The CTA and DWI risk findings for postoperative new stroke in patients with ATAAD were totally different in the DWI (+) or DWI (-) group. Multivariate analysis showed that the retrograde aAO dissection with thrombosis of the false lumen, the aortic arch entry, the coronary artery involvement, and preoperative hypotension were independent risk predictors for postoperative stroke in patients with ATAAD with normal brain. In patients with ATAAD with preoperative cerebral infarction in DWI, only lesions distributed ≥ 3 lobes in the unilateral hemisphere were an independent risk factor for postoperative new stroke.
Preoperative cerebral malperfusion in patients with ATAAD was a predictor for postoperative stroke and detrimental outcome.[6] However, assessment of cerebral malperfusion may not be accurate only based on symptoms and signs as well as the dissection of the supraaortic branches without intracranial imaging evidence, which may further lead to unreliable prediction of postoperative stroke. The DWI may be the best imaging modality to assess cerebral infarction. In case of emergency, however, fewer patients with ATAAD undergo this test prior to surgery. Therefore, few studies may obtain direct evidence of brain abnormalities before surgery in patients with ATAAD. All patients with ATAAD in this study underwent preoperative cranial DWI and postoperative CT. Evaluation of cerebral infarction resulting from cerebral hypoperfusion prior to surgery and postoperative new stroke is accurate. Evaluation of preoperative risk factors for postoperative stroke based on imaging information is also accurate.
In this study, preoperative acute cerebral infarction resulting from cerebral hypoperfusion is frequent and is found in 24.1% of the brains, which is higher than the results in previous studies.[17–19] This may be related to the fact that the majority of the patients with ATAAD in this study had neurological symptoms and signs. Our results, showing a percentage of 18.4% of postoperative stroke in patients with ATAAD, are similar to those reported in a previous study.[1] A total of 31% (13/42) of patients with ATAAD with preoperative cerebral infarction develop postoperative new stroke, further indicating that preoperative cerebral malperfusion highly correlated with postoperative stroke. Moreover, it is perhaps noteworthy that 14.4% (19/174) of the patients with ATAAD with normal brain also presented postoperative stroke.
In the DWI (-) cohort, our data suggest that the retrograde aAO dissection with thrombosis of the false lumen, the aortic arch entry, and dissection involving the coronary artery, as well as preoperative hypotension are independent risk predictors for postoperative stroke in patients with ATAAD. Previous studies indicated that hypotension and aortic cross-clamp time are predictors for postoperative stroke and neurological dysfunction.[6, 20, 21] Unexpectedly, aortic cross-clamp time is not an independent risk predictor for postoperative stroke in this study, but it is significantly longer in patients with ATAAD with postoperative stroke (113.1 ± 35.3 min) than in subjects without stroke (95.6 ± 19.0 min, P = 0.002 ). Our previous study confirmed that retrograde aAO dissection is an independent predictor of postoperative permanent neurological dysfunction (PND) in patients with ATAAD. This condition is characterized by an entry tear in the aortic arch and descending aorta, and thrombus in the false lumen owing to the integrated intimal flap in aAO. The present study further accurately confirms that the retrograde aAO dissection with thrombosis of the false lumen is one of the risk predictors for postoperative stroke in patients with ATAAD with normal brain, but not in those with infarcted brain. The key point of this CTA finding was the thrombus in the false lumen, and almost all of the patients with retrograde aAO dissection had thrombus in the false lumen. This imaging finding implies a high probability of thrombus flowing into the brain via aortic arch tear during surgical procedure. Thus, particular attention should be given to this imaging finding, which may apprise surgeons of meticulous attention to critical procedural details and avoid the potential risk of postoperative stroke owing to thrombus falling off. The aortic arch entry as a risk factor for postoperative stroke is not unexpected. The potential cause may be similar to the CTA finding of retrograde aAO dissection with thrombosis of the false lumen. An aortic arch entry may enable the pre- and intraoperative microthrombus flow more easily into the craniocervical arteries via the tear point, resulting in subsequent cerebral artery occlusion and cerebral infarction. The CTA finding of dissection involving the coronary artery as a risk factor for postoperative stroke is unexpected. Coronary artery bypass grafting is associated with postoperative neurological complications, including stroke, with an incidence of 2.6–7.6%.[22, 23] Thus, one might speculate that postoperative stroke might be associated with longer surgical time due to additional coronary artery bypass grafting.
Although the distribution characteristics of preoperative cerebral lesions are rarely described in previous reports of ATAAD, this study demonstrates that cerebral lesions distributed ≥ 3 lobes in the unilateral hemisphere and number of cerebral lesions > 5 were significantly more common in patients with ATAAD with postoperative stroke in the DWI (+) group. Cerebral lesions distributed ≥ 3 lobes in the unilateral hemisphere were also an independent predictor for postoperative new stroke in patients with ATAAD with preoperative cerebral lesions. It is perhaps noteworthy that all 9 cases of lesions distributed ≥ 3 lobes in the unilateral hemisphere were in the right hemisphere, which may be due to right CCA dissection that was observed in 6 cases. The presence of DWI finding of cerebral lesions ≥ 3 lobes in the unilateral hemisphere implies that the lesions are multiple and widely distributed, with more possibility of cerebral hypoperfusion leading to postoperative new stroke. More than 5 infarction lesions in the brain, may be localized in one lobe, despite the high number. These imaging findings may help to individualize the optimized surgical strategy including brain protection techniques. For patients with ATAAD with preoperative cerebral lesions ≥ 3 lobes in the right hemisphere but without information of the circle of Willis, an anterograde bilateral selective cerebral perfusion may be better than unilateral cerebral perfusion.
This study has several limitations. First, it was a retrospective study with selection bias, and the follow-up period was limited. Second, this is a single-center data with limited preoperative DWI samples and limited number of postoperative new stroke. Larger multicenter studies may be necessary to determine the real imaging risk findings for postoperative new stroke in patients with ATAAD with different preoperative status. Third, preoperative cerebral DWI examination was not often available in emergency situations. However, analysis based on imaging presence or absence of cerebral infarction may provide more accurate evaluation of preoperative risk factors for postoperative new stroke in patients with ATAAD with normal or abnormal neurological status.