There is an impression among cardiothoracic surgeons that the technique of profound hypothermic circulatory arrest (PHCA) is associated with an increased bleeding tendency compared to conventional bypass surgery. In addition to the recognized factors contributing to the hemorrhagic tendency seen in moderate hypothermic cardiopulmonary bypass (CPB), it is likely that the lower temperature utilized in PHCA may exacerbate platelet dysfunction. In this report, platelet counts and functions at the same cardiopulmonary bypass time were compared in human PHCA surgery (hypothermia group, n=16) and moderate hypothermic cardiopulmonary bypass surgery (control group, n=20). Mean platelet count corrected by hematocrit in the hypothermia group at 2h of CPB was significantly lower than in the control group (3.7×10⁴μl vs. 11.4×10⁴/μl, p<0.0001). In the hypothermia group, there were significant increases in the percentage of GMP-140 (P-selectin)-positive platelets (11.8% vs. 8.3%, p=0.0091) at 1h of CPB, and also in microparticles (24.8% vs. 10.5%, p<0.0001) and aggregated platelets (3.4% vs. 1.4%, p=0.0058) at 2h of CPB. Profound hypothermic circulatory arrest used in surgery for aortic arch aneurysm or dissection may cause irreversible platelet dysfunction and contribute to hemorrhagic tendency during the surgery. To minimize platelet dysfunction during CPB, the lowest blood temperature should be maintained above 15°C.

Seven patients with congenital heart defects suffered from multiple major hemorrhages from the lung after surgery and 5 of them died at 8 to 54 postoperative days because of respiratory insufficiency. In a patient with tetralogy of Fallot associated with pulmonary atresia, bleeding occured after the second shunt operation, presumably from rupture of bronchial collateral vessels. The clinical diagnoses of the other 6 patients were coarctation of the aorta (CoA) with common atrioventricular canal (CAVC) in 1, triple shunt in 1, persistent truncus arteriosus in 2, total anomalous pulmonary venous connection in 1 and CAVC in 1. Subclavian flap aortoplasty was performed without pulmonary artery banding in the patient with CoA and CAVC, whereas complete repair was performed in the other 5 patients. As these patients were associated with severe pulmonary hypertension preoperatively and 4 of them encountered pulmonary hypertensive crisis, the hemorrhage from the lung may be related to pre and postoperative high pressure of the pulmonary artery. Dilatation and rupture of the pulmonary capillary net was demonstrated in the patient with CoA and CAVC. These findings suggest the hypothesis that bleeding occurred due to rupture of the capillary net as a result of transmission of high pressure. Major bleeding from the lung is a rare but catastrophic complication after repair of congenital heart defects. As the treatment is difficult, early surgical intervention and treatment of postoperative pulmonary hypertension are important in complex lesions with severe pulmonary hypertension.

The incidence of ventricular subepicardial aneurysm following myocardial infarction is quite low. We report a case of subepicardial aneurysm that was diagnosed on postoperative pathohistologic examination. A 69-year-old man was admitted to our hospital because of left ventricular aneurysm following myocardial infarction. The patient had left main trunk disease, triple-vessel coronary artery desease and low output syndrome. Under cardiopulmonary bypass with the heart arrested, the aneurysm was resected and the defect was closed. The suture line was reinforced using Teflon felt and GRF glue. A saphenous vein graft was anastmosed to the left anterior descending artery. On pathohistologic examination, the wall of the aneurysm was found to be composed of fibrotic tissue, myocardial fibers, medium-sized pericardial arteries, epicardium and fibrin thrombi. We diagnosed this as subepicardial aneurysm.