Ann Thorac Surg 2006;81:909
© 2006 The Society of Thoracic Surgeons
Original article: Cardiovascular
Invited commentary
Peter Haan, MD, PhD
Department of Anesthesiology, Onze Lieve Vrouwe Gasthuis, PO Box 95500, Amsterdam, 1090 HM, the Netherlands
(Email: p.dehaan{at}olvg.nl).
Lower limb neurologic deficits are a devastating complication of thoracoabdominal aortic aneurysm (TAAA) repair, and result from a prolonged or permanent interruption of blood supply to the spinal cord. Protective measures try to preserve spinal cord perfusion (ie, cerebrospinal fluid drainage, reattachment of intercostals arteries, distal aortic perfusion, and maintaining adequate proximal and distal pressures, in combination with monitoring spinal cord function with motor evoked potentials. However, if a period of spinal cord ischemia can not be avoided, it would be advantageous if adjuncts were available that enhance neuronal tolerance and improve neuronal survival after a temporary interruption of blood supply. If blood flow to the spinal cord can not be restored during the procedure, protective measures operate in the small watershed area of the infarction and are probably of small significance in the spinal cord.
The neuroprotective effect of permissive or induced mild hypothermia is well established in the experimental setting, but may be complicated by a deterioration of hemostasis, cardiac arrhythmias, and postoperative infections in the clinical situation.
The role of pharmacologic interventions during TAAA surgery has to be established. At best the tolerable duration of temporary spinal cord ischemia can be increased. The article by Reece and associates [1] clearly describes that the systemic route of administration of the adenosine A2A agonist ATL-146e improved functional and immunohistochemical outcomes in a porcine model of temporary spinal cord ischemia. The search for the golden pharmacologic neuroprotective bullet extends several decades. The majority of putative neuroprotective agents are hampered for clinical use by serious side effects. Moreover, in clinical stroke, apparently promising neuroprotective pharmacologic agents were not effective in large clinical studies, although experimental results showed significant improved outcomes. The lack of effectiveness is probably due partly to differences in between animal models and the clinical situation, but it can also be attributed to flaws in the preclinical studies. Indeed systematic review of experimental studies in stroke revealed serious flaws in the methodology and did not show convincing evidence to substantiate the decision to perform clinical trials. Consequently, guidelines were suggested for animal studies in stroke that should be adapted prior to starting a clinical study of a potential neuroprotective agent. If adjusted for TAAA surgery and experimental spinal cord ischemia a modified version of these guidelines may be of use in experimental spinal cord ischemia:
- 1 Blinded drug administration and blinded outcome evaluation, which are essential precautions against bias in clinical trials should be valued equally in animal studies.
- 2 Monitoring physiologic parameters.
- 3 Group size based on a-priori power calculations.
- 4 Assessment of both histopathologic and functional outcomes.
- 5 Outcome assessment in the acute phase (up to 6 days) and in the chronic phase (up to 30 days).
These recommendations may be of use in order to avoid overoptimistic expectations of proposed neuroprotective agents in the clinical application during TAAA surgery.
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References
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- Reece TB, Okonkwo DO, Ellman PI. Comparison of systemic and retrograde delivery of adenosine A2A agonist for attenuation of spinal cord injury after thoracic aortic cross-clamping Ann Thorac Surg 2006;81:902-909.[Abstract/Free Full Text]
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