Time for systematic tackling the disastrous effect of stroke in type A aortic dissection surgery

Stroke is a severe complication in acute type A aortic dissection (ATAAD). In a real-world study, Bossone and IRAD collaborators detected a 6% incidence of stroke in patients presenting with ATAAD, which resulted in a surgical hospital mortality of 31%.1 In a more previous IRAD study, Evangelista et al. reported major brain injury at the onset of dissection in 10% of ATAAD. Arch vessel involvement was more frequent among patients with stroke (68%). Furthermore, arch vessel involvement was associated with twofold or threefold higher mortality depending on the presence of cerebrovascular accident or coma. Even in this cohort, surgery was found to be a protective factor against hospital mortality in patients with preoperative brain injury (odds ratio, 0.058; p < .001).2 In the contemporary NORCAAD study, the pre-, intra-, and postoperative possible stroke scenarios added up to an overall stroke incidence of almost 16% and the associated surgical mortality to 27%.3 In this issue of the Journal, Fichadiya et al.4 present their basic work to improve the current understanding of precise neuroanatomical characteristics, mechanisms of injury, and clinical severity of stroke when it is detected after ATAAD surgery. They hypothetise, that attempts to reduce stroke through changes in intraoperative surgical technique will be ineffective if the etiology and pathogenesis is not fully understood. In their retrospective review within a single-center observational study, 189 consecutive ATAAD patients undergoing surgical treatment between 2006 and 2015 were analyzed. Thirty-eight patients had stroke (20%) and clinical evaluation as well as neuroimaging was done by stroke neurologists, which contrasts many studies with cardiac surgeons themselves judging the presence of stroke and underdetecting the incidence by factor 2–3. The observed 30-day mortality was 21%. All neurovascular findings were ischemic in nature, 42% bihemispheric, the remaining unilateral lesions had near equal distribution on right or left hemisphere. Sixty percent had isolated anterior circulation involvement, 2.6% were posterior. Fifty percent were watershed infarcts, 10% had large vessel occlusion (LVO). Forty percent of the LVO had preoperative carotid artery and left subclavian artery dissection. Etiology was 58% purely embolic, 26% as purely hypoperfusion, 11% mixed, and 5% unknown. Importantly, there was no relationship between preoperative cerebral malperfusion, surgical approach or intraoperative neuroprotection with stroke mechanism or stroke laterality. At 30 days postoperatively, 66% of stroke patients had at least moderate disability according to the modified Rankin Scale and 20% of those died. From this data the authors conclude that preoperative—as well as early postoperative neuroimaging can help to detect lesions amenable to modern endovascular therapy (EVT) with the possibility for mechanical thrombectomy in case of LVO. In their series, 10% of stroke patients would have been eligible for this treatment option. From my point of view we have to differentiate between factors which can be influenced and those not. Certainly, the patient's condition at arrival at the tertiary care center is such a noninfluenceable factor. From that point on, real-world conditions contrast with an ideal world of specialized centers for aortic disease treatment, we all should aim for: With 24/7 skilled aortic teams consisting of cardiothoracic surgeons, cardiologists, anesthetists, interventionalists and, as suggested by the authors of the commented paper, stroke neurologists, who are either awaiting the patient or are readily available on call. With the patient suspected for acute aortic syndrome arriving in a hybrid operating theater, life-threatening time loss by passing the patient through an emergency room can be avoided. Thus immediate expert diagnosis confirmation or refutation with the patient already on the operating table is possible, ready for intervention and/or operation.5 The modern equipment with angiographic imaging modality and CT technology allows exact pre- and postoperative control imaging to rule out or confirm severe malperfusion situations, differentiating between dynamic or static obstruction affecting the therapeutic decision making. Due to the dynamic situation with a 1%–2% mortality rate per hour, a remote CT scan, often hours old and sometimes of minor quality, can be controlled and updated. For example, in case of static carotid artery occlusion this knowledge helped us to immediately go for carotid artery replacement with a polyester tube graft which itself could be connected to one of the arterial lines of the extracorporeal circulation circuit for continuous unhampered brain perfusion while fixing the dissected thoracic aorta. Anesthesia can be managed that way, that in a stable hemodynamic situation after surgery, a brief wake up phase on the intensive care unit can be initiated to control motor function and consciousness in patients coming in with motor deficits, or even coma. Early reintervention within hours after onset of ATAAD for any kind of life-threatening or debilitating cerebral malperfusion can be opened, like the endovascular treatment option in case of LVO in the brain.6 With the presented basic data, Fichadiya et al. added valuable information about the underlying neuroanatomical pathologies and damaging pathways to better design the treatment startegies of cerebral injury in ATAAD, no matter if this takes place pre-, intra-, or postoperatively. All other confounding aspects of this complex scenario in ATAAD like cannulation sites, perfusion strategies, with or without hypothermic circulatory arrest, the dimension of surgery including root repair techniques, hemiarch versus total arch replacement with or without frozen elephant trunk, concomitant surgery for additional cardiac pathologies, or debranching techniques and finally the upcoming endovascular arch repair techniques, are a matter of intense scrutiny worldwide. Hopefully, all those international efforts can be synchronized to jointly develop a consensus and strategy for treatment variations in ATAAD.7 Open access funding enabled and organized by Projekt DEAL.