Disappearance of glycoprotein Ib from the platelet surface in pericardial blood during cardiopulmonary bypass.

OBJECTIVES: Several investigators have reported decreased expression of glycoprotein Ib on the platelet surface during coronary artery bypass grafting, but others could not confirm this finding. Because platelet glycoprotein Ib functions as an adhesion receptor for von Willebrand factor and other adhesive proteins, this decreased expression may explain excessive postoperative blood loss. In this study the expressions of glycoprotein Ib and other platelet activation markers were studied in the systemic and pericardial blood of seven patients undergoing coronary artery bypass grafting. Pericardial blood was recently shown to have high activation levels of fibrinolytic and coagulation pathways; we hypothesized that this local blood activation might be paralleled by extensive platelet activation and associated disappearance of glycoprotein Ib. METHODS: Expression of platelet surface antigens was determined by whole-blood double-label flow cytometry. RESULTS: Glycoprotein Ib expression in systemic blood decreased 10% (p = 0.03) from preoperative levels at the start of cardiopulmonary bypass and 30% (p = 0.04) before release of the aortic crossclamp. Expression in pericardial blood at these times decreased by 50% and 51%, respectively (p = 0.003, p = 0.009). No changes were observed in the expression of the platelet activation antigens CD62P (P-selectin, indicating platelet alpha-granular release) and CD63 (indicating lysosomal release) or in binding of monoclonal antibody PAC-1 (detecting the fibrinogen-binding receptor conformation of the glycoprotein IIb-IIIa complex). CONCLUSION: Glycoprotein Ib disappeared from the platelet surface during bypass grafting, most notably in pericardial blood. No increased expression of CD62P, CD63, or PAC-1 was found, indicating the absence of general platelet activation.

Cell-derived microparticles generated in patients during cardiopulmonary bypass are highly procoagulant.

BACKGROUND: Microparticles from platelets and other cells have been extensively studied and characterized in vitro. Although the level of platelet-derived microparticles is elevated in a variety of diseases, including cardiac surgery, virtually nothing is known about their functions in vivo. The aim of the present study was to investigate the procoagulant properties of microparticles generated in vivo. METHODS AND RESULTS: In 6 patients at the end of cardiopulmonary bypass, 14.8 x 10(9)/L (median; range, 9.7 to 27.4 x 10(9)/L) platelet-derived microparticles were present in pericardial blood, whereas blood obtained from the systemic circulation contained 1.6 x 10(9)/L (median; range, 0.4 to 8.9 x 10(9)/L) of such microparticles, as determined by flow cytometry. Microparticles stained positively for phosphatidylserine as determined with labeled annexin V. In contrast to systemic blood, pericardial blood contained not only microparticles of platelet origin but also microparticles that originated from erythrocytes, monocytes, or granulocytes, and other hitherto unknown cellular sources. Plasma prepared from pericardial blood and to a lesser extent plasma from systemic blood obtained at the same time, stimulated formation of thrombin in vitro. This activity of pericardial plasma was lost after removal of its microparticles by high-speed centrifugation, whereas the corresponding microparticle pellet was strongly procoagulant. The generation of thrombin in vitro involved a tissue factor/factor VII-dependent and factor XII-independent pathway. CONCLUSIONS: This study is the first to demonstrate that microparticles generated in vivo can stimulate coagulation.

An ambiguous case of chordal rupture. erroneous diagnosis of echocardiography. case report.

A patient is described, in whom a sessile endocardial mass was diagnosed by echocardiography after a history of progressive dyspnoea. The tumor appeared to be attached to the mitral valve suspension apparatus and it was seen to be fluttering in the outflow tract of the left ventricle. During surgery, mucoid degenerated and ruptured chordae were resected. The actual size of the chordae was very small in relation to the tumor seen by echocardiography. The possible etiology and the echocardiographic pitfalls are discussed.

Systolic and diastolic pressure-volume relationships during cardiac surgery.

Seven patients undergoing elective coronary artery bypass surgery were studied to assess left ventricular (LV) performance by pressure-volume loops. LV pressure was measured by micromanometry and instantaneous LV volume by a conductance catheter. Continuous pressure-volume relationships were determined during preload reduction before and after cardiopulmonary bypass (CPB). End-systolic elastance (Ees), as the slope of the end-systolic pressure-volume relationship (ESPVR), and diastolic elastance (Ed) were calculated from these interventions. Changes in position of the Ees were assessed at V75, the value of LV end-systolic volume at 75 mm Hg of LV pressure. From pre-CPB to post-CPB, Ees increased in three patients with a decrease of V75 in two patients, and Ees decreased in four patients with a concomitant increase in V75. Ed increased significantly (P less than 0.01) following CPB, demonstrating a decrease of ventricular distensibility. It is concluded that continuous measurement of LV pressure-volume relationships using the conductance catheter is feasible and may be a useful tool to estimate LV performance during cardiac surgery.