Hypotensive resuscitation is a safe strategy for use in the trauma population and results in a significant reduction in blood product transfusions and overall IV fluid administration. Specifically, resuscitating patients with the intent of maintaining a target minimum MAP of 50 mm Hg, rather than 65 mm Hg, significantly decreases postoperative coagulopathy and lowers the risk of early postoperative death and coagulopathy. These preliminary results provide convincing evidence that support the continued investigation and use of hypotensive resuscitation in the trauma setting.

After antireflux surgery, most patients with Barrett's enjoy long-lasting relief of reflux symptoms, and nearly all patients consider themselves cured or improved. Mild symptoms recur in one fifth. Importantly, dysplasia regressed in nearly half of the patients in whom it was present before surgery, intestinal metaplasia disappeared in 14% of patients, and high-grade dysplasia and adenocarcinoma were prevented in all.

Atrial fibrillation (AF) is a common arrhythmia and is associated with significant morbidity and mortality. The pathogenesis of AF remains incompletely understood and management remains a difficult task. Over the past decade there has been accumulating evidence implicating inflammation in the pathogenesis of AF. Inflammation appears to play a significant role in the initiation and perpetuation of AF as well as the prothrombotic state associated with AF. Inflammatory biomarkers (C-reactive protein and interleukin-6) have been shown to be associated with the future development, recurrence and burden of AF, and the likelihood of successful cardioversion. Therapies directed at attenuating the inflammatory burden appear promising. Animal and clinical studies have evaluated statins, angiotensin-converting enzyme inhibitors/angiotensin-II receptor blockers, and corticosteroids for the treatment or prevention of AF. The purpose of this review is to provide current evidence on the relationship between inflammation and AF and potential therapies available to modulate the inflammatory state in AF.

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