Postoperative Atrial Fibrillation: A Review

Abstract

Atrial fibrillation (AF) in the postoperative phase is a manifestation of numerous factors, including surgical stress, anesthetic effects, and underlying cardiovascular conditions. The resultant cardiac hyperactivity can induce new onset or exacerbate existing AF. A common phenomenon, postoperative atrial fibrillation (POAF) affects nearly 40% of patients and is associated with longer hospitalization stays, and increased mortality, heart failure, stroke, and healthcare costs. Areas of controversy in POAF include whether to anticoagulate patients who have short-lived POAF, especially given their higher bleeding risk in the postoperative period, and the identification of patients who would benefit the most from preventive drug therapy for POAF. This review discusses the pathophysiology and management of POAF, and strategies to reduce its occurrence.

Keywords: anticoagulation; atrial fibrillation; bleeding risk; direct-acting anticoagulants; perioperative; stroke; warfarin.

Figure 1

Risk factors of postoperative atrial fibrillation. These risk factors are important to address before surgery to minimize the incidence of POAF. Structural changes including atrial stretching by long-standing OSA result in the replacement of cardiomyocytes with pathological fibrosis which predisposes to conduction variation, and increased vulnerability to reentry pathway. Advanced age is the biggest independent risk factor for the development of POAF through atrial structural changes such as atrial dilatation consequently resulting in reduced refractoriness. Patient comorbidities, inIcluding modifiable ones, such as hypertension and obesity, and non-modifiable comorbidities, like advanced age and male sex, all play a pivotal part in chronic inflammation and remodeling which increase the risk of developing POAF. Changes at the cellular level through various mechanisms all aid in increasing the risk of POAF. Post-surgical inflammation which peaks at 48 h results in cytokines such as IL-1β resulting in an immense inflammatory response leading to the downregulation of gap junction proteins such as Connexin 40 and 43 which are essential in the propagation of action potentials across cardiac myocytes, causing arrhythmogenic state. Chronic intermittent hypoxia as seen in OSA patients causes increased expression of hypoxia-inducible factor-1α (HIF). HIF upregulates the expression nuclear factor-κB causing remodeling, and pathological changes. Hypomagnesemia is one of the major electrolytes known to increase atrial ectopy by promoting fibrosis through the activation of fibroblasts into myofibroblasts by TRPM7 expression.

Figure 2

The pathophysiology of POAF is multifactorial and is influenced by modifiable and non-modifiable risk factors. Electrolyte disturbances, including hypomagnesemia, have been shown to activate TRPM7 channels responsible for activating fibroblasts to myofibroblast, resulting in fibrosis of the physiological cardiac myocytes, increasing the risk of POAF. Pericardial effusion is a common occurrence after coronary artery bypass graft and cytokine-mediated inflammation leads to the development of effusion, which increases the risk of POAF. Post-operation inflammation is a physiological response including released cytokines that mediate the inflammatory process. IL-1β is a major pro-inflammatory marker that results in inflammation of the cardiomyocyte which predisposes to slowing of cardiac conduction along with variation in the conduction and it is this mechanism that increases the chance of POAF. Connexin 40 and 43 are gap junction proteins expressed in the atria that are downregulated in inflammation, leading to decreased conduction velocity and arrhythmogenesis. Myocardial ischemia can result in atrial infarction, and ischemia is arrhythmogenic. Atrial stretching is another pathological change that occurs through various mechanisms, such as fluid shifts, as seen in hypervolemia, direct structural changes noted post-surgery, and long-standing comorbidities including hypertension, chronic obstructive pulmonary disease, and obesity.

Figure 3

This figure illustrates the spectrum of medications commonly used to manage POAF. They are mainly categorized by rate control agents, rhythm control agents, and NSAIDs. Each class of medication addresses a different aspect of POAF management. The choice of medication depends on individual patient factors, including the severity of the arrhythmia, underlying comorbidities, and risk of adverse effects.

Figure 4

Algorithmic approach to POAF management. The process begins with the identification and diagnosis of POAF. Upon diagnosis, the initial step involves assessing the hemodynamic stability of the patient. If the patient is hemodynamically unstable, immediate synchronized cardioversion is indicated. For hemodynamically stable patients, the algorithm proceeds to evaluate the rate versus rhythm control strategy based on the duration and symptoms of POAF. Further steps include the consideration of anticoagulation therapy, determined by assessing thromboembolic risk and further outpatient management.

Figure 5

Algorithm for anticoagulation and bridging in POAF. The type of anticoagulation is determined based on patient preference, bleeding risks, and indications. Historically, warfarin is used for bridging in high-risk thromboembolism groups per American College of Clinical Pharmacy/American Heart Association recommendations. Note that if these high-risk factors are not present then bridging is advised against as there is an increased incidence of bleeding and adverse cardiovascular events with no significant benefit.