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J Thorac Cardiovasc Surg 2002;123:742-755
© 2002 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology (CSP)

Limitation of thrombin generation, platelet activation, and inflammation by elimination of cardiotomy suction in patients undergoing coronary artery bypass grafting treated with heparin-bonded circuits

From the Division of Cardiothoracic Surgery, Department of Surgery, University of Washington School of Medicine, Seattle, Wash.

Received for publication May 5, 2001. Revisions requested July 9, 2001; revisions received Aug 27, 2001. Accepted for publication Sept 16, 2001. Address for reprints: Gabriel S. Aldea, MD, Associate Professor, Division of Cardiothoracic Surgery, Department of Surgery, University of Washington, PO Box 356310, 1959 NE Pacific St, Seattle, WA 98195-3166 (E-mail: aldea{at}u.washington.edu).

Objective: Reports evaluating the efficacy of heparin-bonded circuits to blunt inflammation, platelet dysfunction, and thrombin generation in response to cardiopulmonary bypass have varied. We hypothesized that this variability may in part be related to the use of cardiotomy suction, which has been demonstrated to reintroduce procoagulant and proinflammatory factors into the systemic circulation during cardiopulmonary bypass. A prospective, randomized study was undertaken to evaluate the specific effects of cardiotomy suction.
Methods: Thirty-six patients undergoing first-time, nonemergency coronary artery bypass grafting with cardiopulmonary bypass were randomly assigned to one of three treatment groups: group I, non-heparin-bonded circuits with the use of cardiotomy suction (n = 12); group II, Duraflo II (BCR-3500; Jostra Bentley Corp, Irvine, Calif) heparin-bonded circuits with cardiotomy suction (n = 12); and group III, Duraflo II heparin-bonded circuits without cardiotomy suction (n = 12). Thrombin generation, neutrophil activation (polymorphonuclear elastase), platelet activation (ß-thromboglobulin), and neuronal injury (neuron-specific enolase) were analyzed by enzyme-linked immunosorbent assays after cardiopulmonary bypass and compared with prebypass levels. Results are presented as mean ± SEM.
Results: Prebypass levels of all markers were similar among treatment groups. However, postbypass levels were significantly and consistently highest in group I relative to groups II and III. Thrombin generation levels were 5.0 ± 0.9 nmol/L in group I, 3.0 ± 0.6 nmol/L in group II, and 1.5 ± 0.1 nmol/L in group III (P < .05 vs group II and P < .001 vs group I). Polymorphonuclear elastase levels were 307 ± 64 µg/L in group I, 128 ± 24 µg/L in group II (P < .05 vs group I), and 75 ± 14 µg/L in group III (P < .001 vs group I). ß-Thromboglobulin levels were 2692 ± 401 IU/mL in group I, 912 ± 99 IU/mL in group II (P = .001 vs group I), and 646 ± 133 IU/mL in group III (P = .001 vs group I). Neuron-specific enolase levels were 9.8 ± 0.9 ng/mL in group I, 10.5 ± 1.6 ng/mL in group II, and 4.2 ± 0.5 ng/mL in group III (P = .001 vs groups I and II).
Conclusions: Use of cardiotomy suction resulted in significant increases in thrombin, neutrophil, and platelet activation, as well as the release of neuron-specific enolase, after cardiopulmonary bypass. Limiting increases in these markers would be best accomplished by eliminating cardiotomy suction and routinely using heparin-bonded circuits whenever possible.

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