Preoperative high lymphocyte-to-monocyte ratio is associated with intraoperative type I endoleak in patients with TAA with TEVAR

Abstract

Objectives

Various inflammatory factors are closely associated with the incidence of thoracic aortic aneurysms (TAAs). Furthermore, the severity of inflammation is closely related to the absolute value and proportion of each leukocyte subgroup. Only few reports have analyzed the importance of lymphocyte–monocyte ratio (LMR) as a potential inflammatory marker in vascular diseases. Therefore, we aimed to investigate the effect of peripheral blood LMR on thoracic endovascular aortic repair (TEVAR) in patients with TAA.

Methods

A retrospective study of the clinical data collected in our hospital between January 2016 and January 2021 was performed on 162 patients with TAA treated with TEVAR, based on the inclusion and exclusion criteria for patient selection. Based on whether the patient had the clinical symptoms at admission and the occurrence of type I endoleaks during operation, patients were divided into two groups, respectively: an intraoperative type I endoleak group (n = 34) and a group without intraoperative type I endoleak (n = 128), and a group with clinical symptoms (n = 31) and a group without clinical symptoms (n = 131). The clinical data of these two groups were compared, the free from second intervention rates related to endoleak and the preoperatively LMR of the two groups was calculated. LMR was calculated preoperatively. Receiver-operating characteristic curve analysis was used to determine the cut-off for preoperative LMR values. Based on the cut-off point, patients were divided into a high LMR group (n = 34) and a low LMR group (n = 128). The clinical data of the two groups were compared, and further stratified analysis was performed.

Results

A total of 162 patients were included in the analysis. All patients were successfully implanted with a thoracic aorta stent graft. The preoperative LMR level and postoperative endoleak-related secondary intervention rate were higher in the type I endoleak group than those in the group without intraoperative type I endoleaks. The preoperative C-reactive protein (CRP) level of patients with TAA with clinical symptoms was higher than that of asymptomatic patients. There was a negative correlation between preoperative CRP and LMR levels. In addition, in symptomatic or asymptomatic patients, the LMR level was associated with the occurrence of intraoperative type I endoleaks. After excluding the influence of type of endografts, our results showed that the clinical symptoms did not affect the occurrence of the intraoperative type I endoleak, and patients with intraoperative type I endoleak had a higher rate of postoperative secondary intervention.

Conclusion

Patients with TAA with type I endoleaks during TEVAR had an increased rate of secondary intervention related to endoleaks. Patients with TAA with high LMR levels before TEVAR were more likely to have endoleaks during operation.

Keywords

Thoracic aortic aneurysm lymphatic–monocyte ratio endoleak TEVAR C-reactive protein

Introduction

Thoracic aortic aneurysm (TAA) is a chronic disease that may present with acute and critical condition, in which pathological dilation of normal thoracic vessels occurs to more than 1.5 times their normal diameter. Some patients seek medical treatment owing to chest or back pain, hoarse voice, or difficulty in swallowing. If not treated in time, the compression symptoms or ruptured aneurysm caused by this disease condition will endanger the patient’s life at any time.^1–3 Based on previous studies, the causes of TAA include atherosclerosis, hypertension, infection, immune system diseases, and vascular wall lesions.⁴ Recent studies have shown that multiple inflammation-related factors are closely associated with the pathogenesis of TAAs.^5,6 The main pathological manifestations of TAA are continuous dilation of the artery caused by the invasion of inflammatory cells, destruction of the middle elastic protein matrix, inflammatory cell infiltration in the aortic wall, thrombosis in the lumen, and elevated C-reactive protein (CRP) levels.^7–9 In the progression of TAA, the expression of inflammatory cells within the aneurysmal wall increased and the serum proinflammatory cytokines were elevated. The aortic wall inflammation infiltrated by lymphocytes, monocytes, macrophages, neutrophils, and other inflammatory cells can promote the expression of immune cells, proteases, and cell adhesion molecules, and release reactive oxygen species. At the same time, inflammatory cells can also promote the apoptosis of aortic smooth muscle cells and eventually lead to the degeneration of the aortic wall. These inflammatory processes will eventually lead to the progression of aortic aneurysms.¹⁰

A number of studies have confirmed that changes in the level of systemic inflammatory markers are closely related to the risk of various cardiovascular diseases.¹¹ In recent years, white blood cells have been proposed to be associated with the prognosis of cardiovascular diseases or can be used as biomarkers to evaluate the prognosis of cardiovascular diseases.¹² In the process of inflammation, an elevated mononuclear cell count in peripheral blood is a sign of a severe inflammatory response. In some cardiovascular diseases, although the number of WBCs may still be within the normal range, leukocyte subtypes such as L–M ratio can still be effectively used to predict the level of atherosclerosis in patients.¹³ The lymphocyte–monocyte ratio (LMR), which is a novel, simple, and inexpensive inflammatory marker, is calculated by dividing the absolute lymphocyte count by the monocyte count in a differential sample of the complete blood count. LMR integrates two subtypes of white blood cells, whose ratio is determined by the relative value of lymphocyte count, representing the immune protection mechanism and monocyte count, reflecting the degree of inflammation. It was regarded as a stable and effective marker of inflammation, which would comprehensively and systematically reflect the immune inflammatory state of the body.¹⁴ Therefore, in the TAA, the LMR level would also be helpful for clinically relevant outcomes of the TEVAR.

Surgical treatment is the standard treatment for TAA. In recent years, with the development of endovascular technology, some patients with permissive anatomical conditions can choose endovascular interventions for vascular repair,¹⁵ especially when the aneurysm is located in the distal segment of the thoracic aorta arch or the descending aorta. Intracavitary isolation technology with coated stents can be used to isolate aneurysm lumens without extracorporeal circulation. Stent-covered intraluminal isolation technology can be used to complete the isolation of the cavity under non-external circulation conditions. It can reduce the risk of rupture, avoid thoracotomy trauma and surgical complications, improve treatment safety, reduce perioperative mortality, and provide several benefits for patients who cannot tolerate thoracotomy.^16,17 Studies have shown that the LMR is related to the severity of coronary artery disease and is considered a risk factor for atherosclerosis.¹³ Despite the clear association between LMR and atherosclerosis, few reports have evaluated the significance of LMR in vascular disorders. Therefore, we hypothesized that due to the increased atherosclerotic and inflammatory burden, the LMR level would be related to the inflammatory response of TAA patients, which then may further influence the intraoperative operation of thoracic endovascular aortic repair (TEVAR).

Methods

Participants

Between January 2016 and January 2021, 162 consecutive patients underwent TEVAR for TAA in our department (Figure 1). All patients were diagnosed with thoracic aortic aneurysm by CT angiography (CTA) before operation. Inclusion criterion was patients diagnosed preoperatively with TAA requiring intervention (with the following anatomical conditions: The length where the stent can be anchored at the proximal end of the aneurysm neck is greater than 2 cm, the angulation of the aneurysm neck is less than 60°, the shape of the aneurysm neck is regular, and the configuration is straight or nearly straight). Exclusion criteria were previous aortic surgery, planned major surgery (patients with severe thoracic aortic disease requiring staged treatment or hybrid surgery treatment), incomplete pathological data, patients who died before arrival at the hospital or in the emergency department, and known serious concomitant illness associated with life expectancy of less than 1 year. All patients voluntarily chose TEVAR and signed an informed consent form following an explanation of the surgical risks. All TEVAR procedures were carried out by the same group of surgeons. Our study followed the standard of reporting by the 2010 reporting standards for thoracic endovascular aortic repair.

Figure 1.

Diagram of study population.

Variables and definitions

The variables included in the study included age, gender, acute and chronic problems at the admission (e.g., coronary heart disease, diabetes, hypertension, and stroke), diameter of the lumen, length of hospital stay, secondary intervention, and LMR. Hematological specimens were collected within 24 h after admission and within 2 days before the operation for blood cell count and classification; the count of monocytes and lymphocytes was further obtained. Blood LMR is calculated by dividing the absolute value of blood lymphocytes by the absolute value of blood mononuclear cells. The cut-off point value of LMR was obtained by ROC analysis.

Follow-up

Follow-up was conducted by special person, using outpatient service, email, and telephone. All patients underwent CTA examination at 1 week, 3 months, and every year after operation to evaluate the patency of the subject’s stent graft, whether there was an endoleak or changes in the aneurysm cavity. In this study, the survival time free from second intervention related to endoleaks is the time from the day of surgery to the day the patient undergoes secondary intervention due to the endoleak.

Statistical analysis

All statistical analyses were performed using the Statistical Package for Social Science (SPSS) version 23.0 for Windows (IBM, Chicago, IL, USA). The results were expressed as percentages or as the means ± standard deviation (SD) unless otherwise noted. The distribution of clinicopathological data was summarized by the descriptive statistical method. Data were analyzed using the chi-squared test, Fisher’s exact test or student’s t-test. The receiver-operating characteristic (ROC) curve was calculated to assess the reliability of the LMR level to predict the type I endoleak during the TEVAR. The area under the curve (AUC) was also measured, shown as the absolute value and 95% confidence interval (95% CI). Preoperative LMR was divided into low (< 4.0) and high (> 4.0) values on the basis of the results of a receiver-operating characteristic curve analysis. The survival rate was calculated according to the Kaplan–Meier method, and the Kaplan–Meier method was used to draw the survival curve. The survival rate was compared using the log-rank test. When p < 0.05, it shows that the difference is statistically significant.

Results

Patient population

There were 162 patients with TAA in the entire group, including 133 men (82.1%) and 29 women (17.9%) with an average age of 63.36 ± 12.30 years. The intraoperative type I endoleak rate (only the intraoperative rate and some then had additional interventions during the operation, not including patients who leave the OR with type I endoleaks) was 20.98%, and the postoperative endoleak-related secondary intervention rate (all patients followed up) was 2.56%. Symptoms were defined as patients with dysphagia, hoarseness, chest pain, or back pain. Among the patients included in this study, 31 and 131 patients had TAA-related and no clinical symptoms, respectively (Table 1).

Table 1.

Patient characteristics by symptom in the TEVAR.

	Overall		Symptom		No symptom		p
	No.	%	No.	%	No.	%	p
Overall	162	100	31	19.14	131	80.86	—
Age, years, mean (SD.)	63.36	(12.30)	62.90	(13.78)	63.47	(11.98)	0.820
Sex	—	—	—	—	—	—	0.420
Female	29	17.90	4	12.90	25	19.10	—
Male	133	82.10	27	88.10	106	81.90	—
Hypertension	—	—	—	—	—	—	0.888
Yes	108	66.67	21	67.74	87	66.41	—
No	54	33.33	10	33.26	44	33.59	—
Diabetes	—	—	—	—	—	—	0.991
Yes	21	12.96	4	12.90	17	12.98	—
No	141	87.04	27	88.10	114	87.02	—
Coronary heart disease	—	—	—	—	—	—	0.735
Yes	28	17.28	6	19.35	22	16.79	—
No	134	82.72	25	80.65	109	83.21	—
Stroke	—	—	—	—	—	—	0.255
Yes	17	10.49	5	16.13	12	9.16	—
No	145	89.51	26	83.87	119	90.84	—
Endoleak	—	—	—	—	—	—	0.219
Yes	34	20.99	4	12.90	30	22.90	—
No	128	79.01	27	88.10	101	77.10	—
Re-intervention	—	—	—	—	—	—	0.325
Yes	4	2.56	0	—	4	3.05	—
No	152	97.44	31	100	127	96.95	—
Type of the endograft	—	—	—	—	—	—	0.456
Captivia	74	45.68	18	58.06	56	42.75	—
CTAG	36	22.22	6	19.35	30	22.90	—
ZenithTX2	8	4.94	2	6.45	6	4.58	—
Valiant	29	17.90	4	12.90	25	19.08	—
Else	15	9.26	1	3.23	14	10.69	—
LMR, mean (SD.)	3.81	2.54	3.10	1.30	3.97	2.73	0.086
CRP, mean (SD.)	41.04	(4.04)	30.77	(13.15)	11.47	(3.14)	0.038
Diameter, mean (SD.)	2.09	(3.48)	50.32	(17.25)	48.19	(14.14)	0.485
LOS, mean (SD.)	48.59	(14.75)	4.23	(2.73)	3.77	(2.76)	0.409

LMR, lymphocyte–monocyte ratio; CRP, C-reactive protein; LOS, length of stay.

Univariate analysis for symptoms and intraoperative type I endoleaks

The results of univariate analysis for symptoms showed that the CRP level was the factor affecting the clinical symptoms of TAA patients. However, in our study, sex, age, maximal aortic diameter, preoperative hypertension, diabetes, coronary heart disease, and stroke history were not significantly correlated with clinical symptoms (p > 0.05). In addition, clinical symptoms had no effect on intraoperative type I endoleaks, re-intervention, and length of hospital stay (p > 0.05). The differences in clinical data between the two patient groups are shown in Table 1.

The results of univariate analysis showed that the preoperative peripheral blood LMR level was significantly related to intraoperative type I endoleaks. However, in our study, sex, age, maximal aortic diameter, whether the aneurysm is ruptured, type of the endograft, preoperative hypertension, diabetes, coronary heart disease, and stroke history were not significantly correlated with intraoperative type I endoleak (p > 0.05). In addition, the occurrence of type I endoleaks during the operation was related to the second intervention related to endoleaks during the postoperative follow-up period, with a statistically significant difference. Intraoperative type I endoleaks had no effect on the length of hospital stay. Binary logistic analysis suggested that LMR was an independent risk factor for postoperative type I endoleaks. The differences in clinical data between the two patient groups are shown in Table 2.

Table 2.

Patient characteristics by intraoperative endoleaks in the TEVAR.

	Overall	Endoleak	No endoleak	p	HR (95% CI)	p
Overall	162	34	128	—	—	—
Age	63.36 ± 12.30	60.35 ± 14.68	64.16 ± 11.53	0.109	—	—
Sex	—	—	—	0.585	—	—
Female	29	5	24	—	—	—
Male	133	29	104	—	—	—
Hypertension	—	—	—	0.495	—	—
Yes	108	21	87	—	—	—
No	54	13	41	—	—	—
Diabetes	—	—	—	0.734	—	—
Yes	21	5	16	—	—	—
No	141	29	112	—	—	—
Coronary heart disease	—	—	—	0.950	—	—
Yes	28	6	22	—	—	—
No	134	28	106	—	—	—
Stroke	—	—	—	0.786	—	—
Yes	17	4	13	—	—	—
No	145	30	115	—	—	—
Symptom	—	—	—	0.219	0.29 (0.21–4.08)	0.360
Yes	31	4	27	—	—	—
No	131	30	101	—	—	—
Re-intervention	—	—	—	0.009	—	—
Yes	4	3	1	—	—	—
No	152	31	121	—	—	—
Rupture	—	—	—	0.242	—	—
Yes	5	0	5	—	—	—
No	157	34	123	—	—	—
Type of the endograft	—	—	—	0.557	—	—
Captivia	74	15	59	—	—	—
cTAG	36	9	27	—	—	—
ZenithTX2	8	1	7	—	—	—
Valiant	29	4	25	—	—	—
Else	15	5	10	—	—	—
LMR	3.80 ± 2.54	5.17 ± 4.42	3.44 ± 1.57	0.031	1.98 (1.11–3.51)	0.021
CRP	15.94 ± 29.63	15.98 ± 36.16	15.93 ± 28.67	0.996	1.02 (0.99–1.05)	0.107
Diameter	48.59 ± 14.75	49.66 ± 15.97	48.29 ± 14.43	0.634	1.03 (0.96–1.09)	0.423
LOS	3.86 ± 2.75	4.62 ± 3.58	3.66 ±	0.070	—	—

LMR: lymphocyte–monocyte ratio, CRP: C-reactive protein, LOS: length of stay.

Intraoperative type I endoleaks related to secondary intervention

We performed survival analysis on all patients to clarify whether the intraoperative type I endoleak in patients with TAA undergoing TEVAR treatment affects the free-from-secondary-intervention time without dependency on secondary interventions due to the endoleak during the follow-up period. The 3-year free-from-secondary-intervention rate was lower in patients with intraoperative type I endoleak than those patients without intraoperative type I endoleaks (p < 0.05, Figure 2).

Figure 2.

Kaplan–Meier analysis for endoleak-free secondary intervention according to the preoperative LMR.

LMR level predicts the incidence of intraoperative type I endoleaks

To explore the relationship between the preoperative peripheral blood LMR level and the incidence of intraoperative type I endoleaks in patients with TAA undergoing TEVAR treatment, we analyzed the predictive value of the preoperative LMR level for the occurrence of intraoperative type I endoleaks using receiver-operating characteristic (ROC) curve analysis. The area under the ROC curve demonstrated that the preoperative LMR level has a potential predictive value for intraoperative type I endoleaks during TEVAR (Figure 3(a), Supplementary Table 1). In addition, we also analyzed the predictive value of the preoperative LMR level for the clinical symptoms using receiver-operating characteristic (ROC) curve analysis. The area under the ROC curve showed that the preoperative LMR level maybe has a potential predictive value for the clinical symptoms in TAA patients (Figure 3(b)).

Figure 3.

Receiver-operating characteristic analysis of the sensitivity and specificity of the predictive value of LMR for TAA patient with TEVAR (A) and with symptom (B), respectively.

Stratification analysis of the effect of LMR level and intraoperative type I endoleaks on clinical characteristics of patients based on clinical symptoms

To explore the relationship between inflammation, LMR levels, and patients' clinical symptoms, we conducted a stratified analysis based on the presence of accompanying clinical symptoms at the time of patient admission (Tables 3 and 4). The results showed that the CRP levels of patients with clinical symptoms were higher than those of patients without clinical symptoms (p = 0.038, Figure 4(a)). Patients with low LMR levels in this study had larger aneurysm lumen diameters (p < 0.01, Figure 4(b), Supplementary Table 2, p = 0.005) and were more likely to develop clinical symptoms (Supplementary Table 2, p = 0.032). In addition, the preoperative peripheral blood LMR levels of the patients were negatively correlated with CRP (Figure 4(c)). The results of the stratified analysis for LMR or intraoperative type I endoleaks all showed that regardless of the presence or absence of clinical symptoms, the LMR level of preoperative peripheral blood was related to the occurrence of intraoperative type I endoleaks (Tables 3 and 4). In addition, the results of the stratified analysis for intraoperative type I endoleaks showed that patient absence of clinical symptoms with intraoperative type I endoleaks was more likely to occur during re-intervention (Table 4). To further explore the effects of the type of endografts, we conducted the stratified analysis of the influence of clinical symptoms on intraoperative type I endoleak and the influence of intraoperative type I endoleaks on the 3-year free-from-secondary-intervention rate. After excluding the influence of type of endografts, our results showed that the clinical symptoms did not affect the occurrence the intraoperative type I endoleak, and patients with intraoperative type I endoleaks had a higher rate of postoperative secondary intervention (Supplementary Table 3).

Table 3.

Stratification analysis the effect of LMR level on clinical characteristics of patients by whether there are clinical symptoms.

	Symptom			No symptom
	High LMR	Low LMR	p	High LMR	Low LMR	p
Overall	7	24	—	57	74	—
Age	61.71 ± 14.93	63.25 ± 13.74	0.800	59.11 ± 13.77	66.82 ± 9.17	0.000
Sex	—	—	0.247	—	—	0.341
Female	7	20	—	44	62	—
Male	0	4	—	13	12	—
Hypertension	—	—	0.038	—	—	0.07
Yes	7	14	—	33	54	—
No	0	10	—	24	20	—
Diabetes	—	—	0.160	—	—	0.464
Yes	2	2	—	6	11	—
No	5	22	—	51	63	—
Coronary heart disease	—	—	0.074	—	—	0.031
Yes	3	3	—	5	17	—
No	4	21	—	52	57	—
Stroke	—	—	0.309	—	—	0.634
Yes	2	3	—	6	6	—
No	5	21	—	51	68	—
Re-intervention	—	—	—	—	—	0.445
Yes	0	0	—	1	3	—
No	7	23	—	54	68	—
Endoleak	—	—	0.007	—	—	0.038
Yes	3	1	—	18	12	—
No	4	23	—	39	62	—
Diameter	44.17 ± 9.01	52.28 ± 18.89	0.287	44.62 ± 13.31	51.04 ± 14.24	0.011
CRP, mean (SD.)	2.13 ± 1.62	39.17 ± 51.41	0.252	6.61 ± 11.23	14.39 ± 24.16	0.234
LOS, mean (SD.)	3.86 ± 1.77	4.33 ± 2.97	0.692	3.49 ± 1.99	3.99 ± 3.22	0.310

Table 4.

Stratification analysis the effect of endoleaks on clinical characteristics of patients by whether there are clinical symptoms.

	Symptom			No symptom
	Endoleak	No endoleak	p	Endoleak	No endoleak	p
Overall	4	27	—	30	101	—
Age	56.75 ± 19.10	63.81 ± 13.05	0.347	60.83 ± 14.34	64.25 ± 11.15	0.172
Sex	—	—	0.409	—	—	0.701
Female	0	23	—	5	20	—
Male	4	4	—	25	81	—
Hypertension	—	—	0.739	—	—	0.397
Yes	3	18	—	18	69	—
No	1	9	—	12	32	—
Diabetes	—	—	0.018	—	—	0.581
Yes	2	2	—	3	14	—
No	2	25	—	27	87	—
Coronary heart disease	—	—	0.096	—	—	0.564
Yes	2	4	—	4	18	—
No	2	23	—	26	83	—
Stroke	—	—	0.605	—	—	0.856
Yes	1	4	—	3	9	—
No	3	23	—	27	92	—
Re-intervention	—	—	—	—	—	0.012
Yes	—	—	—	3	1	—
No	4	26	—	27	100	—
Type of the endograft	—	—	0.101	—	—	0.860
Captivia	2	16	—	13	43	—
cTAG	1	5	—	8	22	—
ZenithTX2	0	2	—	1	5	—
Valiant	0	4	—	4	21	—
Else	1	0	—	4	10	—
High LMR	—	—	0.007	—	—	0.038
Yes	3	1	—	18	12	—
No	4	23	—	39	62	—
Diameter	41.10 ± 11.91	51.80 ± 17.70	0.257	50.80 ± 16.25	47.35 ± 13.39	0.247
CRP, mean (SD.)	39.03 ± 26.45	33.14 ± 48.48	0.823	17.92 ± 38.15	10.03 ± 14.43	0.581
LOS, mean (SD.)	3.75 ± 2.06	4.30 ± 2.84	0.715	4.73 ± 3.74	3.49 ± 2.34	0.029

LMR: lymphocyte–monocyte ratio, CRP: C-reactive protein, LOS: length of stay.

Figure 4.

The relationship between CRP and LMR, and clinical symptoms in the TAA. (A) The levels of the CRP between the TAA patient with or without clinical symptoms. (B) The lumen diameter between the TAA patient with low LMR or high LMR. (C) The levels of LMR and CRP showed the negative correlation in the TAA.

Discussion

Since Dake et al. first used TEVAR to treat TAAs in 1994, this relatively simple technique has been widely used as it results in lesser trauma, low surgical mortality, fast recovery, and high success rate.^18,19 However, complications after TEVAR, such as endoleaks, stroke, and retrograde Stanford A aortic dissection after TEVAR, are common.²⁰ Among them, an endoleak is the most common complication after TEVAR and is the main reason for postoperative intervention, with an incidence rate of 5%–29%.^21,22 Continuous endoleaks lead to increased pressure in the aneurysm cavity, expansion of the aneurysm, and rupture of the aneurysm. Endoleaks after TEVAR are a high-risk factor for postoperative death in patients.²³ Sampaio et al.²⁴ found that the presence of a type I or type II endoleak during TEVAR significantly increases the likelihood of a postoperative endoleak and should prompt a high degree of suspicion during follow-up.

Univariate analysis of intraoperative type I endoleaks showed that patients with high preoperative peripheral blood LMR levels were more likely to have an intraoperative type I endoleak, and stratified analysis showed that LMR levels affected the incidence of intraoperative type I endoleaks in both patients with and without clinical symptoms. Moreover, patients with intraoperative type I endoleaks had a higher rate of secondary interventions related to endoleaks during the follow-up period. Studies have shown that a variety of inflammation-related factors is closely related to the pathogenesis of TAAs.^5,25 Several inflammatory cells play an important role in this process. In the process of chronic inflammation, the number of lymphocytes decreases due to apoptosis. As an important part of the inflammatory response, monocytes are activated by different growth factors and proinflammatory cytokines.²⁶ Low levels of LMR suggest a more serious inflammatory reaction. In this study, patients with low LMR levels may have more aortic wall inflammatory responses and thickening. Therefore, the stent graft during surgery is more likely to stick to the aortic wall when stretched. The corresponding incidence of intraoperative type I endoleaks was also reduced. Interestingly, intraoperative correction of proximal endoleaks did not decrease the rate of endoleaks of the same type and location during the follow-up period or the need for re-intervention. The explanation for this observation is not clear; however, one could speculate that the local anatomic factors implicated in the failure to obtain an immediately efficient seal after deployment continued to exert their deleterious action in the postoperative period.

In addition, patients with low LMR levels in this study had larger aneurysm lumen diameters and were more likely to develop clinical symptoms. The preoperative peripheral blood LMR levels of the patients were negatively correlated with CRP. Furthermore, patients with clinical symptoms had high CRP levels. Studies have shown that there are a number of leukocyte infiltrations in human AAA tissues, among which the most important cell type is monocytes.²⁷ Similarly, in TAA, a lower LMR indicates severe vascular wall inflammation and degradation of the extracellular matrix. This in turn leads to severe TAA lesions and clinical symptoms associated with larger lumen diameters. Song et al.²⁸ showed that the levels of a variety of inflammatory indicators such as CRP, procalcitonin, and LMR were related to the severity of chronic inflammation in the lungs of patients and were significantly related to the prognosis of patients. Feitelson et al. showed that liver cell necrosis and inflammation caused by hepatitis B virus infection can stimulate the surrounding liver tissue for a long time and promote the occurrence of liver cancer. The preoperative LMR level is of certain significance in the prognostic risk stratification model of patients undergoing radical resection of liver cancer.²⁹ Studies have shown that some inflammatory markers in peripheral blood can be used in the diagnosis of AD or as a tool for evaluating prognosis.^30–32 Elevated inflammatory markers such as CRP and white blood cells can classify the short-term mortality risk of AD patients.³⁰ Among them, white blood cell subtype (WBC) has been widely used as a classic indicator for the prognosis of cardiovascular diseases.³³ With the progress of research, increasing evidence shows that inflammation plays an important role in the occurrence and development of TAAs.^6,22 As an indicator of systemic inflammation, LMR is also a routine and economical detection index for patients, which can provide a reference for the clinical treatment of patients to a certain extent.

There are a few limitations to this study. First, patients with other preoperative inflammatory diseases (e.g., pneumonia) were excluded from this study to ensure the consistency of the status of all patients before blood draw. Therefore, the results of this study may not be suitable for the clinical treatment of patients with TAA who also suffer from inflammatory diseases. Second, due to the small number of patients with acute rupture or dissection in this study, relevant statistical analysis of this part of the data (the rupture or had emergency surgery) could not be carried out. Third, the sample size of this study was not large enough; the limitation of inclusion and exclusion criteria and the clinical data collection was not detailed enough, which led to the incomplete analysis of risk factors and failed to find the other potential risk factors affecting intraoperative type I leakage. Fourth, the data of patients included in this study could not be compared over time. From the current conditions, we cannot compare the results through covariance ANCOVA by measuring changes over time in both control conditions. Nevertheless, this is the first study to show that patients with TAA having intraoperative type I endoleaks during TEVAR have an increased rate of postoperative endoleak-related secondary intervention. In addition, patients with TAA with high levels of peripheral blood LMR before surgery are more likely to have type I endoleaks during surgery. The findings of this study will help clinicians choose effective inflammatory markers in their work practice, as a part of the preoperative prognosis stratification and postoperative follow-up, and will help guide the individualized treatment of patients with TAA.

Supplemental Material

sj-pdf-1-vas-10.1177_17085381211039939 – Supplemental Material for Preoperative high lymphocyte-to-monocyte ratio is associated with intraoperative type I endoleak in patients with TAA with TEVAR

Supplemental Material, sj-pdf-1-vas-10.1177_17085381211039939 for Preoperative high lymphocyte-to-monocyte ratio is associated with intraoperative type I endoleak in patients with TAA with TEVAR by Xin-sheng Xie, Yu-fei Zhao, Dan-dan Xu, En-ci Wang, Xiao-long Shu, Da-qiao Guo, Wei-guo Fu and Li-xin Wang in Vascular

Footnotes

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article: This work was supported by the National Natural Science Foundation of China (grant number: 81970412), Shanghai Municipal Science and Technology Commission Innovation Fund (grant number: 18441902400), Xiamen Municipal Health Science And Technology Program Fund (grant number: 3502Z20194034), Zhongshan hospital’s Talents Supporting Plan (grant number:2019ZSGG11), Xiamen Branch, Zhongshan hospital, Fudan University’s incubation project (grant number:2019ZSXMYS20), Health and Health Scientific Research Talent Training Project of Fujian Province (grant number 2019-1-92) and Science and Technology Plan Project of Quanzhou (grant number 2019N032S).

Ethical approval

All procedures performed involving human participants were in accordance with the ethical standards of the institutional research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. The present study was reviewed and approved y the Ethics Committee of the Zhongshan Hospital, Fudan University.

ORCID iD

Li-xin Wang

Supplementary Material

Supplementary material for this article is available online.

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Supplementary Material

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