Page 94 - Read Online

Page 8 of 21 Calafiore et al. Vessel Plus 2023;7:18 https://dx.doi.org/10.20517/2574-1209.2023.42

ACP allows continuous cerebral perfusion throughout HCA; however, the manipulation of arch vessels
(including dissection, clamping, or directly cannulation of the ostia of the arch vessels) can dislodge debris
from the vessels or introduce air into the cerebral circulation, causing cerebral embolism. A study based on
magnetic resonance imaging demonstrated that patients with no clinical symptoms had more embolic
lesions after ACP than after RCP .
[36]
SACP can perfuse the brain during a period of CA, but the presence of moderate or severe atherosclerotic
plaques inside the common carotid arteries can cause embolic strokes. The use of UCP needs manipulation
of the origin of the brachiocephalic trunk and of the LCCA (both need to be clamped with possible
fragmentation of atherosclerotic plaques, if present).

[37]
A major risk factor for non-focal encephalopathy, including generalized seizures and PND , is
leukoaraiosis [32,38] . This term describes abnormalities of the white matter, appearing as patchy or confluent
subcortical and periventricular hypodensity on computed tomography or hyperintensity on magnetic
resonance imaging. These silent brain lesions are often seen in elderly patients with hypertension and
diabetes, with or without a prior history of stroke or dementia.

The emerging widespread addition of FET during total arch replacement seems to increase the prevalence
of postoperative NDs, mostly embolic in origin. Berger et al. reported a ND rate of 16.8% in 250 patients
[33]
undergoing arch replacement for acute and chronic aortic pathologies . The rate rose to 35.7% in patients
undergoing arch replacement for chronic aneurysms. In all cases, moderate hypothermia and bilateral SCP
were routinely used. In another clinical picture, where the procedure was performed at a rectal temperature
[39]
of 20-25 °C (likely DHCA) and ACP (LSA was ligated), the stroke rate was 8.6% . In three meta-analyses,
the prevalence of stroke was 7.6% , 7.7% , and 7.1% , respectively.
[42]
[41]
[40]
Spinal cord injury (SCI) can be related to a lack of LSA perfusion or the use of FET with different
mechanisms. Perfusing the LSA avoids malperfusion of the left vertebral artery (steal syndrome) but also
allows to perfuse continuously the anterior spinal artery via cervical and left thoracic collaterals. There are
pieces of evidence in human that ACP, including LSA perfusion, only partially perfuses the upper thoracic
cord via collateral circulation from vertebral arteries, but blood flow by ACP does not reach the lower
[43]
thoracic cord . In an experimental setting, Etz et al. also concluded that ACP provides insufficient spinal
flow below T8/T9 . A recent anatomical study emphasized the necessity of perfusing the four suppliers
[44]
[45]
of spinal cord (LSA, thoracic segmental arteries, lumbar segmental arteries, and internal iliac arteries) to
avoid SCI.

SCI represents a major drawback of FET surgery. Berger et al. reported a prevalence of 1.2% after FET, but
other studies reported higher prevalence rates ranging from 5.6% to 24% [33,39,43,46,47] . Three meta-analyses
reported a prevalence of 4.7% , 3.5% , and 6.5% , respectively. Lower body CA duration represents a risk
[42]
[41]
[40]
factor for SCI. In a small group of patients who underwent ACP at 28 °C and lower body CA > 60 min,
[48]
paraplegia rose to 18.2% vs. 1.2% when lower body CA was 60 min or less . Another important point is the
[40]
length of the FET. If longer than 15 cm, extending beyond T8, it is a risk factor for SCI . This was
demonstrated experimentally as well . In addition, proximalization of FET to zone 0 can reduce SCI,
[49]
thereby reducing the occlusion of the intercostal vessels .
[50]
During lower body CA, it is important to recognize that cooling protects the lower spinal cord better than
ACP .
[51]