Inflammation, oxidative stress and postoperative atrial fibrillation in cardiac surgery

Abstract

Postoperative atrial fibrillation (POAF) is a common complication of cardiac surgery that occurs in up to 60% of patients. POAF is associated with increased risk of cardiovascular mortality, stroke and other arrhythmias that can impact on early and long term clinical outcomes and health economics. Many factors such as disease-induced cardiac remodelling, operative trauma, changes in atrial pressure and chemical stimulation and reflex sympathetic/parasympathetic activation have been implicated in the development of POAF. There is mounting evidence to support a major role for inflammation and oxidative stress in the pathogenesis of POAF. Both are consequences of using cardiopulmonary bypass and reperfusion following ischaemic cardioplegic arrest. Subsequently, several anti-inflammatory and antioxidant drugs have been tested in an attempt to reduce the incidence of POAF. However, prevention remains suboptimal and thus far none of the tested drugs has provided sufficient efficacy to be widely introduced in clinical practice. A better understanding of the cellular and molecular mechanisms responsible for the onset and persistence of POAF is needed to develop more effective prediction and interventions.

Atrial Fibrillation Initiated by Early Afterdepolarization-Mediated Triggered Activity during Acute Oxidative Stress: Efficacy of Late Sodium Current Blockade

“…Increased systemic and atrial myocardial oxidative stress is often observed in post-operative patients with new onset (acute) paroxysmal AF (POAF) [3,4] with an incidence of up to 50% [5]. Diverse etiological factors such as fibrosis [6,7] and increased Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) activity [8,9] among others, are thought to play a key role in the initiation of oxidative AF [4,10]. While the causative and signaling factors of oxidative AF are reasonably well identified, the mechanism of spontaneous initiation (i.e., not induced by electrical stimulation) of acute oxidative AF in experimental and human studies, remains undefined [10].…”

O2‐09‐05: Coronary Artery Bypass Graft Surgery and Dementia Risk in the Cardiovascular Health Study

“…Hypoperfusion during surgery affects the washout of microemboli and is linked to brain ischemia and infarction. 34 CABG markedly increases cytokine levels as part of the systemic inflammatory response, 35 which may in turn increase the risk of dementia. 36 Given that our results suggest the increased dementia risk associated with CABG takes >1 year to become apparent, it is possible that these mechanisms reduce brain reserve and increase vulnerability to dementia by accelerating cognitive decline.…”

“…CABG is increasingly performed in older adults who are at risk of dementia. 2 In a study of 326 adults aged 55 years and older, prevalence of dementia was markedly increased 7.5 years after CABG and amounted to 30.7% [95% confidence interval (CI), [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40]. 3 However, it remains unclear whether any increased risk of dementia associated with CABG is a consequence of the procedure, CAD itself, the progression of underlying disease, or a combination of these factors.…”

Myocardial Ischemia-Reperfusion Injury: The Perioperative Application and Cardiac Protective Potential of Ginsenoside Preparations

“…It is generally known that inflammation response also plays a fundamental role in the progression of MI/R injury (34,35). Following reperfusion, a large amount of inflammatory cells (including polymorphonuclear neutrophils and monocytes/ macrophages) aggregate and cause the release of inflammatory mediators (including cytokines, chemokines, adhesion molecules, and other inflammatory molecules) in the infarcted myocardium (36)(37)(38).…”