Pericardial Effusion Provoking Atrial Fibrillation After Cardiac Surgery
- Gaudino M, Di Franco A, Rong LQ, et al.
- Pericardial Effusion Provoking Atrial Fibrillation After Cardiac Surgery: JACC Review Topic of the Week. J Am Coll Cardiol 2022;79:2529-2539.
This state-of-the-art review outlines various aspects of postoperative atrial fibrillation (POAF) following cardiac surgery and the possible role of pericardial effusion-mediated inflammation. The following are key points to remember:
- POAF is the most common complication after cardiac surgery, affecting 19-30% of surgical patients.
- POAF can result in major adverse outcomes including increased rates of mortality, stroke, heart failure, hospitalizations, and medical costs, which are estimated to exceed $2 billion per year in the United States.
- Increasing evidence suggests that postoperative pericardial effusion and localized pericardial inflammation can trigger POAF. Several small studies suggest that >75% of patients develop a postoperative pericardial effusion. The incidence of POAF was significantly higher in patients with a pericardial effusion (27%) compared to patients without an effusion (11%).
- Higher incidence of POAF is seen in older patients, male sex, prior AF, congestive heart failure, hypertension, obesity, chronic obstructive pulmonary disease (COPD), and following mitral valve surgery.
Pathophysiology of POAF:
- POAF is typically caused by an acute trigger related directly to surgery in combination with an underlying predisposition. Triggers for POAF can be divided into three groups according to their timing in relation to surgery.
- Preoperative factors: The pre-existing atrial substrate is affected by age, genetics, hypertension, COPD, prior AF, obesity, and structural abnormalities, in particular valvular heart disease.
- Perioperative factors related to the actual surgery such as direct atrial injury from cannulation, and cardiopulmonary bypass. Higher rates of POAF are seen with increased cross-clamp time, bicaval cannulation, use of cardiopulmonary bypass (CPB), and left ventricular venting via the pulmonary veins.
- Postoperative factors: Ischemia and reperfusion can cause reactive oxygen species and dysregulation of calcium homeostasis. CPB can induce systemic inflammation, which can lead to conduction disturbances. Last, increased sympathetic tone postoperatively results in higher heart rates and more atrial triggered activity.
- Interventions aimed at suppressing these POAF triggers have included prophylactic antiarrhythmics, colchicine, steroids, statins, magnesium, and postoperative atrial overdrive pacing. Nonetheless, the incidence of POAF remains high.
New Etiopathogenetic Hypothesis for Mechanisms Triggering POAF:
- Pericardial effusion and inflammation: Mediastinal blood within the pericardial space can result in a pro-oxidant and proinflammatory environment with breakdown products, an activated coagulation cascade, and oxidative burst. Several studies have shown that POAF incidence can be reduced by surgical drainage of the pericardium in the postoperative period.
- Periatrial fat metabolic activity and autonomic neuromodulation: Postoperative inflammation and oxidative stress directly affects the pulmonary veins and ganglionated plexi situated within the periatrial fat pads. Periatrial fat is metabolically active tissue, which is believed to modulate atrial rhythms through autonomic regulation as well as paracrine secretion of cytokines and adipokines. Epicardial ablation or CaCl2 injection of the ganglionated plexi has shown to significantly reduce rates of POAF.
- Cardiac surgery procedures which include opening the pericardium have a higher incidence of POAF, likely due to direct mechanical compression. However, even small amounts of blood in the pericardium without hemodynamic compromise can induce POAF through inflammation and oxidative stress.
- Oxidative stress can occur when reactive oxygen species (typically the H2O2 produced by white blood cells) cause lipid peroxidation of the atrial cell membranes and periatrial fat pads, resulting in membrane disruption, mitochondrial dysfunction, intracellular Ca2+ overload, and ultimately apoptosis and necrosis.
- Both pericardiectomy and hemopericardium result in a highly inflammatory and pro-oxidant milieu, in close proximity to the atria.
- Activation of the coagulation cascade and platelets by mediastinal blood can further trigger an inflammatory response through interleukin activation, and clot breakdown from shed blood can further ignite periatrial inflammation.
- Several randomized controlled trials have evaluated the incidence of POAF following a posterior pericardiotomy (allowing for drainage from the pericardium into the left pleural space) with the largest single-center study finding that the incidence of POAF was 17% versus 32% in the non-pericardiotomy group (p < 0.001).
- Genetic predisposition: Polymorphisms in the -174G/C IL-6 promoted gene variant have been shown to modulate the postsurgical inflammatory response and result in the development of POAF.
- Postoperative pericardial effusion and resultant localized inflammation seem to be key components in triggering POAF.
- POAF and clinical AF are likely two separate entities with different pathophysiologic mechanisms. However, POAF is generally considered an early predictor of developing eventual clinical AF.
- Further studies are needed to test prophylactic strategies to prevent POAF. Recent evidence suggests that minimizing retained blood in the pericardial and mediastinal space is associated with a significant reduction in the incidence of POAF.
Clinical Topics: Arrhythmias and Clinical EP, Cardiac Surgery, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Pericardial Disease, Prevention, Valvular Heart Disease, Implantable Devices, EP Basic Science, Genetic Arrhythmic Conditions, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Cardiac Surgery and Arrhythmias, Cardiac Surgery and Heart Failure, Cardiac Surgery and VHD, Acute Heart Failure, Interventions and Structural Heart Disease, Hypertension, Stress
Keywords: Anti-Arrhythmia Agents, Arrhythmias, Cardiac, Atrial Fibrillation, Cardiac Surgical Procedures, Cardiopulmonary Bypass, Genetics, Heart Failure, Heart Valve Diseases, Hypertension, Inflammation, Obesity, Oxidative Stress, Pericardial Effusion, Pericardiectomy, Postoperative Period, Pulmonary Disease, Chronic Obstructive, Reperfusion, Secondary Prevention, Stroke
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