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Calafiore et al. Vessel Plus 2023;7:18 https://dx.doi.org/10.20517/2574-1209.2023.42 Page 9 of 21

Cognitive decline has not been studied often, but it can occur in more than 20% of the patients who had no
[34]
stroke by 7 days after extubation .
[34]
Delirium can be present alongside ischemic strokes . However, when it comes to non-focal NDs, which
have a multifactorial origin, determining whether delirium is an expression of encephalopathy poses a
challenge. Nevertheless, its incidence can be as high as 36% in patients without postoperative stroke .
[34]
NEUROPROTECTION
Before circulatory arrest: straight DHCA [Table 2]
Reducing the cerebral temperature to 18-20 °C has been, in the past, the only way to protect the brain. The
institution of deep hypothermia gave the possibility to repair the aortic arch, partially or totally. First
[52]
proposed by Borst et al. in 1964 , DHCA was, for a long time, and still is, a method used by many
surgeons. EEG monitoring is not necessary, as it was demonstrated that most patients achieve EEG silence
[53]
after 45 min of cooling when a nasopharyngeal temperature of 15-20 °C is reached .

The cerebral flow is roughly 50 mL per 100 gr and the energy produced is mainly required to maintain
[54]
+
+
Na homeostasis, which is largely governed by the Na /K - ATPase pump . Hypothermia decreases
[55]
+
cerebral blood flow, but also cerebral oxygen consumption, glucose utilization and brain metabolism, so this
[56]
decrease is not harmful. Brain metabolism reduces by 5%-6% for every degree of decrease in temperature .
[57]
Hypothermia significantly reduces extracellular levels of excitatory neurotransmitters , the release of
which is temperature dependent, as even mild levels of hypothermia exert an inhibitory effect [58,59] . Another
mechanism by which hypothermia promotes the survival of neurons is through the interaction with glycine.
Excitatory amino acids, through receptor activation, increase Ca++ influx into the cell. Some receptors
[60]
require the presence of glycine to be activated . Hypothermia significantly decreases brain glycine levels
after ischemia, thus decreasing hyperexcitability by glutamate [61,62] .

Straight DHCA has been shown to be a safe approach at many centers. Adding ACP or RCP to DHCA does
not seem to add any advantage, at least in non-complex surgery . In 490 patients, including total arch
[63]
replacement and AAD, Ziganshin et al. reported a prevalence of stroke of 1.6%, 1.3% (6/478) if DHCA was
[64]
< 50 min and 16.7% (2/12) if ≥ 50 min (this latter subgroup included only for the 2.4% of the cases) .
Damberg et al. demonstrated that, in elective non-dissected patients, 10-year survival after DHCA was not
[65]
different from the normal reference population .
Neurocognitive function after straight DHCA was explored by Chau et al. in 33 patients who did not need
DHCA and 29 who did . The prevalence of patients who showed some cognitive decline was not related to
[66]
DHCA (13/33 vs. 11/29, P = 1.00). In patients who needed DHCA, cognitive decline was not correlated with
CA time. Nevertheless, only three patients had a CA time > 40 min and all experienced cognitive decline.

In a prospective randomized study on neurocognitive function in patients where DHCA, straight or with
ACP or with RCP, was used, Svensson et al. found no neurocognitive advantage in adding ACP or RCP to
DHCA . On the contrary, straight DHCA patients performed better than RCP patients in 5 of 7 and better
[67]
than ACP patients in 9 of 9 postoperative subscores. The same group , analyzing 403 patients who had
[68]
undergone hemiarch or arch surgery, found that the ACP added to DHCA was a risk factor for
neurocognitive decline at multivariate analysis.