Modulation of systemic inflammatory response after cardiac surgery.

Cardiac surgery and cardiopulmonary bypass initiate a systemic inflammatory response largely determined by blood contact with foreign surfaces and the activation of complement. It is generally accepted that cardiopulmonary bypass initiates a whole-body inflammatory reaction. The magnitude of this inflammatory reaction varies, but the persistence of any degree of inflammation may be considered potentially harmful to the cardiac patient. The development of strategies to control the inflammatory response following cardiac surgery is currently the focus of considerable research efforts. Diverse techniques including maintenance of hemodynamic stability, minimization of exposure to cardiopulmonary bypass circuitry, and pharmacologic and immunomodulatory agents have been examined in clinical studies. This article briefly reviews the current concepts of the systemic inflammatory response following cardiac surgery, and the various therapeutic strategies being used to modulate this response.

Surgery for functional tricuspid regurgitation: current techniques, outcomes and emerging concepts.

Functional tricuspid regurgitation is the most frequent cause of tricuspid insufficiency and is often secondary to left-sided valve diseases. The correction of left-sided valve diseases without concomitant repair of functional tricuspid regurgitation is associated with significant late morbidity and mortality. This occurs on account of progressive right ventricular dysfunction and increasing need for reoperation. Recent years have seen a surge in surgery for functional tricuspid regurgitation. Several techniques are available to correct functional tricuspid regurgitation. These include the stitch annuloplasty, such as semicircular (classical De Vega repair) or simple lateral annuloplasty (Kay), novel techniques such as edge-to-edge or clover technique and suture bicuspidization technique, use of flexible and rigid prosthetic rings or 3D rings, flexible prosthetic bands, and use of artificial chordae with polytetrafluoroethylene sutures for anterior and septal ticuspid leaflet pathology. Whereas the short-term outcomes of these techniques are satisfactory, the majority are limited in the mid- and long term by unacceptably high rates of residual and/or recurrent regurgitation. A better understanding of the mechanisms of functional tricuspid regurgitation will help explain the failure of current techniques and be a help to modify existing surgical techniques or develop new techniques.