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Ann Thorac Surg 1997;64:1218-1219
© 1997 The Society of Thoracic Surgeons


Correspondence

Stroke From Heparin-Coated Circuits and Reduced Systemic Anticoagulation

Mrinal K. Dewanjee, PhD

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-111–labeled 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.

References

  1. Kuitunen AH, Heikkila LJ, Salmenperra MT. Cardiopulmonary bypass with heparin-coated circuits and reduced systemic anticoagulation. Ann Thorac Surg 1997;63:438–44.
  2. Dewanjee MK, Wu SM, Kapadvanjwala M, et al. Reduction of platelet thrombi and emboli by L-arginine during cardiopulmonary bypass in a pig model. J Thrombosis Thrombolysis 1996;3:343–60.
  3. Dewanjee MK, Belinskiy V, Holland JFW, et al. Effect of thoracotomy and cardiopulmonary bypass on activated platelet and neutrophil dynamics and platelet-emboli in a pig model. J Thrombosis Thrombolysis 1996;3:195–208.
  4. McKhann GM, Goldsborough MA, Borowicz LM Jr, et al. Predictors of stroke risk in coronary artery bypass patients. Ann Thorac Surg 1997;63:516–21.
  5. Hope AF, Heyns AdP, Lotter MG, et al. Kinetics and site of sequestration of In-111 labeled human platelets during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1981;81:880–6.
  6. Peterson KA, Dewanjee MK, Kaye MP. Fate of indium-111 labeled platelets during cardiopulmonary bypass performed with membrane and bubble oxygenators. J Thorac Cardiovasc Surg 1982;84:39–43.
  7. Dewanjee MK, Tago M, Josa M, Fuster V, Kaye MP. Quantification of platelet retention in aortocoronary femoral vein bypass graft in dogs treated with dipyridamole and aspirin. Circulation 1984;69:350–6.
  8. Palatianos GM, Dewanjee MK, Robinson RP, Hsu LH, Kaiser G. Quantitation of platelet loss with indium-111 labeled platelets in a hollow-fiber membrane oxygenator and arterial filter during extracorporeal circulation in a pig model. Trans ASAIO 1989;35:667–70.
  9. Palatianos GM, Dewanjee MK, Kapadvanjwala M. Cardiopulmonary bypass with a surface-heparinized extracorporeal perfusion system. Trans ASAIO 1990;36:M476–9.
  10. Dietrich WD, Dewanjee S, Prado R, Watson BD, Dewanjee MK. Transient platelet accumulation in the rat brain after common carotid artery thrombosis: an 111In-labeled platelet study. Stroke 1993;24:1534–40.



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