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Lou et al. Vessel Plus 2022;6:38  https://dx.doi.org/10.20517/2574-1209.2021.108  Page 7 of 9

               the proximal edge of the endograft in the suture line. The TEVAR-first approach consisted of emergent
               TEVAR followed by delayed central aortic repair.

               Patients who presented with hemodynamic instability, cardiac tamponade/hemopericardium, respiratory
               distress, intractable chest pain, stroke, coronary malperfusion, or severe aortic insufficiency were excluded
               from consideration of a TEVAR-first approach. In those who underwent TEVAR, additional branch vessel
               stenting was performed until abdominal aortography and femoral artery pressures matched radial artery
               pressures to confirm normal perfusion.


               The limited number of patients in the series precludes any generalizable results. However, the trend was
               towards improved outcomes among patients who received end-organ re-perfusion prior to central aortic
               repair. In the ascending aortic/arch replacement followed by exploratory laparotomy group, 77% of patients
               developed postoperative bowel necrosis or intractable acidosis with an overall mortality of 69.2%. All
               patients in the Ax-Bifem bypass followed by ascending/arch replacement group survived; however, 66%
               needed postoperative renal replacement therapy. In the ascending/arch and concomitant antegrade/TEVAR
               group, the mortality was 80%. Of the 13 patients treated with a TEVAR-first approach, ten survived and
               ultimately underwent central aortic repair. Of these, four patients required additional branch vessel stenting
               for static malperfusion and three patients who underwent aortic repair died for an in-hospital mortality of
               30% after central aortic repair.

               Based on this accumulating experience, a new treatment algorithm for the management of ATAAD with
               mesenteric malperfusion syndrome has been proposed. Once ATAAD with MMP has been diagnosed,
               patients who are hemodynamically stable, free of chest pain, and without evidence of severe aortic
               insufficiency, cardiac tamponade/rupture should be considered for TEVAR with or without additional
               endovascular therapy. If within 24 h of observation, lactate levels have normalized, then the patient should
               undergo central aortic replacement. If lactic acidosis persists, however, these patients should undergo
               exploratory laparotomy, bowel resection and either withdrawal of care or additional delay of aortic
               replacement until their acidosis has resolved. Patients with ATAAD complicated by MMP who are
               hemodynamically unstable, present with evidence of aortic rupture, or intractable chest or abdominal pain
               should proceed with emergent Ax-Bifem bypass with antegrade and retrograde aortic perfusion,
               ascending/arch replacement with antegrade TEVAR deployment, followed by Ax-Bifem bypass completion.


               Hybrid techniques with central aortic repair at the same time as endovascular management of distal
               malperfusion syndromes are also emerging [25,26] , and there have been case reports of successful results of
               ATAAD with MMP management in hybrid operating rooms using interventional techniques to re-establish
               end-organ malperfusion first, followed by aortic root repair, total arch replacement with debranching, and
               retrograde stent graft implantation. The benefit of this approach is the ability to first relieve visceral and
               lower extremity malperfusion and subsequently prevent aortic rupture during the same operation.


               CONCLUSIONS
               In summary, malperfusion involving any vascular bed and organ system complicates acute aortic dissections
               and significantly impacts morbidity and mortality. Malperfusion syndrome itself results in an inflammatory
               cascade that mediates end-organ injury, which can persist even after aortic repair. Many types of
               malperfusion syndromes are effectively treated with central aortic repair. These include coronary
               malperfusion as well as cases of ATAAD complicated by stroke and coma. While the available data are
               limited, they do suggest that the presence of brain malperfusion or cerebral dysfunction is not a
               contraindication to surgical intervention. In these specific patient populations, early intervention is
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