Early mortality and morbidity after surgical treatment for acute type A aortic dissection (AAAD) has remained high over the last decades despite technical improvements and is still in the range of 10–30% [1–6]. The most important risk factor for this still high early mortality is the preoperative status of the patients [4, 7]. Especially end-organ malperfusion contributes significantly to perioperative death and is present in approximately one-third of all patients with acute aortic dissection [3, 7–9]. Coronary, cerebral, visceral and lower extremity malperfusion syndromes are most often associated with type A dissection. A significant surgical dilemma is the treatment of AAAD patients with preoperative cerebral malperfusion [7]. Intimal tears in the proximal aorta often up to 37% [10] result in the involvement of the supra-aortic branches. Consequently, the impaired flow in the brainsupplying arteries is, besides coronary arteries, the most frequent form of malperfusion [7]. The reported incidence of neurological deficit before surgery in AAAD varies between 14% [7] and 20% [11]. The general surgical strategy in AAAD patients is directed towards (i) cannulation and perfusion of the true lumen, (ii) perfusion of all body regions intraoperatively, (iii) a certain degree of hypothermia, (iv) avoiding aortic cross-clamp during distal repair (open distal anastomosis), (v) avoiding changing arterial cannulation site and uncertain de-airing manoeuvres when resuming total body perfusion after distal aortic repair and (vi) unrestricted global perfusion postoperatively. To develop an individual surgical plan for those patients with supra-aortic malperfusion, preoperative assessment of the extent of dissection and type of malperfusion is of utmost importance. This assessment is usually done with computed tomography angiography (CTA) preoperatively, which translates to only a few minutes of delay on the way to the operating theatre and is just as important for the surgical outcome as surgical experience [6, 12]. Malperfusion can be further validated intraoperatively by using transoesophageal echocardiography (TEE), orbital Doppler and near-infrared spectroscopy (NIRS) [9]. One has to keep in mind, however, that NIRS does not provide information in the basilar artery region [9]. There is an ongoing debate about the best surgical strategy for AAAD in general and even more for the high-risk subgroup of patients with cerebral malperfusion [9]. Despite a consensus that the true lumen of the arterial system should be cannulated [13], the approaches vary considerably. This lack of evidence to enable any recommendations for the choice of surgical methods is related to the fact that randomized studies in AAAD (with wide variations of pathologies) are very unlikely to be performed. Even though a meta-analysis of 14 papers between axillary artery and femoral artery perfusion has shown that axillary arterial perfusion had a significantly lower complication rate [14], routes that are currently advocated for AAAD include subclavian (right and left) cannulation, common carotid artery (right and left) cannulation [15, 16], cannulation of the innominate artery, peripheral cannulation of a non-dissected artery (femoral), ascending aortic cannulation (Fig. 1) [17] or apex of the left ventricle (transapical). There is also no agreement about optimal protection (e.g. temperature) during circulatory arrest; however, even the best method of protection would be useless if the cerebral perfusion and other end-organ perfusion have not been restored during cardiopulmonary bypass (CPB) and aortic repair. In this ‘Great Debate’, different approaches are being described and the rationale for doing so is explained by world-known experts in this field. Special emphasis will be placed on common carotid, subclavian and innominate artery cannulation for antegrade cerebral perfusion (ACP). The rationale of retrograde cerebral perfusion (RCP) during selective cerebral perfusion is also described.
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