Key result
Atrial fibrillation pathophysiology involves immunothrombosis, inflammation, and oxidative stress, with management relying on rhythm control, rate control, and anticoagulation strategies.
This review summarizes the pathophysiology of atrial fibrillation, highlighting the roles of inflammation and oxidative stress, and outlines current management strategies including rhythm and rate control.
Affirms standard AF management; leaves open immunomodulatory trials as hypothesis-generating.
Atrial fibrillation is a common supraventricular arrhythmia which affects approximately 1% to 4% of the global population. Atrial fibrillation is more common in older individuals; the prevalence of AF increases sharply in those over 80 years old. Atrial fibrillation is the most common cardiac arrythmia and is associated with costly cardiovascular morbidity such as stroke and heart failure. Inflammation has been implicated in the pathophysiology of various cardiac, as well as non-cardiac, diseases that are comorbid with atrial fibrillation. Heart failure and cardiomyopathy are associated with a 4-6-fold increase in atrial fibrillation prevalence. Inflammation has been implicated in the pathophysiology of heart failure and modulates the cell signaling activation patterns associated with fibrosis, apoptosis and hypertrophy; these are all forms of cardiac remodeling that, when they occur at the atrial level, predispose to atrial fibrillation. Rhythm control strategy should be preferred in symptomatic patients due to paroxysmal pattern of atrial fibrillation and the presence of a hyperdynamic circulation. -blockers is effective in reducing symptoms when rhythm control is not possible Indicated also for HF; Calcium channel blockers (verapamil, diltiazem): Effective in reducing symptoms when rhythm control is not possible and Digoxin: Second line therapy when -blockers or calcium channel blockers are not tolerated.
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Gudisa Bereda (2022) conducted a review in Atrial Fibrillation. Atrial Fibrillation Management was evaluated. Atrial fibrillation pathophysiology involves immunothrombosis, inflammation, and oxidative stress, with management relying on rhythm control, rate control, and anticoagulation strategies.
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