Post-operative atrial fibrillation: a maze of mechanisms

Abstract

Post-operative atrial fibrillation (POAF) is one of the most frequent complications of cardiac surgery and an important predictor of patient morbidity as well as of prolonged hospitalization. It significantly increases costs for hospitalization. Insights into the pathophysiological factors causing POAF have been provided by both experimental and clinical investigations and show that POAF is ‘multi-factorial’. Facilitating factors in the mechanism of the arrhythmia can be classified as acute factors caused by the surgical intervention and chronic factors related to structural heart disease and ageing of the heart. Furthermore, some proarrhythmic mechanisms specifically occur in the setting of POAF. For example, inflammation and beta-adrenergic activation have been shown to play a prominent role in POAF, while these mechanisms are less important in non-surgical AF. More recently, it has been shown that atrial fibrosis and the presence of an electrophysiological substrate capable of maintaining AF also promote the arrhythmia, indicating that POAF has some proarrhythmic mechanisms in common with other forms of AF. The clinical setting of POAF offers numerous opportunities to study its mechanisms. During cardiac surgery, biopsies can be taken and detailed electrophysiological measurements can be performed. Furthermore, the specific time course of POAF, with the delayed onset and the transient character of the arrhythmia, also provides important insight into its mechanisms.This review discusses the mechanistic interaction between predisposing factors and the electrophysiological mechanisms resulting in POAF and their therapeutic implications.

Severe sepsis and cardiac arrhythmias

“…Furthermore, abnormalities in calcium handling have been demonstrated in animal models in response to endotoxin application (28)(29)(30)(31). Increased intracellular calcium is associated with shortening of atrial refractory period and elicited triggered activity by the way of delayed afterdepolarizations therefore putting patients at high risk of cardiac arrhythmias (26,32).…”

Cardiac aging and heart disease in humans

“…The implication of β-adrenergic signaling in atrial fibrillation is less clear. However, in post-operative atrial fibrillation-one of the most frequent complications of cardiac surgery-sympathetic activation has been shown to contribute to the onset of the arrhythmia, by altering atrial refractoriness and promoting ectopic activity (Maesen et al 2012). …”

Evaluation of Risk Factors for Atrial Fibrillation Occurring After Coronary Bypass Surgery

“…Leitch ve arkadaşlarının yaptığı çalışmaya göre, yaştaki her 10 yıllık artış, AF riskini %70 oranında arttırmaktadır (16) . İlerlemiş yaşın özellikle, nodal lifl erin kaybı, sinoatrial noda fi bröz ve adipöz dokunun artması, atriyal dilatasyon, fokal ventriküler fi brozis gelişimi ve atriumda interstisyel amiloid depositlerinin oluşma-sı gibi yapısal değişikliklere neden olarak AF gelişiminde etkili olabileceği vurgulanmıştır (5,17) . Cinsiyetin ise temel olarak postoperatif AF gelişiminde etkili olmadığı bildirilmiştir (18) .…”

“…Diyabet ise infl amatuvar süreçler sonunda hem direk hem de oluşan mikroanjiopati ve nöropati gibi sekonder patolojilerle indirek olarak AF gelişiminde etkili olabilmektedir (5,(18)(19)(20)(21) . KOAH'lı hastalarda ise yüksek AF prevelansını işaret eden raporlar mevcuttur.…”

“…Diğer yandan operasyon sonrası AF gelişmesinin hastanede yatış süresini uzattığı ve 3 kat artmış tromboemboli riski gibi sekonder patolojilere yol açarak ek morbidite ve mortalite riski oluşturduğu saptanmıştır (3) . Postoperatif AF gelişmindeki temel elektrofi zyolojik mekanizmanın atriyal refraktör odaklardan uyarıların ışınsal olarak dağılımı sonucu meydana gelen reentry olduğuna inanılmaktadır (4,5) . Uniform olmayan atriyal odaklara sahip hastalarda cerrahi girişimin bu hassas yapıları etkileyerek AF gelişimini tetiklediği düşünülmektedir (4) .…”