The Effect of Surface Roughness on Activation of the Coagulation System and Platelet Adhesion in Rotary Blood Pumps

Abstract

The surface roughness of left ventricular assist devices (LVADs) is important for the biocompatibility of blood pumps. However, little is known about the effect of surface roughness on the antithrombogenicity of the device. The present study investigated the effect of surface roughness on the activation of the coagulation system and platelet adhesion in an impeller-type blood pump. Three identical Baylor Gyro 710 centrifugal blood pumps (Baylor College of Medicine, Houston, TX, USA) were manufactured with impeller surface roughness of 0.05, 0.2, and 0.4 microm, respectively, as determined by a stylus profilometer and by scanning electron microscopy. Whole blood was anticoagulated (1-IU heparin/mL, ACT 250 s) and circulated for 60 min in an artificial circulatory system, simulating LVAD perfusion (5-L/min flow against 100 mm Hg). Enzyme-linked immunosorbent assays were developed to quantify fibrinogen- and von Willebrand factor (vWf) adsorption as well as platelet adhesion directly on the impellers of the pumps. Levels of prothrombin fragment F1.2 and thrombin-antithrombin (TAT) complex were measured in order to quantify activation of coagulation. Compared with the 0.05-microm surface, platelet adhesion was 40 and 76% higher on the 0.2- and 0.4-microm surface, respectively (P < 0.01). The evaluation of adsorbed fibrinogen and vWf showed significant higher protein antigen levels on the rougher surfaces (P < 0.01). Furthermore, nonpulsatile perfusion activated the coagulation system. By contrast, the surface roughness had no significant influence on plasma prothrombin F1.2 fragment- and TAT concentrations. Antithrombogenicity was significantly reduced in pumps with inferior metal-finishing quality.

Early Diagnosis of Acquired von Willebrand Syndrome (AVWS) is Elementary for Clinical Practice in Patients Treated with ECMO Therapy

“…Furthermore, the activated partial thromboplastin time (aPTT) was slightly prolonged in most of the ECMO patients (15/18) due to the effects of anticoagulation with heparin. pared to that noted on surfaces with a lower grade of roughness 20) , and coating artificial surfaces with swellable polymers has the potential to minimize platelet activation in perfusion models 21) . The extent of AVWS appears to be more pronounced in patients with ECMO and VAD than in those with aortic stenosis.…”

Novel nanostructured biomaterials: implications for coronary stent thrombosis

“…This finding is in agreement with data from a study on the influence of surface roughness on the activation of coagulation and platelet adhesion on continuous flow blood pumps. 39 In their study, Linneweber et al showed that surface roughness greater than 50 nm stimulates platelet adhesion and fibrinogen adsorption, indicating a reduction in anti-thrombogenicity in devices with rougher metal finishes. 39 What is remarkable is the fact that both carbon-(without nanotubes) and titanium-based films showed a timedependant increase in surface roughness (R rms ) depending on platelet adhesion and aggregation onto the substrates.…”

“…39 In their study, Linneweber et al showed that surface roughness greater than 50 nm stimulates platelet adhesion and fibrinogen adsorption, indicating a reduction in anti-thrombogenicity in devices with rougher metal finishes. 39 What is remarkable is the fact that both carbon-(without nanotubes) and titanium-based films showed a timedependant increase in surface roughness (R rms ) depending on platelet adhesion and aggregation onto the substrates. In contrast, the bare CNT/DLC nanocoatings had high R rms values due to the CNT bundles, but this then decreased because of the platelet adhesion during time.…”

Successful Treatment of Rotary Pump Thrombus With the Glycoprotein IIb/IIIa Inhibitor Tirofiban

“…7 The surface roughness of the LVAD and shear forces within the device contribute to platelet activation in rotary blood pumps. 8 This, together with the persistent inflammatory state and endothelial activation observed after ventricular support, 9 results in platelet aggregation mediated primarily by the interaction of activated platelet glycoprotein IIb/IIIa receptors with fibrinogen and von Willebrand factor to form an organized platelet-rich thrombus. 10 These so-called "white thrombi" differ from "red thrombi" that are rich in fibrin and trapped red blood cells, which are generally treated with anticoagulants.…”