Cardiac surgery causes direct trauma to cardiac tissue, breaches the pericardium, and disrupts the normal composition of the fluid largely produced from the myocardial interstitium and epicardial and visceral pericardium. This leaves the heart exposed to pericardial fluid (PCF) and mediastinal contents comprising inflammatory cells and their products that now bathe the heart. This can potentially have adverse effects on the thin-walled atria leading to postoperative atrial fibrillation (AF).¹ After cardiac surgery, the pericardium remains open, and chest drains are routinely placed to prevent fluid accumulation around the heart. Here, we describe the concentration and trajectory of blood proinflammatory factors in the PCF after cardiac surgery over time. The study protocol was approved by the University of Alabama at Birmingham. Institutional Review Board approval and informed consent were obtained from all patients.

PCF (n=19) was collected immediately after pericardiotomy (time 0) and from the pericardial drains at times 4, 12, 24, and 48 hours after surgery. The patient population (mean age, 60±3 years) included 26.3% women and 26.3% blacks undergoing cardiac surgery (coronary artery bypass graft, n=14; coronary artery bypass graft+valve procedure, n=3; valve procedure alone, n=2). Patients with ventricular assist devices, AF surgery, thoracic aorta surgery, and AF within 6 months prior were excluded. All participants who had valve replacement (with or without coronary artery bypass graft) underwent on-pump surgeries. Of the patients undergoing coronary artery bypass graft only, 7 underwent on-pump and 7 underwent off-pump surgeries. Blood samples were collected in parallel with PCF.

ELISA analysis² revealed that neutrophil products (myeloperoxidase and neutrophil-gelatinase–associated lipocalin), neutrophil chemotactic factors (C-X-C motif chemokine ligand 6 and interleukin-8), and cardiac inflammatory factors (tumor necrosis factor-α and oncostatin M) were manyfold higher in PCF than in blood over the 4- to 48-hour time course after cardiac surgery (Figure A). Matrix metallopeptidase-9 (MMP-9), a major product of neutrophils, was significantly higher in blood than in PCF at time 0, but quickly rose in PCF to 2.6-, 2.3-, and 2.7-fold higher than in blood at 4, 12, and 24 hours, respectively. Mast cell chymase activity was increased at 4, 12, and 24 hours in comparison with time 0, whereas MMP-9 activity, which is activated by chymase, was significantly higher than time 0 throughout the 48 hours postsurgery