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

Maquelin, Kyra N.; Berckmansb, René J.; Nieuwland, Rienk; Schaapb, Marianne C.L.; Have, Klaas ten; Eijsman, L.; Sturk, Augueste

doi:10.1016/s0022-5223(98)70416-7

Cited by 21 publications

(23 citation statements)

References 25 publications

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“…The contribution of platelet defects, and specifically that of attenuation of GP1b expression [25], to whole blood hemostasis has been a long-standing consideration in on-pump CPB surgery, where TEG analysis on whole blood is employed to predict post-surgical bleeding [26], [27], and off-pump coronary artery bypass surgery led to lower platelet activation defects than on-pump surgery [28].…”

Section: Resultsmentioning

confidence: 99%

Abnormal Whole Blood Thrombi in Humans with Inherited Platelet Receptor Defects

et al. 2012

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To delineate the critical features of platelets required for formation and stability of thrombi, thromboelastography and platelet aggregation measurements were employed on whole blood of normal patients and of those with Bernard-Soulier Syndrome (BSS) and Glanzmann’s Thrombasthenia (GT). We found that separation of platelet activation, as assessed by platelet aggregation, from that needed to form viscoelastic stable whole blood thrombi, occurred. In normal human blood, ristocetin and collagen aggregated platelets, but did not induce strong viscoelastic thrombi. However, ADP, arachidonic acid, thrombin, and protease-activated-receptor-1 and -4 agonists, stimulated both processes. During this study, we identified the genetic basis of a very rare double heterozygous GP1b deficiency in a BSS patient, along with a new homozygous GP1b inactivating mutation in another BSS patient. In BSS whole blood, ADP responsiveness, as measured by thrombus strength, was diminished, while ADP-induced platelet aggregation was normal. Further, the platelets of 3 additional GT patients showed very weak whole blood platelet aggregation toward the above agonists and provided whole blood thrombi of very low viscoelastic strength. These results indicate that measurements of platelet counts and platelet aggregability do not necessarily correlate with generation of stable thrombi, a potentially significant feature in patient clinical outcomes.

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Section: Resultsmentioning

confidence: 99%

Abnormal Whole Blood Thrombi in Humans with Inherited Platelet Receptor Defects

et al. 2012

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“…These MP originate from various cell types and initiate coagulation via a tissue factor and factor VII(a)-dependent mechanism in vitro [2,15,24] and thrombus formation in vivo [25]. One could have expected that retransfusion of pericardial blood, i.e.…”

Section: Discussionmentioning

confidence: 99%

“…Inclusion criteria were elective coronary artery bypass surgery, body surface area > 1.66 m 2 and preoperative hemoglobin levels > 7.5 mmol/l. Exclusion criteria were combined valve surgery or aneurysmectomy, redo operations, insulin-dependent diabetes mellitus, renal or hepatic dysfunction, preoperative coagulopathics, preoperative intra-aortic balloon pumping and protocol violation (complications).…”

Section: Patientsmentioning

confidence: 99%

“…Initially, this activation was predominantly attributed to contact of blood with the body foreign surface of the extracorporeal bypass circuit of the heart lung machine [1]. More recently, smaller extracorporeal circuits and improved surface coatings have been developed with improved biocompatibility [2][3][4]. Despite these improvements, however, blood is still activated during the CPB.…”

Section: Introductionmentioning

confidence: 99%

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Retransfusion of pericardial blood does not trigger systemic coagulation during cardiopulmonary bypass

Goor

Nieuwland

Rutten

et al. 2007

European Journal of Cardio-Thoracic Surgery

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Objective: During cardiopulmonary bypass (CPB), systemic coagulation is believed to become activated by blood contact with the extracorporeal circuit and by retransfusion of pericardial blood. To which extent retransfusion activates systemic coagulation, however, is unknown. We investigated to which extent retransfusion of pericardial blood triggers systemic coagulation during CPB. Methods: Thirteen patients undergoing elective coronary artery bypass grafting surgery were included. Pericardial blood was retransfused into nine patients and retained in four patients. Systemic samples were collected before, during and after CPB, and pericardial samples before retransfusion. Levels of prothrombin fragment F 1+2 (ELISA), microparticles (flow cytometry) and non-cell bound (soluble) tissue factor (sTF; ELISA) were determined. Results: Compared to systemic blood, pericardial blood contained elevated levels of F 1+2 , microparticles and sTF. During CPB, systemic levels of F 1+2 increased from 0.28 (0.25-0.37; median, interquartile range) to 1.10 (0.49-1.55) nmol/l ( p = 0.001). This observed increase was similar to the estimated (calculated) increase ( p = 0.424), and differed significantly between retransfused and non-retransfused patients (1.12 nmol/l vs 0.02 nmol/l, p = 0.001). Also, the observed systemic increases of platelet-and erythrocyte-derived microparticles and sTF were in line with predicted increases ( p = 0.868, p = 0.778 and p = 0.205, respectively). Before neutralization of heparin, microparticles and other coagulant phospholipids decreased from 464 mg/ml (287-701) to 163 mg/ml (121-389) in retransfused patients ( p = 0.001), indicating rapid clearance after retransfusion. Conclusion: Retransfusion of pericardial blood does not activate systemic coagulation under heparinization. The observed increases in systemic levels of F 1+2 , microparticles and sTF during CPB are explained by dilution of retransfused pericardial blood. #

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“…During the last 20 years, significant improvements have been made in anaesthesia, surgery and biocompatibility of the extracorporeal circuits, resulting in reduced activation of blood, decreased blood loss, diminished inflammation and a faster post-operative recovery of patients. [1][2][3][4] Based on these improvements, one might expect a reduction in the incidence and severity of cognitive dysfunction after bypass surgery.…”

Section: Introductionmentioning

confidence: 99%

Improvement of cognitive test performance in patients undergoing primary CABG and other CPB-assisted cardiac procedures

Goor

Saxby²,

et al. 2008

Perfusion

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Cardiac surgical procedures assisted by cardiopulmonary bypass (CPB) impair cognitive functions. Several studies, however, showed that cognitive functions were unaffected in patients undergoing either primary coronary artery bypass grafting (CABG) or more complex surgery assisted by CPB. Therefore, we conducted a straightforward study to compare patient groups who differed significantly in terms of risk factors such as prolonged CPB times. Consecutive patients (n = 54) were included, undergoing either non-primary CABG, e.g. valve and/or CABG, (n = 30) or primary CABG (n = 24), assisted by CPB. Cognitive function was determined pre-operatively on the day of hospital admission, and post-operatively after one and six months using the Cognitive Drug Research computerized assessment battery. Data from the fourteen individual task variables were summarized in four composite scores: Power of Attention (PoA), Continuity of Attention (CoA), Quality of Episodic Memory (QoEM), and Speed of Memory (SoM). In the non-primary CABG patients, both CoA and QoEM improved after 1 month (p = 0.001 and p = 0.016, respectively), whereas, after 6 months, CoA (p = 0.002), QoEM (p = 0.002) and SoM (p < 0.001) were improved. In primary CABG patients, CoA improved at one month after surgery (p = 0.002) and, after six months, not only CoA (p = 0.003), but also QoEM and SoM were improved (p = 0.001 and p = 0.030, respectively). The test performance was similar in non-primary and primary CABG patients after surgery. Our present study shows a post-operative improvement of cognitive composite scores after cardiac surgery assisted by CPB in both non-primary CABG and in primary CABG patients.

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

Abstract: 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.

Cited by 21 publications

References 25 publications

Abnormal Whole Blood Thrombi in Humans with Inherited Platelet Receptor Defects

Abnormal Whole Blood Thrombi in Humans with Inherited Platelet Receptor Defects

Retransfusion of pericardial blood does not trigger systemic coagulation during cardiopulmonary bypass

Improvement of cognitive test performance in patients undergoing primary CABG and other CPB-assisted cardiac procedures

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