Effects of ε-Aminocaproic Acid and Aprotinin on Leukocyte–Platelet Adhesion in Patients Undergoing Cardiac Surgery

2004 ◽  
Vol 100 (2) ◽  
pp. 225-233 ◽  
Author(s):  
Philip E. Greilich ◽  
Chad F. Brouse ◽  
Christine S. Rinder ◽  
Brian R. Smith ◽  
Bernardo A. Sandoval ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Platelet Activation ◽  
Platelet Adhesion ◽  
Relative Effectiveness ◽  
Aminocaproic Acid ◽  
Saline Control ◽  
Plasmin Activity ◽  
Double Blind ◽  
Cd11b Expression ◽  
D Dimer

Background The administration of aprotinin during cardiopulmonary bypass (CPB) is hypothesized to decrease activation of leukocytes and platelets and possibly reduce their adhesion. Although epsilon-aminocaproic acid (EACA) shares the ability of aprotinin to inhibit excessive plasmin activity after CPB, its effect on leukocyte and platelet activation and leukocyte-platelet (heterotypic) adhesion is largely unknown. This study was performed to determine the relative effectiveness of the antifibrinolytics, aprotinin and EACA, at reducing leukocyte and platelet activation and leukocyte-platelet conjugate formation in patients undergoing CPB. Methods Thirty-six patients scheduled to undergo cardiac surgery with CPB were randomized in a double-blind fashion to receive EACA, aprotinin, or saline (placebo). Markers of plasmin activity (D-dimer concentrations), platelet activation (CD62P), leukocyte activation (CD11b), and leukocyte-platelet adhesion (monocyte- and neutrophil-platelet conjugates) were measured before, during, and after CPB. Results Platelet CD62P (P-selectin), monocyte CD11b, and monocyte-platelet conjugates were all significantly increased (compared with baseline) in the saline group during and after CPB. Despite equivalent reductions in D-dimer formation in patients receiving EACA (P < 0.0001) and aprotinin (P < 0.0001), decreases in platelet CD62P and monocyte CD11b expression were incomplete (not significantly different from saline control). In contrast, peak monocyte-platelet conjugate formation was significantly reduced by both EACA (P = 0.026) and aprotinin (P = 0.039) immediately after CPB. Conclusions EACA seems to be as effective as aprotinin at reducing peak monocyte-platelet adhesion after CPB. Furthermore, inhibition of excessive plasmin activity seems to influence monocyte-platelet adhesion. The findings suggest that monocyte-platelet conjugate formation may be a useful marker of monocyte and platelet activation in this clinical setting.

Hemostatic Parameters and Platelet Activation Marker Expression in Cyanotic and Acyanotic Pediatric Patients Undergoing Cardiac Surgery in the Presence of Tranexamic Acid

2000 ◽  
Vol 83 (01) ◽  
pp. 54-59 ◽  
Author(s):  
Elena Levin ◽  
John Wu ◽  
John Alexander ◽  
Clayton Reichart ◽  
Suvro Sett ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Blood Loss ◽  
Tranexamic Acid ◽  
Platelet Activation ◽  
Pediatric Patients ◽  
Factor Xiiia ◽  
Congenital Defects ◽  
Plasma Factor ◽  
Pai 1 ◽  
D Dimer

SummaryWe have investigated hemostatic parameters including platelet activation in 56 pediatric patients with or without cyanosis undergoing cardiopulmonary bypass (CPB) and cardiac surgery to repair congenital defects. Patients were participants in a study assessing the effects of tranexamic acid on surgery-related blood loss. Parameters monitored included blood loss, prothrombin F1.2, thrombin-antithrombin complexes, t-PA, PAI-1, plasminogen, fibrin D-dimer, and plasma factor XIII. Additionally, flow cytometry monitored platelet degranulation (P-selectin or CD63), as well as surface-bound fibrinogen, von Willebrand factor and factor XIIIa. Cyanotic patients had evidence of supranormal coagulation activation as both fibrin D-dimer and PAI-1 levels were elevated prior to surgery. While the extent of expression of Pselectin or CD63 was not informative, platelet-associated factor XIIIa was elevated in cyanotic patients at baseline. In both patient groups, CPB altered platelet activation state and coagulation status irrespective of the use of tranexamic acid.

The Effect of Desmopressin on Reducing Blood Loss in Cardiac Surgery – A Meta-Analysis of Double-Blind, Placebo-Controlled Trials

1995 ◽  
Vol 74 (04) ◽  
pp. 1064-1070 ◽  
Author(s):  
Marco Cattaneo ◽  
Alan S Harris ◽  
Ulf Strömberg ◽  
Pier Mannuccio Mannucci
Keyword(s):  
Cardiac Surgery ◽  
Blood Loss ◽  
Meta Analysis ◽  
Postoperative Blood Loss ◽  
Controlled Trials ◽  
Double Blind ◽  
Double Blind Placebo ◽  
Transfusion Requirements ◽  
The Mean ◽  
Excessive Blood Loss

SummaryThe effect of desmopressin (DDAVP) on reducing postoperative blood loss after cardiac surgery has been studied in several randomized clinical trials, with conflicting outcomes. Since most trials had insufficient statistical power to detect true differences in blood loss, we performed a meta-analysis of data from relevant studies. Seventeen randomized, double-blind, placebo-controlled trials were analyzed, which included 1171 patients undergoing cardiac surgery for various indications; 579 of them were treated with desmopressin and 592 with placebo. Efficacy parameters were blood loss volumes and transfusion requirements. Desmopressin significantly reduced postoperative blood loss by 9%, but had no statistically significant effect on transfusion requirements. A subanalysis revealed that desmopressin had no protective effects in trials in which the mean blood loss in placebo-treated patients fell in the lower and middle thirds of distribution of blood losses (687-1108 ml/24 h). In contrast, in trials in which the mean blood loss in placebo-treated patients fell in the upper third of distribution (>1109 ml/24 h), desmopressin significantly decreased postoperative blood loss by 34%. Insufficient data were available to perform a sub-analysis on transfusion requirements. Therefore, desmopressin significantly reduces blood loss only in cardiac operations which induce excessive blood loss. Further studies are called to validate the results of this meta-analysis and to identify predictors of excessive blood loss after cardiac surgery.

scholarly journals Is ε-Aminocaproic Acid as Effective as Aprotinin in Reducing Bleeding With Cardiac Surgery?

Circulation ◽  
1999 ◽  
Vol 99 (1) ◽  
pp. 81-89 ◽  
Author(s):  
John J. Munoz ◽  
Nancy J. O. Birkmeyer ◽  
John D. Birkmeyer ◽  
Gerald T. O’Connor ◽  
Lawrence J. Dacey
Keyword(s):  
Cardiac Surgery ◽  
Aminocaproic Acid

scholarly journals Monocyte Functional Responsiveness After PSGL-1–Mediated Platelet Adhesion Is Dependent on Platelet Activation Status

2008 ◽  
Vol 28 (8) ◽  
pp. 1491-1498 ◽  
Author(s):  
Stylianos Bournazos ◽  
Jillian Rennie ◽  
Simon P. Hart ◽  
Keith A.A. Fox ◽  
Ian Dransfield
Keyword(s):  
Platelet Activation ◽  
Platelet Adhesion ◽  
Functional Responsiveness ◽  
Activation Status

Abstract 803: Diesel Exhaust Inhalation Enhances Thrombus Formation In Man

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Andrew J Lucking ◽  
Magnus Lundback ◽  
Nicholas L Mills ◽  
Dana Faratian ◽  
Fleming Cassee ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Air Pollution ◽  
Platelet Activation ◽  
Diesel Exhaust ◽  
Intermittent Exercise ◽  
Ex Vivo ◽  
Thrombus Formation ◽  
Ex Vivo Model ◽  
Double Blind

Background: Transient exposure to traffic-derived air pollution may be a trigger for acute myocardial infarction although the mechanism is unclear. The aim of this study was to investigate the effect of diesel exhaust inhalation on thrombus formation in man using an ex vivo model of thrombosis. Methods and Results: In a double-blind randomized cross-over study, 20 healthy volunteers were exposed to diluted diesel exhaust (300 μg/m3) or filtered air during intermittent exercise for 1 or 2 hours. Thrombus formation, coagulation, platelet activation and inflammatory markers were measured at 2 and 6 hours after exposure. Thrombus formation was measured using the Badimon ex vivo perfusion chamber at low (212 /s) and high (1,690 /s) shear rates with porcine aortic tunica media as the thrombogenic substrate. Specimens were fixed, stained and thrombus area measured using computerized planimetry. Compared to filtered air, diesel exhaust increased thrombus formation in the low and high shear chambers by 24.2% (p<0.001) and 19.1% (p<0.001) respectively. This increased thrombogenicity was seen at two and six hours, and using two different types of diesel exposure. Although there were no effects on coagulation variables, diesel exhaust inhalation increased platelet-neutrophil (6.5% to 9.2%; P<0.05) and platelet-monocyte (21.0% to 25.0%; P<0.05) aggregates 2 hours following exposure. Conclusions: Inhalation of diesel exhaust increases ex vivo thrombus formation and causes platelet activation in man. These findings provide a potential mechanism that links exposure to traffic-derived air pollution with acute atherothrombotic events including acute myocardial infarction.

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