| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Ann Thorac Surg 2005;79:2038-2039
© 2005 The Society of Thoracic Surgeons
Division of Cardiothoracic Surgery, University of Washington School of Medicine, Box 356310, 1959 NE Pacific St, AA115, Seattle, WA 98195-6310
(E-mail: aldea{at}u.washington.edu).
Despite many theoretical opportunities and possibilities, the goal of complete attenuation of inflammation and ischemia reperfusion injury after cardiopulmonary bypass (CPB) by a single strategy remains elusive. This may reflect the primal teleological redundancy of the inflammatory and coagulation systems and requires a fundamental change in our often overly simplistic uni-dimensional approaches to these problems. At its extreme, this appreciation leads to a nihilistic intellectual pessimism that concludes that perturbations after artificial perfusions are unavoidable and severe and that CPB should be abandoned whenever possible. This position ignores many of the theoretical and pragmatic advances that were made in the field of artificial perfusion in the past 4 decades. It also ignores the overwhelming clinical observation that most patients tolerate these perturbations without major, catastrophic, adverse or long-term consequences. Inflammation and activation of the coagulation system are closely linked [1] and have been shown to be attenuated by altering circuit configuration (closed circuit, membrane oxygenator, soft flow, low-shear cannulas), composition (heparin-bonded biocompatible circuits), technique (limitations and elimination of cardiotomy suction whenever possible) [2], adjuvant anti-complement and anti-inflammatory drugs (pexelizumab, aprotinin) [3, 4], as well as leukofiltration. Each technique in isolation has modest, if any effects, and has to be combined with other "best practice" strategies to be of clinical relevance.
This report by Dr Salamonsen and colleagues presents the largest prospective randomized report to date (n = 300) investigating the clinical efficacy of leukofiltration of all five inflow and outflow points into the CPB circuit and patient ("total leukocyte control") on short-term clinical outcomes after routine CABG. The authors conclude that although the technology is safe (no increase bleeding or infection), it failed to demonstrate any significant impact on clinical outcomes. The authors have dealt well with the limitations of prior studies: small sample size, unblinded "controls," heterogeneous patient populations (mixing valve patients with CABG, acutely ischemic patient with nonemergent cases, possible adjuvant effects of other anti-inflammatory strategies (such as the use of aprotinin), circuit composition and bypass techniques. They also acknowledge the possibility of "filter exhaustion" and the possible effect of the timing of their filtration strategies, raising the question of whether the use of the terms total leukocyte control is a misnomer.
The overwhelming problem for this approach and many others is our current inability to carefully measure and account for how an individual patient will respond to artificial perfusion. We, along with others, have demonstrated an enormous variability in this response. This mirrors our clinical experiences that some patients have minimal perturbation after prolonged CPB, whereas others have profound disturbances after even a brief CPB run. Whenever we see a study demonstrating lack of clinical effect of a theoretically promising strategy (and even a positive initial study with negative subsequent reports), we wonder whether experimental treatment was applied to a high or low enough risk group. Phrasing it another way, was individual biological variability fully and equally accounted for in the study design? Except with extreme physiologic circumstances, such as organ transplantation with massive expected ischemia reperfusion, our ability to predict these variable responses in an individual patient remains poor. These variability in biological responses are poorly understood and do not correlate well with standard preoperative demographic and physiologic profiling such as age, gender, ejection fraction, urgency, New York Heart Association functional class, and so forth. We are beginning to understand the importance of profiling biological diversity as markers of longer term outcomes [5, 6]. Similarly, we need to focus our research efforts to better understand and stratify patients’ vascular biologic profiles before choosing a specific treatment strategy; doing this may avoid the current relatively crude, blind and potentially expensive, broad, and unfocused application of mechanical, technical, and pharmacologicl approaches to a biologically diverse patient population. Perhaps one day this will allow tailored judicious design of the right combinations of strategies for an individual patient.
 |
References |
|---|
 Top References |
|---|
This article has been cited by other articles:
|
|
 |
|
  S. Gunaydin, K. Ayrancioglu, E. Dikmen, K. Mccusker, V. Vijay, T. Sari, T. Tezcaner, and Y. Zorlutuna Clinical effects of leukofiltration and surface modification on post-cardiopulmonary bypass atrial fibrillation in different risk cohorts Perfusion, July 1, 2007; 22(4): 279 - 288. [Abstract] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
