Postoperative atrial fibrillation (POAF) is a common, expensive and potentially morbid complication following cardiac surgery. POAF occurs in around 35% of cardiac surgery cases and has a peak incidence on postoperative day 2. Patients who develop POAF incur on average $10 000-$20 000 in additional hospital treatment costs, 12-24 h of prolonged ICU time, and an additional 2 to 5 days in the hospital. POAF has been identified as an independent predictor of numerous adverse outcomes, including a 2- to 4-fold increased risk of stroke, reoperation for bleeding, infection, renal or respiratory failure, cardiac arrest, cerebral complications, need for permanent pacemaker placement, and a 2-fold increase in all-cause 30-day and 6-month mortality. The pathogenesis of POAF is incompletely understood but likely involves interplay between pre-existing physiological components and local and systemic inflammation. POAF is associated with numerous risk factors including advanced age, pre-existing conditions that cause cardiac remodelling and certain non-cardiovascular conditions. Clinical management of POAF includes both prophylactic and therapeutic measures, although the efficacy of many interventions remains in question. This review provides a comprehensive and up-to-date summary of the pathogenesis of POAF, outlines current clinical guidelines for POAF prophylaxis and management, and discusses new avenues for further investigation.

The immune system, despite its complexity, is maintained at a relative steady state. Mechanisms involved in maintaining lymphocyte homeostasis are poorly understood; however, recent availability of transgenic (Tg) and knockout mouse models with altered balance of lymphocyte cell populations suggest that cytokines play a major role in maintaining lymphocyte homeostasis. We show here that transforming growth factor (TGF)-β plays a critical role in maintaining CD8+ T cell homeostasis in a Tg mouse model that specifically overexpresses a dominant negative TGF-β II receptor (DNRII) on T cells. DNRII T cell Tg mice develop a CD8+ T cell lymphoproliferative disorder resulting in the massive expansion of the lymphoid organs. These CD8+ T cells are phenotypically “naive” except for the upregulation of the cell surface molecule CD44, a molecule usually associated with memory T cells. Despite their dominance in the peripheral lymphoid organs, CD8+ T cells appear to develop normally in the thymus, suggesting that TGF-β exerts its homeostatic control in the peripheral immune system.

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