Thoracic endovascular aneurysm repair (TEVAR) has become the first-line therapy for treating descending aortic pathologies with low mortality and complication rates [1]. The latter may be caused by treatment failure due to the absence of technical success, disease progress or device failure during the follow-up, or perioperative ischaemic events. The 2 most frequently reported ischaemic events after TEVAR comprise stroke and paraplegia whose absence is widely regarded as an important treatment quality indicator. The rise of complex arch procedures with a considerably higher stroke risk than standard TEVAR has sensitized the community regarding ischaemic complications and led to an undeclared anti-stroke campaign emphasizing the role of graft de-airing and the use of carbon dioxide flushing, the use of embolic protection devices and the reduction of wire manipulation in the aortic arch [2, 3]. As for spinal cord ischaemia (SCI), the importance of the left subclavian artery revascularization, the limited aortic coverage length, the staged TEVAR approach in extensive aortic disease or other preconditioning strategies for the SCI have been established or proposed to reduce the incidence of this disabling complication. As an example of the neurological risk evaluation, recently published results of the SUMMIT database in our journal showed a 7% risk of post-TEVAR ischaemic neurological injury and identified the graft deployment proximal to the Left subclavian artery (LSA) and the procedural duration as the main risk factors for stroke, while age and renal function impairment were reported as major risk factors for SCI [4]. However, beyond the neurological complications, the ischaemic event rates of the end organs are not well established. How common is the end-organ and limb ischaemia after TEVAR? Which risk factors are associated with ischaemic events and what are their effects on early and mid-term mortality?

The multicentre retrospective observational study by Franchin et al. with robust methodology offers new insights into the sphere of organ ischaemia after TEVAR [5]. The study included 255 patients of whom 11% developed perioperative end-organ ischaemia. The authors clearly demonstrated that almost half of the ischaemic events affected the limbs, myocardium, visceral organs or kidneys. The incidence of stroke and SCI was 5% in the overall cohort.

Furthermore, the authors reported prolonged hospitalization and impaired early and mid-term survival in patients with ischaemic complications. Interestingly, stroke-associated mortality was not observed, whereas 5 of the 6 deceased individuals in the ‘ischaemic’ group had a direct causal relation with the visceral or spinal ischaemic events. This observation implies once more the importance of spinal cord protection, but also the meaning of visceral organ malperfusion in view of early mortality.

It is scarcely surprising that the authors identified the presence of severe aortic arch wall atheroma and ‘shaggy aortas’ as the main risk factors for ischaemic events, which may indicate the major source and the embolic pathomechanism of organ infarction in their study.

Despite all mentioned embolism prevention and ischaemic protection strategies, the identification of the aortic wall atheroma and thrombus during the planning and the diligent patient selection process for TEVAR treatment remains the most effective method to prevent ischaemic complications and thus to improve perioperative outcomes. The age, co-morbidities and patients’ life expectancy need to be correlated with the risk of perioperative organ ischaemia and finally with the indication for TEVAR. Given that ischaemic complications may go along with a disastrous impairment of quality of life and reduced survival after the intervention, the thresholds for elective TEVAR repair should be raised in patients with high embolic risk, particularly for indications at a lower level of evidence.

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