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.

OBJECTIVE The Cox-Maze IV procedure (CMPIV) has been established as the gold standard for surgical ablation, however late outcomes using current consensus definitions of treatment failure have not been well described. In order to compare to reported outcomes of catheter-based ablation, we report our institutional outcomes of patients who underwent a left-sided or biatrial CMPIV at five years of follow up. METHODS Between January 2002 and September 2014, data were collected prospectively on 576 patients with AF who underwent a CMPIV(n= 532) or left-sided CMPIV(n= 44). Perioperative variables and long-term freedom from AF on and off AADs were compared in multiple subgroups. RESULTS Follow up at any time point was 89%. At five years, overall freedom from AF was 78% (93/119) and freedom from AF off AADs was 66% (77/177). There were no differences in freedom from AF on or off AADs at 1, 2, 3, 4, and 5 years between patients with paroxysmal AF(n=204) and patients with persistent/long-standing persistent AF(n=305), or between those who underwent stand-alone and those who received a concomitant CMP. Duration of preoperative AF and hospital length of stay were the best predictors of failure at 5 years. CONCLUSIONS The outcomes of the CMPIV remain good at late follow up. The type of preoperative AF or the addition of a concomitant procedure did not affect late success. The results of the CMPIV remain superior to those reported for catheter ablation and other forms of surgical AF ablation, especially for patients with persistent or long-standing AF.

The effects of estrogen deficiency on the loss of cardioprotection with advancing age are complex and poorly understood. A major focus of the current study was to uncover a cardioprotective role for rapid, nongenomic estrogen receptor (ER) signaling in the aged female myocardium. We hypothesized that selective ERalpha activation in aged females would reduce infarct size in part, through reversal of age-associated reductions in mitochondrial protein kinase Cepsilon (PKCepsilon). Hearts isolated from adult (6 month old) and aged (23-24 months old) female F344 rats with ovaries removed (n = 20 per group) were subjected to ischemia/reperfusion (47 min global ischemia). Rats were injected sc with the ERalpha agonist propylpyrazole triol (PPT) or vehicle 45 min before heart isolation (5 microg/kg). Infarct size was greatest in aged vs. adult ovariectomized rats, significantly reduced by PPT, and the protection reversed by prior administration of the ER inhibitor ICI 182,780 (3 mg/kg). Increased ERalpha particulate targeting occurred after PPT in conjunction with reversal of age-related reductions in nuclear PKCepsilon, mitochondrial PKCepsilon and pAkt (P < 0.05). PPT also increased mRNA levels for the PKCepsilon anchoring protein, receptor for activated C kinase2 (RACK2; P < 0.05). Our data suggest, for the first time, that selective ERalpha activation reduces ischemic injury in the aged, estrogen-deficient heart through a mechanism involving nongenomic redistribution of ERalpha and PKCepsilon activation. A novel feed-forward transcriptional mechanism to potentially enhance PKCepsilon-RACK2 interactions was also observed. Collectively, our findings may provide key insight into developing targeted therapeutic interventions in postmenopausal women to reduce ischemia/reperfusion injury, including selective ERalpha mimetics.