Effect of Prolonged Hypothermic Cardiopulmonary Bypass, Heparin, and Protamine on Platelet: A Small-Group Study

AbstractCardiopulmonary bypass (CPB) is associated with platelet dysfunction (PD), an important cause of postoperative bleeding. The etiology of PD is not completely understood. We mapped the platelets' function during CPB to determine the etiology of PD. Platelets activation, measured by procaspase activating compound-1 and P-selectin expression (CD62P), after activation by adenosine diphosphate and thrombin receptor activator peptide, were decreased by protamine. Changes during CPB were insignificant. Platelet-leukocyte aggregation was increased by CPB but not by protamine. Platelet apoptosis marker, annexin V, was increased by protamine. Changes during CPB were insignificant. Our findings demonstrate that protamine given after CPB plays a central role in PD and count decrease.

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Clot Impedence As An Indicator Of Platelet Dysfunction Following Cardiopulmonary Bypass

10.1055/s-0038-1652394 ◽

1981 ◽

Author(s):

A Saleem ◽

D H Yawn ◽

S A Saleh ◽

E S Crawford

Keyword(s):

Cardiopulmonary Bypass ◽

Blood Sample ◽

Platelet Function ◽

Postoperative Bleeding ◽

Coagulation Factors ◽

Initial Slope ◽

Platelet Dysfunction ◽

Number Of Patients ◽

Precision Evaluation ◽

Surgical Bleeding

Post-operative bleeding following cardiopulmonary bypass remains a serious problem. Recent studies have indicated platelet dysfunction may be responsible for altered hemostasis in a significant number of patients. Although evaluation of coagulation factors can usually be done with speed and precision, evaluation of platelet function is time-consuming. We have evaluated a clot impedence device (Sonoclot®, Sieneo Inc., Colorado) to measure platelet function. The device measures and records the clot impedence to a vibrating probe as the blood sample clots and retracts. In our evaluation of healthy subjects, we found the initial slope of the impedence curve and the entire retraction phase are influenced by the number of platelets. Extrapolating this information to the patients undergoing cardiovascular bypass, we found 7 out of 11 patients with postoperative bleeding had poor retraction phase in spite of an adequate platelet count. This suggested platelet dysfunction. All seven patients achieved satisfactory hemostasis after platelet transfusion. This was correlated with a normal clot impedence study. Four patients with normal clot impedence were found to have surgical bleeding. The test is easy to perform and the result is available within fifteen minutes of drawing the blood sample. In our hands, the measurement of clot impedence appears to be a reliable adjunct in the etiological diagnosis of post-operative bleeding.

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Whole blood platelet aggregation kinetics under cardiopulmonary bypass: A pilot study

The International Journal of Artificial Organs ◽

10.1177/0391398819882440 ◽

2019 ◽

Vol 43 (3) ◽

pp. 208-214

Author(s):

Tobias Petzold ◽

Erik Bagaev ◽

Helen Herzog ◽

Frank Born ◽

Dominik Hoechter ◽

...

Keyword(s):

Cardiopulmonary Bypass ◽

Platelet Aggregation ◽

Life Support ◽

Platelet Reactivity ◽

Extracorporeal Life Support ◽

Adenosine Diphosphate ◽

Thrombin Receptor ◽

Electrode Impedance ◽

Platelet Counts ◽

Impedance Aggregometry

Assessing the platelets’ functional status during surgery on cardiopulmonary bypass is challenging. This study used multiple electrode impedance aggregometry (Multiplate®) to create a timeline of platelet aggregation changes as induced by cardiopulmonary bypass in antiplatelet-naive patients undergoing elective surgery for mitral valve regurgitation. We performed six consecutive measurements (T1: pre-operatively, T2: after heparinization, T3: 3 min after establishment of cardiopulmonary bypass, T4: immediately after administration of cardioplegia, T5: 5 min after administration of cardioplegia, and T6: 45 min after administration of cardioplegia). Platelet aggregation was determined after stimulation with 3.2-μg/mL collagen, 6.4-μM adenosine diphosphate, and 32-μM thrombin receptor activating peptide. Five patients were included (age: 64 ± 10 years, one female). We observed a decrease in hematocrit levels by −17.1% ± 3.7% (T1 vs T6) with a drop after establishment of cardiopulmonary bypass (T2 vs T3) and slightly decreasing platelet counts by −6.2% ± 7.7% (T1 vs T6). Immediately after establishment of cardiopulmonary bypass (T2 vs T3), we observed reduced platelet aggregation responses for stimulation with adenosine diphosphate (−19.7% ± 12.8%) and thrombin receptor activating peptide (−19.3% ± 6.3%). Interestingly, we found augmented platelet aggregation for all stimuli 45 min after administration of cardioplegia (T5 vs T6) with the strongest increase for collagen (+83.4% ± 42.8%; adenosine diphosphate: +39.0% ± 37.2%; thrombin receptor activating peptide: +34.5% ± 18.5%). Thus, after an initial drop due to hemodilution upon establishment of cardiopulmonary bypass, platelet reactivity increased over time which was not outweighed by decreasing platelet counts due to mechanical platelet destruction and absorption. These findings have implications for rational transfusion, peri-operative antiplatelet therapy, and for the management of patients on other extracorporeal support, such as extracorporeal life support or extracorporeal membrane oxygenation.

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Nitroglycerin and Sodium Nitroprusside: Potential Contributors to Postoperative Bleeding?

The Heart Surgery Forum ◽

10.1532/hsf98.20111109 ◽

2012 ◽

Vol 15 (2) ◽

pp. 92 ◽

Cited By ~ 4

Author(s):

Donald Clark ◽

Stephanie Tesseneer ◽

Curtis G. Tribble

Keyword(s):

Cardiac Surgery ◽

Cardiopulmonary Bypass ◽

Sodium Nitroprusside ◽

Platelet Activation ◽

Postoperative Bleeding ◽

Antihypertensive Agents ◽

Platelet Inhibition ◽

Clinical Consequence ◽

Platelet Dysfunction ◽

Knowing That

Postoperative bleeding is common in patients undergoing cardiac surgery with cardiopulmonary bypass. Most cases of severe postoperative bleeding not due to incomplete surgical hemostasis are related to acquired transient platelet dysfunction mediated by platelet activation during contact with the synthetic surfaces of the cardiopulmonary bypass equipment. Antihypertensive agents nitroglycerin and sodium nitroprusside have been shown to have platelet inhibitory properties, yet the clinical consequence in terms of postoperative bleeding has been little studied. Knowing that cardiopulmonary bypass causes platelet dysfunction, it is prudent for physicians to be aware of the additional platelet inhibition caused by these commonly used antihypertensive agents.

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A Comparison of Defective Platelet Count and Aggregation between the Valve Replacement and Cyanotic Congenital Heart Cases during Cardiopulmonary Bypass

Perfusion ◽

10.1177/026765918700200202 ◽

1987 ◽

Vol 2 (2) ◽

pp. 87-95

Author(s):

Yan-Ji Gu ◽

Yi-Shan Wang ◽

Chun-Xiu Ye

Keyword(s):

Platelet Count ◽

Cardiopulmonary Bypass ◽

Platelet Aggregation ◽

Valve Replacement ◽

Congenital Heart ◽

Postoperative Bleeding ◽

Significant Negative Correlation ◽

Platelet Dysfunction ◽

Group A ◽

The Mean

Platelet count and ADP-induced platelet aggregation were studied in 10 single valve replacement (VR) patients and 10 cyanotic congenital heart disease (CCHD) patients undergoing cardiopulmonary bypass (CPB). The mean platelet count dropped to 78% in VR group and 73% in CCHD group at 30 minutes CPB as compared with the prebypass levels (being corrected for haemodilution). The mean prebypass platelet aggregation value was 65·5% ± 7·5% (Mean ± SEM) in VR group and 56·5% ± 5·2% in CCHD group; the values dropped to 54·2% ± 4·5% and 28·2% ± 4·8% respectively in VR and CCHD groups ( P < 0·01) at 30 minutes CPB. Both groups had a slight further drop at the end of the CPB, but only CCHD group had a further drop in platelet aggregation function after protamine administration. Mean plasma haemoglobin was much higher in the CCHD group than that in VR group at the termination of the bypass ( P < 0·05). Increased blood transfusion volumes were needed and greater blood losses noticed in the CCHD group. A significant negative correlation ( r = 0·5044. P < 0·05) was found between platelet function measured at the termination of CPB and postoperative bleeding. Cardiopulmonary bypass in patients with CCHD appears to be associated with greater platelet dysfunction and this results in more serious haemostatic defects after CPB. It is necessary to have further studies of the defective haemorrhagic status in these patients. More advanced perfusion techniques should be applied to preserve platelets during cardiopulmonary bypass.

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Effect of Cardiopulmonary Bypass Machine on the Platelet Function Testing.

10.21203/rs.3.rs-45350/v1 ◽

2020 ◽

Author(s):

Khalid A. AlSaleh ◽

Rashed B. AlBakr ◽

Turki B. AlBacker ◽

Rakan AlNazer ◽

Abdulkareem Almomen ◽

...

Keyword(s):

Cardiac Surgery ◽

Cardiopulmonary Bypass ◽

Platelet Function ◽

Clinical Decision Making ◽

Complete Blood Count ◽

Artery Bypass ◽

Postoperative Bleeding ◽

Inverse Correlation ◽

Platelet Dysfunction ◽

Significant Difference

Abstract Background: Bleeding during coronary artery bypass surgery is a leading cause of mortality. Several factors have been associated with bleeding, platelet dysfunction being the most significant.Objective: to assess the effect of cardiopulmonary bypass machine (CPB) during cardiac surgery on platelet function using Platelet Function Analyzers (PFA-100), and Multiplate Electrode Aggregometry (MEA), and correlating that with a drop in Hemoglobin (Hb).Methods: Whole blood samples were collected preoperative and sixty minutes intraoperatively of different cardiac procedures utilizing (CPB) and tested for platelet function by PFA-100 and MEA. Complete blood count was measured using an automated hematology analyzer.Results: A significant difference was found between pre- and intraoperative ADP and EPI measurement in PFA-100, where preoperative PFA-ADP values displayed the ability to predict the intra-op drop in Hb (P–value 0.01, correlation coefficient 0.4699). At the same time, pre-op MEA- Ristocetin and TRAP showed an inverse correlation with an intra-op drop in Hb (-0.31 and -0.36). Conclusion: The current study reported significant changes in platelet dysfunction in cardiac surgeries with CPB, measured by two modalities PFA-100, and MEA. While PFA-100 and MEA both detected the changes in platelet dysfunction due to CPB, PFA-100 results were sensitive and positively predicted intra-op Hb drop as compared to MEA. There was a significant change in Hb one hour into the CPB, indicating that platelet transfusion might help decrease Intra- and postoperative bleeding independent of the platelet count as they are dysfunctional. PFA-100 results can be relied upon for distinction of high-risk cardiac surgery patients for bleeding and can be used for clinical decision making to improve patient outcome.

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Platelets from children are hyper-responsive to activation by thrombin receptor activator peptide and adenosine diphosphate compared to platelets from adults

British Journal of Haematology ◽

10.1111/bjh.13153 ◽

2014 ◽

Vol 168 (4) ◽

pp. 526-532 ◽

Cited By ~ 15

Author(s):

Christina Yip ◽

Matthew D. Linden ◽

Chantal Attard ◽

Paul Monagle ◽

Vera Ignjatovic

Keyword(s):

Adenosine Diphosphate ◽

Thrombin Receptor ◽

Receptor Activator

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Aprotinin: is it prothrombotic?

Perfusion ◽

10.1177/026765910101600510 ◽

2001 ◽

Vol 16 (5) ◽

pp. 401-409 ◽

Cited By ~ 3

Author(s):

M Poullis ◽

R C Landis ◽

K M Taylor

Keyword(s):

Platelet Aggregation ◽

Platelet Activation ◽

Mechanism Of Action ◽

Adenosine Diphosphate ◽

Platelet Membrane ◽

Calcium Flux ◽

Thrombin Receptor ◽

Proteolytic Activation ◽

Agonist Peptide ◽

Receptor Family

Controversy continues as to whether aprotinin (Trasylol) is prothrombotic. The recent discovery of the thrombin receptor family, known as the protease-activated receptor family (PAR) has been essential in aiding our understanding of the mechanism of action of aprotinin. Our results show that aprotinin has no effect on platelet aggregation induced by adrenaline, adenosine diphosphate, phorbol-12-myristate-13-acetate, collagen or PAR 1 agonist peptide. However, aprotinin inhibits thrombin-induced platelet activation as assessed by macroaggregation, microaggregation and platelet membrane calcium flux. Aprotinin inhibits proteolytic activation of platelets, but platelets can still be activated by non-proteolytic mechanisms.

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