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Ann Thorac Surg 1997;64:1218-1219
© 1997 The Society of Thoracic Surgeons
Division of Physiology, Bioengineering and Nuclear Medicine, Department of Veterinary Biosciences, College of Veterinary Medicine, 3215 Vmbs Bldg, University of Illinois at Urbana-Champaign, 2001 S Lincoln Ave, Urbana, Il 61802, e-mail:dewanjee{at}uiuc.edu
To the Editor:
I read with considerable interest the article about the effect of heparin-coating of a Univox oxygenator, arterial filter, and components of cardiopulmonary bypass circuits on the thromboembolic complications [1]. In a small series of 30 men undergoing saphenous vein bypass grafting with low-dose heparin and a heparin-bonded circuit, 2 patients suffered stroke. A low-dose L-arginine infusion (2 mg kg-1 min-1) during cardiopulmonary bypass was found to reduce emboli in the brain and lungs significantly; this experimental observation is crying out loud for a clinical trial [14].
A meaningful measurement of clinically relevant end points, eg, thrombi and emboli, can be measured with autologous indium-111labeled platelets. My colleagues and I have made quantitative measurements of the dose of anticoagulants and platelet inhibitors in the acute and chronic phase of cardiovascular intervention and thrombogenicity of cardiovascular prostheses in several animal models and patients. We were able to predict clinical outcome from animal studies, with a high degree of accuracy [59]. We have also shown [2, 3, 810] that heparin-bonding to the components of the cardiopulmonary bypass circuit, including the oxygenator and arterial filter, did not decrease adherent platelet thrombi to the oxygenator and filter or trapped emboli in the brain and lungs [8, 9]. Clinical studies by Kuitunen and associates [1] confirmed our initial observation made in the pig model. From our sham-thoracotomy studies, we also observed that contact of platelets with subendothelial collagen and the interaction of factor VII of plasma proteins with tissue factor present on adventitial cells during surgical incision of thoracotomy or sternotomy without cardiopulmonary bypass increased the emboli in the brain by 50-fold and emboli in the lungs fourfold in pigs [3].
The role of the extrinsic coagulation pathway on formation of platelet thrombi and emboli during surgical intervention is underemphasized. Studies over the last 20 years have indicated that the design improvements of oxygenators significantly decreased oxygenator-adherent thrombi from 25% in the bubble oxygenator to 10% in the silicone membrane oxygenator to 3% in the intraluminal blood flow oxygenator to 0.3% in the extraluminal blood flow oxygenator. In the absence of treatments to prevent thrombosis induced by tissue factor activation, it is necessary to maintain a high level of heparin to keep the activated coagulation time greater than 400 seconds. We agree with the conclusion about the need for adequate heparinization before and during cardiopulmonary bypass in spite of heparin coating of the components of the extracorporeal circuit.
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