL-37 that were closely linked with AF subgroups.

Background The adipokines, secreted from adipose tissue or body fats, are also called adipocytokines which are cytokines, cell signaling proteins or cell–cell communication. However, AF is a common cardiac arrhythmia in which the heart beats so fast by abnormal beating and is a serious public health disease associated with increased heart failure, systemic thromboembolism, and death. Adipokines are cardiovascular disease (CVD) mediators or biomarkers that affect the heart as well as blood vessels, by increasing the cardiac contractility and action potential duration, which result in the extent of left ventricular and atrial remodeling. Main body Google Scholar, PubMed, and science direct were used to review the literature. Many keywords were used for searching the literature such as Adipokines, Leptin, Apelin, Adiponectin, Omentin-1, Chemerin, CTRP3, TNF-α, IL-6, IL-10, and AF. According to the literature, much more data are available for numerous adipokines, but this review article only has taken few major adipokines which played their major role in Atrial Fibrillation. The review article did not limit the time frame. Conclusion In conclusion, adipokines play a significant role in the development and progress of atrial fibrillation. Also, there are major adipokines such as adiponectin, apelin, C1q/TNF-Related Protein 3 (CTRP3), Chemerin, Omentin-1, interleukin-6, Leptin, TNF-α, resistin, and interleukin-10, which played their pathophysiological role in atrial fibrillation by causing cardiac hypertrophy, increasing the cardiac contractility and action potential duration, atrial fibrosis, electrical and structural remodeling of atrial tissue.