Abstract 18989: Determination of Optimal Coronary Flow for the Preservation of “Donation After Circulatory Death” Heart
Introduction: Transplantation of hearts from donation after circulatory death donors (DCD) have the potential to increase the number of transplants. However, DCD hearts undergo an extended period of warm ischemia and necessitate use of ex-vivo machine perfusion preservation after recovery. The minimum flow needed to meet basal oxygen demand (DCRIT) and the necessary machine perfusion conditions to achieve this are unknown for perfused DCD hearts.
Aim: To determine the DCRIT of DCD hearts during midthermic perfusion preservation.
Methods: Sprague Dawley adult male rats were anesthetized, intubated, heparinized (500 U/rat) and paralyzed with vecuronium (2 mg/rat). The DCD protocol was observed by withdrawal of ventilatory support. After circulatory death, 30 min of “stand-off” time was observed. DBD rats were continuously ventilated. Hearts (DBD n=8, DCD n=4) were perfused on Langendorff mode, with an oxygenated preservation solution at 15oC starting at a flow index of 300 mL/min*100g, decreasing it by 40 ml*100g/min every 10 min. Inflow (aortic- Ao) and outflow (inferior vena cava- IVC) perfusate samples were collected serially to assess the myocardial oxygen consumption index (MVO2), O2 extraction ratio ([PO2Ao-PO2IVC]/PO2Ao*100), troponin I (TnI) and lactate production.
Results: The basal MVO2 and oxygen extraction ratio were higher in DCD hearts compared to DBD hearts, indicating higher metabolic demands or a debt repayment (Table). DCD hearts had higher perfusion pressures. The DCRIT for DCD hearts was 132±2 ml*100g /min, significantly higher than that for DBD hearts, indicating a need for a higher flow to maintain basal MVO2. Lactate and TnI in the IVC effluent were increased in the DCD group indicating signs of warm ischemic damage.
Conclusions: DCD hearts sustain warm ischemic damage and manifest higher metabolic needs compared to DBD hearts. At 15oC, DCD hearts need to be perfused at a higher flow than the DBD hearts to sustain a flow independent MVO2.
Author Disclosures: S. Toldo: None. J.F. Torrado Arrosa: None. A.G. Mauro: None. E. Mezzaroma: None. H. Reichstetter: None. A. Abbate: None. V. Kasirajan: None. M.J. Mangino: None. M. Quader: None.
- © 2016 by American Heart Association, Inc.