A cardioprotective preservation strategy employing ex vivo heart perfusion facilitates successful transplant of donor hearts after cardiocirculatory death

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• 作者：Christopher W. White ; Ayyaz Ali ; Devin Hasanally ; Bo Xiang ; Yun Li ; Paul Mundt ; Matthew Lytwyn ; Simon Colah ; Julianne Klein ; Amir Rav ; i ; Rakesh C. Arora ; Trevor W. Lee ; Larry Hryshko ; Stephen Large ; Ganghong Tian ; Darren H. Freed
• 关键词：Ex vivo heart perfusion ; heart transplantation ; donation after cardiocirculatory death ; DCD ; ischemia-reperfusion injury ; adenosine-lidocaine cardioplegia
• 刊名：The Journal of Heart and Lung Transplantation
• 出版年：2013
• 出版时间：July, 2013
• 年：2013
• 卷：32
• 期：7
• 页码：734-743
• 全文大小：3462 K

文摘

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Background

Ex vivo heart perfusion (EVHP) has been proposed as a means to facilitate the resuscitation of donor hearts after cardiocirculatory death (DCD) and increase the donor pool. However, the current approach to clinical EVHP may exacerbate myocardial injury and impair function after transplant. Therefore, we sought to determine if a cardioprotective EVHP strategy that eliminates myocardial exposure to hypothermic hyperkalemia cardioplegia and minimizes cold ischemia could facilitate successful DCD heart transplantation.

Methods

Anesthetized pigs sustained a hypoxic cardiac arrest and a 15-minute warm ischemic standoff period. Strategy 1 hearts (S1, n = 9) underwent initial reperfusion with a cold hyperkalemic cardioplegia, normothermic EVHP, and transplantation after a cold hyperkalemic cardioplegic arrest (current EVHP strategy). Strategy 2 hearts (S2, n = 8) underwent initial reperfusion with a tepid adenosine-lidocaine cardioplegia, normothermic EVHP, and transplantation with continuous myocardial perfusion (cardioprotective EVHP strategy).

Results

At completion of EVHP, S2 hearts exhibited less weight gain (9.7 ¡À 6.7 [S2] vs 21.2 ¡À 6.7 [S1] g/hour, p = 0.008) and less troponin-I release into the coronary sinus effluent (4.2 ¡À 1.3 [S2] vs 6.3 ¡À 1.5 [S1] ng/ml; p = 0.014). Mass spectrometry analysis of oxidized phosphatidylcholines in post-transplant myocardium revealed less oxidative stress in S2 hearts. At 30 minutes after wean from cardiopulmonary bypass, post-transplant systolic (pre-load recruitable stroke work: 33.5 ¡À 1.3 [S2] vs 19.7 ¡À 10.9 [S1], p = 0.043) and diastolic (isovolumic relaxation constant: 42.9 ¡À 6.7 [S2] vs 65.2 ¡À 21.1 [S1], p = 0.020) function were superior in S2 hearts.

Conclusion

In this experimental model of DCD, an EVHP strategy using initial reperfusion with a tepid adenosine-lidocaine cardioplegia and continuous myocardial perfusion minimizes myocardial injury and improves short-term post-transplant function compared with the current EVHP strategy using cold hyperkalemic cardioplegia before organ procurement and transplantation.