Skip to main content
Download PDF
Download ePub

The risk factors of postoperative cognitive dysfunction in patients undergoing carotid endarterectomy: an updated meta-analysis

Journal of Cardiothoracic Surgery volume 18, Article number: 309 (2023) Cite this article

Abstract

Objective

The purpose of the current meta-analysis was to determine the incidence and risk factors to provide a scientific basis for prevention and treatment of postoperative cognitive dysfunction (POCD) after carotid endarterectomy (CEA).

Methods

Relevant articles published before October 2022 were searched from Pubmed/MEDLINE, Cochrane and Embase databases. The outcomes were the incidence and risk factors for POCD. A random-effects model was applied to estimate the overall odds ratios (ORs) and mean differences (MDs) for all risk factors through STATA 14.0 and RevMan 5.4. The quality of eligible studies was evaluated by Newcastle–Ottawa Scale (NOS) as previously described.

Results

A total of 22 articles involving 3459 CEA patients were finally identified. The weighted mean incidence of POCD was 19% (95% confidence intervals (95% CI) 0.16–0.24, P < 0.001). Of the 16 identified risk factors, hyperperfusion (OR: 0.54, 95% CI 0.41–0.71) and degree of internal carotid artery (ICA) stenosis (OR: 5.06, 95% CI 0.86–9.27) were the potential risk factors of POCD, whereas patients taking statins preoperative had a lower risk of POCD (OR: 0.54, 95% CI 0.41–0.71). Subgroup analysis revealed that the risk of POCD at 1 month after CEA was higher in patients with diabetes (OR: 1.70, 95% CI 1.07–2.71).

Conclusion

The risk factors of POCD were hyperperfusion and degree of ICA stenosis, while diabetes could significantly increase the incidence of POCD at 1 month after surgery. Additionally, preoperative statin use could be a protective factor for POCD following CEA.

Peer Review reports

Introduction

Stroke is the most common cause of disability and death in the world, killing about 12 million people each year [1]. The carotid artery is one of the most common sites of atherosclerosis, and 30% of ischemic strokes originate in the carotid artery [2]. CEA is one of the main effective interventions for patients with severe carotid stenosis to reduce stroke, which is associated with various postoperative complications, including POCD. POCD, defined as a significant decrease in cognitive ability after surgery or anesthesia, is mainly associated with serious surgical outcomes, overall declined quality of life, prolonged hospitalization and even increased mortality [3]. Recently, a study indicated that the incidence of POCD in patients undergoing CEA was from 6 to 30%, and cognitive decline at 3 months in patients might be a risk factor for poor long-term survival [4]. Therefore, systematic identification of risk factors is essential for doctors and nurses to develop prevention strategies to reduce the incidence of POCD following CEA.

Different from other surgery, the mechanism of POCD after CEA might be closely associated to existed cerebrovascular lesions and the specificity of the surgical procedure. Recently, Arba et al. [5] found that cerebral small vessel disease might play a relevant role in developing cognitive impairment after CEA. A previous study indicated that the occurrence of POCD was related to covert stroke caused by cerebral microembolism during surgery [6]. Moreover, several studies confirmed that extension of cross-clamping duration and postoperative hyperperfusion could be associated with the incidence of POCD following CEA [7, 8]. There is accumulating evidence indicating that POCD is complex and multifactorial, the interaction between predisposing and precipitating factors plays a vital role in developing POCD. A meta-analysis by Aceto et al. [9] first reported the risk factors of POCD in patients undergoing CEA, while the limitations stemmed from the heterogeneity of the included studies, such as cognitive function assessment and cohort size. Furthermore, several new observational studies reported risk factors of cognitive decline after CEA recently [4, 6, 10]. Therefore, it is necessary to update the meta-analysis of POCD-related risk factors following CEA.

In the present meta-analysis, we will systematically review the incidence and perioperative risk factors for POCD following CEA by comparing with the prior articles, to provide more accurate guidance for routine screening risk factors, which may be beneficial to early interventions of at-risk individuals.

Materials and methods

Search strategy

The present meta-analysis was based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement [11], which was performed following a pre-established protocol registered on PROSPERO (CRD 42023388096). A systematic search was conducted on PubMed/MEDLINE, the Cochrane Library and Embase database for all relevant articles published from the database inception to October 25, 2022. The search strategy was based on the search components as follows: “carotid endarterectomy” and “cognitive function”, which also composed of all relevant words to these search terms through the MeSH database and expert opinions (refer to search strategy details in Additional file 1: Appendix 1).

Study selection

All original English prospective and retrospective studies including cohort, case–control, cross-sectional, etc. were considered qualified for inclusion criteria, which assessed cognitive functions in patients before and after CEA. We excluded review articles, meta-analyses, conference abstracts, comments and case reports/case series. Moreover, the reported outcomes should be odd ratios (ORs) of risk factors with 95% confidence intervals (95% CI).

All records containing titles and abstracts were inputted into Endnote X9 and repeating items were expurgated. Then, we screened titles and abstracts of the remaining studies according to inclusion criteria. The full texts of potentially included articles were further obtained and assessed by two reviewers to identify studies meeting the selection criteria independently. Any different opinions were identified by discussion, with the participation of a third author if necessary. In addition, all relevant reviews screened by the original search and the reference lists were assessed for additional eligible studies.

Data extraction and quality evaluation

We extracted details of the eligible studies, such as the first name of author, study type, year and country of publication, patient characteristics (mean or median age, percentage of female, percentage of preoperatively symptomatic patients and diabetes), methodological standards (cognitive assessment criteria and time of preoperative and postoperative cognitive assessment), Outcome measures(sample size, ORs or MD with 95% confidence intervals of risk factors and incidence of POCD when reported). Variables represented by median and quartile were converted to mean standard deviation [12]. All data was extracted by two reviewers independently, and disagreements were resolved by discussion (with a third author if necessary). The quality of eligible articles was assessed through the Newcastle–Ottawa scale (for cohort studies) [13].

Data synthesis and statistical analysis

POCD incidence was shown as proportion of the case in total sample and pooled as proportional-weighted estimates. Review Manager 5.4 and STATA 14.0 software were used to conduct the meta-analysis. Odds ratios (ORs) with 95% confidence intervals (CIs) were applied to express effect-size for dichotomous data, while mean difference (MD) and 95%CIs were used to show continuous data. If data on risk factors for studies was incomplete, the effect estimate was shown as log[OR] with standard error. First, we performed a heterogeneity test on identified studies through I2 test. A fixed effects model was applied to conduct the meta-analysis if there was no heterogeneity (P > 0.1 or I2 < 50%) in the eligible studies. If there was significant heterogeneity (P < 0.1 or I2 ≥ 50%), a random effects model was applied for the meta-analysis. Publication bias was assessed as quality through Egger’s tests. A value of P < 0.05 was identified statistically significant.

Results

Study selection

The original literature searched from three databases produced 2350 records. 2022 studies remained when 328 duplicate records were removed. Then, 1986 studies excluded according to titles and abstracts, and the full texts of 36 relevant studies were accessed and reviewed. Finally, a total of 22 observational studies, published between 2001 and 2021, were identified for further qualitative and quantitative synthesis. The database screening process was shown in Fig. 1.

Fig. 1
figure 1

Flow diagram of study select

Full size image

Study characteristics and quality evaluation

The characteristics of the eligible articles were shown in Table 1. 22 prospective and retrospective studies, including a total of 3459 adult patients undergoing CEA. Among them, 20 articles were cohort studies and 2 were case–control studies. A total of 9 studies (42.9%) assessed the cognitive function at 3 days after surgery, 8 studies (38.1%) at one month and 4 studies (19%) at one year after surgery. The sample size of these eligible articles ranged from 36 to 585. The mean age of participants was 68.39 ± 8.03 years old, and the ratio of male to female participants was 2528: 931. For quality evaluation, all eligible studies with NOS scores were more than 6, so the quality of these eligible articles was reliable (studies with NOS scores details can be found in Additional file 1: Appendix 3).

Table 1 Characteristics of observational studies included in the meta-analysis (n = 22)
Full size table

POCD incidence rate

Incidence of POCD was reported in 21 studies, in total of 3413 patients. The weighted mean incidence of POCD was 19% (95% CI 0.16–0.24), as indicated in Fig. 2. Nevertheless, the result of synthesized incidence lacked reliability due to heterogeneity was significant (I2 = 93.1%, P < 0.001). The result of subgroup analysis showed that incidence of POCD at 3 days, 1 month, 1 year after surgery was 32% (I2 = 55.9%, 95% CI 0.28–0.37, P = 0.02), 13% (I2 = 41.2%, 95% CI 0.12–0.15, P = 0.104), 13% (I2 = 0%, 95% CI 0.11–0.15, P = 0.49), respectively.

Fig. 2
figure 2

Forest plot of studies (n = 21) evaluating POCD incidence after CEA

Full size image

Patient-related risk factors for POCD

The pooled odds ratios (ORs) and mean difference (MD) of 16 risk factors with their heterogeneity test and confidence intervals results were summarized in Table 2.

Table 2 Results of meta-analysis on patient-related and procedure-related risk factors for POCD (continuous and dichotomous variables)
Full size table

Patient-related risk factors were demonstrated in 18 observational articles (shown in Table 1 and Table 2). The results revealed that the degree of ICA stenosis (OR: 5.06, 95% CI 0.86–9.27) could be the potential risk factor for POCD. Although the result lacked credibility because its heterogeneity was significant (I2 = 62%, P = 0.02), subsequent sensitivity analysis revealed that the degree of ICA stenosis was still a risk factor for POCD (OR: 3.25, 95% CI 0.45–6.06, I2 = 0%, P = 0.02), as shown in Fig. 3. Besides, patients taking statins preoperative had a lower risk of POCD (OR: 0.54, 95% CI 0.41—0.71, I2 = 0%, P < 0.001), as illustrated in Fig. 4. No significant differences were founded in age, sex, BMI, education years, diabetes, dyslipidemia, previous MI, hypertension, smoking, contralateral stenosis and preoperative symptoms, ORs and 95%CI were summarized in Table 2. The subgroup analysis indicated that diabetes could significantly increase the incidence of POCD at 1 month after surgery. (OR: 1.70, 95% CI 1.07—2.71, I2 = 0%, P = 0.02), as shown in Figs. 5 and 6.

Fig. 3
figure 3

Forest plot and sensitivity analysis of studies (n = 4) reporting mean degree of ICA stenosis in patients undergoing CEA

Full size image
Fig. 4
figure 4

Forest plot of studies (n = 7) reporting preoperative use of statins in patients undergoing CEA

Full size image
Fig. 5
figure 5

Forest plot of studies reporting diabetes (n = 17) in patients undergoing CEA

Full size image
Fig. 6
figure 6

Forest plot of subgroup analysis of studies reporting diabetes (n = 17) in patients undergoing CEA

Full size image

Procedure-related risk factors for POCD

There were 6 articles reporting hyperperfusion, 2 articles evaluating selective shunting placement and 9 studies assessing cross-clamping duration. The result of our analysis indicated that the risk of POCD increased in patients with hyperperfusion after CEA (OR: 38.67, 95% CI 19.32–77.38, I2 = 0%, P < 0.00001) as shown in Table 2 and Fig. 7. Selective shunting placement and cross-clamping duration were not significant risk factors for POCD in patients following CEA.

Fig. 7
figure 7

Forest plot of studies (n = 6) reporting presence/absence of hyperperfusion in patients undergoing CEA

Full size image

Publication bias assessment

The Egger's coefficient bias of POCD incidence (P = 0.3) and each factor relevant studies did not indicate the presence of publication bias: age (P = 0.891), sex (P = 0.939), diabetes (P = 0.518), dyslipidemia (P = 0.699), hypertension (P = 0.913), preoperative symptoms (P = 0.092), and cross-clamping duration (P = 0.299) ( The result of Egger's test details can be found in Additional file 11 Appendix 2).

Discussion

Postoperative cognitive dysfunction is a severe neurological complication after carotid endarterectomy and contributes to a variety of adverse outcomes, such as longer hospital stays and decrease in life quality [14]. However, there is no evidence indicating that specific treatments could cure POCD currently. Early identification of relative factors might play a vital role in reducing the incidence of POCD after CEA. Compared to the meta-analysis of 2020 [9], we included 7 additional studies published since then and added data from an additional 739 patients. Besides, we added some indicators that might be related to POCD, such as education years, degree of ICA stenosis and others. Finally, a total number of 3459 patients with CEA and 16 risk factors based on 22 studies were identified for meta-analysis. The potential risk factors of POCD were hyperperfusion and degree of ICA stenosis, while diabetes could significantly increase the incidence of POCD 1 month after surgery. What’s more, preoperative statin use could be a protective factor for POCD following CEA.

In the present article, the pooled incidence of POCD after CEA was 19% (95% CI 0.16–0.24), which was consistent with the result in a previous study (6–36%) [4]. Similar to previous studies, the heterogeneity of the synthetic incidence was significant (I2 = 93.1%, P < 0.001), which might be related to the adjustment for confounding factors in the most of included studies [15, 16]. Furthermore, we conducted subgroup analysis, which revealed the incidence of POCD at 3 days, 1 month, 1 year after CEA were 32%, 13% and 13% respectively. However, another meta-analysis reported the incidence of cognitive decline at 1 month (20.5%) was higher than our result, which might be related to baseline characteristics, sample size and diagnostic criteria in the included studies [9].

The result of this article revealed that hyperperfusion was a significant risk factor for POCD after CEA. Cerebral hyperperfusion, a dramatic increase in cerebral blood flow (CBF) exceeded the metabolic requirements of the brain tissue, could cause cerebral oedema or intracerebral haemorrhage. Hyperperfusion post-CEA was defined as a 100% increase or greater in CBF compared with preoperative values. CBF was measured by single-photon emission computerized tomography (SPECT) scanning before and after CEA in included articles. Some studies indicated that asymptomatic hyperperfusion could also lead to postoperative cortical neural damage and resulted in cognitive decline [17, 18]. There are several possibilities to explain the relationship of hyperperfusion and cognitive decline after CEA. Firstly, T2-weighted MR imaging on CBF showed hyperintense lesions in the region corresponding to hyperperfusion, which indicated the existence of cytotoxic edema [19]. Secondly, significant cerebral ischemia caused by embolism or clamping of the ICA during CEA can contribute to reperfusion hyperemia [10].

Moreover, different from the meta-analysis of 2020 [9], we found that the degree of ICA stenosis could be another risk factor for POCD after CEA. Although the result lacked credibility because of its significant heterogeneity (I2 = 62%, P = 0.02), subsequent sensitivity analysis revealed that the degree of ICA stenosis was still a significant risk factor for POCD. We found the study by Zhang et al. [20] might have a major impact on the heterogeneity in the result, which might be associated with the inconsecutive subjects and the small sample in the study. The main mechanism by carotid stenosis contributed to POCD might be related to the impaired cognition before surgery caused by hypoperfusion [21]. Previous study indicated that patients with unilateral carotid stenosis of 70% produced poorer cognitive function such as verbal memory and executive function, which was likely attributed to chronic hypoperfusion and microemboli from unstable carotid plaques, while cognitive impairment preoperative had been proved to be related to POCD [22, 23]. Besides, cerebral hypoperfusion induced by carotid stenosis was also thought to accelerate amyloid and tau deposition, which might be another potential link with POCD [24].

From this meta-analysis, We did not find significant relationships between patient-related factors and POCD, such as age, sex, hypertension and others. Age is a well known risk factor for POCD in patients undergoing cardiac and noncardiac surgery [25, 26]. The discrepancy from the current findings might be due to the fact that participants included in identified studies were all elderly. Besides, as previously mentioned, cross-clamping duration was an independent risk factor for POCD [20]. Conversely, our meta‐analysis showed that cross-clamping duration was not related to the occurrence of POCD after CEA, which may be associated with the adjustment for confounders.

Although there were no significant differences in diabetes, the subgroup analysis indicated that diabetes could significantly increase the incidence of POCD 1 month after surgery. Similarly, in a retrospective review of more than 6000 CEA patients, Tu et al. [27] verified that diabetes independently predicts stroke or death within 30 days of surgery. However, the association between diabetes and POCD is controversial. Diabetes, analyzed by HbA1c, was considered as a predisposing factor for POCD in several studies [28, 29], while others did not [4, 8]. Although the exact mechanism was unclear, glycemic variables was considered to play an important role in developing POCD [30]. Hyperglycemia is both a cause and result of inflammation, while neuroinflammation is an important mechanism for development of POCD, which may explain the relationship between hyperglycemia and POCD [31, 32].

Another interesting result demonstrated that statin use preoperative was a protective factor for POCD following CEA, which consistent with conclusions of previous meta-analysis [9]. Statins, known as lipid-lowering drugs, might reduce POCD risk due to lower cholesterol levels. Nevertheless, there was no significant association between dyslipidaemia and POCD in our study. According to the pleiotropic effect of statins, we speculated that statins might exert neuroprotective effects through other pathways. A previous research suggested that statins play a neuroprotective role through anti-inflammatory and regulating nitric oxide production to attenuate the ischemic reperfusion injury of asymptomatic patients after CEA [33]. In the present article, we did not analyze the effects of different types and duration of statin use on POCD. Therefore, it would be interesting to explore the effect of pre-operative treatment duration with statins on prevention of POCD after CEA.

There are some limitations in the current meta-analysis. Firstly, the absence of standardisation to define POCD may limit the precision of the analysis. Secondly, the time of evaluating cognitive function is only within 1 year after CEA in included studies, which may lead to errors in the incidence of POCD. Finally, some other risk factors such as frailty, anesthesia method and data on middle cerebral artery Doppler are not considered in this study.

Conclusions

The potential risk factors of POCD were hyperperfusion and the degree of ICA stenosis, while diabetes could significantly increase the incidence of POCD 1 month after surgery. What’s more, preoperative statin use could be a protective factor for POCD following CEA. In order to develop accurate prevention strategies, surgeons and nursing staff should have a comprehensive understanding of POCD after CEA. This meta-analysis can help them systematically identify risk factors.

Availability of data and materials

The original contributions presented in the study are included in the article/Suplementary Material; further inquiries can be directed to the corresponding author.

Abbreviations

POCD:

Postoperative cognitive dysfunction

CEA:

Carotid endarterectomy

ORs:

Odds ratios

MDs:

Mean differences

NOS:

Newcastle–Ottawa Scale

CI:

Confdence interval

ICA:

Internal carotid artery

CAS:

Carotid artery stenting

BMI:

Body mass index

CBF:

Cerebral blood flow

References

  1. Krishnamurthi RV, Ikeda T, Feigin LV. Global, regional and countryspecific burden of ischaemic stroke, intracerebral haemorrhage and subarachnoid haemorrhage: a systematic analysis of the global burden of disease study 2017. Neuroepidemiology. 2020;54:171–9.

    Article  PubMed  Google Scholar 

  2. Kolominsky-Rabas PL, Weber M, Gefeller O, Neundoerfer B, Heuschmann PU. Epidemiology of ischemic stroke subtypes according to TOAST criteria: incidence, recurrence, and longterm survival in ischemic stroke subtypes: a populationbased study. Stroke. 2001;32:2735–40.

    Article  CAS  PubMed  Google Scholar 

  3. Thiele RH, Theodore DJ, Gan TJ. Outcome of organ dysfunction in the perioperative period. Anesth Analg. 2021;133:393–405.

    Article  PubMed  Google Scholar 

  4. Relander K, Hietanen M, Nuotio K, Ijäs P, Tikkala I, et al. Cognitive dysfunction and mortality after carotid endarterectomy. Front Neurol. 2021;11: 593719.

    Article  PubMed  PubMed Central  Google Scholar 

  5. Arba F, Vit F, Nesi M, Rinaldi C, Silvestrini M, et al. Carotid revascularization and cognitive impairment: the neglected role of cerebral small vessel disease. Neurol Sci. 2022;43:139–52.

    Article  PubMed  Google Scholar 

  6. Capoccia L, Sbarigia E, Rizzo A, Mansour W, Speziale F. Silent stroke and cognitive decline in asymptomatic carotid stenosis revascularization. Vascular. 2012;20:181–7.

    Article  PubMed  Google Scholar 

  7. Kamenskaya OV, Loginova IY, Lomivorotov VV. Brain oxygen supply parameters in the risk assessment of cerebral complications during carotid endarterectomy. J Cardiothorac Vasc Anesth. 2017;31:944–9.

    Article  PubMed  Google Scholar 

  8. Igarashi S, Ando T, Takahashi T, Yoshida J, Kobayashi M, et al. Development of cerebral microbleeds in patients with cerebral hyperperfusion following carotid endarterectomy and its relation to postoperative cognitive decline. J Neurosurg. 2021;1:1–7.

    Google Scholar 

  9. Aceto P, Lai C, De Crescenzo F, Crea MA, Di Franco V, et al. Cognitive decline after carotid endarterectomy systematic review and meta-analysis. Eur J Anaesthesiol. 2020;37:1066–74.

    Article  PubMed  Google Scholar 

  10. Zhang LM, Li Y, Zhang YT, Zhang BX, Wang JZ, et al. Decrease of coronal optic nerve sheath diameter is associated with postoperative cognitive decline in patients undergoing carotid endarterectomy. J Cardiothorac Vasc Anesth. 2021;35:2355–62.

    Article  PubMed  Google Scholar 

  11. Booth A, Clarke M, Ghersi D, Moher D, Stewart L. An international registry of systematic-review protocols. Lancet. 2011;377:108–9.

    Article  PubMed  Google Scholar 

  12. Luo D, Wan X, Liu J, Tong T. Optimally estimating the sample mean from the sample size, median, mid-range, and/or mid-quartile range. Stat Methods Med Res. 2018;27:1785–805.

    Article  PubMed  Google Scholar 

  13. Wells GA, Shea B, O’Connell D. The Newcastle-Ottawa scale(NOS) for assessing the quality of nonrandomised studies in metaanalysis. Ottawa: Ottawa Hospital Research Institute. 2011. Available from: http://www.ohri.ca/programs/clinical_epidemiology/oxford.asp.

  14. Park SY, Lee HB. Prevention and management of delirium in critically ill adult patients in the intensive care unit: a review based on the 2018 PADIS guidelines. Acute Crit Care. 2019;34:117–25.

    Article  PubMed  PubMed Central  Google Scholar 

  15. Rong X, Ding ZC, Yu HD, Yao SY, Zhou ZK. Risk factors of postoperative delirium in the knee and hip replacement patients: a systematic review and meta-analysis. J Orthop Surg Res. 2021;16:76.

    Article  PubMed  PubMed Central  Google Scholar 

  16. Wang X, Yu D, Du Y, Geng J. Risk factors of delirium after gastrointestinal surgery: A meta-analysis. J Clin Nurs. 2022.

  17. Nanba T, Ogasawara K, Nishimoto H, Fujiwara S, Kuroda H, et al. Postoperative cerebral white matter damage associated with cerebral hyperperfusion and cognitive impairment after carotid endarterectomy: a diffusion tensor magnetic resonance imaging study. Cerebrovasc Dis. 2012;34:358–67.

    Article  PubMed  Google Scholar 

  18. Hirooka R, Ogasawara K, Sasaki M, Fujiwara S, Kuroda H, et al. Magnetic resonance imaging in patients with cerebral hyperperfusion and cognitive impairment after carotid endarterectomy. J Neurosurg. 2008;108:1178–83.

    Article  PubMed  Google Scholar 

  19. Takahashi T, Uwano I, Akamatsu Y, Chida K, Kobayashi M, et al. Prediction of cerebral hyperperfusion following carotid endarterectomy using intravoxel incoherent motion magnetic resonance imaging. J Stroke Cerebrovasc Dis. 2022;32: 106909.

    Article  PubMed  Google Scholar 

  20. Zhang HP, Ma XD, Chen LF, Yang Y, Xu BN, et al. Cognitive function after carotid endarterectomy: early decline and later recovery. Turk Neurosurg. 2016;26:833–9.

    PubMed  Google Scholar 

  21. Porcu M, Cocco L, Saloner D, Suri JS, Montisci R, et al. Extracranial carotid artery stenosis: the effects on brain and cognition with a focus on resting-state functional connectivity. J Neuroimaging. 2020;30:736–45.

    Article  PubMed  Google Scholar 

  22. Silvestrini M, Paolino I, Vernieri F, Pedone C, Baruffaldi R, et al. Cerebral hemodynamics and cognitive performance in patients with asymptomatic carotid stenosis. Neurology. 2009;72:1062–8.

    Article  CAS  PubMed  Google Scholar 

  23. Greaves D, Psaltis PJ, Davis DHJ, Ross TJ, Ghezzi ES, et al. Risk factors for delirium and cognitive decline following coronary artery bypass grafting surgery: a systematic review and meta-analysis. J Am Heart Assoc. 2020;9: e017275.

    Article  PubMed  PubMed Central  Google Scholar 

  24. Koike MA, Green KN, Blurton-Jones M, LaFerla FM. Oligemic hypoperfusion differentially affects tau and amyloid-β. Am J Pathol. 2010;177:300–10.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Chen H, Mo L, Hu H, Ou Y, Luo J, et al. Risk factors of postoperative delirium after cardiac surgery: a meta-analysis. J Cardiothorac Surg. 2021;16:113.

    Article  PubMed  PubMed Central  Google Scholar 

  26. Janssen TL, Alberts AR, Hooft L, Mattace-Raso F, Mosk CA, et al. Prevention of postoperative delirium in elderly patients planned for elective surgery: systematic review and meta-analysis. Clin Interv Aging. 2019;14:1095–117.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  27. Tu JV, Wang H, Bowyer B, Green L, Fang J, Kucey D. Risk factors for death or stroke after carotid endarterectomy: observations from the Ontario carotid endarterectomy registry. Stroke. 2003;34:2568–73.

    Article  PubMed  Google Scholar 

  28. Mocco J, Wilson DA, Komotar RJ, Zurica J, Mack WJ, et al. Predictors of neurocognitive decline after carotid endarterectomy. Neurosurgery. 2006;58:844–50.

    Article  CAS  PubMed  Google Scholar 

  29. Kotfis K, Szylińska A, Listewnik M, Brykczyński M, Ely EW, et al. Diabetes and elevated preoperative HbA1c level as risk factors for postoperative delirium after cardiac surgery: an observational cohort study. Neuropsychiatr Dis Treat. 2019;15:511–21.

    Article  PubMed  PubMed Central  Google Scholar 

  30. Berger M, Terrando N, Smith SK, Browndyke JN, Newman MF. Neurocognitive function after cardiac surgery. Anesthesiology. 2018;129:829–51.

    Article  PubMed  Google Scholar 

  31. Tsalamandris S, Antonopoulos AS, Oikonomou E, Papamikroulis GA, Vogiatzi G, et al. The role of inflammation in diabetes: current concepts and future perspectives. Eur Cardiol. 2019;14:50–9.

    Article  PubMed  PubMed Central  Google Scholar 

  32. Li Z, Zhu Y, Kang Y, Qin S, Chai J. Neuroinflammation as the underlying mechanism of postoperative cognitive dysfunction and therapeutic strategies. Front Cell Neurosci. 2022;16: 843069.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  33. van der Most PJ, Dolga AM, Nijholt IM, Luiten PG, Eisel UL. Statins: mechanisms of neuroprotection. Prog Neurobiol. 2009;88:64–75.

    Article  PubMed  Google Scholar 

  34. Robison TR, Heyer EJ, Wang S, Caccappolo E, Mergeche JL, et al. Easily screenable characteristics associated with cognitive improvement and dysfunction after carotid endarterectomy. World Neurosurg. 2019;121:e200–6.

    Article  PubMed  Google Scholar 

  35. Heyer EJ, Mergeche JL, Wang S, Gaudet JG, Connolly ES. Impact of cognitive dysfunction on survival in patients with and without statin use following carotid endarterectomy. Neurosurgery. 2015;77:880–7.

    Article  PubMed  Google Scholar 

  36. Heyer EJ, Mergeche JL, Stern Y, Malone HR, Bruce SS, et al. Apolipoprotein E-ε4 polymorphism and cognitive dysfunction after carotid endarterectomy. J ClinNeurosci. 2014;21:236–40.

    CAS  Google Scholar 

  37. Sussman ES, Kellner CP, Mergeche JL, Bruce SS, McDowell MM, et al. Radiographic absence of the posterior communicating arteries and the prediction of cognitive dysfunction after carotid endarterectomy. J Neurosurg. 2014;121:593–8.

    Article  PubMed  Google Scholar 

  38. Heyer EJ, Mergeche JL, Bruce SS, Connolly ES. Does cognitive dysfunction after carotid endarterectomy vary by statin type or dose? Int J brain Cogn Sci. 2013;2:57–62.

    PubMed  PubMed Central  Google Scholar 

  39. Saito H, Ogasawara K, Nishimoto H, Yoshioka Y, Murakami T, et al. Postoperative changes in cerebral metabolites associated with cognitive improvement and impairment after carotid endarterectomy: a 3T proton MR spectroscopy study. Am J Neuroradiol. 2013;34:976–82.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  40. Takahashi Y, Ogasawara K, Matsumoto Y, Kobayashi M, Yoshida K, et al. Changes in cognitive function after carotid endarterectomy in older patients: comparison with younger patients. Neurol Med Chir. 2013;53:353–9.

    Article  Google Scholar 

  41. Yoshida KK, Ogasawara K, Kobayashi M, Yoshida K, Kubo Y, et al. Improvement and impairment in cognitive function after carotid endarterectomy: comparison of objective and subjective assessments. Neurol Med Chir. 2012;52:154–60.

    Article  Google Scholar 

  42. Gaudet JG, Yocum GT, Lee SS, Granat A, Mikami M, et al. MMP-9 levels in elderly patients with cognitive dysfunction after carotid surgery. J ClinNeurosci. 2010;17:436–40.

    CAS  Google Scholar 

  43. Chida K, Ogasawara K, Suga Y, Saito H, Kobayashi M, et al. Postoperative cortical neural loss associated with cerebral hyperperfusion and cognitive impairment after carotid endarterectomy 123I-iomazenil SPECT study. Stroke. 2009;40:448–53.

    Article  PubMed  Google Scholar 

  44. Soinne L, Helenius J, Tikkala I, Saimanen E, Salonen O, et al. The effect of severe carotid occlusive disease and its surgical treatment on cognitive functions of the brain. Brain Cogn. 2009;69:353–9.

    Article  PubMed  Google Scholar 

  45. Ogasawara K, Yamadate K, Kobayashi M, Endo H, Fukuda T, et al. Postoperative cerebral hyperperfusion associated with impaired cognitive function in patients undergoing carotid endarterectomy. J Neurosurg. 2005;102:38–44.

    Article  PubMed  Google Scholar 

  46. Sahlein DH, Heyer EJ, Rampersad A, Winfree CJ, Solomon RA, et al. Failure of intraoperative jugular bulb S-100B and neuron-specific enolase sampling to predict cognitive injury after carotid endarterectomy. Neurosurgery. 2003;53:1243–50.

    Article  PubMed  Google Scholar 

  47. Connolly ES, Winfree CJ, Rampersad A, Sharma R, Mack WJ, et al. Serum S100B protein levels are correlated with subclinical neurocognitive declines after carotid endarterectomy. Neurosurgery. 2001;49:1076–82.

    PubMed  Google Scholar 

Download references

Acknowledgements

All authors appreciated for the support from Hebei General Hospital.

Author information

Authors and Affiliations

  1. Department of Anesthesiology, Hebei General Hospital, Shijiazhuang, China

    Jinhua He, Ran Duan, Huanhuan Zhang, Meng Zhang, Meinv Liu, Xiaoqian Wu & Jianli Li

  2. Clinical Laboratory, Hebei General Hospital, Shijiazhuang, 050051, China

    Peng Qiu

Authors
  1. Jinhua He
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Ran Duan
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Peng Qiu
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Huanhuan Zhang
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Meng Zhang
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Meinv Liu
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Xiaoqian Wu
    View author publications

    You can also search for this author in PubMed Google Scholar

  8. Jianli Li
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

The following authors made contributions to this manuscript: design or idea of the study: JHH and JLL; data extraction: JHH, RD and PQ; conducting meta-analysis: RD, HHZ and MZ; drafting the manuscript: JHH, JLL and MNL; revision of the article: all participating authors. All authors contributed to the article and approved the submitted version.

Corresponding author

Correspondence to Jianli Li.

Ethics declarations

Ethics approval and consent to participate

Ethical approval for this study was not necessary because the study was a review of existing literature and did not involve the processing of any individual patient data.

Consent for publication

Not applicable.

Competing interests

The authors declare no conficts of interest.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary Information

Additional file 1

: Search Strategy and Supplemental Tables and Figures.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

He, J., Duan, R., Qiu, P. et al. The risk factors of postoperative cognitive dysfunction in patients undergoing carotid endarterectomy: an updated meta-analysis. J Cardiothorac Surg 18, 309 (2023). https://doi.org/10.1186/s13019-023-02428-6

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s13019-023-02428-6

Keywords

Journal of Cardiothoracic Surgery

ISSN: 1749-8090

Contact us