
==== Front
Ann Med
Ann Med
Annals of Medicine
0785-3890
1365-2060
Taylor & Francis

39268588
10.1080/07853890.2024.2402950
2402950
Version of Record
Research Article
Cardiology & Cardiovascular Disorders
Evaluation of silent brain injury in patients undergoing aorto-ostial coronary stent implantation
U. Yildirim et al.
https://orcid.org/0000-0002-8848-8711
Yildirim Ufuk a
Kara Abdulkadir a
https://orcid.org/0000-0002-5103-0141
Uyanik Muhammet b
Kocasari Ahmet Onur a
Cinar Ahmet a
Coksevim Metin a
Avci Bahattin c
Soylu Korhan a
Gulel Okan a
a Department of Cardiology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey
b Department of Cardiology, Carsamba State Hospital, Samsun, Turkey
c Department of Biochemistry, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey
CONTACT Ufuk Yildirim ufukyildirim2715@yahoo.com.tr Department of Cardiology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey
13 9 2024
2024
13 9 2024
56 1 24029503 10 2023
30 4 2024
6 6 2024
KnowledgeWorks Global Ltd.12 9 2024
published online in a building issue12 9 2024
© 2024 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group
2024
The Author(s)
https://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

Abstract

Background

Aorto-ostial (AO) coronary interventions may be associated with multiple problems, including the potential embolization of atherothrombotic debris into the aorta and systemic circulation. Such embolization could theoretically lead to stroke or silent brain injury (SBI). In this study, we aimed to investigate whether there is an increased risk of SBI in patients undergoing AO stent implantation.

Methods

Fifty-five consecutive patients undergoing AO stenting and 55 consecutive patients undergoing non-AO stenting were included. Venous blood samples were obtained before and 12 h after the procedure to measure neuron-specific enolase (NSE), which is a sensitive marker of brain injury. Newly developed NSE elevation after the procedure in an asymptomatic patient was defined as SBI.

Results

SBI was detected in 24 (43.6%) patients in the AO stenting group and 17 (30.9%) patients in the non-AO stenting group (p = .167). Although the SBI rates were statistically comparable between the groups, the presence of significant (≥50%) AO stenosis was found to be an independent predictor of SBI in multivariate logistic regression analysis [odds ratio (OR) 2.856; 95% confidence interval (CI) 1.057-7.716; p = .038]. A longer procedure time was another independent predictor for the development of SBI (OR 1.037; 95% CI 1.005-1.069; p = .023).

Conclusion

This study suggests that AO stenting may be associated with an increased risk of SBI if the lesion in the ostium is significant.

Keywords

Aorto-ostial stenting
silent brain injury
neuron-specific enolase
The authors declare that no funding was received for conducting this study.
==== Body
pmcIntroduction

Aorto-ostial (AO) coronary interventions present many challenges for interventional cardiologists. Some of these challenges include inability to engage, pressure dampening, difficulty in stent placement and inability to re-engage after stent implantation [1]. Another possible problem that may be associated with AO interventions is the potential embolization of atherothrombotic debris into the aorta and systemic circulation. Such embolization could theoretically lead to stroke or silent brain injury (SBI). The definition of SBI is based on evidence of neuronal injury in the absence of clinically apparent stroke or transient ischemic attack (TIA) [2]. Evidence of neuronal injury can be demonstrated mainly with the use of imaging modalities [2] but an acute injury can also be detected by biochemical markers such as neuron-specific enolase (NSE) [3]. NSE is an intracytoplasmic enzyme found in neurons that can be detected in serum approximately 2 h after acute neuronal injury, reaches a peak level at about 12 h, and remains positive for about 3 days [4]. Serum NSE levels have been employed to predict acute brain injury in various conditions affecting the brain directly (e.g. stroke and traumatic brain injury) or indirectly (e.g. cardiac arrest, cardiopulmonary bypass, and neonatal hypoxia) [3–11]. The risk of SBI detected by serum NSE elevation has been shown to increase in patients undergoing coronary stent implantation for acute or chronic coronary syndromes [12–16]. In this study, we aimed to investigate whether there is a further increased risk of SBI in patients undergoing AO stent implantation and to identify baseline and procedural characteristics that may be associated with the development of SBI.

Methods

Fifty-five consecutive patients who underwent AO stenting and 55 consecutive patients who underwent non-AO stenting were included in this prospective, single-centre, observational study. The AO stenting group consisted of patients with ≥70% stenosis in whom the stent protruded 1-2 mm into the aorta according to the operator’s decision for complete coverage of the plaque in the ostium (Figure 1). The non-AO stenting group consisted of patients with ≥70% stenosis who underwent stent implantation in a coronary vessel, but not within 3 mm of the aortic ostia. The exclusion criteria were as follows: baseline NSE elevation, ST-segment elevation myocardial infarction, hemodynamic instability, left ventricular ejection fraction (LVEF) <40%, severe aortic stenosis, chronic total occlusion (CTO) as the target lesion, percutaneous treatment of multiple unrelated lesions, atrial fibrillation, prior stroke or TIA, degenerative central nervous system (CNS) disorders, CNS or neuroendocrine tumours and symptomatic peripheral arterial diseases.

Figure 1. (a). Critical lesion involving the proximal and mid segments of the RCA with approximately 30% stenosis in the ostium.

RCA, right coronary artery. (b). The RCA after the implantation of 2 stents overlapping. The proximal stent was protruded 1-2 mm into the aorta for complete coverage of the plaque in the ostium.

RCA, right coronary artery.

The baseline patient characteristics were recorded. Age, sex, smoking status and body mass index were noted. History of hypertension, diabetes, prior myo­cardial infarction, prior percutaneous coronary intervention (PCI) and prior coronary artery bypass grafting (CABG) were assessed. Glycated haemoglobin, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglyceride levels at presentation were noted. The glomerular filtration rate (GFR) was estimated using the Modification of Diet in Renal Disease formula. Patients with GFR <60 mL/min/1.73 m2 for at least 3 months were considered to have chronic kidney disease [17]. LVEF was calculated using the modified Simpson method. The diagnosis at admission was recorded as non-ST-segment elevation acute coronary syndrome or chronic coronary syndrome.

Aspirin (300 mg) was given orally to all patients at admission. The P2Y12 inhibitor was loaded after imaging of the coronary anatomy. Unfractionated heparin 70/100 IU/kg was administered at the beginning of PCI to obtain activated clotting times of 250–350 s. Pre-dilation and post-dilation were performed in all target lesions. Additionally, in all patients undergoing AO stent implantation, ostium flaring was performed by inflating a balloon half-way in the stent and half-way in the aorta [1]. Access site, P2Y12 inhibitor choice, guiding catheter size, number and length of stents implanted, kissing balloon (KB) inflation or bifurcation stenting (BS) with two stents if necessary were left to the operator’s discretion. The number of diseased vessels was defined as the number of major epicardial coronary arteries with ≥50% stenosis and was recorded as 1, 2 or 3. Diameter stenosis was assessed visually. Significant AO stenosis was defined as ≥50% stenosis within 3 mm of the orifice engaged by the guiding catheter. Calcification more than just spots in the ostium engaged by the guiding catheter was noted as moderate or severe AO calcification [18]. The reference vessel diameter (RVD) was accepted as the diameter reached by the stent or post-dilation balloon, whichever was higher. The target vessel, native or in-stent target lesion, contrast volume, and procedure time were also recorded.

Venous blood samples were obtained before and 12 h after the procedure for NSE measurements. NSE levels were measured using a human NSE enzyme-linked immunosorbent assay (ELISA) kit (Sunredbio, Shanghai, China). The absolute change in NSE was calculated by subtracting the baseline NSE level from the postprocedural NSE level. The intra- and inter-assay coefficients of variability were <10% and <12%, respectively. The upper reference limit of normal for the kits, determined by the manufacturer, was 20 ng/mL. NSE within normal limits before the procedure and >20 ng/mL after the procedure in an asymptomatic patient was defined as SBI.

The research data were uploaded and analysed using the Statistical Package for Social Sciences (SPSS) version 25, for which a copyright license was obtained. Descriptive statistics for categorical variables are presented as frequencies and percentages. The chi-square test or Fisher’s exact test in case of any cells with an expected count of less than 5 in the crosstabs, was used to compare categorical variables. The Kolmogorov–Smirnov test was applied to determine whether the numerical variables were normally distributed. Descriptive statistics are expressed as mean ± standard deviation for numerical variables with a normal distribution and as median (minimum-maximum) for those without a normal distribution. An independent samples t-test was used to compare numerical variables with a normal distribution, and Levene’s test was utilized to check the equality of variances. The Mann–Whitney U-test was used to compare numerical variables without a normal distribution. Multivariate logistic regression analysis was performed to identify the independent predictors of NSE elevation after the procedure. All baseline and procedural characteristics evaluated in the study were subjected to univariate analysis, and variables with p < 0.1 in the univariate analysis were subjected to multivariate analysis. In this study, no data were missing, and the statistical significance level was set at p < 0.05.

Results

The stenting procedure was successful in all patients included in the study, with <30% residual stenosis and Thrombolysis In Myocardial Infarction (TIMI) grade 3 flow. TIA, stroke, or death were not observed in any of the patients during hospitalization, and no patients were subjected to magnetic resonance imaging (MRI) after PCI.

SBI was detected in 24 (43.6%) patients in the AO stenting group and 17 (30.9%) patients in the non-AO stenting group (p = 0.167). The baseline NSE was similar between the groups, but the postprocedural NSE and the absolute change in NSE were significantly higher in the AO stenting group (p = 0.021 and p = 0.007, respectively). The baseline characteristics of the AO and non-AO stenting groups were comparable. Among the procedural characteristics, access site, number of diseased vessels, native or in-stent target lesion, diameter stenosis, moderate or severe AO calcification, guiding catheter size, total stent length per lesion, KB inflation, BS with 2 stents, and procedure time were similar. The target vessel was the right coronary artery (RCA) in 31 (56.4%), left main coronary artery (LM) in 22 (40.0%), and saphenous vein graft (SVG) in 2 (3.6%) patients in the AO stenting group, whereas it was the left anterior descending artery in 22 (40.0%), left circumflex artery in 15 (27.3%), RCA in 15 (27.3%), LM in 2 (3.6%), and SVG in 1 (1.8%) patient in the non-AO stenting group (p <. 001). Significant AO stenosis was present in 22 (40.0%) patients in the AO stenting group, but none of the patients in the non-AO stenting group had significant AO stenosis (p <. 001). The P2Y12 inhibitor was significantly different between the groups (p = .015). The RVD, number of stents per lesion, and contrast volume were significantly higher in the AO stenting group (p <. 001, p = .019, and p = .031, respectively) (Table 1).

Table 1. Comparison of baseline and procedural characteristics, and SBI rates of AO and non-AO stenting groups.

Variable	AO stenting (n = 55)	Non-AO stenting (n = 55)	P	
Age (year)	64.3 ± 10.6	64.2 ± 8.6	0.968	
Sex	Male (%*)	30 (54.5)	35 (63.6)	0.332	
Female (%*)	25 (45.5)	20 (36.4)	
Smoking	Current (%*)	15 (27.3)	13 (23.6)	0.628	
Past (%*)	15 (27.3)	12 (21.8)	
Never (%*)	25 (45.5)	30 (54.5)	
Hypertension (%*)	32 (58.2)	36 (65.5)	0.432	
Diabetes (%*)	27 (49.1)	27 (49.1)	1.000	
HbA1c (%)	6.0 (5.1-11.6)	6.3 (5.3-12.9)	0.108	
Total cholesterol (mg/dL)	185.2 ± 48.6	176.1 ± 46.6	0.337	
LDL cholesterol (mg/dL)	113.7 ± 45.1	101.7 ± 40.5	0.159	
HDL cholesterol (mg/dL)	41 (22–67)	40 (22–88)	0.311	
Triglyceride (mg/dL)	123 (47–1145)	136 (65–461)	0.114	
Body mass index (kg/m2)	27.5 (19.6–37.1)	27.6 (21.6–39.0)	0.335	
Chronic kidney disease (%*)	10 (18.2)	8 (14.5)	0.606	
GFR (mL/min/1.73 m2)	82.4 ± 22.4	83.1 ± 22.6	0.866	
Prior MI (%*)	26 (47.3)	20 (36.4)	0.246	
Prior PCI (%*)	22 (40.0)	26 (47.3)	0.442	
Prior CABG (%*)	9 (16.4)	3 (5.5)	0.067	
LVEF (%)	55 (40-73)	55 (40-70)	0.505	
Diagnosis at admission	NSTE-ACS (%*)	19 (34.5)	17 (30.9)	0.684	
CCS (%*)	36 (65.5)	38 (69.1)	
Access site	Radial (%*)	26 (47.3)	33 (60.0)	0.181	
Femoral (%*)	29 (52.7)	22 (40.0)	
Number of diseased vessels	1 (%*)	20 (36.4)	30 (54.5)	0.152	
2 (%*)	30 (54.5)	22 (40.0)	
3 (%*)	5 (9.1)	3 (5.5)	
Target vessel	LM (%*)	22 (40.0)	2 (3.6)	<0.001	
LAD (%*)	0	22 (40.0)	
LCX (%*)	0	15 (27.3)	
RCA (%*)	31 (56.4)	15 (27.3)	
SVG (%*)	2 (3.6)	1 (1.8)	
Native/in-stent	Native (%*)	53 (96.4)	51 (92.7)	0.679	
In-stent (%*)	2 (3.6)	4 (7.3)	
Diameter stenosis (%)	85 (70–100)	90 (70–100)	0.552	
Significant AO stenosis (%*)	22 (40.0)	0	<0.001	
Moderate or severe AO calcification (%*)	5 (9.1)	3 (5.5)	0.716	
P2Y12 inhibitor	Prasugrel (%*)	17 (30.9)	5 (9.1)	0.015	
Ticagrelor (%*)	6 (10.9)	6 (10.9)	
Clopidogrel (%*)	32 (58.2)	44 (80.0)	
Guiding catheter size	6Fr (%*)	37 (67.3)	42 (76.4)	0.289	
7Fr (%*)	18 (32.7)	13 (23.6)	
Reference vessel diameter (mm)	4.3 (2.8–5.7)	3.3 (2.7–5.2)	<0.001	
Number of stents per lesion	1.4 ± 0.6	1.2 ± 0.4	0.019	
Total stent length per lesion (mm)	32 (12–81)	23 (12–78)	0.090	
KB inflation (%*)	10 (18.2)	7 (12.7)	0.429	
BS with 2 stents (%*)	4 (7.3)	4 (7.3)	1.000	
Contrast volume (mL)	130 (50-230)	100 (40-270)	0.031	
Procedure time (min)	33.8 ± 14.4	31.9 ± 14.1	0.493	
Baseline NSE (ng/ mL)	9.76 ± 3.28	9.24 ± 3.28	0.413	
Postprocedural NSE (ng/ mL)	16.3 (3.8-86.1)	10.4 (3.2-88.2)	0.021	
Absolute change in NSE (ng/ mL)	5.9 (−1.8–71.3)	0.1 (−1.8–78.9)	0.007	
SBI (%*)	24 (43.6)	17 (30.9)	0.167	
AO: aorto-ostial; BS: bifurcation stenting; CABG: coronary artery bypass grafting; CCS: chronic coronary syndrome; Fr: French; GFR: glomerular filtration rate; HbA1c: glycated haemoglobin; HDL: high-density lipoprotein; KB: kissing balloon; LAD: left anterior descending artery; LCX: left circumflex artery; LDL: low-density lipoprotein; LM: left main coronary artery; LVEF: left ventricular ejection fraction; MI: myocardial infarction; NSE: neuron-specific enolase; NSTE-ACS: non-ST-segment elevation acute coronary syndrome; PCI: percutaneous coronary intervention; RCA: right coronary artery; SBI: silent brain injury; SVG: saphenous vein graft.

* Column percentage.

When comparing the baseline and procedural characteristics of patients with and without SBI, patients with SBI were more likely to have significant AO stenosis and longer procedure times (p = 0.018 and p = 0.025, respectively) (Table 2).

Table 2. Comparison of baseline and procedural characteristics of patients with and without SBI.

Variable	SBI (+) (n = 41)	SBI (-) (n = 69)	P	
Age (year)	65 (39–89)	65 (32–83)	0.582	
Sex	Male (%*)	28 (68.3)	37 (53.6)	0.130	
Female (%*)	13 (31.7)	32 (46.4)	
Smoking	Current (%*)	9 (22.0)	19 (27.5)	0.395	
Past (%*)	13 (31.7)	14 (20.3)	
Never (%*)	19 (46.3)	36 (52.2)	
Hypertension (%*)	23 (56.1)	45 (65.2)	0.341	
Diabetes (%*)	25 (61.0)	29 (42.0)	0.055	
HbA1c (%)	6.7 (5.2–12.9)	6.1 (5.1–11.6)	0.216	
Total cholesterol (mg/dL)	186.0 ± 56.6	177.5 ± 41.5	0.421	
LDL cholesterol (mg/dL)	110.3 ± 50.0	106.1 ± 38.8	0.659	
HDL cholesterol (mg/dL)	41 (22–88)	41 (22–64)	0.797	
Triglyceride (mg/dL)	130 (52–1145)	131 (47–461)	0.956	
Body mass index (kg/m2)	27.4 (21.1–37.1)	27.6 (19.6–39.0)	0.670	
Chronic kidney disease (%*)	8 (19.5)	10 (14.5)	0.491	
GFR (mL/min/1.73 m2)	83.7 ± 23.0	82.1 ± 22.2	0.734	
Prior MI (%*)	19 (46.3)	27 (39.1)	0.458	
Prior PCI (%*)	20 (48.8)	28 (40.6)	0.402	
Prior CABG (%*)	6 (14.6)	6 (8.7)	0.358	
LVEF (%)	51 (40–73)	55 (40–70)	0.278	
Diagnosis at admission	NSTE-ACS (%*)	11 (26.8)	25 (36.2)	0.310	
CCS (%*)	30 (73.2)	44 (63.8)	
Access site	Radial (%*)	23 (56.1)	36 (52.2)	0.690	
Femoral (%*)	18 (43.9)	33 (47.8)	
Number of diseased vessels	1 (%*)	17 (41.5)	33 (47.8)	0.828	
2 (%*)	21 (51.2)	31 (44.9)	
3 (%*)	3 (7.3)	5 (7.2)	
Target vessel	LM (%*)	8 (19.5)	16 (23.2)	0.405	
LAD (%*)	8 (19.5)	14 (20.3)	
LCX (%*)	3 (7.3)	12 (17.4)	
RCA (%*)	20 (48.8)	26 (37.7)	
SVG (%*)	2 (4.9)	1 (1.4)	
Native/in-stent	Native (%*)	39 (95.1)	65 (94.2)	1.000	
In-stent (%*)	2 (4.9)	4 (5.8)	
Diameter stenosis (%)	90 (70–100)	85 (70–100)	0.119	
Significant AO stenosis (%*)	13 (31.7)	9 (13.0)	0.018	
Moderate or severe AO calcification (%*)	4 (9.8)	4 (5.8)	0.468	
P2Y12 inhibitor	Prasugrel (%*)	7 (17.1)	15 (21.7)	0.823	
Ticagrelor (%*)	5 (12.2)	7 (10.1)	
Clopidogrel (%*)	29 (70.7)	47 (68.1)	
Guiding catheter size	6Fr (%*)	30 (73.2)	49 (71.0)	0.808	
7Fr (%*)	11 (26.8)	20 (29.0)	
Reference vessel diameter (mm)	3.8 (2.7–5.2)	3.8 (2.7–5.7)	0.748	
Number of stents per lesion	1.4 ± 0.6	1.2 ± 0.5	0.139	
Total stent length per lesion (mm)	28 (12-81)	24 (12-78)	0.178	
KB inflation (%*)	5 (12.2)	12 (17.4)	0.466	
BS with 2 stents (%*)	3 (7.3)	5 (7.2)	1.000	
Contrast volume (mL)	120 (50-230)	110 (40-270)	0.717	
Procedure time (min)	33 (15-92)	29 (12-61)	0.025	
AO: aorto-ostial; BS: bifurcation stenting; CABG: coronary artery bypass grafting; CCS: chronic coronary syndrome; Fr: French; GFR: glomerular filtration rate; HbA1c: glycated haemoglobin; HDL: high-density lipoprotein; KB: kissing balloon; LAD: left anterior descending artery; LCX: left circumflex artery; LDL: low-density lipoprotein; LM: left main coronary artery; LVEF: left ventricular ejection fraction; MI: myocardial infarction; NSTE-ACS: non-ST-segment elevation acute coronary syndrome; PCI: percutaneous coronary intervention; RCA: right coronary artery; SBI: silent brain injury; SVG: saphenous vein graft.

* Column percentage.

Although the SBI rates were statistically comparable between the AO and non-AO stenting groups, the presence of significant AO stenosis was found to be an independent predictor of SBI development in multivariate logistic regression analysis [odds ratio (OR) 2.856; 95% confidence interval (CI) 1.057–7.716; p = 0.038]. Subgroup analysis revealed that 13 (59.1%) of 22 patients with significant AO stenosis who underwent AO stent implantation developed SBI. A longer procedure time was another independent predictor of SBI according to the multivariate analysis (OR 1.037; 95% CI 1.005–1.069; p = 0.023) (Table 3).

Table 3. Predictors of SBI in multivariate logistic regression analysis.

Variable	OR (95% CI)	P	
Diabetes	1.949 (0.851–4.463)	0.115	
Significant AO stenosis	2.856 (1.057–7.716)	0.038	
Total stent length per lesion	1.019 (0.992–1.047)	0.171	
Procedure time	1.037 (1.005–1.069)	0.023	
AO: aorto-taostial; CI: confidence interval; OR: odds ratio; SBI: silent brain injury.

AQ1: Please provide significance of bold values in Tables 1, 2 and 3.

Discussion

In the present study, the SBI rates were statistically comparable between patients who underwent AO and non-AO stent implantation. However, the presence of significant AO stenosis in the ostium engaged by the guiding catheter was an independent predictor of SBI. A longer procedure time was another independent predictor of SBI development.

According to the results of our study, the SBI rates tended to be higher in patients who underwent AO stent implantation, but the difference was not statistically significant. Significant AO stenosis, which was present in 40% of the patients in the AO stenting group but not in any of the patients in the non-AO stenting group, was independently associated with the development of SBI. In the AO stenting group, the SBI rate was 59.1% in patients with significant AO stenosis, whereas it was 33.3% in those without significant AO stenosis, which was very similar to the SBI rate in the non-AO stenting group. In other words, the tendency for SBI in the AO stenting group was due to a subgroup with significant AO stenosis. This may be associated with the potential embolization of atherothrombotic debris from the coronary ostium into cerebral circulation. In addition, the higher SBI rate in the subgroup with significant AO stenosis may be due to technical issues rather than the lesions themselves. Aggressive catheter manipulations to engage the ostium with significant AO stenosis may cause plaque mobilization from the ascending aorta [19]. Pressure dampening associated hypotension may play a role in the development of SBI [20]. While the catheter is disengaged from the coronary ostium to avoid pressure dampening, embolization may occur during the removal of equipment contaminated with atherothrombotic fragments. Contrast injections and even saline flush while the catheter is slightly disengaged may lead to embolization of small thrombi formed at the tip of the catheter into cerebral circulation [21]. In a similar setting, contrast-induced vasoconstriction [22] and air embolism [23] in the cerebral vessels may also contribute to the development of SBI. These are possible explanations why significant AO stenosis may be an independent predictor of SBI.

A longer procedure time was also independently associated with SBI development in our study, in line with previous studies [16,24]. It is reasonable to assume that the risk of thrombus formation and plaque mobilization may increase as the procedure is prolonged. Although not statistically significant, patients with SBI were more likely to have diabetes in our study. However, in the multivariate analysis, diabetes was not an independent predictor of SBI development. In another study we conducted previously, the rate of SBI detected by serum NSE elevation was higher when stenting CTO lesions compared with stenting non-CTO lesions (59.7% vs. 39.1%). The findings of the aforementioned study suggested that diabetes might also be an independent predictor of SBI [15].

Our findings imply that utmost care should be taken to prevent atheromatous plaque and thrombus embolization in patients with significant AO stenosis under­going AO stent implantation. In addition, avoiding prolonged PCI procedures, if possible, may reduce the risk of SBI. The cumulative effects of SBI have been shown to be associated with various psychiatric and neurological disorders and even increased mortality [25–29]. To our knowledge, this is the first study to associate the presence of significant AO stenosis with SBI development in patients undergoing AO stent implantation.

There are extracerebral sources of NSE such as red blood cells, platelets, and lymphocytes [30,31]. The reliability of NSE as a marker for brain injury in situations where there are manipulations taking place in the bloodstream, as occurs in interventional coronary procedures, may be compromised due to the potential for contamination from blood. For instance, in the context of cardiac surgery with cardiopulmonary bypass, the elevated levels of NSE have been primarily attributed to the release of haemolysed erythrocytes [32]. Coronary stenting is a less invasive procedure, and the potential for NSE contamination from blood may be less significant. However, the possibility of invisible haemolysis still exists, which could result in elevated NSE levels [33]. This is a limitation of the study, and further research is required to elucidate this issue.

Our study also had other limitations. First, this was a single-centre study with a relatively small sample size. Second, SBI was not confirmed by MRI, which is the recommended method for detecting ischemic brain injury [2]. However, NSE has been shown to have similar efficacy to MRI in detecting brain injury, with a sensitivity of approximately 90% [5,34]. Finally, some variables with the potential to affect SBI rates were not similar between the groups. Probably because LM stenting was more common, prasugrel as the choice of P2Y12 inhibitor was more frequent in the AO stenting group compared to the non-AO stenting group. The number of stents per lesion and contrast volume were higher in the AO stenting group. Although not statistically significant, a history of prior CABG was more common, and the total stent length per lesion was higher in the AO stenting group. However, none of these variables were independently associated with SBI development according to the logistic regression analysis.

Conclusion

This study suggests that AO stenting may be associated with an increased risk of SBI if the lesion in the ostium is significant.

Author contributions

UY, MU, MC, BA, KS, and OG were involved in the conception and design of the work. UY, AK, AOK, AC, and BA made substantial contributions to the acquisition, analysis, or interpretation of data for the work. UY drafted the article. AK, MU, AOK, AC, MC, BA, KS, and OG revised the article critically for intellectual content. All authors approved the final version to be published. All authors agreed to be accountable for all aspects of the work.

Ethical statement

The study was approved by the Ondokuz Mayis University Clinical Research Ethics Committee (decision date: March 13, 2020; decision number: 2020/107).

Consent to participate

Written informed consent was obtained from all the patients included in the study.

Disclosure statement

The authors report there are no competing interests to declare.

Data availability statement

The data that support the findings of this study are available from the corresponding author, UY, upon reasonable request.
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