Cardiac surgery elicits pericardial inflammatory responses that are distinct compared with postcardiopulmonary bypass systemic inflammation.

Objectives: Cardiac surgery using cardiopulmonary bypass contributes to a robust systemic inflammatory process. Local intrapericardial postsurgical inflammation is believed to trigger important clinical implications, such as postoperative atrial fibrillation and postsurgical intrathoracic adhesions. Immune mediators in the pericardial space may underlie such complications. Methods: In this prospective pilot clinical study, 12 patients undergoing isolated coronary artery bypass graft surgery were enrolled. Native pericardial fluid and venous blood samples (baseline) were collected immediately after pericardiotomy. Postoperative pericardial fluid and venous blood samples were collected 48-hours after cardiopulmonary bypass and compared with baseline. Flow cytometry determined proportions of specific immune cells, whereas multiplex analysis probed for inflammatory mediators. Results: Neutrophils are the predominant cells in both the pericardial space and peripheral blood postoperatively. There are significantly more CD163lo macrophages in blood compared with pericardial effluent after surgery. Although there are significantly more CD163hi macrophages in native pericardial fluid compared with baseline blood, after surgery there are significantly fewer of these cells present in the pericardial space compared with blood. Postoperatively, concentration of interleukin receptor antagonist 6, and interleukin 8 were significantly higher in the pericardial space compared with blood. After surgery, compared with blood, the pericardial space has a significantly higher concentration of matrix metalloproteinase 3, matrix metalloproteinase 8, and matrix metalloproteinase 9. The same trend was observed with transformational growth factor ß. Conclusions: Cardiac surgery elicits an inflammatory response in the pericardial space, which differs from systemic inflammatory responses. Future work should determine whether or not this distinct local inflammatory response contributes to postsurgical complications and could be modified to influence clinical outcomes.

Right Mini-Thoracotomy Beating-Heart Mitral Valve Replacement With a SAPIEN 3 Valve for Severe Circumferential Mitral Annular Calcification.

Mitral annular calcification (MAC) is a degenerative process that can cause mitral valve stenosis. Conventional surgical mitral valve replacement (MVR) for MAC with mitral stenosis can be challenging and associated with significant risk. Open surgical MVR with a transcatheter valve can offer an alternative in select situations. When such a strategy is not feasible, a beating-heart, mini-thoracotomy MVR with a SAPIEN 3 transcatheter heart valve can be considered. The novel teaching point of this case is use of an alternative approach for managing severe mitral stenosis secondary to MAC, when conventional surgical and transcatheter strategies are not safe or possible.

La calcification de l'anneau mitral (CAM) est un processus dégénératif qui peut causer la sténose mitrale. Le remplacement valvulaire mitral (RVM) par intervention chirurgicale traditionnelle lors de CAM associée à la sténose mitrale peut être complexe et est associé à un risque important. Le RVM à cœur ouvert par cathéter peut être une solution dans certaines situations. Lorsque cette stratégie n'est pas faisable, le RVM à cœur battant par mini-thoracotomie à l'aide d'une valve cardiaque SAPIEN 3 par cathéter peut être envisagé. Le nouveau point à retenir de ce cas est l'utilisation d'une autre approche pour prendre en charge la sténose mitrale grave secondaire à la CAM, lorsque les stratégies d'intervention chirurgicale traditionnelle et de cathétérisme ne sont pas sûres ou possibles.

Comprehensive characterization of the postoperative pericardial inflammatory response: Potential implications for clinical outcomes.

Objective: There is a paucity of data on the inflammatory response that takes place in the pericardial space after cardiac surgery. This study provides a comprehensive assessment of the local postoperative inflammatory response. Methods: Forty-three patients underwent cardiotomy, where native pericardial fluid was aspirated and compared with postoperative pericardial effluent collected at 4, 24, and 48 hours' postcardiopulmonary bypass. Flow cytometry was used to define the levels and proportions of specific immune cells. Samples were also probed for concentrations of inflammatory cytokines, matrix metalloproteinases (MMPs), and tissue inhibitors of metalloproteinases (TIMPs). Results: Preoperatively, the pericardial space mainly contains macrophages and T cells. However, the postsurgical pericardial space was populated predominately by neutrophils, which constituted almost 80% of immune cells present, and peaked at 24 hours. When surgical approaches were compared, minimally invasive surgery was associated with fewer neutrophils in the pericardial space at 4 hours' postsurgery. Analysis of the intrapericardial concentrations of inflammatory mediators showed interleukin-6, MMP-9, and TIMP-1 to be highest postsurgery. Over time, MMP-9 concentrations decreased significantly, whereas TIMP-1 levels increased, resulting in a significant reduction of the ratio of MMP:TIMP after surgery, suggesting that active inflammatory processes may influence extracellular matrix remodeling. Conclusions: These results show that cardiac surgery elicits profound alterations in the immune cell profile in the pericardial space. Defining the cellular and molecular mediators that drive pericardial-specific postoperative inflammatory processes may allow for targeted therapies to reduce immune-mediated complications.