Normothermia Does Not Improve Postoperative Hemostasis Nor Does it Reduce Inflammatory Activation

Background:

Despite its common acceptance in clinical practice, the effective benefits of normothermic systemic perfusion during coronary artery bypass operations are far from established.

Methods:

A total of 113 patients undergoing primary isolated coronary artery bypass were randomly assigned to normothermic (37°C) or hypothermic (26°C) systemic perfusion. The clinical course of the patients was prospectively recorded, and several inflammatory and fibrinolytic markers (C-reactive protein, fibrinogen, interleukin 6, plasminogen activator inhibitor 1, prothrombin time, activated partial thromboplastin time, platelets, and white blood cell counts) were determined before surgical intervention; 24, 48, and 72 hours thereafter; and at hospital discharge.

Results:

Postoperatively, 2 in-hospital deaths occurred in the normothermic series and none in the hypothermic series. Four patients had a myocardial infarction, 1 had respiratory insufficiency, 1 had to be reoperated on for graft malfunction, and none had renal insufficiency in the hypothermic group versus 1 patient with each of these complications in the normothermic series. Mean blood loss in the first 24 hours was 766 ± 223 mL in the normothermic group and 740 ± 220 mL in the hypothermic group. None of these differences was statistically significant. Similarly, no significant difference in the postoperative level of any of the measured variables at any time point was evident between the patients in the normothermic and hypothermic groups.
 

Conclusion:

Normothermic systemic perfusion does not influence the clinical course or the extent of inflammatory and hemostatic activation in patients undergoing primary isolated coronary artery bypass.

Mario Gaudino, MD^a,
Roberto Zamparelli, MD^b,
Felicita Andreotti, MD^c,
Francesco Burzotta, MD^c,
Licia Iacoviello, MD^d,
Franco Glieca, MD^a,
Maria Benedetta Donati, ^d,
Attilio Maseri, MD^c,
Rocco Schiavello, MD^b,
Gianfederico Possati, MD^a

From the Departments of Cardiac Surgery,^a Cardiac Anaesthesiology,^b and Cardiology,^c Catholic University, Rome, and “Angela Valenti” Laboratory of Genetic and Enviromental Risk Factors for Thrombotic Disease,^d Department of Vascular Medicine and Pharmacology, Consorzio Mario Negri Sud, Santa Maria Imbaro, Italy.

Received for publication April 26, 2001. Revisions requested June 13, 2001; revisions received Sept 26, 2001. Accepted for publication Oct 3, 2001.

Address for reprints: Mario Gaudino, MD, Divisione di Cardiochirurgia, Policlinico Universitario A. Gemelli, Largo A. Gemelli 8, 00168 Rome, Italy (E-mail: [email protected]).