Ann Thorac Surg 2003;75:1910-1911
© 2003 The Society of Thoracic Surgeons
Original article: cardiovascular
Invited commentary
Tetsuya Ueno, MDa
a Department of Cardiovascular Surgery, Ureshino National Hospital, 2436 Ureshino-machi Fujitsu-gunSaga 843-0393, Japan
e-mail: tueno{at}ureshino-hp-mo.jp
Perioperative cerebral protection in aortic operations requiring deep hypothermic circulatory arrest (DHCA) to avoid stroke and severe neurocognitive dysfunction remains one of the biggest concerns for cardiovascular surgeons.
No matter how much attention has been paid to avoiding emboli during such operations, stroke can still accidentally occur, possibly due to disease-related factors. Neurocognitive dysfunction is multifactorial and more complicated. Possible causes of neurocognitive dysfunction are reported to be cerebral ischemia and the consequent accumulation of anaerobic metabolic substances, reactive hyperemia immediately after reperfusion, release of toxic amino acids, and explosive exacerbation of inflammatory responses that are related to contact between blood and the bypass circuit, and are considerably suppressed under deep hypothermia. All of these factors may contribute to consequent cerebral edema in the primarily damaged region and secondary damage in surrounding penumbra through a compartment phenomenon.
A large number of experimental and clinical investigations addressing the beneficial and adverse effects of DHCA have been performed in the last decade. Currently, more attention is being shifted to the rewarming, or postischemia reperfusion, phase after DHCA. Pokela and colleagues have already presented the negative impacts of prolonged (14 hours) mild hypothermia (32°C) after DHCA through similarly well-designed experimental protocols as the present study [1]. They performed another in-depth investigation addressing the impact of a much shorter period (2 hours) of mild topical hypothermia by head cooling.
Contrary to previously published articles that support the significance of post-DHCA mild hypothermia for the reduction of cerebral complications [2, 3], they did not demonstrate a significant neuroprotective effect of short-period topical hypothermia. Why are these results contradictory? Because of the period of mild hypothermia after DHCA; because of the method of head cooling, internally by perfusion versus externally by packing the head with icepacks, and because of the rewarming rate after DHCA.
Their present study shows that the beneficial and favorable effects of mild topical hypothermia on brain tissue oxygenation, intracranial pressure, and similar factors are spoiled by detrimental metabolic outcomes due to altered brain vasoregulation. This does not simply deny the beneficial effects of mild hypothermia, but addresses the important question of whether the detrimental effects can be minimized under different conditions. In their experiment, several conditions differ considerably from clinical conditions, including an unacceptably longer DHCA time (75 minutes) and rapid rewarming rate (10°C increase in 15 minutes in figure 3), which must be modified to mimic practical aortic operations using DHCA. We look forward to many more exciting results from their sophisticated investigations.
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References
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- Romsi P., Heikkinen J., Biancari F., et al. Prolonged mild hypothermia after experimental hypothermic circulatory arrest in a chronic porcine model. J Thorac Cardiovasc Surg 2002;123:724-734.[Abstract/Free Full Text]
- Hagl C., Ergin M.A., Galla J.D., et al. Neurologic outcome after ascending aorta-aortic arch operations: effect of brain protection technique in high-risk patients. J Thorac Cardiovasc Surg 2001;121:1107-1121.[Abstract/Free Full Text]
- Ehrlich M.P., McCullough J., Wolfe D., et al. Cerebral efects of cold reperfusion after hypothermic circulatory arrest. J Thorac Cardiovasc Surg 2001;121:923-931.[Abstract/Free Full Text]
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