Clinical features and survival analysis of non-hypertensive aortic dissection patients post-thoracic endovascular aortic repair: a 10-year retrospective study
Introduction
Aortic dissection (AD) is a relatively rare but extremely serious medical emergency characterized by sudden onset, rapid progression, and high mortality (1). It occurs when an tear that allows the blood to separate the intimal and medial layers, creating a dissection flap that divides the true lumen from a newly formed false lumen (2). Thoracic endovascular aortic repair (TEVAR) can significantly reduce short-term mortality compared with traditional aortic replacement surgery, resulting in shorter surgical time and less trauma (3,4).
However, a variety of aortic adverse events (AAEs) after TEVAR remains a life-threatening limitation, which has caused less satisfactory aortic remodeling and more questioned points. The past decades have witnessed a growing number of biomarkers and risk factors investigated to refine stratification of preoperative patients and prediction of postoperative AAEs (5-8). Hypertension has been shown to be the most prevalent complication for AD with nearly 43.3% of AD patients suffered from hypertension in J-SCH study and 57.7% in the UK Biobank Study (9). However, the previous data also indicate that there are still more than 30% of AD patients without hypertension. The clinical characteristics and predictors for AAEs after TEVAR of non-hypertensive AD patients remain unclear.
In this retrospective study, cases of AD undergone TEVAR in our center are included to clarify the clinical characteristics of non-hypertensive AD and predictive indicators of AAEs, aiming to further refine the management of AD. We present this article in accordance with the STROBE reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-24-318/rc).
Methods
Patients and data collection
This retrospective cohort study screened 1,281 consecutive patients who had received standard TEVAR between January 2012 and December 2020. Cases were excluded if they had AD secondary to trauma (n=23), diagnosed as syndromic AD (n=70), or confirmed as repeat admission cases (n=300). Data were collected only when patients were first admitted to the hospital. Cases of AD admitted for TEVAR were identified from the electronic surgical records and imaging databases of Changhai Hospital in China. AD was diagnosed by clinician according to physical examination and image examination. The standardized procedure for TEVAR had been described in previous studies and the selection of stents was left to the vascular surgeon (10,11).
For all eligible patients (n=888), the false lumen thrombosis status was assessed by computed tomography angiography (CTA). The patients’ baseline and clinical characteristics, such as demographic and examination data, were retrospectively collected from medical charts and electronic medical records on admission. Fasting glucose was obtained from the results of the glucose tolerance test (OGTT). Data regarding the cardiac structure and function were collected from the echocardiographic results.
The study was conducted in accordance with the Declaration of Helsinki (as revised in 2013). The study was approved by the Central Ethics Committee of Shanghai Changhai Hospital Ethics Committee (Y2020-042) and individual consent for this retrospective analysis was waived. The study design and patient inclusion process are shown in Figure 1.
Definition and grouping
Patients were categorized as type A aortic dissection (TAAD) when the ascending aorta was involved and otherwise classified as type B aortic dissection (TBAD) according to the classical Stanford classification system (12). In this study, AD had been traditionally defined as “acute” during the first 2 weeks after symptom onset and “chronic” when beyond the second week. Deaths ascribed to AD or aortic rupture were confirmed by at least 1 of the following: autopsy, operation, death certificate, or radiologic imaging.
The neutrophil-to-lymphocyte ratio (NLR) was defined as the number of neutrophils divided by the number of lymphocytes. The monocyte-to-lymphocyte ratio (MLR) was defined as the number of monocytes divided by the number of lymphocytes. The platelet-to-lymphocyte ratio (PLR) was defined as the number of platelets divided by the number of lymphocytes.
Non-hypertension was defined as systolic or diastolic blood pressure (SBP/DBP) ≤140/90 mmHg on admission and no hypertension medication has been taken, and an increase in blood pressure after surgery may be due to surgical stress and is not defined as hypertension. The remaining 888 patients after TEVAR were divided into two groups based on hypertension: a non-hypertension group (non-hp, n=255) and a hypertension group (hp, n=633).
Propensity score matching (PSM)
Propensity score (PS), the intervention-assigned probability based on given covariates, were designed and implemented to eliminate confounding effects in multiple clinical analyses and retrospective studies (13,14). PSM was performed to partly eliminate the discrepancies between two cohorts of patients in our study, thus making the baseline information compatible and avoiding the potential selection bias (15). The clinical data and follow-up analysis were based upon only those patients who are successfully matched.
Follow-up
Standardized follow-up procedures were performed at 3 months, 6 months and then annually after TEVAR. Direct phone contact and readmission records review were performed to ascertain the precise outcomes for each patient. For living patients who did not follow-up with our center, efforts were made to obtain recent medical records from their referring physicians. Repeated clinical imaging with CTA was performed whenever possible at the first follow-up. The follow-up duration ended at the death or termination time (December 2021) and the endpoint of this study was the occurrence of postoperative AAEs after TEVAR.
Follow-up of all-cause mortality was initiated upon admission. Any instances of AAEs, including endoleak, distal aortic expansion, distal stent-induced new entry (dSINE), retrograde type A aortic dissection (RTAD), arterial rupture and death (ARD) and evidence of vital organ ischemia (VOI) were recorded.
Statistical analysis
Continuous variables were presented as means with standard deviation (SD) or as median with interquartile range (IQR) and compared by the t-test or the Mann-Whitney U test. Categorical variables were presented as number with percentage and compared using either the Pearson’s Chi-squared test or Fisher’s exact test. The nearest-neighbor matching ratio between the non-hypertensive patients and the hypertensive patients was 1:2, with the difference between PS (caliper width) was at most 0.05 to avoid pairing different individuals. Variables with statistical differences in patients’ baseline characteristics were included as predictive variables for PSM. Kaplan-Meier analysis was used to assess the differences in time-to-event endpoints, and the log-rank test was used to distinguish Kaplan-Meier curves. To identify potential risk factors as far as possible, variables with P values less than 0.2 in univariate analysis were included in univariate Cox proportional hazards regression analysis to preliminarily analyze the risk factors for AAEs. Variables with statistical significance (P<0.05) in univariate Cox analysis were included in multivariate Cox regression analysis to estimate the risk factors of AAEs. Statistical analyses were performed using SPSS software version 26.0 (IBM Corp., Armonk, NY, United States) and variables with two-sided P<0.05 were considered statistically significant.
Results
Patient population and baseline characteristics
A total of 888 AD patients who had received TEVAR were remained for research after exclusion, with a mean age of 59.88±13.05 years old, including 694 (78.15%) males and 194 (21.85%) females. All patients were divided into two groups according to hypertension criteria: 255 (28.71%) patients without hypertensive condition and 633 (71.29%) patients with hypertension. The baseline characteristics of the two groups of patients are shown in Table 1. The proportion of males in the non-hypertensive group (72.2% vs. 80.6%, P=0.006) and the mean age of onset (55.17±14.95 vs. 59.08±13.34 years, P=0.001) were lower than those in the hypertensive group. The proportion of patients with smoking (P<0.001), diabetes (P=0.03) and renal failure (P<0.001) was also lower in the non-hypertensive group, but there was no significant difference in the proportion of patients with alcohol history (P=0.42), family history of cardiovascular disease (P=0.75), atrial fibrillation (P=0.89), dissection stage (P=0.35) and false lumen thrombosis (P=0.01).
Table 1
Variables | Before PSM study cohort | Matched study cohort | |||||
---|---|---|---|---|---|---|---|
Non-hp (n=255) | hp (n=633) | P value | Non-hp (n=207) | hp (n=367) | P value | ||
Basic information | |||||||
Male | 184 (72.2) | 510 (80.6) | 0.006* | 171 (82.6) | 286 (77.9) | 0.18 | |
Age (years) | 55.17±14.95 | 59.08±13.34 | 0.001* | 57.29±14.43 | 58.57±13.46 | 0.34 | |
Medical history | |||||||
Smoking | 55 (21.6) | 220 (34.8) | <0.001* | 54 (26.1) | 100 (27.2) | 0.76 | |
Drinking | 28 (11) | 82 (12.9) | 0.42 | 28 (13.5) | 37 (10.1) | 0.21 | |
Family history of cardiovascular disease | 3 (1.2) | 6 (0.9) | 0.75 | 0 | 2 (0.5) | 0.74 | |
Atrial fibrillation | 21 (8.2) | 54 (8.5) | 0.89 | 18 (8.7) | 32 (8.7) | 0.99 | |
Diabetes | 11 (4.3) | 53 (8.4) | 0.03* | 11 (5.3) | 25 (6.8) | 0.48 | |
Renal failure | 43 (16.9) | 210 (33.2) | <0.001* | 31 (15.0) | 56 (15.3) | 0.93 | |
Stanford classification | 0.007* | 0.02* | |||||
A | 98 (38.4) | 184 (29.1) | 79 (38.2) | 104 (28.3) | |||
B | 157 (61.6) | 449 (70.9) | 128 (61.8) | 263 (71.7) | |||
Stage | 0.35 | 0.64 | |||||
Acute | 174 (68.2) | 452 (71.4) | 146 (70.5) | 252 (68.7) | |||
Chronic | 81 (31.8) | 181 (28.6) | 61 (29.5) | 115 (31.3) | |||
False lumen thrombosis | 25 (9.8) | 88 (13.9) | 0.01 | 19 (9.2) | 48 (13.1) | 0.16 |
Values are presented as n (%) or mean ± SD. *, P<0.05. AD, aortic dissection; hp, hypertension; PSM, propensity score matching; SD, standard deviation.
In addition, type A dissection accounted for a higher proportion in the non-hypertensive group than the hypertensive group (38.4% vs. 29.1%, P=0.007), and the difference was still statistically significant (38.2% vs. 28.3%, P=0.02) after matching the baseline characteristics of the two groups with PS in which 207 cases in the non-hypertensive group and 367 cases in the hypertensive group were matched. However, there was no other significant difference after matching.
We further divided the 888 patients before PSM matching by genders and analysis the age distribution of patients in the two groups respectively. As shown in Figure 2, the proportion of non-hypertensive group in male patients under 40 years old and female patients under 60 years old was higher than that in hypertensive group.
Preoperative examination characteristics of matched cohort
For the patients with matched baseline characteristics after PSM, preoperative examination results are shown in the Table 2. Compared with the hypertensive group, the non-hypertensive group presented lower in fasting glucose (P<0.001) but higher in lymphocyte counts (P=0.02) and monocyte ratio (P=0.01). In addition, the non-hypertensive group showed smaller in ascending aorta diameter (AoAsc) (P<0.001), aortic root diameter (AoRoot) (P<0.001), fractional shortening (FS) (P<0.001) and left ventricular ejection fraction (P<0.001), but larger in left and right ventricular volume (P=0.008 and P=0.007).
Table 2
Variables | Non-hp (n=207) | hp (n=367) | P value |
---|---|---|---|
Fasting glucose (mmol/L) | 6.36 (4.90–7.61) | 7.01 (5.4–8.00) | <0.001* |
Cholesterol (mmol/L) | 4.47 (3.70–5.07) | 4.44 (3.88–4.91) | 0.87 |
Triglyceride (mmol/L) | 1.55 (0.84–1.79) | 1.4 (0.94–1.76) | 0.10 |
HDL (mmol/L) | 1.19 (0.96–1.38) | 1.19 (0.96–1.36) | 0.82 |
LDL (mmol/L) | 2.58 (2.00–3.04) | 2.59 (2.08–3.04) | 0.78 |
Serum urea (mmol/L) | 6.61 (4.90–7.80) | 6.87 (5.44–7.90) | 0.07 |
Serum creatinine (μmol/L) | 91.43 (68.96–102.36) | 97.07 (72.00–111.51) | 0.06 |
Uric acid (mmol/L) | 0.34 (0.28–0.39) | 0.35 (0.30–0.40) | 0.07 |
WBC (×109/L) | 9.64 (6.65–11.75) | 9.48 (6.61–11.50) | 0.69 |
Lymphocyte (×109/L) | 1.39 (0.93–1.63) | 1.26 (0.81–1.60) | 0.02* |
Monocyte (×109/L) | 0.7 (0.46–0.93) | 0.64 (0.40–0.83) | 0.06 |
Neutrophil (×109/L) | 7.44 (4.28–9.64) | 7.47 (4.44–9.85) | 0.82 |
Platelets (×109/L) | 201.56 (148.00–238.00) | 193.97 (144.00–230.00) | 0.44 |
Lymphocyte ratio | 16.38 (8.29–22.80) | 15.81 (7.91–21.90) | 0.69 |
Monocyte ratio | 7.71 (6.00–9.75) | 7.09 (5.60–8.80) | 0.01* |
Neutrophil ratio | 73.99 (65.90–83.20) | 75.56 (67.00–85.00) | 0.16 |
NLR | 7.67 (2.84–8.76) | 8.26 (3.06–11.53) | 0.11 |
MLR | 0.62 (0.31–0.73) | 0.59 (0.33–0.75) | 0.83 |
PLR | 172.31 (102.26–204.41) | 184.96 (113.56–222.94) | 0.09 |
INR | 1.12 (1.00–1.20) | 1.10 (1.00–1.11) | 0.08 |
PT (s) | 14.36 (13.30–14.90) | 14.20 (13.30–14.60) | 0.13 |
APTT (s) | 40.66 (36.40–43.25) | 41.02 (35.30–42.70) | 0.14 |
TT (s) | 17.86 (15.00–18.60) | 16.30 (15.19–18.00) | 0.34 |
FIB (g/L) | 4.30 (2.78–5.67) | 4.18 (2.95–5.19) | 0.81 |
FDP (μg/mL) | 18.06 (4.90–23.47) | 19.45 (4.79–23.67) | 0.61 |
D-Dimer (mg/mL) | 4.49 (0.96–5.88) | 4.65 (1.07–6.86) | 0.24 |
AoAsc (cm) | 3.53 (2.83–4.09) | 3.72 (3.33–4.07) | <0.001* |
AoRoot (cm) | 2.24 (2.09–2.40) | 2.39 (2.14–2.60) | <0.001* |
Pulmonary trunk (cm) | 2.40 (2.14–2.60) | 2.41 (2.20–2.60) | 0.70 |
Left atrium (mL) | 51.13 (39.91–61.36) | 49.27 (40.64–58.35) | 0.91 |
Right atrium (mL) | 39.78 (28.94–47.85) | 36.16 (28.00–45.00) | 0.28 |
Left ventricular volume (mL) | 98.89 (72.00–119.23) | 86.21 (68.61–101.15) | 0.008* |
Right ventricular volume (mL) | 35.08 (28.00–41.00) | 31.79 (23.12–40.08) | 0.007* |
FS% | 31.85 (30.00–35.05) | 35.70 (32.00–38.73) | <0.001* |
LVEF% | 59.85 (56.78–65.05) | 65.25 (60.10–69.01) | <0.001* |
Values are presented as median (25th to 75th percentile). *, P<0.05. AD, aortic dissection; hp, hypertension; HDL, high density lipoprotein; LDL, low density lipoprotein; WBC, white blood cell; NLR, neutrophil to lymphocyte ratio; MLR, monocyte to lymphocyte ratio; PLR, platelet to lymphocyte ratio; INR, international normalized ratio; PT, prothrombin time; APTT, activated partial thromboplastin time; TT, thrombin time; FIB, fibrinogen; FDP, fibrinogen degradation product; AoAsc, ascending aorta diameter; AoRoot, aortic root diameter; FS, fractional shortening; LVEF, left ventricular ejection fraction.
There were no statistically significant differences between two groups in cholesterol (P=0.87), triglyceride (P=0.10), high density lipoprotein (HDL) (P=0.82), low density lipoprotein (LDL) (P=0.78), serum urea (P=0.07), serum creatinine (P=0.06), uric acid (P=0.07), white blood cell (P=0.69), monocyte (P=0.06), neutrophil (P=0.82), platelets (P=0.44), NLR (P=0.11), MLR (P=0.83), PLR (P=0.09), PT (P=0.13), INR (P=0.08), APTT (P=0.14), thrombin time (TT) (P=0.34), fibrinogen (FIB) (P=0.81), fibrin degradation products (FDPs) (P=0.61), D-Dimer (P=0.24), pulmonary trunk diameter (P=0.70), left and right atrium volume (P=0.91 and P=0.28).
Follow-up and AAEs
AAEs of matched AD patients are shown in Table 3. Excluding 29 patients lost to follow-up, 545 patients completed follow-up with 184 recorded AAEs during the study period, including 71 instances in non-hypertensive patients and 103 instances in hypertensive patients. The mean time survive from AAEs in the non-hypertensive group was lower (36.65±2.08 vs. 42.74±1.41, P=0.01) but the 5-year adverse event ratio was higher (37.4% vs. 29.0%, P=0.05) than those in the hypertensive group. The incidence of endoleak (P=0.92), distal aortic expansion (P=0.11), ARD (P=0.16) and VOI (P=0.28) between the groups was not seen statistically significant. Kaplan-Meier survival analysis curve showed that the 5-year percentage of non-hypertensive group spared AAEs was significantly lower than that of hypertensive group (70.4% vs. 62.6%, P=0.02), as shown in Figure 3.
Table 3
Variables | Non-hp (n=190) | hp (n=355) | P value |
---|---|---|---|
Mean survival time, month | 36.65±2.08 | 42.74±1.41 | 0.01* |
AAEs | 71 (37.4) | 103 (29.0) | 0.05* |
Endoleak | 10 (5.3) | 18 (5.1) | 0.92 |
Distal aortic expansion | 21 (11.1) | 25 (7.0) | 0.11 |
dSINE | 3 (1.6) | 6 (1.7) | 0.92 |
RTAD | 4 (2.1) | 8 (2.3) | 0.91 |
ARD | 38 (20.0) | 54 (15.2) | 0.16 |
VOI | 14 (7.4) | 18 (5.1) | 0.28 |
Values are presented as mean ± SD or n (%). *, P<0.05. AAEs, aortic adverse events; AD, aortic dissection; hp, hypertension; dSINE, distal stent-induced new entry; RTAD, retrograde type A aortic dissection; ARD, aortic rupture and death; VOI, vital organ ischemia; SD, standard deviation.
Univariate and multivariate Cox proportional hazards regression analyses and predictors for AAEs after TEVAT are presented in Table 4. In the univariate analysis, the risk factors associated with AAEs occurrence were hypertension (P=0.01), type A dissection (P<0.001), serum urea (P=0.02), serum creatinine (P=0.01), monocyte ratio (P<0.001), neutrophil ratio (P=0.002), NLR (P=0.03), INR (P<0.001), PT (P<0.001), AoAsc (P<0.001), AoRoot (P=0.01) and ventriculus sinister volume (P<0.001). However, multivariate Cox regression analysis showed that type A dissection (P<0.001), INR (P=0.01), PT (P=0.03), AoRoot (P<0.001) and left ventricular volume (P<0.001) were major risk factors of the occurrence of AAEs after TEVAR.
Table 4
Variables | Univariable | Multivariable | |||||
---|---|---|---|---|---|---|---|
HR | 95% CI | P value | HR | 95% CI | P value | ||
Hypertension | 1.471 | 1.094–1.978 | 0.01* | 1.227 | 0.886–1.698 | 0.22 | |
Male | 1.028 | 0.721–1.466 | 0.88 | – | – | – | |
Stanford A | 0.359 | 0.268–0.482 | <0.001* | 3.348 | 2.313–4.846 | <0.001* | |
False lumen thrombosis | 0.721 | 0.431–1.205 | 0.21 | – | – | – | |
Fasting glucose | 1.047 | 0.989–1.108 | 0.11 | – | – | – | |
Urea | 1.122 | 1.01–1.122 | 0.02* | 1.023 | 0.944–1.110 | 0.58 | |
Serum creatinine | 1.002 | 1.001–1.004 | 0.01* | 1.000 | 0.997–1.004 | 0.85 | |
Uric acid | 7.027 | 0.273–7.027 | 0.70 | – | – | – | |
Lymphocyte | 0.949 | 0.753–1.195 | 0.70 | – | – | – | |
Monocyte | 0.873 | 0.552–1.381 | 0.56 | – | – | – | |
Monocyte ratio | 0.913 | 0.867–0.961 | <0.001* | 0.949 | 0.891–1.012 | 0.11 | |
Neutrophil ratio | 1.020 | 1.007–1.032 | 0.002* | 1.004 | 0.985–1.023 | 0.71 | |
NLR | 1.030 | 1.002–1.030 | 0.03* | 0.987 | 0.965–1.010 | 0.28 | |
PLR | 1.000 | 0.999–1.002 | 0.75 | – | – | – | |
INR | 4.362 | 2.052–4.362 | <0.001* | 269.197 | 3.46–20,946.462 | 0.01* | |
PT | 1.175 | 1.078–1.175 | <0.001* | 0.595 | 0.369–0.959 | 0.03* | |
APTT | 1.015 | 0.996–1.015 | 0.22 | – | – | – | |
AoAsc | 1.479 | 1.251–1.748 | <0.001* | 0.802 | 0.629–1.023 | 0.08 | |
AoRoot | 1.689 | 1.126–2.532 | 0.01* | 2.446 | 1.542–3.880 | <0.001* | |
Ventriculus sinister | 1.008 | 1.005–1.012 | <0.001* | 1.008 | 1.004–1.012 | <0.001* | |
Ventriculus dexter | 0.992 | 0.981–1.004 | 0.19 | – | – | – | |
FS% | 1.004 | 0.978–1.032 | 0.75 | – | – | – | |
LVEF% | 1.001 | 0.983–1.019 | 0.94 | – | – | – |
*, P<0.05. NLR, neutrophil to lymphocyte ratio; PLR, platelet to lymphocyte ratio; INR, international normalized ratio; PT, prothrombin time; APTT, activated partial thromboplastin time; AoAsc, ascending aorta diameter; AoRoot, aortic root diameter; FS, fractional shortening; LVEF, left ventricular ejection fraction; HR, hazard ratio; CI, confidence interval.
Discussion
Population-based studies reveal that hypertension is widely regarded as an important risk factor leading to AD, but there are more than 30% patients without hypertension whose clinical characteristics are lacking in the relevant studies (9,16). TEVAR has been recognized as a better alternative with superior survival for ADs, but postoperative AAEs such as endoleak, dSINE, and RTAD have undermined the superiorities of TEVAR (17). It is not clear whether preoperative hypertension influences postoperative adverse events for TVEAR.
In this retrospective cohort study, 888 AD patients who had received TEVAR from 2010 to 2020 were included, with 29.71% of the patients not conformed to the hypertension definition. Our results showed a prominent lower proportion of males in the non-hypertensive group than in the hypertensive group, indicating a higher proportion of female in non-hypertensive group. Previous findings have shown that AD patients are predominantly male, with a male-to-female ratio higher than 2:1, but the postoperative outcomes of female worsened than those of male (18).
In addition, our data also showed that the mean age of TEVAR in non-hypertensive AD patients was younger, and the proportion of male under 40 years old and female under 60 years old was higher in non-hypertensive group than that in the hypertensive group. Young AD patients are less likely to have a prior risk factor of hypertension, but they are more often associated with unique risk conditions such as genetic aortopathy or connective tissue disease (19,20). However, cases of recognized syndromic AD have been excluded in our study, which signifying that the pathogenesis of AD without hypertension is still unclear, and more potential pathogenic genes are yet to be discovered for better disease management of AD.
According to past experience and recommendations in guidelines, type B dissection is preferred for endovascular treatment, while type A dissection mainly focuses on surgical treatment (21,22). With the maturity of technology and the development of new branched stent grafts, more and more studies have shown that patients with type A dissection can also enjoy the advantages of TEVAR (23-26). In this study, 31.68% of patients undergone TEVAR was TAAD, while the proportions of type A were both significantly higher in non-hypertensive group than that in hypertensive group before and after the PSM. The univariate and multivariate-adjusted hazard ratios (HRs) associated with classification of Stanford A were related to AAEs. This hazard effect may be attributed to the complex anatomic structure of ascending aorta and fragile attachment of stent graft in type A dissection patients (25).
Hypertension has long been considered as the most common risk factor for AD, but few studies have reported the relationship between hypertension and postoperative adverse events. In our study, univariate Cox analysis of PSM matched cohort significantly showed that hypertension was a risk factor for AAEs, while the risk effect was diminished in multivariate analysis.
Diabetes has long been considered as a risk factor associated with cardiovascular events, however, recent studies have revealed the paradoxical possibility that diabetes may be negatively associated with the presence of AD and postoperative adverse outcomes (27,28). The paradoxical point also supported by our findings that the non-hypertensive dissection group presented a lower preoperative fasting glucose, with a higher incidence of 5-year AAEs and a shorter mean survival than that in hypertensive group.
Elevated inflammatory markers may contribute to the diagnosis of AD and the prediction of postoperative outcome events. Our data showed a higher proportion of macrophages in the non-hypertensive group, in univariable analysis which was diminished in multivariable analysis. But there was no significant difference in inflammatory biomarkers NLR, MLP and PLR between two groups.
The condition of blood coagulation is one of the important indicators for preoperative evaluation. INR has been reported as a significant risk factor of perioperative period for postoperative stroke (29). Our results also showed that INR and PT were important risk factors for AAEs.
Echocardiographic results showed that in the non-hypertensive group, the maximum ascending aorta diameter, AoRoot, and FS were smaller, and the left and right ventricular volumes were larger, which may be related to the changes in cardiac structure and function caused by hypertension (30,31). Cox regression risk analysis showed that AoRoot and left ventricular volume were significant risk factors associated with postoperative adverse events. However, the specific thresholds and predictive effects of AoRoot and left ventricular volume require further evaluation.
Limitations
There are several limitations. First, this is a retrospective study from a single-center, but all included patients had received unified standard TEVAR at our center, which may reduce the influence of potential confounders on the results of the study. Second, patients with type A dissection were included in this study to make our findings more representative, although TEVAR surgery is mainly recommended for patients with type B dissection. Third, our study mainly focused on patients who had undergone TEVAR surgery, and the results may not suitable for patients with open surgery. Fourth, our data revealed risk factors that may be associated with postoperative adverse events, but specific thresholds and predictive effects need to be further evaluated in prospective studies.
Conclusions
Our results show that compared with hypertensive AD, non-hypertensive patients presented with a higher proportion of female and type A classification, and a younger mean age of TEVAR treatment. This suggests that the pathogenesis of non-hypertensive dissection is more inclined to non-hemodynamic factors which need further investigation. Preoperative indicators including Stanford classification, PT, APTT, AoRoot and left ventricular volume were major risk factors for adverse events after TEVAR, which deserve to be further explored and evaluated for its predictive value.
Acknowledgments
Funding: This study was supported by
Footnote
Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jtd.amegroups.com/article/view/10.21037/jtd-24-318/rc
Data Sharing Statement: Available at https://jtd.amegroups.com/article/view/10.21037/jtd-24-318/dss
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Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-24-318/coif). The authors have no conflicts of interest to declare.
Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki (as revised in 2013). The study was approved by the Central Ethics Committee of Shanghai Changhai Hospital Ethics Committee (Y2020-042) and individual consent for this retrospective analysis was waived.
Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.
References
- Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000;283:897-903. [Crossref] [PubMed]
- Isselbacher EM, Preventza O, Hamilton Black J 3rd, et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation 2022;146:e334-482. [Crossref] [PubMed]
- Nienaber CA, Fattori R, Lund G, et al. Nonsurgical reconstruction of thoracic aortic dissection by stent-graft placement. N Engl J Med 1999;340:1539-45. [Crossref] [PubMed]
- Chiu P, Goldstone AB, Schaffer JM, et al. Endovascular Versus Open Repair of Intact Descending Thoracic Aortic Aneurysms. J Am Coll Cardiol 2019;73:643-51. [Crossref] [PubMed]
- Zhao Y, Hong X, Xie X, et al. Preoperative systemic inflammatory response index predicts long-term outcomes in type B aortic dissection after endovascular repair. Front Immunol 2022;13:992463. [Crossref] [PubMed]
- Li D, Peng L, Wang Y, et al. Predictor of false lumen thrombosis after thoracic endovascular aortic repair for type B dissection. J Thorac Cardiovasc Surg 2020;160:360-7. [Crossref] [PubMed]
- Lortz J, Leinburger F, Tsagakis K, et al. Distal Stent Graft Induced New Entry: Risk Factors in Acute and Chronic Type B Aortic Dissections. Eur J Vasc Endovasc Surg 2019;58:822-30. [Crossref] [PubMed]
- Li S, Yang J, Dong J, et al. Neutrophil to lymphocyte ratio and fibrinogen values in predicting patients with type B aortic dissection. Sci Rep 2021;11:11366. [Crossref] [PubMed]
- Hibino M, Otaki Y, Kobeissi E, et al. Blood Pressure, Hypertension, and the Risk of Aortic Dissection Incidence and Mortality: Results From the J-SCH Study, the UK Biobank Study, and a Meta-Analysis of Cohort Studies. Circulation 2022;145:633-44. [Crossref] [PubMed]
- Zhang R, Zhou J, Feng J, et al. Inducing false lumen thrombosis for retrograde type A aortic dissection. J Thorac Cardiovasc Surg 2017;153:57-65. [Crossref] [PubMed]
- Feng J, Lu Q, Zhao Z, et al. Restrictive bare stent for prevention of stent graft-induced distal redissection after thoracic endovascular aortic repair for type B aortic dissection. J Vasc Surg 2013;57:44S-52S. [Crossref] [PubMed]
- Erbel R, Aboyans V, Boileau C, et al. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases: Document covering acute and chronic aortic diseases of the thoracic and abdominal aorta of the adult. The Task Force for the Diagnosis and Treatment of Aortic Diseases of the European Society of Cardiology (ESC). Eur Heart J 2014;35:2873-926. Erratum in: Eur Heart J 2015;36:2779. [Crossref] [PubMed]
- Elze MC, Gregson J, Baber U, et al. Comparison of Propensity Score Methods and Covariate Adjustment: Evaluation in 4 Cardiovascular Studies. J Am Coll Cardiol 2017;69:345-57. [Crossref] [PubMed]
- Bi G, Liang J, Shan G, et al. Propensity Score Matching for Bias Reduction in Genomic Profiling. J Clin Oncol 2022;40:1259-60. [Crossref] [PubMed]
- Deb S, Austin PC, Tu JV, et al. A Review of Propensity-Score Methods and Their Use in Cardiovascular Research. Can J Cardiol 2016;32:259-65. [Crossref] [PubMed]
- Howard DP, Banerjee A, Fairhead JF, et al. Population-based study of incidence and outcome of acute aortic dissection and premorbid risk factor control: 10-year results from the Oxford Vascular Study. Circulation 2013;127:2031-7. [Crossref] [PubMed]
- Zhang L, Zhao Z, Chen Y, et al. Reintervention after endovascular repair for aortic dissection: A systematic review and meta-analysis. J Thorac Cardiovasc Surg 2016;152:1279-1288.e3. [Crossref] [PubMed]
- Nienaber CA, Fattori R, Mehta RH, et al. Gender-related differences in acute aortic dissection. Circulation 2004;109:3014-21. [Crossref] [PubMed]
- Januzzi JL, Isselbacher EM, Fattori R, et al. Characterizing the young patient with aortic dissection: results from the International Registry of Aortic Dissection (IRAD). J Am Coll Cardiol 2004;43:665-9. [Crossref] [PubMed]
- Sherrah AG, Andvik S, van der Linde D, et al. Nonsyndromic Thoracic Aortic Aneurysm and Dissection: Outcomes With Marfan Syndrome Versus Bicuspid Aortic Valve Aneurysm. J Am Coll Cardiol 2016;67:618-26. [Crossref] [PubMed]
- Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the diagnosis and management of patients with thoracic aortic disease: Executive summary: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Anesth Analg 2010;111:279-315. [Crossref] [PubMed]
- Bossone E, LaBounty TM, Eagle KA. Acute aortic syndromes: diagnosis and management, an update. Eur Heart J 2018;39:739-749d. [Crossref] [PubMed]
- Clough RE, Spear R, Van Calster K, et al. Case series of aortic arch disease treated with branched stent-grafts. Br J Surg 2018;105:358-65. [Crossref] [PubMed]
- Petrov I, Stankov Z, Tasheva I, et al. Endovascular Treatment of Acute Aortic Dissection Stanford Type A. JACC Cardiovasc Interv 2018;11:218-9. [Crossref] [PubMed]
- Nienaber CA, Sakalihasan N, Clough RE, et al. Thoracic endovascular aortic repair (TEVAR) in proximal (type A) aortic dissection: Ready for a broader application? J Thorac Cardiovasc Surg 2017;153:S3-S11. [Crossref] [PubMed]
- Qin J, Zhao Z, Liu G, et al. In situ diode laser fenestration of aortic arch stent grafts during thoracic endovascular aortic repair of Stanford type A aortic dissection. EuroIntervention 2019;14:e1854-60. [Crossref] [PubMed]
- de Miguel-Yanes JM, Jiménez-García R, Hernández-Barrera V, et al. Impact of type 2 diabetes mellitus on in-hospital-mortality after major cardiovascular events in Spain (2002-2014). Cardiovasc Diabetol 2017;16:126. [Crossref] [PubMed]
- Liu H, Shi L, Zeng T, et al. Type 2 diabetes mellitus reduces clinical complications and mortality in Stanford type B aortic dissection after thoracic endovascular aortic repair: A 3-year follow-up study. Life Sci 2019;230:104-10. [Crossref] [PubMed]
- Jia H, Huang B, Kang L, et al. Preoperative and intraoperative risk factors of postoperative stroke in total aortic arch replacement and stent elephant trunk implantation. EClinicalMedicine 2022;47:101416. [Crossref] [PubMed]
- Dahan M, Paillole C, Ferreira B, et al. Doppler echocardiographic study of the consequences of aging and hypertension on the left ventricle and aorta. Eur Heart J 1990;11 Suppl G:39-45.
- Hensel KO, Jenke A, Leischik R. Speckle-tracking and tissue-Doppler stress echocardiography in arterial hypertension: a sensitive tool for detection of subclinical LV impairment. Biomed Res Int 2014;2014:472562. [Crossref] [PubMed]