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Purpose To our knowledge, there have been no reports focusing on differences of clinical characteristics according to two gross anatomic types of cardiac myxomas. This study evaluated the differences of clinical features, coronary arteriographic findings, and histopathologic findings. Patients and methods Twenty-six patients who underwent surgical excisions for left atrial myxomas were analyzed. According to the gross anatomic types, they were divided into two groups: group 1 having solid and ovoid myxomas (n = 14), and group 2 having soft and papillary myxomas (n = 12). Differences of presenting symptoms, prevalence of brain infarction, coronary angiographic findings, and histopathologic findings were analyzed. Results An incidence of dyspnea was significantly higher in group 1 (78.6% vs 33.3%, p Conclusions Coronary angiographic findings of tumor-feeding arteries without clusters of tortuous tumor vessels predict a myxoma that is papillary in type. At that time, close attention should be given for the possible existence of silent brain infarction.

Several studies on the effects of cardiopulmonary bypass (CPB) on the reticuloendothelial system (RES) function have been performed previously, but different results have been reported. This study was carried out to determine the effect of CPB on RES function in a canine model simulating clinical CPB. Nine dogs undergoing surgery with CPB were compared with an identical number of dogs subjected to thoracotomy without CPB. A lipid emulsion test was performed in all dogs before and after the surgical procedure to measure RES phagocytic index, i.e., phagocytic function. Kupffer cell iron uptake under conditions of iron loading following CPB was examined histologically, and any ultrastructural changes in the Kupffer cells were observed by electron microscopy. In both groups, the RES phagocytic index showed a significant decline after surgery. However, a comparison of the two groups revealed that there was a significantly greater decrease in the CPB group (P < 0.05). Moreover, histologic evidence of iron uptake in Kupffer cells was strongly suppressed in the CPB group. Electron microscopy of the Kupffer cells showed that the number of phagosomes, especially deformed erythrocytes, increased after CPB. These findings suggest that RES function is significantly impaired following CPB, and an increase in the amount of material, especially deformed erythrocytes, to be processed by the RES is responsible, in part, for the depressed RES phagocytic function. The prevention of hemolysis during CPB may preserve the RES function following CPB.

Fibrinolytic activity is reportedly increased during cardiopulmonary bypass( CPB ), and this increase has been considered to be related to the bleeding complications in open heart surgery. The purpose of this study was to clarify the nature of the fibrinolytic activity duringCPB. Twenty patients with valve replacement or aortocoronary bypass surgery were examined. The following parameters were determined: fibrinogen, plasminogen, fibrinopeptide A( FPA ), fibrinopeptide B β 15-42 ( FPB β15-42 ), and tissue-type plasminogen activator ( t-PA ). For further characterization of the fibrinolytic activity, the fibrin plate method was used. Intrinsic fibrinolytic activity was determined by the assay of the fibrinolytic activity of the kaolin activatedeuglobulin. Extrinsic fibrinolyticactivity was estimated by the assayof Cl-inactivator resistant fibrinolytic activity as well as t-PA. Fibrinogen and plasminogen did not decrease except at the beginning of CPB. FPA was increased significantly during CPB. FPB3 15-42 was also increased to four times the preoperative value at 2 hrs of CPB. The intrinsic fibrinolytic system was activatedonly a short time after the startof CPB. The Cl-inactivator resistant fibrinolytic activity was activated gradually during CPB, reached a maximum level 1 hr after the start of CPB, and returned to the preoperative level within 1 hr after the end of CPB. The changes on t-PA paralleled the course of the Cl-inactivator resistant fibrinolytic activity, indicating that enhanced fibrinolytic activity during CPB is predominantly of extrinsic origin caused by t-PA. We conclude that thrombin activity continues during CPB despite the use of heparin, and thatthe enhanced fibrinolytic activity during CPB is essential because t-PA activates plasminogen predominantly at the sites where fibrin is formed, resulting in the dissolution of the microthrombi formed during CPB.