Models are useful, but they are still only the models …

Dr. Peer with colleagues [1] verifies the hypothesis that mechanical assistance of the pulmonary blood flow in a Norwood circulation can increase systemic blood flow and oxygen delivery. The verification of this hypothesis was not performed in vivo but using a circulatory lumped parameter model, which was developed to simulate a Norwood circulation with 3.5-mm Blalock–Taussig (BT) shunt in a neonate. Irrespective of the topic of the study, the idea to test the physiologic consequences of our surgical procedures using a computational model is not new but still a very attractive concept. The obvious advantage is the avoidance of the patients suffering in the case of a wrong idea, but the main disadvantage (and I think the main limitation of such studies) is underestimation of the biology complexity. Nevertheless, I admire the efforts of the authors to construct such a computational model as well as the new idea alone.

One of the 2 key findings of the study is that the mechanical support of the pulmonary blood flow increases the systemic cardiac output. The increase of the systemic blood flow almost equals the decrease of the BT-shunt flow. This means that the effect of better systemic perfusion is caused only by the reduction of the BT-shunt flow due to competitive flow from the pump (effect of the redistribution of the blood flow). The model does not assess the effect of the reduction of the preload and filling of the ventricle on the systemic cardiac output (relative hypovolaemia in the systemic circulation). The authors analyze 4 different amount of assisted pulmonary blood flow: 200, 400, 600 and 800 ml/min and in each case the systemic blood flow increases linearly. If we take 800 ml/min from the right atrium of a newborn heart (even if we assume that there is an additional inflow bladder with a volume of 25 ml as designed in the presented model) and pump to the pulmonary circulation, the question is, if there is still enough blood to fill the single ventricle? The model should predict when the filling of the ventricle (preload) would be a limiting factor for the systemic blood flow and even a cause for a reversal flow through the BT shunt.

The second important issue regarding the assisted pulmonary blood flow in a newborn could be the in vivo consequences of the huge (non-pulsatile) pulmonary blood flow and possible difficulties in weaning from the assisted pulmonary circulation. The common atrium is very effectively unloaded in the presented model (so the pulmonary venous congestion in the lungs is not possible) but a large flow in the pulmonary circulation can have detrimental effect on the lung parenchyma and pulmonary vascular resistance. This problem is very important from the perspective of the future Fontan pathway, as the main precondition for an effective Fontan circulation is a low/normal pulmonary vascular resistance.

Once again, I admire the work of the authors and I am looking forward to see the animal model study to test the idea and to develop this inspiring concept.

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