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.
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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