No abstract

Pulmonary arterial thrombosis among adults with Eisenmenger syndrome is common and relates to older age, biventricular dysfunction, and slow pulmonary artery blood flow rather than degree of cyanosis or coagulation abnormalities. Further work to define treatment efficacy is needed.

Iron deficiency is common in cyanotic adults but does not alter viscosity. Hyperviscosity symptoms are associated with a higher Hct-adjusted viscosity independent of cell size or iron stores. Higher Hct is associated with better exercise capacity. Further work to understand the origin of hyperviscosity symptoms is warranted.

No abstract

SummaryThere is growing evidence that the tissue factor/factor VIIa pathway of coagulation is enhanced during cardiopulmonary bypass. Hitherto, available evidence has suggested that upregulated monocyte bound tissue factor is made available, either in the blood collected from the site of surgery or on circulating cells. However, cellular upregulation is slow, while generation of factor VIIa in blood collected from the pericardial cavity is rapid. We have therefore investigated the possibility of an alternative source of tissue factor, plasma (as opposed to cellular) tissue factor in blood samples taken from the central vein catheter (systemic circulation) and collected from the pericardial cavity during cardiopulmonary bypass. Six patients undergoing first time cardiopulmonary bypass grafting were studied. Tissue factor antigen was found to be rapidly elevated (by 15 min) in the pericardial plasma, ∼5-fold above systemic levels (p <0.004). Similar elevations were found in markers of coagulation activation, factor VIIa antigen (p = 0.066), prothrombin fragment F1+2 (p <0.003) and thrombin-antithrombin complex (p <0.03). To explore whether plasma tissue factor was (or had been) functionally active, factor VIIa was measured also with the soluble tissue factor functional assay after removal of heparin. Functional factor VIIa activity fell significantly in the systemic circulation, probably due to the heparin-induced increase (∼15-fold) in tissue factor pathway inhibitor (TFPI), but was elevated in pericardial blood compared with that taken from the central line catheter (p <0.006). These results demonstrate that both components of the activation complex for the extrinsic pathway of coagulation are rapidly generated in pericardial blood during bypass.

Abstract-Several recent studies have proposed that coagulation is triggered during cardiopulmonary bypass surgery by extrinsic pathway activation involving factor VIIa generation, but the methodology was indirect. Therefore, 12 patients were studied during routine cardiac and cardiopulmonary bypass surgery. Samples were taken before, during, and after bypass from the perfusate, from the aorta (retrograde cardiac drainage), pericardium, and collected suction fluid originating from the whole operative field. These samples were analyzed by enzyme-linked immunosorbent assay for 2-chain factor VIIa, by prothrombin F 1ϩ2 assay, by thrombin-antithrombin (TAT) assay, and for heparin concentration. Factor VIIa, F 1ϩ2 , and TAT levels in samples from the pericardium were greatly elevated (mean, 0.92 to 1.01, 227 to 334, and 399 to 526 g/L, respectively; preoperative mean, 0.33, 32.3, and 1.90 g/L, respectively; PϽ0.05 for all), whereas levels in suction fluid were less consistently high. Factor VIIa and both F 1ϩ2 and thrombin-antithrombin levels in samples from the aorta, pericardium, and suction fluid were significantly correlated (rϭ0. 57, PϽ0.001, nϭ111; and rϭ0.51, PϽ0.001, nϭ105, respectively), and all were inversely correlated with heparin levels (rϾϪ0.35, PϽ0.001, nϾ92). There was no evidence of factor VIIa generation in the circuit during bypass surgery, and both F 1ϩ2 and thrombin-antithrombin levels rose only Ϸ2-fold, probably because heparin levels were higher than they were in the pericardium (PϽ0.05). We concluded that appreciable activation of factor VII occurs on the pericardium and that this is associated with increased thrombin generation. Ineffective local heparinization may be partly responsible. These results suggest that pericardium-induced activation of factor VII should be the target of anticoagulant strategies during cardiopulmonary bypass surgery. (Arterioscler Thromb Vasc Biol. 1999;19:248-254.)

We evaluated the effectiveness, ease of use and safety of five machines for blood salvage during coronary artery surgery. All were equally effective in concentrating red cells. We measured haemoglobin, packed cell volume, free haemoglobin, white cells, neutrophil elastase, platelets, thrombin-antithrombin complex (TAT), prothrombin activation peptide F1.2, fibrin degradation product (d-dimers), tissue plasminogen activator (tPA) and heparin in wound blood, in washed cell suspensions and in a unit of bank blood prepared for each patient. All machines were equally safe and easy to use and were equally effective in removing heparin and the physiological components measured. There were no adverse effects on patients. Clotting factors are severely depleted both in salvaged blood, even before washing, and in bank blood. Cell savers are a valuable adjunct to coronary artery surgery, but careful monitoring of coagulation is required when the volumes of either bank blood or salvaged blood are large.

In patients with cyanosis from congenital heart disease, erythropoiesis is governed by many factors that can alter the expected relation between the oxygen saturation (O(2sat)) and hemoglobin concentration. We sought to define the relation between the O(2sat) and hemoglobin in such patients and to predict an ideal hemoglobin concentration for a given O(2sat). Adults with congenital heart defects and cyanosis were studied prospectively using blood tests and exercise testing. Nonoptimal hemoglobin was defined as any evidence of inadequate erythropoiesis (i.e., iron, folate, or vitamin B(12) deficiency, increased erythropoietin, reticulocytosis, or a right-shifted oxygen-hemoglobin curve). For patients without these factors, a linear regression equation of hemoglobin versus O(2sat) was used to predict the optimal hemoglobin for all patients. Of the 65 patients studied, 21 met all the prestudy criteria for an optimal hemoglobin. For all patients, no correlation was found between O(2sat) and hemoglobin (r = -0.22). However, a strong linear correlation was found for those meeting the criteria for optimal hemoglobin (r = -0.865, p <0.001). The optimal hemoglobin regression equation was as follows: predicted hemoglobin = 57.5 - (0.444 × O(2sat)). A negative correlation was found between the hemoglobin difference (predicted minus measured) and exercise duration on cardiopulmonary exercise testing (r = -0.396, p = 0.005) and the 6-minute walk distance (r = -0.468, p <0.001). In conclusion, a strong relation between O(2sat) and hemoglobin concentration can be shown in stable cyanotic patients and used to predict an optimal hemoglobin. This relation might be useful in defining functional anemia in this group.