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.