IntechOpen

Home > Books > Advances in Vascular Surgery [Working Title]

Open access peer-reviewed chapter - ONLINE FIRST

Unilateral Antegrade Cerebral Perfusion during Aortic Arch Repair

Written By

Boris Kozlov and Dmitri Panfilov

Submitted: 01 May 2024 Reviewed: 07 May 2024 Published: 18 June 2024

DOI: 10.5772/intechopen.1005746

Advances in Vascular Surgery IntechOpen
Advances in Vascular Surgery Edited by Dario Buioni

From the Edited Volume

Advances in Vascular Surgery [Working Title]

Dr. Dario Buioni and Dr. Carlo Bassano

Chapter metrics overview

8 Chapter Downloads

View Full Metrics
Advertisement

Abstract

Circulatory arrest is one of the most crucial timeframes during aortic arch surgery due to the increased ischemic risk for inner organs, including the brain. In this regard, the issue of intraoperative cerebral protection is of great importance. Despite the fact that antegrade cerebral perfusion is the preferred neuroprotective strategy during aortic arch surgery, including the frozen elephant trunk procedure, the choice of the best perfusion technique for cerebral protection is still a matter of debate. We conducted a comprehensive analysis of cerebral status in 97 patients who underwent total arch repair using the frozen elephant trunk technique under moderate hypothermia and unilateral cerebral perfusion via an innominate artery. Our analysis, including intraoperative monitoring of cerebral oximetry, the incidence of postoperative neurological deficit and cognitive impairment, and added assessment of a neuronal injury marker level (neuron-specific enolase), demonstrates the high efficacy and safety of unilateral antegrade cerebral perfusion via an innominate artery.

Keywords

  • unilateral cerebral perfusion
  • innominate artery
  • neurological deficit
  • neuron-specific enolase
  • cognitive impairment

1. Introduction

It is known that aortic arch surgery requires temporary interruption of cerebral circulation [1]. However, the safe period of such a maneuver is only 4–5 minutes, which is not enough to perform an adequate aortic arch reconstruction. Therefore, certain measures are required to ensure cerebral protection during aortic arch surgery. The main components of neuroprotection include systemic hypothermia leading to a decrease of cerebral metabolism, and cerebral perfusion during circulatory arrest (CA), allowing the delivery of energy substrates, oxygen, and, at the same time, the removal of metabolites.

1.1 Hypothermic circulatory arrest

Systemic hypothermia is distinguished into several degrees with the following temperature ranges: mild (28.1–34°C), moderate (20.1–28°C), severe (20–14°C), and deep (≤ 14°C) [2]. The degree of hypothermic protection is still a highly controversial issue. In fact, with a hypothermia level deeper by 10°C, cellular metabolism slows down by 5–7% [3]. Consequently, neuronal activity decreases proportionally to body temperature. Thus, with hypothermia at 15–17°C, cellular metabolism decreases approximately by six times (to 12–25% of the metabolic rate at normothermia), and at a temperature of 10–12°C, it shows electrocerebral silence. However, numerous studies found that the absence of electrical cerebral activity can also be observed at higher temperatures (up to 27°C) [3, 4].

Despite all the advantages, including cerebral protection, avoidance of clamping, a bloodless and motionless operative field, and no need for additional perfusion equipment, the safe time provided by hypothermia is limited [5]. Thus, deep hypothermia protects from cerebral ischemia for a period of up to 30–40 minutes [2, 3, 6]. Hypothermia of longer than 40 minutes was found to lead to increased neurological complications, and in cases of over 65 minutes, the risk of mortality was significantly higher [7, 8]. Additionally, with deep hypothermia, there is an increased risk of bleeding, as well as cardiac, respiratory, and renal complications due to the development of endothelial dysfunction caused by prolonged cardiopulmonary bypass (CPB) [4, 5, 6].

The necessity to reduce complications required altering the strategy for protecting from ischemia. Di Eusanio et al. [9] analyzed their own surgical experience performed under deep and moderate hypothermia amplified with antegrade cerebral perfusion (ACP). The authors noted that the postoperative rate of deaths and strokes decreased in moderate hypothermia. Vallabhajosyula et al. and Gong et al. made similar conclusions [10, 11]. Thus, increasing body temperature during aortic arch surgery was found to reduce the number of complications related to deep hypothermia. However, moderate hypothermia alone does not provide safety due to the time limit, which does not exceed 10–20 minutes, because of increased cerebral oxygen consumption. As a result, there is a need for additional perfusion support during aortic arch operations [2].

1.2 Cerebral perfusion

To date, there are several neuroprotective strategies during aortic arch repair: retrograde cerebral perfusion (RCP) as well as uni- and bilateral antegrade cerebral perfusion [5, 6, 12].

1.2.1 Retrograde cerebral perfusion

Retrograde cerebral perfusion provides cerebral protection by perfusing cold oxygenated blood into the superior vena cava, maintaining a flow rate of 500 ml/min and a pressure of no lower than 25–30 mm Hg. The opening of internal jugular vein valves, which are the primary venous drain for the human brain, is ensured only under these conditions [13, 14]. There is compelling evidence that retrograde cerebral perfusion may provide neuroprotection not only through the support of cerebral metabolism but also by expelling emboli from the cerebral vasculature [15, 16]. According to Rylski et al. [15], retrograde cerebral perfusion is superior in the prevention of focal neurological deficits during “short” aortic arch procedures (<40 min). However, some data demonstrate opposite outcome. Thus, temporary neurological deficit (agitation, delirium) with retrograde cerebral perfusion has been reported in 12.8–25.1% and the incidence of permanent neurological events (stroke) was observed in 2.8–13.5% of cases [17, 18]. Moreover, a number of papers did not reveal significant differences in neurological complication rates between isolated hypothermic circulatory arrest and retrograde cerebral perfusion [19, 20].

The relatively low degree of cerebral protection during RCP is due to some of its peculiarities. Thus, up to 90% of blood is shunted through arterio-venous and veno-venous shunts into the inferior vena cava, the functionality of which increases during hypothermia [5, 21]. Cerebral edema is another negative factor resulting from conditions of high perfusion pressure [6, 16, 17]. Fluid extravasation due to high hydrostatic pressure leads to increased perivascular pressure and compressed parenchymal arterioles, causing cerebral edema followed by delirium development [13, 14]. Attempts to reduce perfusion pressure in the experiment have demonstrated the ineffectiveness of such perfusion. It has been shown that in primates, RCP for up to 60 minutes duration with the maintenance of perfusion pressure around 20 mm Hg provides only 1% of the cerebral flow from antegrade values [13].

Additionally providing of RCP is limited in patients with occlusive disease of supra-aortic vessels. This entity causes cerebral edema development due to positive (even residual) pressure in the arterial system. For this reason, RCP is less effective and even dangerous in these patients [22].

Thus, the role of retrograde perfusion in cerebral protection during aortic arch repair is still controversial, mostly due to the high risk of neurocognitive disorders (up to 40%) [1, 23]. To date, most clinics have abandoned the use of this type of cerebral protection and have focused their efforts on antegrade cerebral perfusion [24, 25].

1.2.2 Antegrade cerebral perfusion

Antegrade cerebral perfusion was popularized by Bachet and Guilmet in Europe and Kazui in Asia. The fundamental difference between ACP from RCP is in the cerebral blood supply via a physiological route, namely through supra-aortic vessels instead of the superior vena cava. A significant advantage of ACP is a longer safe period of circulatory arrest (up to 90 minutes) at a higher body temperature. Antegrade cerebral perfusion allows for better elimination of metabolites as well as lower biomarker levels of cerebral damage [5, 7, 26], consequently reducing hospital mortality and stroke rate [27]. To date, uni- and bilateral approaches are proposed for ACP during aortic arch surgery.

Bilateral antegrade cerebral perfusion is the most physiological approach, providing blood supply to the brain through both carotid arteries. On the other side, unilateral ACP possibility is based on cerebral multiple ways of cross-perfusion. An important role in collateral cerebral circulation is played by the ophthalmic artery, leptomeningeal vessels, and external carotid arteries [28, 29, 30, 31]. Alongside this, the role of the Circle of Willis remains unclear. Thus, Urbanski et al. [32] revealed that up to 40% of patients have abnormalities in the Circle of Willis. However, in these cohorts, flow velocity was recorded in the contralateral middle cerebral artery during unilateral ACP. This indicates collateral pathways function that ensures adequate perfusion of both cerebral hemispheres.

Taking these circumstances into account, the choice of the best strategy is still debated. Malvindi et al. [33] analyzed the results of 3548 patients and concluded that bilateral perfusion provides greater safety during prolonged circulatory arrest (> 50 minutes) compared to unilateral perfusion. Others consider it mandatory to provide bilateral ACP during complex aortic arch repair, ensuring the most physiological cerebral perfusion [34, 35].

Meanwhile, a meta-analysis (6788 patients) conducted by Angeloni et al. [36] demonstrated the superiority of unilateral perfusion over bilateral perfusion in terms of the incidence of postoperative neurological complications (5.8 versus 6.9%, p = 0.53) and mortality (7.6 versus 9.8%; p = 0.19). A possible explanation of the increase of temporary and permanent neurologic deficit in patients with bilateral ACP related to additional manipulations with supra-aortic vessels that lead to increased risk of embolism. At the same time, unilateral ACP may prevent neurological complications by high-velocity retrograde flow from the supra-aortic vessels.

Zierer et al. [37] showed a comparable 30-day mortality rate and two times higher stroke rate after bilateral ACP compared to unilateral cerebral perfusion (4 versus 2%, p = 0.06). Supporting the theory of unilateral ACP superiority, Özatik et al. [31] showed that the levels of cerebral damage markers (S-100 protein and neuron-specific enolase), as well as lactate, pH, glucose, and blood oxygen, do not differ significantly between different hemispheres with unilateral cerebral perfusion. Moreover, it has been shown that prolonged unilateral perfusion, even more than 60 minutes, is not accompanied by a significant increase either in early mortality or cerebral complications [38, 39].

However, Tong et al. [40], comparing outcomes of bilateral and unilateral ACP, did not reveal any advantages of one technique over the other regarding 30-day mortality and neurologic complications. Moreover, the findings of a meta-analysis conducted by Tian et al. [41] served as additional evidence for the adequacy of unilateral perfusion. They found that both unilateral and bilateral cerebral perfusion techniques do not significantly differ in neurological outcomes or mortality.

To sum up, currently, the effects of uni- and bilateral ACP remain controversial and require further investigations.

1.2.3 Arterial cannulation

A number of arterial cannulation sites for antegrade cerebral perfusion have been described in the literature. The optimal site depends on thoracic aortic pathology, including anatomical features of the patient, surgical conditions, and the experience of the surgical team.

In the mid-90s, Sabik et al. [42] were the first who suggested subclavian artery for arterial cannulation site during thoracic aortic surgery. Subclavian artery cannulation allows to provide antegrade flow during cardiopulmonary bypass, as well as adequate antegrade cerebral perfusion within circulatory arrest [43, 44]. The disadvantages of this approach include the impossibility of initiating cardiopulmonary bypass if the artery diameter is too small or has subclavian stenosis or thrombosis [15, 43, 45]. Overall, the incidence of complications related to inadequate perfusion, vascular complications, and brachial plexus injuries is up to 14%. Moreover, the need to replace the arterial cannula with an alternative site is required in 11% of cases [46].

Cannulation of the common carotid artery is considered another option, especially in emergency cases. According to Rylski et al. [15], the common carotid artery has an advantage over the subclavian artery, primarily due to its larger diameter and convenient anatomy. In addition, a cannula placed into the carotid artery allows for lower pressure from the pump of the heart-lung machine. On the other hand, obstacles in the aortic arch lead to an increase in blood flow and pressure in the arterial system. This, in turn, can cause over-perfusion and cerebral damage. Hence, it necessitates additional cannulation, which eliminates all the advantages of common carotid artery cannulation.

An alternative option to central aortic cannulation is the cannulation of the innominate artery (IA), which allows for antegrade cerebral perfusion within circulatory arrest, avoiding high pump pressure due to the larger size of the vessel [47, 48, 49]. IA cannulation does not require an additional skin incision, which enables good visual control of the cannulation site. Additionally, there is no risk of neural plexus injuries [50]. Nevertheless, the IA is not suitable for cannulation when dissected or if its arterial wall is severe atheromatous [51].

The body of evidence regarding the efficacy and safety of cerebral perfusion via the innominate artery is sparse. Thus, we conducted a comprehensive analysis of cerebral status in 97 patients who underwent total arch repair using the frozen elephant trunk (FET) technique under moderate hypothermia and unilateral cerebral perfusion via the innominate artery.

Advertisement

2. Surgical techniques

2.1 Technique of unilateral cerebral perfusion via innominate artery

After median sternotomy IA up to its bifurcation is mobilized. After the administration of a 1 mg/kg heparin dose, the artery is side-clamped. The IA is opened to decrease the arterial pressure in the right radial artery by no more than 50% and to decrease the right hemisphere cerebral oximetry not lower than 20% compared to the baseline values. Then, an anastomosis is performed using a continuous 5–0 Prolene suture with an 8–10 mm vascular graft in an end-to-side fashion. After washing off possible debris and eliminating air from the vascular graft, it is connected to the arterial line of the CPB circuit (Figures 1 and 2).

Figure 1.

Side clamp of the IA in a schematic diagram (left image) and intraoperative image (right image).

Figure 2.

The arterial line of the CPB circuit connecting to the innominate artery in a schematic diagram (left image) and intraoperative image (right image).

Very rarely, when the side clamp of the IA is considered technically impossible or unsafe, IA was cross-clamped with flow interruption.

During the entire procedure, cerebral oximetry is carefully monitored using the near-infrared spectroscopy (NIRS), while maintaining mean arterial pressure at 50–60 mmHg in both radial arteries.

Mannitol and hydrocortisone are administered intraoperatively to prevent cerebral edema, which can ensue due to temperature gradient.

Unilateral cerebral perfusion is carried out through the IA while the left common carotid artery and left subclavian artery are clamped. The flow rate is 8–10 ml/kg/min maintaining the mean blood pressure at 50–70 mm Hg under 25–28°C degrees. Based on an experimental study of cerebral metabolism and histopathologic findings in dogs, Tanaka et al. [52] assumed that the aforementioned values provide about 50% of the physiologic flow rate, which is sufficient for intraoperative cerebral protection.

However, taking into account the unilateral cerebral perfusion, which directly supplies blood to only one hemisphere, a decrease in the NIRS values in the opposite hemisphere of more than 10% from the baseline forced us to increase the flow to 13–15 ml/kg/min.

Technically, connecting the arterial line to the IA using a side graft has several advantages: (i) no additional arterial cannulation site for CPB; (ii) visual control of the graft inside the surgical field promotes bleeding control from the anastomosis; (iii) ensuring the correct measurement of arterial pressure in the right radial artery since there is no cannula in the lumen of the vessel.

The strategy of IA cannulation for aortic arch pathology has always been used in our practice and is considered to be safe and effective since no serious complication has been encountered when using the IA as an arterial port for either CPB or ACP. Cannulation of the IA with a side graft allows for eliminating artery lumen occlusion with a cannula, turbulent flow around the cannula, as well as reducing unnecessary trauma to the fragile wall of the IA.

Other groups have also obtained excellent results with IA cannulation. Huang et al. [53] used сannulation of the IA with a side graft. The authors reported five (10.9%) patients with diagnosed temporal neurological deficit (TND) in the early postoperative period, without any stroke. Di Eusanio et al. [54] used a similar technique for IA cannulation for either CPB or ACP. In 55 patients, only 1 (1.8%) patient had TND. Preventza et al. [55] analyzed the results of aortic arch procedures, including those performed with IA cannulation with a graft sewn in an end-to-side fashion. Postoperatively, 3 (4.4%) patients had a stroke. It is worth noting that only one patient had an irreversible neurological deficit; the other two patients underwent partial neurological recovery. Additionally, 7 (10.3%) patients had postoperative delirium.

Meanwhile, Ji et al. [56] cannulated the innominate artery directly in 68 patients. The cannula tip was oriented toward the aortic arch during the period of CPB, and it was turned cranially during lower body circulatory arrest with ACP. The authors reported no neurologic events after the surgery.

Svensson et al. [23], analyzing results of 1336 operations, diagnosed only 1 (4.2%) case of stroke using direct IA cannulation. The authors noted that IA cannulation with a side graft can be considered a more preferable option for preventing neurologic complications compared to direct arterial cannulation. Moreover, this technique is considered easier and safer to use than direct artery cannulation.

Taking into account the aforementioned features of different arterial cannulation sites for uACP, we adopted IA cannulation on a regular basis during aortic arch surgery, regardless of the condition of alternative arteries. From our point of view, IA cannulation is more advantageous compared to other arterial sites in light of the benefit-risk ratio. Specifically, the innominate artery, as a relatively large brachiocephalic vessel, provides a higher volumetric blood flow rate without high blood pressure compared to other arterial cannulation sites (subclavian, carotid artery, or axillary artery) additionally to the technical advantages listed above.

2.2 FET implantation technique

The FET procedure was performed according to a surgical management procedure adopted in our clinic [57]. The sequence of the surgical steps during the operation was the same for all patients. In brief, surgical repair is conducted under moderate lower body circulatory arrest (25–28°C) and unilateral ACP via the innominate artery. A hybrid graft with a diameter of 24–30 mm is implanted in all cases. The length of the stent graft was 150 mm only. After establishing CPB, body cooling is started. Once the target temperature is achieved, lower body circulatory arrest with ACP is initiated. Then the aortic arch is opened and resected. The stent graft is implanted in the descending aorta, and fixed to the aortic tissue by continuous Prolene 4/0 suture without oversizing. Cerebrospinal fluid drainage and pressure monitoring are not performed. The distal aortic anastomosis is performed in Z2 or Z3 and depends on the patients’ anatomical features and the technical possibilities encountered during the operation. Subsequently, re-implantation of the supra-aortic vessels is performed using one of the known techniques. After ACP is stopped, the CPB is reinstituted with warming of the patient’s body. The proximal aorta is reconstructed during rewarming, and, if necessary, concomitant cardiac procedures are performed.

Advertisement

3. Study population

A retrospective single-center study was conducted. Between March 2012 and December 2022, a total of 311 aortic arch repairs were performed in our center. In this cohort, 97 patients underwent the FET procedure using the E-vita Open Plus hybrid graft (Jotec GmbH, Hechingen, Germany) and MedEng (MedEng, Penza, Russia). Detailed demographics and comorbidities of analyzed patients are shown in Table 1.

VariablePatients (n = 97)
Age, years54.5 [51; 63]
Male, n (%)68 (70.1%)
Height, cm173 [166; 178]
Weight, kg94 [64.5; 101]
BMI, kg/m229.3 [21.9; 33.1]
BSA, m22.1 [1.8; 2.2]
Aortic dissection, n (%)80 (82.5%)
Degenerative aneurysm, n (%)17 (17.5%)
Hypertension, n (%)65 (67%)
Diabetes mellitus, n (%)7 (7.2%)
COPD, n (%)10 (10.2%)
Creatinine, mg/dl10 [8.9; 12.2]
CAD, n (%)15 (15.5%)
LVEF, %61 [57.5; 66]
Redo surgery, n (%)9 (9.3%)

Table 1.

Demographics and comorbidities.

BMI – body mass index, BSA – body surface area, COPD – chronic obstructive pulmonary disease, CAD – coronary artery disease, LVEF – left ventricle ejection fraction. Categorical variables are presented as n (%). Continuous data are described as median with the [25th; 75th] percentiles.

Advertisement

4. Neurological results of antegrade unilateral cerebral perfusion via an innominate artery

4.1 Cerebral oximetry

As known, regional cerebral oximetry (rSO2) is a safe, robust, and operator-independent method for assessing the adequacy of cerebral oxygen balance [58]. The method is based on a local measurement of the oxygemoglobin/deoxyhemoglobin ratio (according to the modification of Beer-Lambert law) mainly in venous blood [59]. Cerebral oximetry values in normothermic settings ranged from 60 to 80%.

Changes in rSO2 in the range of 5–15% were found to correlate with changes in transcranial Doppler-measured cerebral blood flow velocity, electroencephalogram, and somatosensory evoked potentials [59]. A drop in saturation values during CPB below 40–50% (or 65–85% of the baseline) is known to be associated with high neurological complications, a rate confirmed by laboratory, instrumental, and histological findings [59, 60]. Hence, rSO2 is considered as a simple alternative to complex methods for assessing cerebral perfusion during aortic arch surgery.

According to aforementioned statements, we use intraoperative cerebral neuromonitoring of the right and left hemispheres with near-infrared spectroscopy (Invos 5100, Somanetics Corp, USA). Cerebral oximetry values were recorded throughout the entire surgical procedure: (1) at anesthesia induction, (2) at the initiation of CPB, (3) during CA, (4) after weaning from CPB, and (5) at the end of the surgery.

Our analysis showed that the range of intraoperative rSO2 values was from 60 to 70% in both hemispheres during surgery in normal arterial blood gas settings (Figure 3). At different stages of the operation, the difference in rSO2 between the cerebral hemispheres did not exceed 3%. The maximum asymmetry was revealed during circulatory arrest. Moreover, rSO2 values of each hemisphere were stable during the operation without significant differences.

Figure 3.

Intraoperative regional cerebral oximetry of the right and left hemispheres.

In addition, mean blood pressure was monitored in both radial arteries throughout the surgery (Table 2). It is worth emphasizing that blood pressure in the left radial artery as a possible surrogate of efficacy assessment of cerebral perfusion indirectly reflected the blood supply of the left hemisphere, which was derived from cross-hemispheric extra- and intracranial cerebral blood flow during right-sided cerebral perfusion.

VariableBaselineCPB startCACPB
stop		End of surgeryp-value
MBP right RA, mm Hg72
[67;80]		46
[44;51]		47.5
[41;51]		64
[60;67]		70
[64;73]		<0.001
MBP left RA, mm Hg71
[68;79]		40
[37;44]		25.5
[22;30]		63
[60;66]		69
[63;72]		<0.001
Δ, %1.41346.31.61.4
p-value0.740.01<0.0010.900.94

Table 2.

Intraoperative mean blood pressure values.

CPB – cardiopulmonary bypass, CA – circulatory arrest, MBP – mean blood pressure, RA – radial artery.

Right-left asymmetry of intraoperative mean blood pressure (MBP) ranged from 1.4 to 46.3%. MBP asymmetry increasing was observed at the initiation of CPB (13%) and reached a maximum during CA (46.3%).

Comparing rSO2 values and blood pressure asymmetry, there were differences between analyzed parameters at different stages of the operation. During CA, the difference in MBP values was 9.8 times higher (46.3%) than the difference in cerebral oximetry (3%). Nevertheless, despite the MBP in the left radial artery being as low as 25.5 mm Hg, left cerebral hemisphere oxygenation was within the normal range due to adequate cerebral cross-perfusion. Our data are in line with Urbanski et al. [61]. They observed that the MBP value in the radial arteries around 30 mm Hg is considered sufficient for cerebral cross-perfusion during unilateral antegrade cerebral perfusion.

4.2 Neurological deficit

A total of 10 (10.3%) patients had a neurological deficit postoperatively. Of these, 8 (8.2%) cases were reversible: 4 (4.2%) patients had delirium with manifestation within 14 days, and 2 (2.1%) other patients had a transient ischemic attack, which resolved within 12 hours without residual focal neurological deficit. In 2 (2.1%) patients, a non-fatal minor stroke (with a reversible neurological deficit) was recorded; additionally, in 2 (2.1%) patients, a hemorrhagic stroke was observed.

Our findings are consistent with other studies. The incidence of permanent neurological deficit (PND) after innominate cannulation during thoracic aortic surgery varies from 2.4 to 4.5%, and TND is in the range of 3–13.4% [48, 62, 63].

It is known that the duration of CPB, CA, and ACP negatively affects neurological status. However, according to our data, there were no significant differences in ischemic periods in patients with and without neurological deficits (Table 3). In an attempt to elucidate the impact of the duration of CPB, circulatory arrest, and ACP on neurological outcomes, we performed a Persons’s correlation analysis. This analysis found weak correlations between the incidence of neurological deficit and the duration of CPB (0.073, p = 0.4782), CA (−0.146, p = 0.1560), and ACP (0.15, p = 0.1456). Thus, in our patients, these variables did not influence the neurological status.

DurationWithout neurological deficit (n = 87)Neurological deficit (n = 10)p-value
PNDTND
CPB, min216 [180; 308]230 [212; 270]230 [215; 280]0.144
Lower body CA, min44 [25; 53]47.3 [44; 53]51.5 [45; 57]0.475
uACP55 [47;69]47.3 [44; 53]51.5 [45; 57]0.155

Table 3.

Duration of ischemic periods in patients with or without neurological deficit.

ACP – unilateral antegrade cerebral perfusion; CA – circulatory arrest; CPB – cardiopulmonary bypass; TND – temporary neurological deficit (including transient ischemic attack, delirium), PND – permanent neurological deficit (stroke).

4.3 Neuron-specific enolase

As known any conventional instrumental methods for evaluating postoperative cerebral damage are widely used due to their reproducibility but not accuracy. Thus, to overcome this issue, an analysis of neuron-specific markers has been proposed [64]. In contrast to well-known S100 and S100B proteins, the most reliable and specific marker reflecting cerebral damage is a neuron-specific enolase (NSE) [65]. One study [66] showed that serum NSE level within 24 hours after surgery is a useful predictor of neurologic injury onset and severity. It has been demonstrated that NSE level significantly correlated with the extent of stroke, which is in line with our results. However, to date, there is a lack of data regarding the changes of NSE values during thoracic aortic surgery in different grade of neurological deficit.

Striving to assess the cerebral damage grade in patients who underwent the frozen elephant trunk procedure, we assessed NSE serum levels by measuring an enzyme immunoassay before and after surgery in every patient. Venous blood assays were collected in the operating room before skin incision and 24 hours after surgery. Blood serum was centrifuged at 3000 rpm for 60 minutes to prevent the leakage of NSE from blood cells, with subsequent evaluation of results. NSE values between 0 and 9.9 μg/L were considered normal.

Pre- and postoperative NSE serum levels in patients without neurological deficit, with TND and PND, are presented in Figure 4.

Figure 4.

Pre- and postoperative NSE serum levels in patients without neurological deficit (ND), with TND and PND.

Patients without postoperative neurological deficit based on clinical assessment showed a 1.9-fold increase in NSE level (from 1.8 to 3.4 μg/L) after surgery compared to the baseline. However, despite statistically significant increase in postoperative NSE value (p < 0.001), its level did not exceed the normal range.

NSE levels in patients with postoperative TND increased by 5.6 times compared to the baseline and amounted to 6.2 [5.2; 6.6] μg/l. The difference between pre-and postoperative results was statistically significant (p < 0.001); however, NSE values were within the normal range.

In contrast to our aforementioned results, the NSE value in patients with postoperative PND was 10.74 [9.9; 11.8] μg/l, which exceeded the normal range. In this group of patients, a 6.7-fold increase in NSE value from baseline was recorded with a statistically significant difference (p < 0.001).

Our results suggested that NSE level might correlate with the severity of postoperative neurological deficit in patients who underwent aortic arch surgery. Our findings are supported by Kimura et al. [66] who demonstrated a similar correlation.

4.4 Cognitive assessment

To date, there is a focus on strong cerebral damage such as TND (i.e., delirium) and PND (i.e., stroke) when assessing postoperative neurological outcomes after thoracic aortic surgery. However, it is not the one manifestation that could worsen the quality of life. Recently, postoperative cognitive dysfunction, characterized as a mild neurological disorder, has become a paramount concern [67]. This kind of neurological deficit can manifest with poor attention, memory, speech, and other cognitive impairments, diagnosed by validated neurological screening tests [68, 69].

At present, the Montreal Cognitive Assessment (MoCA) has been proposed as one of the best tools for detecting the mild cognitive impairments compared to other tests [70]. Hence, it has been successfully used in patients who have suffered a stroke or underwent cardiac surgery [71]. This test assesses abstraction, language, memory, attention, and orientation abilities.

The test takes into account the patient’s initial level of education, as it adds value when comparing patients with initially different levels of cognitive reserve, which serves to maintain functional and structural properties of the brain to compensate and minimize cognitive failure after strokes, injuries, chronic cerebrovascular, neurodegenerative diseases or due to age-related changes [72].

All of the patients scheduled for surgery passed the MoCA test preoperatively. After the surgery, 10 (10.3%) patients with documented TND or PND were excluded from the assessment of cognitive function. In total, data from 87 (89.7%) patients were analyzed. The score of every patient was recorded. Evaluating the severity of cognitive postoperative cognitive dysfunction the ‘normal’ cutoff was 26 points: scores > 26 indicated no cognitive impairment (normal test), and scores < 26 indicated mild cognitive impairment [73].

In the analyzed patients with complete data, mean preoperative MoCA score was 24 [21, 25]. The “normal” cutoff was attained by 53 (60.9%) of 87 patients.

The postoperative MoCA score in the analyzed patients was 26 [1, 26]. The “normal” cutoff was reached by 57 (65.5%) out of 87 patients. According to our analysis, postoperative patients’ cognitive function was comparable to preoperative parameters, i.e., without an increasing rate of cognitive impairment.

In detail, there was an increase in attention (p = 0.012) and orientation (p = 0.009) abilities, as well as improvements in both short-term (p = 0.491) and long-term (p < 0.001) memory after surgery compared to the preoperative status. Simultaneously, we observed non-inferior postoperative values of language and abstraction abilities. Taking these results into account, we assume that ACP via innominate artery during aortic arch surgery is not associated with a decline of cognitive function or additional postoperative mental disorders.

Advertisement

5. Conclusion

Unilateral cerebral perfusion via the innominate artery during aortic arch repair is associated with a low incidence and severity of neurological deficit, minor changes in intraoperative cerebral oximetry in both hemispheres, and the absence of significant cerebral damage without a decline in postoperative cognitive function.

Advertisement

Acknowledgments

The authors would like to thank Elena Kim for her contribution to the manuscript editing.

Advertisement

Conflict of interest

The authors declare no conflict of interest.

References

  1. 1. Apostolakis E, Koletsis EN, Dedeilias P, Kokotsakis JN, Sakellaropoulos G, Psevdi A, et al. Antegrade versus retrograde cerebral perfusion in relation to postoperative complications following aortic arch surgery for acute aortic dissection type A. Journal of Cardiac Surgery. 2008;23:480-487. DOI: 10.1111/j.1540-8191.2008.00587.x
  2. 2. Yan TD, Bannon PG, Bavaria J, Coselli JS, Elefteriades JA, Griepp RB, et al. Consensus on hypothermia in aortic arch surgery. Annals of Cardiothoracic Surgery. 2013;2(2):163-168. DOI: 10.3978/j.issn.2225-319X.2013.03.03
  3. 3. Ziganshin BA, Elefteriades JA. Deep hypothermic circulatory arrest. Annals of Cardiothoracic Surgery. 2013;2(3):303-315. DOI: 10.3978/j.issn.2225-319X.2013.01.05
  4. 4. Englum BR, Andersen ND, Husain AM, Mathew JP, Hughes GC. Degree of hypothermia in aortic arch surgery – Optimal temperature for cerebral and spinal protection: Deep hypothermia remains the gold standard in the absence of randomized data. Annals of Cardiothoracic Surgery. 2013;2(2):184-193. DOI: 10.3978/j.issn.2225-319X.2013.03.01
  5. 5. Bashir M, Shaw M, Desmond M, Kuduvalli M, Field M, Oo A. Cerebral protection in hemi-aortic arch surgery. Annals of Cardiothoracic Surgery. 2013;2(2):239-244. DOI: 10.3978/j.issn.2225-319X.2013.02.04
  6. 6. Misfeld M, Mohr FW, Etz CD. Best strategy for cerebral protection in arch surgery - antegrade selective cerebral perfusion and adequate hypothermia. Annals of Cardiothoracic Surgery. 2013;2(3):331-338. DOI: 10.3978/j.issn.2225-319X.2013.02.05
  7. 7. Luehr M, Bachet J, Mohr FW, Etz CD. Modern temperature management in aortic arch surgery: The dilemma of moderate hypothermia. European Journal of Cardio-Thoracic Surgery. 2014;45(1):27-39. DOI: 10.1093/ejcts/ezt154
  8. 8. Bachet J. Open repair techniques in the aortic arch are still superior. Annals of Cardiothoracic Surgery. 2018;7(3):328-344. DOI: 10.21037/acs.2018.05.05
  9. 9. Di Eusanio M, Wesselink RMJ, Morshuis WJ, Dossche KM, Schepens MAAM. Deep hypothermic circulatory arrest and antegrade selective cerebral perfusion during ascending aorta – Hemiarch replacement: A retrospective comparative study. The Journal of Thoracic and Cardiovascular Surgery. 2003;125:849-854. DOI: 10.1067/mtc.2003.8
  10. 10. Vallabhajosyula P, Jassar AS, Menon RS, Komlo C, Gutsche J, Desai ND, et al. Moderate versus deep hypothermic circulatory arrest for elective aortic transverse hemiarch reconstruction. The Annals of Thoracic Surgery. 2015;99:1511-1517. DOI: 10.1016/j.athoracsur.2014.12.067
  11. 11. Gong M, Ma W-G, Guan X-L, Wang L-F, Li J-C, Lan F, et al. Moderate hypothermic circulatory arrest in total arch repair for acute type A aortic dissection: Clinical safety and efficacy. Journal of Thoracic Disease. 2016;8(5):925-933. DOI: 10.21037/jtd.2016.02.75
  12. 12. Englum BR, He X, Gulack DC, Ganapathi AM, Mathew JP, Brennan JM, et al. Hypothermia and cerebral protection strategies in aortic arch surgery: A comparative effectiveness analysis from the STS adult cardiac surgery database. European Journal of Cardio-Thoracic Surgery. 2017;52(3):492-498. DOI: 10.1093/ejcts/ezx133
  13. 13. Ueda Y. A reappraisal of retrograde cerebral perfusion. Annals of Cardiothoracic Surgery. 2013;2(3):316-325. DOI: 10.3978/j.issn.2225-319X.2013.01.02
  14. 14. Kin N, Ono N, Mori Y, Ninagawa J, Yamada Y. Increased cerebrovascular resistance after retrograde cerebral perfusion: A Doppler study. BioScience Trends. 2012;6(5):276-282. DOI: 10.5582/bst.2012.v6.5.276
  15. 15. Rylski B, Urbanski PP, Siepe M, Beyersdorf F, Bachet J, Gleason TG, et al. Operative techniques in patients with type a dissection complicated by cerebral malperfusion. European Journal of Cardio-Thoracic Surgery. 2014;46:156-166. DOI: 10.1093/ejcts/ezu251
  16. 16. Girardi LN, Shavladze N, Sedrakyan A, Neragi-Miandoab S. Safety and efficacy of retrograde cerebral perfusion as an adjunct for cerebral protection during surgery on the aortic arch. The Journal of Thoracic and Cardiovascular Surgery. 2014;148:2927-2935. DOI: 10.1016/j.jtcvs.2014.07.024
  17. 17. Estrera AL, Miller CC III, Lee T-Y, Shah P, Safi HJ. Ascending and transverse aortic arch repair. The impact of retrograde cerebral perfusion. Circulation. 2008;118(Suppl. 1):S160-S166. DOI: 10.1161/circulationaha.107.757419
  18. 18. Perreas K, Samanidis G, Dimitriou S, Kalogris P, Balanika M, Antzaka C, et al. Outcomes after ascending aorta and proximal aortic arch repair using deep hypothermic circulatory arrest with retrograde cerebral perfusion: Analysis of 207 patients. Interactive Cardiovascular and Thoracic Surgery. 2012;15:456-461. DOI: 10.1093/icvts/ivs252
  19. 19. Reich DL, Uysal S. Con: Retrograde cerebral perfusion is not an optimal method of neuroprotection in thoracic aortic surgery. Journal of Cardiothoracic and Vascular Anesthesia. 2003;17(6):768-769. DOI: 10.1053/j.jvca.2003.09.021
  20. 20. Aziz SA. Total circulatory arrest and retrograde cerebral perfusion during ascending aorta and arch surgery. The Journal of Egyptian Society of Cardiothoracic Surgery. 2005;13(1-2):39-43
  21. 21. Griepp RB, Griepp EB. Perfusion and cannulation strategies for neurological protection in aortic arch surgery. Annals of Cardiothoracic Surgery. 2013;2(2):159-162. DOI: 10.3978/j.issn.2225-319X.2013.03.12
  22. 22. Pochettino A, Cheung AT. Pro: Retrograde cerebral perfusion is useful for deep hypothermic circulatory arrest. Journal of Cardiothoracic and Vascular Anesthesia. 2003;17(6):764-767. DOI: 10.1053/j.jvca.2003.09.020
  23. 23. Svensson LG, Blackstone EH, Rajeswaran J, Sabik JF III, Lytle BW, Gonzalez-Stawinski G, et al. Does the arterial cannulation site for circulatory arrest influence stroke risk? The Annals of Thoracic Surgery. 2004;78:1274-1284. DOI: 10.1016/j.athoracsur.2004.04.063
  24. 24. Gutsche JT, Feinman J, Silvay G, Patel PA, Ghadimi K, Landoni G, et al. Practice variations in the conduct of hypothermic circulatory arrest for adult aortic arch repair: Focus on an emerging European paradigm. Heart, Lung and Vessels. 2014;6(1):43-51
  25. 25. Augoustides JGT, Patel P, Ghadimi K, Choi J, Yue Y, Silvay G. Current conduct of deep hypothermic circulatory arrest in China. HSR Proceedings in Intensive Care & Cardiovascular Anesthesia. 2013;5(1):25-32
  26. 26. Li B, Zhu Y, Liu A, Lu W, Su J, Zhang J, et al. Selective antegrade cerebral perfusion reduces brain injury following deep hypothermic circulatory arrest in the piglets’ model by decreasing the levels of protein SUMO2/3-ylation. International Journal of Clinical and Experimental Medicine. 2014;7(11):4562-4571
  27. 27. Leontyev S, Davierwala PM, Semenov M, von Aspern K, Krog G, Noack T, et al. Antegrade selective cerebral perfusion reduced in-hospital mortality and permanent focal neurological deficit in patients with elective aortic arch surgery. European Journal of Cardio-Thoracic Surgery. 2019;56(5):1001-1008. DOI: 10.1093/ejcts/ezz091
  28. 28. Urbanski PP, Lenos A, Zacher M, Diegeler A. Unilateral cerebral perfusion: Right versus left. European Journal of Cardio-Thoracic Surgery. 2010;37:1332-1337. DOI: 10.1016/j.ejcts.2010.01.006
  29. 29. Akamatsu Y, Nishijima Y, Lee CC, Yang SY, Shi L, An L, et al. Impaired leptomeningeal collateral flow contributes to the poor outcome following experimental stroke in the type 2 diabetic mice. The Journal of Neuroscience. 2015;35(9):3851-3864. DOI: 10.1523/jneurosci.3838-14.2015
  30. 30. Spielvogel D, Tang GHL. Selective cerebral perfusion for cerebral protection: What we do know. Annals of Cardiothoracic Surgery. 2013;2(3):326-330. DOI: 10.3978/j.issn.2225-319X.2013.03.02
  31. 31. Özatik MA, Kocabeyoglu S, Kücüker SA, Saritas A, Altintas A, Kervan Ü, et al. Neurochemical markers during selective cerebral perfusion via the right brachial artery. Interactive Cardiovascular and Thoracic Surgery. 2010;10:948-952. DOI: 10.1510/icvts.2009.228858
  32. 32. Urbanski PP, Lenos A, Blume JC, Ziegler V, Griewing B, Schmitt R, et al. Does anatomical completeness of the circle of Willis correlate with sufficient cross-perfusion during unilateral cerebral perfusion? European Journal of Cardio-Thoracic Surgery. 2008;33:402-408. DOI: 10.1016/j.ejcts.2007.12.021
  33. 33. Malvindi PG, Scrascia G, Vitale N. Is unilateral antegrade cerebral perfusion equivalent to bilateral cerebral perfusion for patients undergoing aortic arch surgery? Interactive Cardiovascular and Thoracic Surgery. 2008;7:891-897. DOI: 10.1510/icvts.2008.184184
  34. 34. Bachet J. I have only 1 brain but 2 hemispheres: Please perfuse both adequately! The Journal of Thoracic and Cardiovascular Surgery. 2017;154:765-766. DOI: 10.1016/j.jtcvs.2017.03.032
  35. 35. Takayama H, Borger MA. Bilateral antegrade cerebral perfusion during aortic dissection surgery: If no harm, then why not? The Journal of Thoracic and Cardiovascular Surgery. 2017;154:776-777. DOI: 10.1016/j.jtcvs.2017.04.030
  36. 36. Angeloni E, Melina G, Refice SK, Roscitano A, Capuano F, Comito C, et al. Unilateral versus bilateral antegrade cerebral protection during aortic surgery: An updated meta-analysis. The Annals of Thoracic Surgery. 2015;99:2024-2031. DOI: 10.1016/j.athoracsur.2015.01.070
  37. 37. Zierer A, Ahmad AE-S, Papadopoulos N, Moritz A, Diegeler A, Urbanski PP. Selective antegrade cerebral perfusion and mild (280°C-300°C) systemic hypothermic circulatory arrest for aortic arch replacement: Results from 1002 patients. The Journal of Thoracic and Cardiovascular Surgery. 2012;144:1042-1050. DOI: 10.1016/j.jtcvs.2012.07.063
  38. 38. Fukunaga N, Saji Y, Kanemitsu H, Koyama T. Prolonged antegrade cerebral perfusion via right axillary artery (≥60 min) does not affect early outcomes in a repair of type a acute aortic dissection. Annals of Thoracic and Cardiovascular Surgery. 2015;21:557-563. DOI: 10.5761/atcs.oa.15-00057
  39. 39. Verhoye J-P, Soulami RB, Fouquet O, Ruggieri VG, Kaladji A, Tomasi J, et al. Elective frozen elephant trunk procedure using the E-Vita open. Plus prosthesis in 94 patients: A multicentre French registry. European Journal of Cardio-Thoracic Surgery. 2017;52(4):733-739. DOI: 10.1093/ejcts/ezx159
  40. 40. Tong G, Zhang B, Zhou X, Tao Y, Yan T, Wang X, et al. Bilateral versus unilateral antegrade cerebral perfusion in total arch replacement for type a aortic dissection. The Journal of Thoracic and Cardiovascular Surgery. 2017;154:767-775. DOI: 10.1016/j.jtcvs.2017.02.053
  41. 41. Tian DH, Wilson-Smith A, Koo SK, Forrest P, Kiat H, Yan TD. Unilateral versus bilateral antegrade cerebral perfusion: A meta-analysis of comparative studies. Heart, Lung & Circulation. 2019;28:844-849. DOI: 10.1016/j.hlc.2019.01.010
  42. 42. Sabik JF, Lytle BW, McCarthy PM, Cosgrove DM. Axillary artery: An alternative site of arterial cannulation for patients with extensive aortic and peripheral vascular disease. The Journal of Thoracic and Cardiovascular Surgery. 1995;109:885-891
  43. 43. Apostolakis EE, Baikoussis NG, Katsanos K, Karanikolas M. Postoperative peri-axillary seroma following axillary artery cannulation for surgical treatment of acute type A aortic dissection. Journal of Cardiothoracic Surgery. 2010;5:43. DOI: 10.1186/1749-8090-5-43
  44. 44. Garg V, Tsirigotis DN, Dickson J, Dalamagas C, Latter DA, Verma S, et al. Direct innominate artery cannulation for selective antegrade cerebral perfusion during deep hypothermic circulatory arrest in aortic surgery. The Journal of Thoracic and Cardiovascular Surgery. 2014;148:2920-2924. DOI: 10.1016/j.jtcvs.2014.07.021
  45. 45. Sabik JF, Nemeh H, Lytle BW, Blackstone EH, Gillinov AM, Rajeswaran J, et al. Cannulation of the axillary artery with a side graft reduces morbidity. The Annals of Thoracic Surgery. 2004;77:1315-1320. DOI: 10.1016/j.athoracsur.2003.08.056
  46. 46. Ayyash B, Tranquilli M, Elefteriades JA. Femoral artery cannulation for thoracic aortic surgery: Safe under transesophageal echocardiographic control. The Thoracic and Cardiovascular Surgeon. 2011;142:1478-1481. DOI: 10.1016/j.jtcvs.2011.04.005
  47. 47. Preventza O, Garcia A, Tuluca A, Henry M, Cooley DA, Simpson K, et al. Innominate artery cannulation for proximal aortic surgery: Outcomes and neurological events in 263 patients. European Journal of Cardio-Thoracic Surgery. 2015;48:937-942. DOI: 10.1093/ejcts/ezu534
  48. 48. Uchino G, Yunoki K, Sakoda N, Saiki M, Hisamochi K, Yoshida H. Innominate artery cannulation for arterial perfusion during aortic arch surgery. Journal of Cardiac Surgery. 2017;32:110-113. DOI: 10.1111/jocs.13091
  49. 49. Kashani A, Doyle M, Horton M. Direct innominate artery cannulation as a sole systemic and cerebral perfusion technique in aortic surgery. Heart, Lung & Circulation. 2019;28(4):67-70. DOI: 10.1016/j.hlc.2018.08.001
  50. 50. Banbury MK, Cosgrove DM. Arterial cannulation of the innominate artery. The Annals of Thoracic Surgery. 2000;69:957. Bachet, 2018
  51. 51. Unal M, Yilmaz O, Akar I, Ince I, Aslan C, Koc F, et al. Brachiocephalic artery cannulation in proximal aortic surgery that requires circulatory arrest. Texas Heart Institute Journal. 2014;41(6):596-600. DOI: 10.14503/THIJ-13-3947
  52. 52. Tanaka H, Kazui T, Sato H, Inoue N, Yamada O, Komatsu S. Experimental study on the optimum flow rate and pressure for selective cerebral perfusion. The Annals of Thoracic Surgery. 1995;59(3):651-657
  53. 53. Huang FJ, Wu Q , Ren CW, Lai YQ , Yang S, Rui QJ, et al. Cannulation of the innominate artery with a side graft in arch surgery. The Annals of Thoracic Surgery. 2010;89:800-803. DOI: 10.1016/j.athoracsur.2009.12.005
  54. 54. Di Eusanio M, Ciano M, Labriola G, Lionetti G, Di Eusanio G. Cannulation of the innominate artery during surgery of the thoracic aorta: Our experience in 55 patients. European Journal of Cardio-Thoracic Surgery. 2007;32:270-273. DOI: 10.1016/j.ejcts.2007.03.050
  55. 55. Preventza O, Bakaeen FG, Stephens EH, Trocciola SM, de la Cruz KI, Coselli JS. Innominate artery cannulation: An alternative to femoral or axillary cannulation for arterial inflow in proximal aortic surgery. The Journal of Thoracic and Cardiovascular Surgery. 2013;145:S191-S196. DOI: 10.1016/j.jtcvs.2012.11.061
  56. 56. Ji S, Yang J, Ye X, Wang X. Brain protection by using innominate artery cannulation during aortic arch surgery. The Annals of Thoracic Surgery. 2008;86:1030-1032. DOI: 10.1016/j.athoracsur.2008.03.044
  57. 57. Kozlov BN, Panfilov DS. False lumen thrombosis after frozen elephant trunk procedure in acute and chronic aortic dissection. The Journal of Cardiovascular Surgery. 2022;63(2):195-201. DOI: 10.23736/S0021-9509.21.11800-2
  58. 58. Bergeron EJ, Mosca MS, Aftab M, Justison G, Reece TB. Neuroprotection strategies in aortic surgery. Cardiology Clinics. 2017;35(3):453-465. DOI: 10.1016/j.ccl.2017.03.011
  59. 59. Zheng F, Sheinberg R, Yee M-S, Ono M, Zheng Y, Hogue CW. Cerebral near-infrared spectroscopy monitoring and neurologic outcomes in adult cardiac surgery patients: A systematic review. Anesthesia and Analgesia. 2013;116:663-676. DOI: 10.1213/ane.0b013e318277a255
  60. 60. Urbanski PP, Lenos A, Kolowca M, Bougioukakis P, Keller G, Zacher M, et al. Near-infrared spectroscopy for neuromonitoring of unilateral cerebral perfusion. European Journal of Cardio-Thoracic Surgery. 2013;43(6):1140-1144. DOI: 10.1093/ejcts/ezs557
  61. 61. Urbanski PP, Lenos A, Lindemann Y, Weigang E, Zacher M, Diegeler A. Carotid artery cannulation in aortic surgery. The Journal of Thoracic and Cardiovascular Surgery. 2006;132:1398-1403. DOI: 10.1016/j.jtcvs.2006.07.024
  62. 62. Harky A, Wong CHM, Chan JSK, Zaki S, Froghi S, Bashir M. Innominate artery cannulation in aortic surgery: A systematic review. Journal of Cardiac Surgery. 2018;33:818-825. DOI: 10.1111/jocs.13962
  63. 63. Preventza O, Price MD, Spiliotopoulos K, Amarasekara HS, Cornwell LD, Omer S, et al. In elective arch surgery with circulatory arrest, does the arterial cannulation site really matter? A propensity score analysis of right axillary and innominate artery cannulation. The Journal of Thoracic and Cardiovascular Surgery. 2018;155(5):1953-1960. DOI: 10.1016/j.jtcvs.2017.11.095
  64. 64. Yuan S-M. Biomarkers of cerebral injury in cardiac surgery. Anadolu Kardiyoloji Dergisi. 2014;14:638-645. DOI: 10.5152/akd.2014.5321
  65. 65. Schaefer ST, Koenigsperger S, Olotu C, Saller T. Biomarkers and postoperative cognitive function: Could it be that easy? Current Opinion in Anaesthesiology. 2019;32(1):92-100. DOI: 10.1097/ACO.0000000000000676
  66. 66. Kimura F, Kadohama T, Kitahara H, Ise H, Nakanishi S, Akasaka N, et al. Serum neuron-specific enolase level as predictor of neurologic outcome after aortic surgery. The Thoracic and Cardiovascular Surgeon. 2020;68(04):282-290. DOI: 10.1055/s-0038-1677511
  67. 67. Newman MF, Grocott HP, Mathew JP, White WD, Landolfo K, Reves JG, et al. Report of the substudy assessing the impact of neurocognitive function on quality of life 5 years after cardiac surgery. Stroke. 2001;32(12):2874-2881
  68. 68. Cumming TB, Bernhardt J, Linden T. The Montreal cognitive assessment short cognitive evaluation in a large stroke trial. Stroke. 2011;42:2642-2644. DOI: 10.1161/Strokeaha.111.619486
  69. 69. Jabagi H, Wells G, Boodhwani M. Commence trial (comparing hypothermic temperatures during hemiarch surgery): A randomized controlled trial of mild vs moderate hypothermia on patient outcomes in aortic hemiarch surgery with anterograde cerebral perfusion. Trials. 2019;20(1):691. DOI: 10.1186/s13063-019-3713-9
  70. 70. Chun CT, Seward K, Patterson A, Melton A, MacDonald-Wicks L. Evaluation of available cognitive tools used to measure mild cognitive decline: A scoping review. Nutrients. 2021;13(11):3974. DOI: 10.3390/nu13113974
  71. 71. Naito Y, Hiraoka A, Himeno M, Chikazawa G, Arimichi M, Yuguchi S, et al. Clinically optimal neuropsycho-logical tests for postoperative cognitive dysfunction in heart valve surgeries. Circulation Journal. 2022;86(11):1719-1724. DOI: 10.1253/circj.CJ-22-0390
  72. 72. Hachinski V, Iadecola C, Petersen RC, Breteler MM, Nyenhuis DL, Black SE, et al. National institute of neurological disorders and stroke–Canadian stroke network vascular cognitive impairment harmonization standards. Stroke. 2006;37:2220-2241. DOI: 10.1161/01.STR.0000237236.88823.47
  73. 73. Fu C, Jin X, Chen B, et al. Comparison of the mini-mental state examination and Montreal cognitive assessment executive subtests in detecting post-stroke cognitive impairment. Geriatrics & Gerontology International. 2017;17:2329-2335. DOI: 10.1111/ggi.13069

Written By

Boris Kozlov and Dmitri Panfilov

Submitted: 01 May 2024 Reviewed: 07 May 2024 Published: 18 June 2024

© The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.