Studies on both humans and animals have found evidence of a link between inflammation and hypertension (HTN).A lower serum calprotectin level was found to be independently related to HTN. The elevated ferritin-HTN link could be mediated by fatty liver disease and insulin resistance (IR). Similarly, fibrinogen was engaged in several processes that may increase the risk of HTN which including hemostasis, coagulation, and the proliferation of smooth muscle cells in the artery wall, and others. Procalcitonin monitoring could be a useful biomarker in inflammation related to atherosclerosis and early-stage HTN. Plasminogen activator 1 (PAI-1) was not just a result of HTN but also contributes to its development. Also, the positive correlation between monocyte chemoattractant protein 1 (MCP-1) levels with blood pressure were found among smokers. The high level of pentraxin 3 (PTX3) was one of the factors of increased blood pressure. Galectin 3 (Gal-3) may contribute to the onset and progression of diastolic dysfunction-complicated HTN. Increased intercellular adhesion molecules (ICAM)/vascular cell adhesion molecule 1 (VCAM-1) ligand expression, along with a drop in soluble cell adhesion molecules (sCAMs) and endocan, points to endothelium deactivation with lower blood pressure, which reduces the adherence of circulatory leukocytes to endothelium and, as a result, lowers the probability of atherosclerosis developing. The circulating levels of soluble VCAM-1 were substantially connected with left ventricular mass indexes (LVMIs) and were higher in uncomplicated essential hypertension (EH) patients with left ventricle (LV) hypertrophy than in those without LV hypertrophy.

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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.

Numerous known risk factors for atrial fibrillation (AF) exist, but few studies have investigated the link between gastrointestinal and liver disorders. Through a variety of pathways, hepatic and gastrointestinal conditions can increase the risk of both prevalent and incident AF. According to numerous studies, liver dysfunction plays a significant role in the pathogenesis of atrial fibrillation. So, this review article aimed to give an overview of how liver function tests played role in the AF. Albumin, alkaline phosphatase, alanine transaminase, aspartate aminotransferase, gamma-glutamyl transferase, serum bilirubin, and prothrombin time were highlighted in the pathogenesis of AF. However, the 5’-nucleotidase test, alpha-fetoprotein test, mitochondrial antibodies test and more, and liver functions test need to find their pathogenesis in AF. The exact mechanism of action of the liver panel was not reported in the pathogenesis of AF. To control the major liver diseases in AF patients, the therapeutic management of liver function tests is required.