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Eur J Cardiothorac Surg 2006;30:263-270
© 2006 Elsevier Science NL

Prevention of TNF-associated myocardial dysfunction resulting from cardiopulmonary bypass and cardioplegic arrest by glucocorticoid treatment

^a Department of Thoracic and Cardiovascular Surgery, University of Göttingen, Germany
^b Department of Anatomy, Division Electron Microscopy, University of Göttingen, Germany
^c Department of Pathology, University of Göttingen, Germany
^d Institute for Pathophysiology, University of Essen Medical School, Germany

Received 28 November 2005; received in revised form 17 March 2006; accepted 11 April 2006.

^_* Corresponding author. Address: Klinik für Thorax-, Herz- und Gefäßchirurgie, Georg-August-Universität Göttingen, Robert-Koch-Strasse 40; 37099 Göttingen, Germany. Tel.: +49 551 39 6001; fax: +49 551 39 6002. (Email: oliver{at}liakopoulos.de).

Objective: Cardiac surgery on cardiopulmonary bypass (CPB) results in progressive myocardial dysfunction, despite unimpaired coronary blood flow, and is associated with increased myocardial tumor necrosis factor- (TNF) expression. We investigated whether anti-inflammatory treatment prevents increased TNF expression and myocardial dysfunction after CPB. Methods and results: Baseline systemic hemodynamics, myocardial contractile function, aortic and coronary blood flow were measured in anesthetized pigs. Then, placebo (PLA; saline; n = 7) or methylprednisolone (MP; 30 mg/kg; n = 6) was infused intravenously and CPB was instituted. Global ischemia was induced for 10 min by aortic cross-clamping, followed by 1 h of cardioplegic cardiac arrest. After declamping and reperfusion, CPB was terminated after a total of 3 h. Measurements were repeated at 15 min, 4 h, and 8 h following termination of CPB. Systemic TNF-plasma concentrations and left ventricular TNF expression were analyzed. With unchanged coronary blood flow in both groups, a progressive loss of myocardial contractile function to 38 ± 2% of baseline (p < 0.01) and cardiac index to 48 ± 6% of baseline (p < 0.01) at 8 h after CPB in PLA was attenuated in MP (myocardial function: 72 ± 3%, p < 0.01 vs PLA; cardiac index: 78 ± 6%, p < 0.05 vs PLA). Systemic TNF was increased at 8 h in PLA compared to MP (243 ± 34 vs 90 ± 34 pg/ml, p < 0.05). Myocardial TNF was increased at 8 h after CPB compared to baseline and MP (p < 0.05). Myocardial TNF immunostaining was more pronounced in PLA than in MP (p < 0.05), with TNF-mRNA localization predominantly to cardiomyocytes. Conclusions: Methylprednisolone attenuates both systemic and myocardial TNF increases and progressive myocardial dysfunction induced by cardiac surgery, suggesting a key role for TNF.

Key Words: Myocardial contractile dysfunction • Inflammation • Steroids • Extracorporal circulation

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