Strategies of myocardial protection for operation in chronic model of cyanotic heart disease

Background. Cyanotic congenital hearts have an increased susceptibility to ischemia and subsequent reperfusion. The role of platelet-activating factor antagonism and mechanical neutrophil depletion with leukocyte-depleting fi lters for control of ischemia-reperfusion injury was assessed in corrective surgical procedures for cyanotic heart disease. Methods. A swine model of cyanotic heart disease was evaluated with three s tudy groups: a control group; a group given a platelet-activating factor an tagonist (PAFA group); and a group with leukocyte-depleting filtration (LDF group). The cyanotic model was created with a left atrial appendage-pulmon ary artery fistula with peripheral banding through a left anterior thoracot omy in weanling swine. The experimental procedure was performed 5 to 7 week s later when body weight was greater than 20 kg and oxygen saturation was 8 5% or less. The corrective procedure was performed through a median sternot omy on cardiopulmonary bypass with repair of the shunt. Myocardial protecti on was accomplished with hypothermic blood-crystalloid (4:1) cardioplegia; the period of ischemic arrest was 90 minutes. In the PAFA group, the platel et-activating factor antagonist CV-6209 was delivered intravenously 15 to 2 0 minutes before aortic crossclamping. In the LDF group, Pall leukocyte-dep leting filters were used in the CPB arterial line. Hemodynamic data were ta ken before operation and 10 and 30 minutes after CPB with impedance ventric ulography. Results. There were four deaths in the control group within 30 minutes afte r CPB; all animals in the treated groups survived longer than 60 minutes (p < 0.05). The ventricular assessment of end-systolic elastance revealed sup erior performance in the LDF group 30 minutes after CPB compared with the c ontrol group (p < 0.05) (controls, 4.0 +/- 9; PAFA group, 6.5 +/- 3.7; and LDF group, 12.0 +/- 4.6). Conclusions. Both leukocyte-depleting filters and platelet-activating facto r antagonism provided myocardial protection, and the filters afforded super ior postoperative myocardial contractility. (C) 1998 by The Society of Thor acic Surgeons.