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Ann Thorac Surg 1999;67:1828
© 1999 The Society of Thoracic Surgeons
a Thermo Cardiosystems Inc., 470 Wildwood, Woburn, MA 01888, USA
To the Editor
I read with interest the article by Baufreton and associates [1] entitled, "Measures to Control Blood Activation During Assisted Circulation." Initially, the promise of a current review of this protean topic raised expectations. However, I was disappointed at the number of references to the very preliminary work of one laboratory [2, 3]. The early findings of Spanier and colleagues [2, 3] have stimulated much interest and, hopefully, an equal amount of basic research into the proinflammatory properties of long-term implantable devices. These early observations raised questions about how best to protect patients. Interestingly, a preliminary report of similar complement and monocyte activation in smooth polyurethane-surfaced devices has been reported by a separate laboratory [4]. Yet another investigator has suggested that the cell-handling methods used in Spanier’s preliminary work might have contributed to the observed monocyte activation. In light of the benchmark clinical outcomes with the textured surface of the HeartMate left ventricular assist device (Thermo Cardiosystems Inc, Woburn, MA) such questions are of dubious relevance to the transplant-ineligible population that will ultimately benefit.
More worrisome is the authors’ assertion of conflicting results regarding the propensity of endothelial cells to populate the textured endovascular surfaces. As with Spanier and colleagues’ work on monocyte activation, the published reports are at best preliminary. Early work by Frazier and colleagues [5] examined cells from the explanted, textured polyurethane diaphragms of 10 HeartMate patients. Of these, only one had been implanted for more than 6 months. In that "long-term" diaphragm, immunocytochemical analysis confirmed the presence of endothelial cells. Many questions regarding the time course and probability of spontaneous endothelial seeding of endovascular surfaces remain. Although other promising areas of research were mentioned, I agree that basic research into biologic linings is critical to the development of thromboresistant devices. Thus, Baufreton and associates produced more than a review article. The work is, in every sense, a call for papers.
Similarly, the authors cannot be faulted for reporting that smooth surfaces might lead to thrombus formation. Nevertheless, clinical studies of multiple smooth polyurethane devices suggest that they are more than possibly thrombogenic [6]. The authors, like many serious academicians and developers of mechanical circulatory assist devices, should consider the possibility that it might not be possible to engineer a smooth, flexible surface that passively coexists with platelets. Fortunately, the next generation of devices will move beyond the smooth polyurethane barrier, leaving textured polyurethane one of the many historic, intuitive leaps that launched long-term circulatory assistance.
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