DISCUSSION
There are many reports on the occurrence of stroke after ATAAD repair. Conzelmann and colleagues examined 2137 cases in the German Registry of Acute Aortic Dissection type A (GERAADA) and reported a mortality rate of 16.9% and a stroke rate of 12.9%. In addition, they reported that the progression of dissection to supra-aortic vessels and the preoperative malperfusion syndrome were risk factors for stroke after ATAAD repair, and that the choice of arterial cannulation site did not contribute to the occurrence of stroke.18 Ghoreishia and colleagues examined the Society of Thoracic Surgeons Adult Cardiac Surgery Database (STS ACSD), and found 17% mortality rate and 13% stroke rate in 7353 patients. They reported that type A repair using axillary arterial cannulation significantly reduced postoperative stroke compared to that using femoral cannulation, and retrograde cerebral perfusion had a lower incidence of stroke than that in deep hypothermic circulatory arrest or selective antegrade cerebral perfusion.14 However, this report did not consider dissection of supra-aortic vessels. Zhao and colleagues examined preoperative CT angiography and preoperative MRI in 281 patients at a single center, and reported that 103 patients (36.7%) had cerebral infarction before ATAAD repair. They concluded that moderate or higher aortic insufficiency, narrowing of the true lumen of the ascending aorta, and dissection of the common carotid artery were risk factors for preoperative stroke.20 However, they did not mention surgical results or postoperative cerebral infarction. In our study of 202 patients, the incidence of stroke after ATAAD repair was almost the same (12%) with the report from GERAADA and STS ACSD, although the mortality rate was better than them. Furthermore, these stroke rate of ATAAD repair was higher than that of total arch replacement for atherosclerotic arch aneurysms in Japanese registry.11,21 In recent years, detailed multi-detector row CT images have been obtained before ATAAD repair in many patients, and a detailed study of dissection into supra-aortic vessels has become possible. Our study is the first report to investigate the dissection progress to supra-aortic vessels in detail and to examine the relationship with postoperative stroke after ATAAD repair. The results of our study showed that only the progression of dissection to BCA was a significant risk factor for postoperative stroke.
Many factors are thought to be associated with the occurrence of stroke in perioperative period of ATAAD repair. One is the hypoperfusion of the area due to severe stenosis or occlusion of the carotid artery. If the thrombosed dissection progresses to BCA and the true lumen is occluded without forming a re-entry, cerebral infarction is predictable. Next, in cases where a re-entry is formed in the periphery of the supra-aortic vessels and supra-aortic vessels have patent false lumen, the thrombus formed in the false lumen can flows through the re-entry into the true lumen. Eight of the 21 patients had a patent false lumen of BCA after ATAAD repair (Figure 2). However, four patients did not have dissection, and nine had thrombosed false lumen without severe stenosis of true lumen. The mechanism of cerebral infarction in these patients cannot be explained by above two mechanisms. And cerebral infarction occurred in both left and right hemispheres, even in the side without dissection of BCA and LCCA.
Although the cerebral artery is the terminal artery, there is a Willis’ circle as left and right communicating arteries. The formation of a Willis’ circle varies greatly between individuals. In patients with a well developed Willis’ circle, even complete occlusion of the carotid artery may not exhibit neurological symptoms. A hypothesis came to our mind. In patients whose perfusion pressure of the unilateral carotid artery rapidly decrease due to acute aortic dissection, even if blood flow to the brain tissue is maintained, a stagnation of the blood flow occurs at the peripheral part of the occluded carotid artery (proximal to Willis’ circle) and a thrombus may be formed. This thrombus may cause bilateral cerebral embolism when blood flow in the carotid artery was restored by central repair for ATAAD. In patients with dissection of BCA, even if true lumen of BCA is not significantly stenotic at the time of CT imaging, it is possible that significant stenosis of true lumen temporarily occurs in the early stage of onset. Currently, we have no data to elucidate this mechanism. Preoperative CT angiography of intracranial arteries should be investigated on ward.
There were some limitations to this study that should be addressed. We didn’t perform central repair in the patients with coma, and they were excluded from this study. This is a single-center study with a small number of cases. ATAAD repair was performed promptly after admitting our hospital, but it was transferred to our hospital after being diagnosed at another hospital in many cases, and the time from onset to ATAAD repair varied. Diagnostic imaging around a Willis’ circle has not yet been performed. The mechanism of cerebral infarction discussed in this study is speculative. In addition, CT and MRI were not performed in all postoperative cases, small cerebral infarction without neurological symptoms may be overlooked.