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2012 annual meeting & cardiothoracic forum - Society for ...

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JOINT ANNUAL MEETING <strong>2012</strong> ABSTRACTS<br />

020 The Right Ventricle Per<strong>for</strong>ms as Well as the Left Ventricle in the<br />

DCD Donor Heart<br />

Authors: Fouad Taghavi 1 C.E. Woods 1 S.R. Large 2 E. Ashley 1 A. Ali 2<br />

1 Stan<strong>for</strong>d University, USA; 2 Papworth Hospital NHS Foundation Trust, United<br />

Kingdom<br />

Objectives: Heart transplantation from DCD donors is not undertaken due to<br />

concerns over ischemic injury. We have demonstrated in animal models that the<br />

DCD heart can be resuscitated and transplanted, however initial right ventricular<br />

(RV) pressure-volume (PV) loops were morphologically abnormal. Myocardial failure<br />

is an important problem after heart transplantation, RV failure is most common,<br />

although its mechanisms remain poorly understood. RV and left ventricle (LV) have<br />

different embryonic origins. To investigate further we compared function of both<br />

RV&LV in control and DCD hearts. To study organ function we used pressure-volume<br />

(PV) loops. To study function at a molecular level we analyzed intracellular calcium<br />

handling and contraction.<br />

Methods: Male Sprague-Dawley rats were subjected to DCD heart resuscitation<br />

using ECMO 15 minutes after circulatory arrest. RV&LV PV loop measurements were<br />

made. Myocytes were isolated separately and loaded with calcium indicator Fluo-5f.<br />

Sarcomere length (SL) was measured during contraction to assess contractility.<br />

Intracellular calcium (deltaF/F) was measured epifluorescently. Sham operated<br />

animals were used as control.<br />

Results: RV function decline mirrored LV function decline from control to DCD with<br />

no statistical differences seen between RV&LV when looking at: end systolic<br />

pressure volume relationship, preload recruitable stroke work and contractility index<br />

(n>7 animals in each group). At a molecular level RV function mirrored LV function<br />

in control and DCD when looking at: myocyte %SL change, speed of contraction and<br />

deltaF/F (n>60 in each group).<br />

Conclusions: Our initial concerns over abnormal RV PV loop morphology in DCD<br />

hearts have been put to rest. The RV does not per<strong>for</strong>m worse than the LV after DCD<br />

heart resuscitation. Even though the RV & LV have different embryonic origins,<br />

measuring LV alone in this model is sufficient in accessing the DCD heart. Our<br />

ef<strong>for</strong>ts must now focus on optimising the DCD heart <strong>for</strong> potential transplantation.<br />

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