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Eur J Cardiothorac Surg 2003;23:898-906
© 2003 Elsevier Science NL

The initial rate of troponin I release post-reperfusion reflects the effectiveness of myocardial protection during cardiac allograft preservation

Heart and Lung Transplant Unit, St. Vincent's Hospital and the Victor Chang Cardiac Research Institute, Sydney, Australia

Received 19 December 2002; received in revised form 10 February 2003; accepted 17 February 2003.

^* Corresponding author. P.O. Box 194, Milsons Point, NSW 2061, Australia. Tel.: +61-4-1222-5138; fax: +61-2-9922-5991
e-mail: j.ryan{at}garvan.unsw.edu.au

Objective: To determine if the initial rate of troponin I release post-reperfusion reflects the effectiveness of myocardial protection during cardiac allograft preservation. Methods: A porcine model of orthotopic heart transplantation was used. Data from two control groups (CON₄ and CON₁₄) and two treatment groups (CAR₄ and CAR₁₄) were analysed. Hearts in CON₄ (n=6) and CAR₄ (n=6) were subjected to 4 h of ischaemia while hearts in CON₁₄ (n=3) and CAR₁₄ (n=6) were subjected to 14 h of ischaemia. All hearts were arrested and stored in the same extracellular preservation solution. Both donor and recipient animals in the CAR₄ and CAR₁₄ groups received a single intravenous dose of cariporide (2 mg/kg), prior to explantation and reperfusion, respectively. Results: Mean (SEM) plasma troponin I levels (µg/ml) 3 h post-reperfusion were: CON₄ 210±52, CAR₄ 68±21, CON₁₄ 633±177, CAR₁₄ 346±93. On multiple linear regression analysis, the rate of troponin I release over the first 3 h post-reperfusion was significantly lower in hearts stored for 4 h compared to hearts stored for 14 h (P<0.0001) and in hearts treated with cariporide compared to control hearts (P=0.0017). Early graft function was superior in hearts treated with cariporide, when compared to control hearts stored for the same period of time. All of the CAR₁₄ hearts could be weaned from cardiopulmonary bypass whereas none of the CON₁₄ could be weaned (6/6 vs. 0/3; P=0.012). While all hearts stored for 4 h could be weaned, contractility, as measured by the preload recruitable stroke work (PRSW) relationship, was significantly better preserved in CAR₄ hearts than in CON₄ hearts (P<0.0001). Conclusions: The initial rate of troponin I release post-reperfusion is determined by the duration of cardiac allograft ischaemia. Altering the myocardial preservation strategy can reduce the rate of release. Such reductions are associated with improvements in early graft function. These findings validate the initial rate of troponin I release post-reperfusion as an end-point when comparing cardiac allograft preservation strategies. In addition, the present study provides indirect evidence that troponin I degradation during ischaemia-reperfusion is related to the accumulation of intracellular calcium.

Key Words: Troponin I • Heart transplantation • Myocardial ischemia • Myocardial reperfusion injury • Myocardial stunning • Sodium–hydrogen antiporter