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• W2000776544 abstract "I read with great interest the excellent article of Gega and colleagues [1Gega A. Rizzo J.A. Johnson M.H. Tranquilli M. Farkas E.A. Elefteriades J.A. Straight deep hypothermic arrest: experience in 394 patients supports its effectiveness as a sole means of brain preservation.Ann Thorac Surg. 2007; 84: 759-767Abstract Full Text Full Text PDF PubMed Scopus (159) Google Scholar] detailing their approach to adult aortic arch repair with straight deep hypothermic circulatory arrest (DHCA). Their results suggest the adequacy of straight DHCA without adjunctive perfusion, especially for arrest times of less than 40 minutes. There was, however, a fourfold increase in stroke risk when the DHCA time exceeded 40 minutes (13.1% vs 3.3% p < 0.01): 62.5% of these strokes were classified as embolic by an experienced neuroradiologist. Because the authors acknowledge in their discussion that retrograde cerebral perfusion is an adjunct for cerebral embolic washout, the following questions arise:1Was retrograde cerebral perfusion used in this series for embolic washout? If so, in what percentage of the patient cohort? Could this be a significant confounder?2If retrograde cerebral perfusion was not used at all, do the results of this series support the need for this perfusion technique to enhance embolic clearance? If so, would the authors suggest it be routine or only in selected cases with stroke predictors such as DHCA time exceeding 40 minutes or severe aortic atheroma, or both. The second consideration is related to the conduct of cooling, because the authors do not specify in the article whether a neuroprotective volatile anesthetic such as desflurane was administered [2Kurth C.D. Priestley M. Watzman H.M. McCann J. Golden J. Desflurane confers neurologic protection for deep hypothermic circulatory arrest in newborn pigs.Anesthesiology. 2001; 95: 959-964Crossref PubMed Scopus (59) Google Scholar]. As a consequence, the following questions arise:1Was a volatile anesthetic administered during cooling in the DHCA protocol? If so, which agent(s) and what dose? What percentage of the study cohort?2If volatile anesthesia was administered during cooling, how might this have affected the outcome results? Major source of bias or not? Would the authors recommend the utility of a volatile anesthetic for neurologic preconditioning during the cooling phase of DHCA? The third consideration is about the possible influence of aprotinin in this series, given the favorable effects on outcome after thoracic aortic surgery reported recently by the same group [3Sedrakyan A. Wu A. Sedrakyan G. Diener-West M. Tranquilli M. Elefteriades J. Aprotinin use in thoracic aortic surgery: safety and outcomes.J Thorac Cardiovasc Surg. 2006; 132: 909-917Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar]. As a consequence, the following questions arise:1What percentage of the cohort was exposed to aprotinin? What was the dosing regimen?2Was aprotinin exposure considered in the reported multivariate analyses? If so, did it achieve statistical significance?3What is the current practice of the authors with respect to aprotinin utilization in aortic arch replacement with DHCA? I congratulate the authors again on an outstanding contribution. I look forward to their feedback about these three considerations. Financial support was provided by the Department of Anesthesiology and Critical Care at the University of Pennsylvania. ReplyThe Annals of Thoracic SurgeryVol. 86Issue 2PreviewWe appreciate Dr Augoustides' [1] kind comments and recognize his personal and institutional experience and insights of cerebral protection in aortic surgery. Full-Text PDF" @default.
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• W2000776544 date "2008-08-01" @default.
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• W2000776544 title "Contemporary Conduct of Adult Deep Hypothermic Circulatory Arrest: Possible Roles of Retrograde Cerebral Perfusion, Anesthetic Preconditioning, and Aprotinin" @default.
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• W2000776544 doi "https://doi.org/10.1016/j.athoracsur.2007.12.016" @default.
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