Prevention of Atrial Fibrillation
Atrial fibrillation (AF) may not be able to be prevented if underlying genetics, COPD, or other irreversible triggers contribute to its emergence. However, reversible causes can and should be addressed by treating any hyperthyroidism, smoking cessation, strict glycemic control in diabetics, weight management to address obesity and obstructive sleep apnea, and other indicated interventions into associated underlying causes.
With an established diagnosis of atrial fibrillation, there are two main goals in preventable intervention:
- Prevention or mitigation of symptoms
- Prevention of arterial thromboembolism
Prevention of Symptoms
Correction of either the rate or rhythm as a first step or–ideally–establishing a normal sinus rhythm can address the symptoms that come from the impaired cardiac output that atrial fibrillation creates. With underlying coronary vascular disease, the tachycardia may cause angina. Other symptoms such as palpitations, dyspnea on exertion, lightheadedness, fatigue, syncope, or generalized malaise can be lessened or eliminated with reestablishing an efficient pumping action.
Prevention of Embolism
With atrial fibrillation’s ineffective pump action in the atria, blood is not effectively pumped into the ventricles as well as with normal sinus rhythm, so this change in fluid dynamics makes more likely coagulation effects that result in thrombi. In the left atrium, such thrombi can break off as emboli and enter the systemic circulation via the left ventricle. This can result in emboli being sent to the cerebral circulation (as an obstructive, ischemic stroke) or peripheral thromboembolism, putting target organs in harm’s way (e.g., mesenteric artery resulting in intestinal ischemia and bowel necrosis).
Thrombus formation is prevented by anticoagulation, and various regimens are determined by whether there already has been an embolic event, the absence of thrombi on echocardiogram, or thrombus presence without emboli to date. Essentially, however, almost all AF patients are anticoagulated, as recommended by the National Institutes of Health, unless there is a contraindication.
Anticoagulation is intervening into the clotting cascade to lengthen the timing and briskness of clot formation, and a therapeutic range is kept constant via surveillance with clotting studies. Newer anticoagulants eliminate the need for routine clotting studies, so in patients taking these, the surveillance parameters are adjusted accordingly.