Neonatal pulmonary vein banding in piglets recapitulates critical aspects of clinical PVS and highlights a pathologic profile consistent with EndMT, supporting the rationale for evaluating therapeutic strategies designed to exploit reversibility of upstream pulmonary vein pathology.

Losartan treatment improved PVS-associated pulmonary hypertension and intimal hyperplasia and might be a beneficial prophylactic therapy for patients at high risk of developing PVS after pulmonary vein surgery.

The number of patients with the failing Fontan physiology is increasing. We tested a novel in situ microaxial pump (Impella) to support the failing atrio-pulmonary Fontan circulation in an acute pig model. A Fontan model was established in eight juvenile pigs by connecting the right atrium to the main pulmonary artery after tricuspid valve destruction. The Impella pump was inserted retrograde from the distal main pulmonary artery into the right atrium. Hemodynamics, blood gas, and echocardiographic data were compared among baseline, pure Fontan physiology (10 minutes), and mechanically assisted Fontan physiology (up to 12 hours). The Impella system generated a blood flow of 75-85 ml/kg/minute in six animals, and 55-65 ml/kg/minute in two animals. The mechanically assisted Fontan attained a significantly higher mean blood pressure (39.6 ± 7 vs. 24.7 ± 3.3 mm Hg, p < 0.01), lower central venous pressure (5 ± 2.4 vs. 12.8 ± 1.7 mm Hg, p < 0.01), and higher mixed venous saturation (60.4 ± 10.8 vs. 23.4 ± 8.4 mm Hg, p < 0.01) compared with pure Fontan physiology. Cardiac output and stroke volume were similar during baseline and mechanically assisted Fontan (p = not significant). This acute pig study demonstrated the feasibility of mechanical circulatory support in the failing Fontan physiology. The in situ microaxial pump maintained cardiac output while increasing blood pressure and reducing venous pressure.

Apoptosis-related mitochondrial dysfunction in postcardioplegic neonatal hearts is mediated by mitochondrial permeability transition pore opening, which is transient and associated with deficits in electron transport. Clinical strategies directed to minimize mitochondrial permeability transition pore opening are likely to improve postoperative myocardial dysfunction after neonatal cardiac surgery.

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