Electrolyte’s imbalance role in atrial fibrillation: Pharmacological management

Abstract

AbstractThe 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.