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Altered aortic arch geometry in patients with type B aortic dissection

Altered aortic arch geometry in patients with type B aortic dissection Abstract Open in new tabDownload slide Open in new tabDownload slide OBJECTIVES This study aims to evaluate differences in proximal aorta geometry and identify specific anatomical predictors of type B aortic dissection (TBAD). METHODS We evaluated computed tomographic angiograms of controls (n = 185) and patients with acute TBAD (n = 173). Using propensity score matching, we created 2 groups of 127 patients. 3mensio Vascular software was used to analyse the computed tomographic angiograms and measure the diameter, length, tortuosity index and angulation of the proximal aorta (divided into ascending aorta and aortic arch). Tortuosity index was calculated by dividing the centre lumen line length of the aortic segment by its shortest length. Angulation was measured by the centre lumen line ‘tangent line angle’. Two independent multivariable models identified significant anatomical associations regarding the tortuosity and angulation geometry. RESULTS Aortic diameter and ascending aorta and aortic arch lengths in TBAD increased significantly. The aortic arch tortuosity was significantly higher in the TBAD group (P < 0.001), with no difference regarding the ascending aorta (P = 0.11). Ascending aorta and aortic arch angulation were significantly higher in the TBAD group (P = 0.01, P < 0.001, respectively). Multivariable analyses showed that increased aortic arch tortuosity and angulation were significant predictors of the development of TBAD [odds ratio (OR) 1.91, 95% confidence interval (CI) 1.40–2.59; P < 0.001 and OR 1.08, 95% CI 1.04–1.12; P < 0.001], respectively. CONCLUSIONS In addition to proximal aorta dilation and elongation, we identified increased aortic arch tortuosity and angulation as possible specific predictors of TBAD. Aortic dissection, Type B aortic dissection, Computed tomographic angiography, Geometrical analysis INTRODUCTION Aortic dissection (AD) is a life-threatening cardiovascular disease that results in a tear in the arterial intimal layer, which allows blood to collect within the medial layer [1]. Previous studies reported that specific geometric features of the proximal aorta, including elongation, angulation and tortuosity, may play important roles in the risk of onset of type A AD (TAAD) [2–6]. More recently, there is also an emerging awareness of the potential detrimental implications of these anatomical characteristics for the development of type B AD (TBAD) [7–10]. Significant elongation of the proximal aorta has been seen in both TAAD and TBAD [3, 9]. Previous studies have demonstrated that ascending aorta elongation was an independent risk factor for TAAD development [2, 3]; however, few studies have evaluated the predictive value of ascending aorta or aortic arch elongation in TBAD patients [9, 10]. Previous studies also demonstrated that the angulation of the ascending aorta plays an independent role in the development of TAAD [4, 5], and, as another important geometrical evaluation method, increased tortuosity in the proximal aorta has been considered a high-level anatomical risk for the development of TAAD [6, 11]. Unfortunately, the lack of consistent reporting methods for the measurement of angulation and tortuosity may have overshadowed the clinical relevance of these features and their important predictive value for TBAD patients. Considering the significant morphology and geometric alterations in the dissected descending aorta [12, 13], evaluating the undissected proximal aorta in TBAD patients may be more feasible regarding investigating geometric differences pre-dissection. Additionally, with advances in medical imaging and more sophisticated algorithms, it is possible to study the complex 3-dimensional geometry of the aorta, especially when analysing the tortuosity and angulation [14]. According to these points and the feasibility of measurement, we aimed to compare proximal aorta geometry in patients with TBAD versus aortas in the control group and to evaluate the significant dimensional differences to identify the independent and specific anatomical predictors of TBAD. MATERIALS AND METHODS Study design This study was approved by our local ethics committee. Obtaining written informed consent was not necessary because of the retrospective, observational nature of the study. Inclusion and exclusion flow charts of the study cohort are shown in Fig. 1. Figure 1: Open in new tabDownload slide Inclusion and exclusion criteria flow chart for the study cohort. TBAD: type B aortic dissection. Figure 1: Open in new tabDownload slide Inclusion and exclusion criteria flow chart for the study cohort. TBAD: type B aortic dissection. All patients diagnosed with acute TBAD were retrospectively enrolled from our medical centre from January 2010 to December 2018. The exclusion criteria were bicuspid aortic valve, connective tissue disease, previous history of aortic surgery, non-A non-B dissection [defined as descending-entry type with entry distally to the left subclavian artery (LSA) and dissection extending into the aortic arch, and arch-entry type with entry between the innominate and LSA] [15, 16]. We also excluded patients with a ‘bovine arch’ because this anatomical configuration is associated with an increased risk of developing thoracic aortic disease [8]. These criteria resulted in including 173 patients with acute TBAD. The control group comprised patients who underwent computed tomography angiography (CTA) for non-vascular emergencies at PLA General Hospital between December 2016 and January 2017. The inclusion criterion was that the ascending aorta and aortic arch were imaged in the scans. Patients with suspected or known aortic disease, ‘bovine arch’, bicuspid aortic valve, connective tissue disease, and those who previously underwent cardiothoracic surgery were excluded. A total of 185 patients met these criteria and were enrolled. Image postprocessing and analysis All enrolled CTA scans were performed using second-generation dual-source computed tomography scanners, and CTA images with a maximum slice thickness of 3 mm were accepted for further processing. All CTAs were imported into the image postprocessing software (3mensio version 8.1; Pie Medical Imaging, Maastricht, Netherlands), which provides dedicated semiautomated vascular segmentation and measurements based on the 3-dimensional centre lumen line (CLL) [17]. Six anatomical landmarks (points A–F) were marked on the stretched image (Fig. 2A and B). ‘Point A’ was located at the sinotubular junction; ‘point B’ was located at the level of the middle ascending aorta; ‘points C and D’ were located at the proximal and distal edge of the innominate artery, respectively; ‘point E’ was located at the distal edge of the left common carotid artery; and ‘point F’ was located at the distal edge of the LSA. The ascending aorta was defined as the aortic segment between ‘points A and C’, the aortic arch was defined as the segment between ‘points C and F’, and the total proximal aorta was defined as the segment between ‘points A and F’. Figure 2: Open in new tabDownload slide Computed tomography angiography measurement process. (A) The centre lumen line of the aorta and the 6 marked anatomical ‘points A–F’. ‘Point A’ is located at the sinotubular junction; ‘point B’ is located at the level of the middle ascending aorta; ‘points C and D’ are located at the proximal and distal edge of the innominate artery, respectively; ‘point E’ is located at the distal edge of the left common carotid artery; and ‘point F’ is located at the distal edge of the left subclavian artery. (B) Centre lumen line length measurement on the stretched view. (C) Angulation measurement of the ascending aorta. (D) Angulation measurement of the aortic arch. Figure 2: Open in new tabDownload slide Computed tomography angiography measurement process. (A) The centre lumen line of the aorta and the 6 marked anatomical ‘points A–F’. ‘Point A’ is located at the sinotubular junction; ‘point B’ is located at the level of the middle ascending aorta; ‘points C and D’ are located at the proximal and distal edge of the innominate artery, respectively; ‘point E’ is located at the distal edge of the left common carotid artery; and ‘point F’ is located at the distal edge of the left subclavian artery. (B) Centre lumen line length measurement on the stretched view. (C) Angulation measurement of the ascending aorta. (D) Angulation measurement of the aortic arch. Diameter and length Aortic diameter was measured on 6 level planes (points A–F) perpendicular to the aorta centreline (Fig. 2B). The lengths of the ascending aorta, aortic arch and total proximal aorta were calculated from the corresponding centreline length (Fig. 2B). Tortuosity index and angulation We calculated the tortuosity index by dividing the length of the CLL by the shortest distance length. Angulation was measured using the CLL ‘tangent angle’ function within the software [14], which was defined as the angle between tangent lines drawn for 2 points along the CLL (Fig. 2C and D). The 2 points correspond to the proximal and distal points of the measured aortic segment. We calculated the tortuosity indexes and angulation for the total proximal aorta, ascending aorta and aortic arch. Measurement reproducibility Measurements were repeated by 2 observers for 40 CTAs randomly selected from the 2 groups to evaluate the interobserver repeatability using the intra-class correlation coefficients and Bland–Altman plots (full details appear in Supplementary Material, Data S1). Statistical analysis Continuous data are expressed as mean ± standard deviation, and categorical data are reported as percentages. Data were tested for normality using the Kolmogorov–Smirnov test, and we used the t-test or Mann–Whitney test to compare each dimension parameter between the TBAD and control groups. The χ2 test or Fisher’s exact probability method was used for differences between frequency and the composition ratio. We then used propensity scores to match the control group using nearest-neighbour matching with a 1:1 ratio. Recognized and potential covariates [age, sex, body surface area (BSA), body mass index (BMI) and hypertension] affecting the aortic dimension were used to calculate the propensity scores [18–20]. Replacement was not allowed, and we set the caliper distance at 0.05. Two models using stepwise logistic regression analyses were created to determine which geometric features were independently associated with TBAD. Model 1 used the covariates aortic diameter, length and the tortuosity index of the aortic segment (Table 3), and model 2 used aortic diameter, length and the angulation of the aortic segment (Table 4). Results were reported as odds ratios (ORs) and 95% confidence intervals (CIs) for the identified risk factors. All reported P-values were 2-sided, and P < 0.05 was considered statistically significant. SPSS 22.0 software (IBM, Armonk, NY, USA) was used for all statistical analyses. RESULTS Overall cohort The baseline characteristics of both groups before propensity score matching are presented in Table 1. Patients with TBAD were significantly younger compared with the control group (52.7 vs 57.8 years, respectively). Furthermore, the TBAD group comprised significantly more men and patients with a larger BSA. There were no differences in the prevalence of hypertension or in BMI measurements between the groups. Table 1: Patient characteristics in the different study groups Variables . Overall cohort . PSM cohort . TBAD (n = 173) . Controls (n = 185) . P-value . Standardized differencea . TBAD (n = 127) . Controls (n = 127) . P-value . Standardized differencea . Age (years) 52.7 ± 11.4 57.8 ± 10.5 <0.001 −46.5 53.8 ± 10.8 56.3 ± 10.9 0.06 −23.0 Male gender 152 (87.9) 106 (57.3) <0.001 72.7 107 (84.3) 106 (83.5) 1 2.2 BMI (kg/m2) 25.5 ± 3.9 25.4 ± 3.3 0.88 2.8 25.5 ± 3.8 25.9 ± 3.3 0.4 −11.2 BSA 1.8 ± 0.2 1.8 ± 0.2 0.005 31.5 1.8 ± 0.2 1.8 ± 0.2 0.48 −5.25 Hypertension 100 (57.8) 98 (53.0) 0.36 9.7 77 (60.6) 68 (53.5) 0.31 14.3 Variables . Overall cohort . PSM cohort . TBAD (n = 173) . Controls (n = 185) . P-value . Standardized differencea . TBAD (n = 127) . Controls (n = 127) . P-value . Standardized differencea . Age (years) 52.7 ± 11.4 57.8 ± 10.5 <0.001 −46.5 53.8 ± 10.8 56.3 ± 10.9 0.06 −23.0 Male gender 152 (87.9) 106 (57.3) <0.001 72.7 107 (84.3) 106 (83.5) 1 2.2 BMI (kg/m2) 25.5 ± 3.9 25.4 ± 3.3 0.88 2.8 25.5 ± 3.8 25.9 ± 3.3 0.4 −11.2 BSA 1.8 ± 0.2 1.8 ± 0.2 0.005 31.5 1.8 ± 0.2 1.8 ± 0.2 0.48 −5.25 Hypertension 100 (57.8) 98 (53.0) 0.36 9.7 77 (60.6) 68 (53.5) 0.31 14.3 Data are presented as mean ± standard deviation and n (%). a Standardized difference is the mean difference divided by the pooled standard deviation, expressed as a percentage. BMI: body mass index; BSA: body surface area; PSM: propensity-score matching; TBAD: type B aortic dissection. Open in new tab Table 1: Patient characteristics in the different study groups Variables . Overall cohort . PSM cohort . TBAD (n = 173) . Controls (n = 185) . P-value . Standardized differencea . TBAD (n = 127) . Controls (n = 127) . P-value . Standardized differencea . Age (years) 52.7 ± 11.4 57.8 ± 10.5 <0.001 −46.5 53.8 ± 10.8 56.3 ± 10.9 0.06 −23.0 Male gender 152 (87.9) 106 (57.3) <0.001 72.7 107 (84.3) 106 (83.5) 1 2.2 BMI (kg/m2) 25.5 ± 3.9 25.4 ± 3.3 0.88 2.8 25.5 ± 3.8 25.9 ± 3.3 0.4 −11.2 BSA 1.8 ± 0.2 1.8 ± 0.2 0.005 31.5 1.8 ± 0.2 1.8 ± 0.2 0.48 −5.25 Hypertension 100 (57.8) 98 (53.0) 0.36 9.7 77 (60.6) 68 (53.5) 0.31 14.3 Variables . Overall cohort . PSM cohort . TBAD (n = 173) . Controls (n = 185) . P-value . Standardized differencea . TBAD (n = 127) . Controls (n = 127) . P-value . Standardized differencea . Age (years) 52.7 ± 11.4 57.8 ± 10.5 <0.001 −46.5 53.8 ± 10.8 56.3 ± 10.9 0.06 −23.0 Male gender 152 (87.9) 106 (57.3) <0.001 72.7 107 (84.3) 106 (83.5) 1 2.2 BMI (kg/m2) 25.5 ± 3.9 25.4 ± 3.3 0.88 2.8 25.5 ± 3.8 25.9 ± 3.3 0.4 −11.2 BSA 1.8 ± 0.2 1.8 ± 0.2 0.005 31.5 1.8 ± 0.2 1.8 ± 0.2 0.48 −5.25 Hypertension 100 (57.8) 98 (53.0) 0.36 9.7 77 (60.6) 68 (53.5) 0.31 14.3 Data are presented as mean ± standard deviation and n (%). a Standardized difference is the mean difference divided by the pooled standard deviation, expressed as a percentage. BMI: body mass index; BSA: body surface area; PSM: propensity-score matching; TBAD: type B aortic dissection. Open in new tab Propensity score matching cohort Age, sex, BSA, BMI and hypertension significantly influenced the proximal aorta dimensions [18–20]; therefore, we included these variables in the model to calculate propensity scores. The propensity scores pre- and postmatching as well as their distribution are presented in Supplementary Material, Fig. S1. Finally, 127 pairs underwent further measurements and comparisons. Aortic diameters In the TBAD group, the ascending aorta was much larger than in controls. Likewise, the aortic arch and the total proximal aorta had larger aortic diameters (all P < 0.05, Table 2). Except for ‘point F’, the aortic diameter of the proximal aorta was ∼10% larger in the TBAD group versus controls. Table 2: Anatomical variables of TBAD patients and controls in the PSM cohort . TBAD (n = 127) . Controls (n = 127) . Mean difference (TBAD-controls) . Mean variance ratio (mean difference/controls × 100%) . P-value . Diameter (cm)  STJ, point A 3.0 ± 0.5 2.7 ± 0.3 0.3 11.1 <0.001  Mid-ascending aorta, point B 3.5 ± 0.6 3.2 ± 0.4 0.3 9.4 <0.001  End-ascending aorta, point C 3.3 ± 0.5 3.0 ± 0.3 0.3 10.0 <0.001  End-INA, point D 3.1 ± 0.5 2.8 ± 0.3 0.3 10.1 <0.001  End-LCCA, point E 2.8 ± 0.5 2.5 ± 0.2 0.3 10.7 <0.001  End-LSA, point F 2.4 ± 0.4 2.3 ± 0.2 0.1 4.3 0.012 Length (cm)  Ascending aorta 7.3 ± 1.1 6.5 ± 0.8 0.8 12.3 <0.001  Aortic arch 3.9 ± 0.7 3.6 ± 0.6 0.3 8.3 <0.001  Total proximal aorta 11.3 ± 1.3 10.2 ± 1.0 1.1 10.7 <0.001 Tortuosity index (%)  Ascending aorta 113.1 ± 4.9 112.2 ± 3.9 NA NA 0.11  Aortic arch 104.2 ± 2.4 102.3 ± 1.3 1.9 1.9 <0.001  Total proximal aorta 126.7 ± 7.3 123.0 ± 4.9 3.7 3.0 <0.001 Angulation (°)  Ascending aorta 83.6 ± 13.2 79.7 ± 10.8 3.9 4.9 0.01  Aortic arch 53.4 ± 13.0 41.7 ± 11.1 11.7 28.1 <0.001  Total proximal aorta 114.8 ± 12.3 103.8 ± 10.0 11.0 10.6 <0.001 . TBAD (n = 127) . Controls (n = 127) . Mean difference (TBAD-controls) . Mean variance ratio (mean difference/controls × 100%) . P-value . Diameter (cm)  STJ, point A 3.0 ± 0.5 2.7 ± 0.3 0.3 11.1 <0.001  Mid-ascending aorta, point B 3.5 ± 0.6 3.2 ± 0.4 0.3 9.4 <0.001  End-ascending aorta, point C 3.3 ± 0.5 3.0 ± 0.3 0.3 10.0 <0.001  End-INA, point D 3.1 ± 0.5 2.8 ± 0.3 0.3 10.1 <0.001  End-LCCA, point E 2.8 ± 0.5 2.5 ± 0.2 0.3 10.7 <0.001  End-LSA, point F 2.4 ± 0.4 2.3 ± 0.2 0.1 4.3 0.012 Length (cm)  Ascending aorta 7.3 ± 1.1 6.5 ± 0.8 0.8 12.3 <0.001  Aortic arch 3.9 ± 0.7 3.6 ± 0.6 0.3 8.3 <0.001  Total proximal aorta 11.3 ± 1.3 10.2 ± 1.0 1.1 10.7 <0.001 Tortuosity index (%)  Ascending aorta 113.1 ± 4.9 112.2 ± 3.9 NA NA 0.11  Aortic arch 104.2 ± 2.4 102.3 ± 1.3 1.9 1.9 <0.001  Total proximal aorta 126.7 ± 7.3 123.0 ± 4.9 3.7 3.0 <0.001 Angulation (°)  Ascending aorta 83.6 ± 13.2 79.7 ± 10.8 3.9 4.9 0.01  Aortic arch 53.4 ± 13.0 41.7 ± 11.1 11.7 28.1 <0.001  Total proximal aorta 114.8 ± 12.3 103.8 ± 10.0 11.0 10.6 <0.001 Values are presented as mean ± standard deviation. Points A–F are illustrated in Fig. 2. INA: innominate artery; LCCA: left common carotid artery; LSA: left subclavian artery; NA: not applicable; PSM: propensity-score matching; STJ: sinotubular junction; TBAD: type B aortic dissection. Open in new tab Table 2: Anatomical variables of TBAD patients and controls in the PSM cohort . TBAD (n = 127) . Controls (n = 127) . Mean difference (TBAD-controls) . Mean variance ratio (mean difference/controls × 100%) . P-value . Diameter (cm)  STJ, point A 3.0 ± 0.5 2.7 ± 0.3 0.3 11.1 <0.001  Mid-ascending aorta, point B 3.5 ± 0.6 3.2 ± 0.4 0.3 9.4 <0.001  End-ascending aorta, point C 3.3 ± 0.5 3.0 ± 0.3 0.3 10.0 <0.001  End-INA, point D 3.1 ± 0.5 2.8 ± 0.3 0.3 10.1 <0.001  End-LCCA, point E 2.8 ± 0.5 2.5 ± 0.2 0.3 10.7 <0.001  End-LSA, point F 2.4 ± 0.4 2.3 ± 0.2 0.1 4.3 0.012 Length (cm)  Ascending aorta 7.3 ± 1.1 6.5 ± 0.8 0.8 12.3 <0.001  Aortic arch 3.9 ± 0.7 3.6 ± 0.6 0.3 8.3 <0.001  Total proximal aorta 11.3 ± 1.3 10.2 ± 1.0 1.1 10.7 <0.001 Tortuosity index (%)  Ascending aorta 113.1 ± 4.9 112.2 ± 3.9 NA NA 0.11  Aortic arch 104.2 ± 2.4 102.3 ± 1.3 1.9 1.9 <0.001  Total proximal aorta 126.7 ± 7.3 123.0 ± 4.9 3.7 3.0 <0.001 Angulation (°)  Ascending aorta 83.6 ± 13.2 79.7 ± 10.8 3.9 4.9 0.01  Aortic arch 53.4 ± 13.0 41.7 ± 11.1 11.7 28.1 <0.001  Total proximal aorta 114.8 ± 12.3 103.8 ± 10.0 11.0 10.6 <0.001 . TBAD (n = 127) . Controls (n = 127) . Mean difference (TBAD-controls) . Mean variance ratio (mean difference/controls × 100%) . P-value . Diameter (cm)  STJ, point A 3.0 ± 0.5 2.7 ± 0.3 0.3 11.1 <0.001  Mid-ascending aorta, point B 3.5 ± 0.6 3.2 ± 0.4 0.3 9.4 <0.001  End-ascending aorta, point C 3.3 ± 0.5 3.0 ± 0.3 0.3 10.0 <0.001  End-INA, point D 3.1 ± 0.5 2.8 ± 0.3 0.3 10.1 <0.001  End-LCCA, point E 2.8 ± 0.5 2.5 ± 0.2 0.3 10.7 <0.001  End-LSA, point F 2.4 ± 0.4 2.3 ± 0.2 0.1 4.3 0.012 Length (cm)  Ascending aorta 7.3 ± 1.1 6.5 ± 0.8 0.8 12.3 <0.001  Aortic arch 3.9 ± 0.7 3.6 ± 0.6 0.3 8.3 <0.001  Total proximal aorta 11.3 ± 1.3 10.2 ± 1.0 1.1 10.7 <0.001 Tortuosity index (%)  Ascending aorta 113.1 ± 4.9 112.2 ± 3.9 NA NA 0.11  Aortic arch 104.2 ± 2.4 102.3 ± 1.3 1.9 1.9 <0.001  Total proximal aorta 126.7 ± 7.3 123.0 ± 4.9 3.7 3.0 <0.001 Angulation (°)  Ascending aorta 83.6 ± 13.2 79.7 ± 10.8 3.9 4.9 0.01  Aortic arch 53.4 ± 13.0 41.7 ± 11.1 11.7 28.1 <0.001  Total proximal aorta 114.8 ± 12.3 103.8 ± 10.0 11.0 10.6 <0.001 Values are presented as mean ± standard deviation. Points A–F are illustrated in Fig. 2. INA: innominate artery; LCCA: left common carotid artery; LSA: left subclavian artery; NA: not applicable; PSM: propensity-score matching; STJ: sinotubular junction; TBAD: type B aortic dissection. Open in new tab Aortic length Compared with controls, the lengths of the ascending aorta, aortic arch and total proximal aorta were significantly longer in the TBAD group, with mean comparative increases of 0.8, 0.3 and 1.1 cm, respectively (all P < 0.001, Fig. 3A and Table 2). Figure 3: Open in new tabDownload slide Morphological and geometrical differences in the proximal aorta between patients with TBAD and controls. (A) Length comparison within different aortic segments. (B) Tortuosity index (%) of the different aortic segments for the control and TBAD groups. (C) Comparison of angulation within different aortic segments. TBAD: type B aortic dissection. Figure 3: Open in new tabDownload slide Morphological and geometrical differences in the proximal aorta between patients with TBAD and controls. (A) Length comparison within different aortic segments. (B) Tortuosity index (%) of the different aortic segments for the control and TBAD groups. (C) Comparison of angulation within different aortic segments. TBAD: type B aortic dissection. Tortuosity index No significant differences were observed between groups for the tortuosity index of the ascending aorta (P = 0.11; Table 2 and Fig. 3B). The tortuosity index values for the aortic arch and total proximal aorta in the TBAD group were significantly higher versus controls (both P < 0.001), with a mean increase in ratio of 1.9% and 3.0%, respectively (Table 2). Angulation Compared with controls, the angulations of the ascending aorta, aortic arch and total proximal aorta were significantly higher in the TBAD group (P = 0.01, P < 0.001 and P < 0.001, respectively), with mean comparative increases of 4.9%, 28.1% and 10.6%, respectively (Fig. 3C and Table 2). Geometric features associated with type B aortic dissection We used binary logistic regression analysis to identify the geometric features that remained independently associated with TBAD. Model 1 identified aortic arch diameter (point D level), ascending aorta length and aortic arch tortuosity index (%) as variables with strong associations with TBAD (Table 3). In addition to aortic arch diameter, both ascending aorta length and aortic arch tortuosity index (%) were independently related to TBAD (OR 3.49, CI 2.01–6.08; P < 0.001 and OR 1.91, CI 1.40–2.59; P < 0.001, respectively). Table 3: Binary logistic regression analysis for the occurrence of TBAD: model 1 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 1 Ascending aorta length (cm) 1.25 0.28 3.49 2.01 6.08 <0.001 Aortic arch tortuosity index (%) 0.64 0.15 1.91 1.40 2.59 <0.001 Aorta diameter in end-INA (point D) (cm) 1.41 0.52 4.12 1.49 11.38 0.006 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 1 Ascending aorta length (cm) 1.25 0.28 3.49 2.01 6.08 <0.001 Aortic arch tortuosity index (%) 0.64 0.15 1.91 1.40 2.59 <0.001 Aorta diameter in end-INA (point D) (cm) 1.41 0.52 4.12 1.49 11.38 0.006 P-value: forwards stepwise method. Initial covariates: ascending aorta and arch length; tortuosity index (%) of the ascending aorta, arch and total proximal aorta (from STJ to LSA); aorta diameter at each point (A–F). Points A–F are illustrated in Fig. 2. INA: innominate artery; LSA: left subclavian artery; STJ: sinotubular junction; TBAD: type B aortic dissection. Open in new tab Table 3: Binary logistic regression analysis for the occurrence of TBAD: model 1 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 1 Ascending aorta length (cm) 1.25 0.28 3.49 2.01 6.08 <0.001 Aortic arch tortuosity index (%) 0.64 0.15 1.91 1.40 2.59 <0.001 Aorta diameter in end-INA (point D) (cm) 1.41 0.52 4.12 1.49 11.38 0.006 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 1 Ascending aorta length (cm) 1.25 0.28 3.49 2.01 6.08 <0.001 Aortic arch tortuosity index (%) 0.64 0.15 1.91 1.40 2.59 <0.001 Aorta diameter in end-INA (point D) (cm) 1.41 0.52 4.12 1.49 11.38 0.006 P-value: forwards stepwise method. Initial covariates: ascending aorta and arch length; tortuosity index (%) of the ascending aorta, arch and total proximal aorta (from STJ to LSA); aorta diameter at each point (A–F). Points A–F are illustrated in Fig. 2. INA: innominate artery; LSA: left subclavian artery; STJ: sinotubular junction; TBAD: type B aortic dissection. Open in new tab When investigating the angulation-related predictors using model 2 (Table 4), in addition to aortic arch diameter and ascending aorta length, aortic arch angulation was independently related to TBAD (OR 1.08, CI 1.04–1.12; P < 0.001). Table 4: Binary logistic regression analysis for the occurrence of TBAD: model 2 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 2 Ascending aorta length (cm) 1.16 0.29 3.18 1.79 5.63 <0.001 Aortic arch angulation (°) 0.07 0.02 1.08 1.04 1.12 <0.001 Aorta diameter in end-INA (point D) (cm) 1.83 0.56 6.22 2.07 18.70 0.001 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 2 Ascending aorta length (cm) 1.16 0.29 3.18 1.79 5.63 <0.001 Aortic arch angulation (°) 0.07 0.02 1.08 1.04 1.12 <0.001 Aorta diameter in end-INA (point D) (cm) 1.83 0.56 6.22 2.07 18.70 0.001 P-value: forward stepwise method. Initial covariates: ascending aorta and aortic arch length; angulation of the ascending aorta and aortic arch; aorta diameter at each point (A–F). Points A–F are illustrated in Fig. 2. INA: innominate artery; LSA: left subclavian artery; STJ: sinotubular junction; TBAD: type B aortic dissection. Open in new tab Table 4: Binary logistic regression analysis for the occurrence of TBAD: model 2 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 2 Ascending aorta length (cm) 1.16 0.29 3.18 1.79 5.63 <0.001 Aortic arch angulation (°) 0.07 0.02 1.08 1.04 1.12 <0.001 Aorta diameter in end-INA (point D) (cm) 1.83 0.56 6.22 2.07 18.70 0.001 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 2 Ascending aorta length (cm) 1.16 0.29 3.18 1.79 5.63 <0.001 Aortic arch angulation (°) 0.07 0.02 1.08 1.04 1.12 <0.001 Aorta diameter in end-INA (point D) (cm) 1.83 0.56 6.22 2.07 18.70 0.001 P-value: forward stepwise method. Initial covariates: ascending aorta and aortic arch length; angulation of the ascending aorta and aortic arch; aorta diameter at each point (A–F). Points A–F are illustrated in Fig. 2. INA: innominate artery; LSA: left subclavian artery; STJ: sinotubular junction; TBAD: type B aortic dissection. Open in new tab DISCUSSION Previous studies demonstrated that the diameter of the descending aorta is insufficient to adequately predict the risk of developing TBAD [21]. The presence of a dilated proximal aorta was also not sufficiently effective and specific [9] because this is also a crucial risk factor predicting TAAD [3, 22]. These findings highlight the need to develop other anatomical and specific factors to identify patients at risk for TBAD. For this purpose, first, we identified the significant dilation, elongation, increased tortuosity and angulation within the proximal aorta in TBAD patients. Second, we demonstrated that the increased tortuosity and angulation of the aortic arch may play independent and specific roles in the development of TBAD. Considering previous studies, several different findings require special attention. Lescan et al. [10] reported significant aortic elongation only in the aortic arch and no significant change in the ascending aorta, whereas Shirali et al. [9] described increased aortic length in the total proximal aorta and ascending aorta, but did not indicate changes in the aortic arch. However, in our study, we saw elongation in both the aortic arch and ascending aorta in TBAD patients. This may be reasonable based on the recognized loss of longitudinal elasticity in the aorta media [23]. Regarding the geometric alteration in the proximal aorta, Shirali et al. [9] investigated the tortuosity of the total proximal aorta between normotensive patients without AD, hypertensive patients without AD and a TBAD group, but reported no significant specific tortuosity differences. However, in our study, we identified greater tortuosity and angulation in the proximal aorta, especially in the aortic arch, in patients with TBAD. This is a reasonable finding that can be explained by the elongated aortic arch in TBAD. Because the aortic arch segment is relatively fixed by the innominate artery and LSA, this may result in increased tortuosity and angulation. Identifying these significant anatomical differences also permits investigating the detailed and specific anatomical predictors of TBAD. Previously, in addition to increased aortic arch diameter, Shirali et al. [9] demonstrated that total aortic length and tortuosity were independent risk factors, but the authors failed to interpret the function of specific segment-related predictors. Lescan et al. [10] reported significant elongation in the aortic arch and not in the ascending aorta, but did not investigate the related predictive value. In our study, significant aortic elongation was observed in both the ascending aorta and aortic arch, with a mean increase of 0.8 and 0.3 cm, respectively. However, only the elongated ascending aorta, not the aortic arch, remained independently associated with TBAD in the multivariate analysis, which validated the hypothesis by Shirali et al. [9] that the elongated ascending aorta may be used as a predictor of AD risk. However, considering the similar role that ascending aorta elongation plays in the development of TAAD [2, 3], other specific geometric features should be considered to predict TBAD risk. Differing from previous studies, in addition to aortic length and diameter, we evaluated detailed aortic segment geometrical comparisons of tortuosity and angulation. Our results showed significantly increased tortuosity and angulation in the aortic arch segment in the TBAD group, with a mean increase in ratio of 1.9% and 28.1%, respectively, which were independent predictors of TBAD in the multivariate analysis. These findings may indicate that severe or greater aortic arch tortuosity and angulation are associated with TBAD independently and specifically. Interestingly, our findings were in accordance with the conclusions of a recent study stating that type III arch configuration is associated with TBAD [7] because type III arch presents peculiar geometric features, namely, a more tortuous and angulated aortic arch [14]. Besides, increased aortic arch tortuosity and angulation better explain the mechanism of TBAD development. Generally, any conditions that increase wall shear stress (WSS) and decrease aorta media degeneration are potential risk factors for TBAD [24]. According to a study by Nathan et al. [25], there were peaks in WSS above the sinotubular junction and distally to the LSA ostium in the normal thoracic aorta. Previous studies demonstrated that greater tortuosity of the proximal aorta leads to stronger helical flow through the distal arch, which increases WSS [11, 26]. According to our results, the area with increased tortuosity was in the aortic arch, not in the ascending aorta, which indicates that increased WSS was present in the segment distally to the aortic arch, following the principles of haemodynamics. Previous studies have confirmed that the magnitude of the haemodynamic forces applied on the aortic wall of Ishimaru zone 3 increased gradually from type I to type III arch configuration [14, 27]. This may suggest that increased aortic arch angulation is accompanied by increased WSS on the zone 3 aortic wall. Under increased WSS, apoptosis in the local smooth muscle cells is accelerated [28], which triggers the formation of tears and the development of TBAD when blood pressure increases suddenly. To some extent, this also explains why entry tears are most often located just distally to the origin of the LSA [29]. However, the specific relationship between altered aortic arch geometry and TBAD requires validation using computer-aided fluid dynamics research. Limitations We recognize that the major limitation in our study was the retrospective design. To confirm a clear causal relationship between altered aorta geometry and dissection, a prospective and longitudinal study is needed; however, given the low incidence rate of TBAD, this would be a challenge. Therefore, we consider our study design combined with modelling of the dimensions to be the best achievable alternative. Second, although we considered that age and other demographic data were homogenous, and we excluded patients with a bovine arch, which is associated with an increased incidence of dissection [8], there may still have been unavoidable selection bias from unknown factors affecting proximal aorta dimensions, such as antihypertensive drug therapy. Third, all the CTA images we used were not electrocardiogram (ECG)-gated, and the CTA maximum slice thickness of 3 mm may impact the measurement accuracy. To minimize measurement error as much as possible, ECG-gated and only thin-slice (1.0 or 1.5 mm) CTA images should be included in future studies. Fourth, patients with TBAD were not enrolled from multicentre studies. Our findings must be validated in multicentre studies involving ethnically diverse populations. CONCLUSION In addition to proximal aorta dilation, significant elongation was seen in both the ascending aorta and aortic arch in TBAD patients. Using advanced tortuosity and angulation measurement approaches based on aorta CLL analysis, we found significant geometric alteration in the proximal aorta in TBAD patients. Increased aortic arch tortuosity and angulation could be independent and specific predictors of TBAD. Further investigations are needed to assess the pathophysiological role and diagnostic value of aortic arch tortuosity and angulation. Conflict of interest: none declared. Author contributions Long Cao: Conceptualization; Data curation; Formal analysis; Investigation; Methodology; Resources; Software; Visualization; Writing—original draft; Writing—review & editing. Weihang Lu: Conceptualization; Data curation; Investigation; Methodology; Resources; Software; Validation; Writing—original draft. Yangyang Ge: Data curation; Formal analysis; Investigation; Methodology; Resources; Validation; Visualization; Writing—original draft. Xinhao Wang: Formal analysis; Investigation; Resources; Software; Validation; Visualization. Yuan He: Data curation; Formal analysis; Investigation; Resources; Supervision. Guoyi Sun: Investigation; Methodology; Resources; Software; Visualization. Jie Liu: Data curation; Formal analysis; Investigation; Methodology; Resources. Xiaoping Liu: Formal analysis; Investigation; Supervision; Writing—review & editing. Xin Jia: Formal analysis; Resources; Software; Supervision; Validation. Jiang Xiong: Formal analysis; Investigation; Methodology; Supervision; Visualization. Xiaohui Ma: Data curation; Formal analysis; Methodology; Software; Visualization. Hongpeng Zhang: Methodology; Resources; Software; Supervision; Writing—review & editing. Lijun Wang: Methodology; Resources; Validation; Visualization. Wei Guo: Conceptualization; Investigation; Methodology; Project administration; Resources; Supervision; Writing—review & editing. REFERENCES 1 Golledge J , Eagle KA. Acute aortic dissection . Lancet 2008 ; 372 : 55 – 66 . Google Scholar Crossref Search ADS PubMed WorldCat 2 Kruger T , Forkavets O, Veseli K, Lausberg H, Vohringer L, Schneider W. Ascending aortic elongation and the risk of dissection . Eur J Cardiothorac Surg 2016 ; 50 : 241 – 7 . 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Google Scholar Crossref Search ADS PubMed WorldCat Abbreviations AD Aortic dissection BMI Body mass index BSA Body surface area CI Confidence interval CLL Centre lumen line CTA Computed tomography angiography LSA Left subclavian artery OR Odds ratio TAAD Type A aortic dissection TBAD Type B aortic dissection WSS Wall shear stress Author notes † Long Cao, Weihang Lu and Yangyang Ge authors contributed equally to this study. © The Author(s) 2020. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Cardio-Thoracic Surgery Oxford University Press

Altered aortic arch geometry in patients with type B aortic dissection

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Oxford University Press
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© The Author(s) 2020. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.
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1010-7940
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1873-734X
DOI
10.1093/ejcts/ezaa102
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Abstract

Abstract Open in new tabDownload slide Open in new tabDownload slide OBJECTIVES This study aims to evaluate differences in proximal aorta geometry and identify specific anatomical predictors of type B aortic dissection (TBAD). METHODS We evaluated computed tomographic angiograms of controls (n = 185) and patients with acute TBAD (n = 173). Using propensity score matching, we created 2 groups of 127 patients. 3mensio Vascular software was used to analyse the computed tomographic angiograms and measure the diameter, length, tortuosity index and angulation of the proximal aorta (divided into ascending aorta and aortic arch). Tortuosity index was calculated by dividing the centre lumen line length of the aortic segment by its shortest length. Angulation was measured by the centre lumen line ‘tangent line angle’. Two independent multivariable models identified significant anatomical associations regarding the tortuosity and angulation geometry. RESULTS Aortic diameter and ascending aorta and aortic arch lengths in TBAD increased significantly. The aortic arch tortuosity was significantly higher in the TBAD group (P < 0.001), with no difference regarding the ascending aorta (P = 0.11). Ascending aorta and aortic arch angulation were significantly higher in the TBAD group (P = 0.01, P < 0.001, respectively). Multivariable analyses showed that increased aortic arch tortuosity and angulation were significant predictors of the development of TBAD [odds ratio (OR) 1.91, 95% confidence interval (CI) 1.40–2.59; P < 0.001 and OR 1.08, 95% CI 1.04–1.12; P < 0.001], respectively. CONCLUSIONS In addition to proximal aorta dilation and elongation, we identified increased aortic arch tortuosity and angulation as possible specific predictors of TBAD. Aortic dissection, Type B aortic dissection, Computed tomographic angiography, Geometrical analysis INTRODUCTION Aortic dissection (AD) is a life-threatening cardiovascular disease that results in a tear in the arterial intimal layer, which allows blood to collect within the medial layer [1]. Previous studies reported that specific geometric features of the proximal aorta, including elongation, angulation and tortuosity, may play important roles in the risk of onset of type A AD (TAAD) [2–6]. More recently, there is also an emerging awareness of the potential detrimental implications of these anatomical characteristics for the development of type B AD (TBAD) [7–10]. Significant elongation of the proximal aorta has been seen in both TAAD and TBAD [3, 9]. Previous studies have demonstrated that ascending aorta elongation was an independent risk factor for TAAD development [2, 3]; however, few studies have evaluated the predictive value of ascending aorta or aortic arch elongation in TBAD patients [9, 10]. Previous studies also demonstrated that the angulation of the ascending aorta plays an independent role in the development of TAAD [4, 5], and, as another important geometrical evaluation method, increased tortuosity in the proximal aorta has been considered a high-level anatomical risk for the development of TAAD [6, 11]. Unfortunately, the lack of consistent reporting methods for the measurement of angulation and tortuosity may have overshadowed the clinical relevance of these features and their important predictive value for TBAD patients. Considering the significant morphology and geometric alterations in the dissected descending aorta [12, 13], evaluating the undissected proximal aorta in TBAD patients may be more feasible regarding investigating geometric differences pre-dissection. Additionally, with advances in medical imaging and more sophisticated algorithms, it is possible to study the complex 3-dimensional geometry of the aorta, especially when analysing the tortuosity and angulation [14]. According to these points and the feasibility of measurement, we aimed to compare proximal aorta geometry in patients with TBAD versus aortas in the control group and to evaluate the significant dimensional differences to identify the independent and specific anatomical predictors of TBAD. MATERIALS AND METHODS Study design This study was approved by our local ethics committee. Obtaining written informed consent was not necessary because of the retrospective, observational nature of the study. Inclusion and exclusion flow charts of the study cohort are shown in Fig. 1. Figure 1: Open in new tabDownload slide Inclusion and exclusion criteria flow chart for the study cohort. TBAD: type B aortic dissection. Figure 1: Open in new tabDownload slide Inclusion and exclusion criteria flow chart for the study cohort. TBAD: type B aortic dissection. All patients diagnosed with acute TBAD were retrospectively enrolled from our medical centre from January 2010 to December 2018. The exclusion criteria were bicuspid aortic valve, connective tissue disease, previous history of aortic surgery, non-A non-B dissection [defined as descending-entry type with entry distally to the left subclavian artery (LSA) and dissection extending into the aortic arch, and arch-entry type with entry between the innominate and LSA] [15, 16]. We also excluded patients with a ‘bovine arch’ because this anatomical configuration is associated with an increased risk of developing thoracic aortic disease [8]. These criteria resulted in including 173 patients with acute TBAD. The control group comprised patients who underwent computed tomography angiography (CTA) for non-vascular emergencies at PLA General Hospital between December 2016 and January 2017. The inclusion criterion was that the ascending aorta and aortic arch were imaged in the scans. Patients with suspected or known aortic disease, ‘bovine arch’, bicuspid aortic valve, connective tissue disease, and those who previously underwent cardiothoracic surgery were excluded. A total of 185 patients met these criteria and were enrolled. Image postprocessing and analysis All enrolled CTA scans were performed using second-generation dual-source computed tomography scanners, and CTA images with a maximum slice thickness of 3 mm were accepted for further processing. All CTAs were imported into the image postprocessing software (3mensio version 8.1; Pie Medical Imaging, Maastricht, Netherlands), which provides dedicated semiautomated vascular segmentation and measurements based on the 3-dimensional centre lumen line (CLL) [17]. Six anatomical landmarks (points A–F) were marked on the stretched image (Fig. 2A and B). ‘Point A’ was located at the sinotubular junction; ‘point B’ was located at the level of the middle ascending aorta; ‘points C and D’ were located at the proximal and distal edge of the innominate artery, respectively; ‘point E’ was located at the distal edge of the left common carotid artery; and ‘point F’ was located at the distal edge of the LSA. The ascending aorta was defined as the aortic segment between ‘points A and C’, the aortic arch was defined as the segment between ‘points C and F’, and the total proximal aorta was defined as the segment between ‘points A and F’. Figure 2: Open in new tabDownload slide Computed tomography angiography measurement process. (A) The centre lumen line of the aorta and the 6 marked anatomical ‘points A–F’. ‘Point A’ is located at the sinotubular junction; ‘point B’ is located at the level of the middle ascending aorta; ‘points C and D’ are located at the proximal and distal edge of the innominate artery, respectively; ‘point E’ is located at the distal edge of the left common carotid artery; and ‘point F’ is located at the distal edge of the left subclavian artery. (B) Centre lumen line length measurement on the stretched view. (C) Angulation measurement of the ascending aorta. (D) Angulation measurement of the aortic arch. Figure 2: Open in new tabDownload slide Computed tomography angiography measurement process. (A) The centre lumen line of the aorta and the 6 marked anatomical ‘points A–F’. ‘Point A’ is located at the sinotubular junction; ‘point B’ is located at the level of the middle ascending aorta; ‘points C and D’ are located at the proximal and distal edge of the innominate artery, respectively; ‘point E’ is located at the distal edge of the left common carotid artery; and ‘point F’ is located at the distal edge of the left subclavian artery. (B) Centre lumen line length measurement on the stretched view. (C) Angulation measurement of the ascending aorta. (D) Angulation measurement of the aortic arch. Diameter and length Aortic diameter was measured on 6 level planes (points A–F) perpendicular to the aorta centreline (Fig. 2B). The lengths of the ascending aorta, aortic arch and total proximal aorta were calculated from the corresponding centreline length (Fig. 2B). Tortuosity index and angulation We calculated the tortuosity index by dividing the length of the CLL by the shortest distance length. Angulation was measured using the CLL ‘tangent angle’ function within the software [14], which was defined as the angle between tangent lines drawn for 2 points along the CLL (Fig. 2C and D). The 2 points correspond to the proximal and distal points of the measured aortic segment. We calculated the tortuosity indexes and angulation for the total proximal aorta, ascending aorta and aortic arch. Measurement reproducibility Measurements were repeated by 2 observers for 40 CTAs randomly selected from the 2 groups to evaluate the interobserver repeatability using the intra-class correlation coefficients and Bland–Altman plots (full details appear in Supplementary Material, Data S1). Statistical analysis Continuous data are expressed as mean ± standard deviation, and categorical data are reported as percentages. Data were tested for normality using the Kolmogorov–Smirnov test, and we used the t-test or Mann–Whitney test to compare each dimension parameter between the TBAD and control groups. The χ2 test or Fisher’s exact probability method was used for differences between frequency and the composition ratio. We then used propensity scores to match the control group using nearest-neighbour matching with a 1:1 ratio. Recognized and potential covariates [age, sex, body surface area (BSA), body mass index (BMI) and hypertension] affecting the aortic dimension were used to calculate the propensity scores [18–20]. Replacement was not allowed, and we set the caliper distance at 0.05. Two models using stepwise logistic regression analyses were created to determine which geometric features were independently associated with TBAD. Model 1 used the covariates aortic diameter, length and the tortuosity index of the aortic segment (Table 3), and model 2 used aortic diameter, length and the angulation of the aortic segment (Table 4). Results were reported as odds ratios (ORs) and 95% confidence intervals (CIs) for the identified risk factors. All reported P-values were 2-sided, and P < 0.05 was considered statistically significant. SPSS 22.0 software (IBM, Armonk, NY, USA) was used for all statistical analyses. RESULTS Overall cohort The baseline characteristics of both groups before propensity score matching are presented in Table 1. Patients with TBAD were significantly younger compared with the control group (52.7 vs 57.8 years, respectively). Furthermore, the TBAD group comprised significantly more men and patients with a larger BSA. There were no differences in the prevalence of hypertension or in BMI measurements between the groups. Table 1: Patient characteristics in the different study groups Variables . Overall cohort . PSM cohort . TBAD (n = 173) . Controls (n = 185) . P-value . Standardized differencea . TBAD (n = 127) . Controls (n = 127) . P-value . Standardized differencea . Age (years) 52.7 ± 11.4 57.8 ± 10.5 <0.001 −46.5 53.8 ± 10.8 56.3 ± 10.9 0.06 −23.0 Male gender 152 (87.9) 106 (57.3) <0.001 72.7 107 (84.3) 106 (83.5) 1 2.2 BMI (kg/m2) 25.5 ± 3.9 25.4 ± 3.3 0.88 2.8 25.5 ± 3.8 25.9 ± 3.3 0.4 −11.2 BSA 1.8 ± 0.2 1.8 ± 0.2 0.005 31.5 1.8 ± 0.2 1.8 ± 0.2 0.48 −5.25 Hypertension 100 (57.8) 98 (53.0) 0.36 9.7 77 (60.6) 68 (53.5) 0.31 14.3 Variables . Overall cohort . PSM cohort . TBAD (n = 173) . Controls (n = 185) . P-value . Standardized differencea . TBAD (n = 127) . Controls (n = 127) . P-value . Standardized differencea . Age (years) 52.7 ± 11.4 57.8 ± 10.5 <0.001 −46.5 53.8 ± 10.8 56.3 ± 10.9 0.06 −23.0 Male gender 152 (87.9) 106 (57.3) <0.001 72.7 107 (84.3) 106 (83.5) 1 2.2 BMI (kg/m2) 25.5 ± 3.9 25.4 ± 3.3 0.88 2.8 25.5 ± 3.8 25.9 ± 3.3 0.4 −11.2 BSA 1.8 ± 0.2 1.8 ± 0.2 0.005 31.5 1.8 ± 0.2 1.8 ± 0.2 0.48 −5.25 Hypertension 100 (57.8) 98 (53.0) 0.36 9.7 77 (60.6) 68 (53.5) 0.31 14.3 Data are presented as mean ± standard deviation and n (%). a Standardized difference is the mean difference divided by the pooled standard deviation, expressed as a percentage. BMI: body mass index; BSA: body surface area; PSM: propensity-score matching; TBAD: type B aortic dissection. Open in new tab Table 1: Patient characteristics in the different study groups Variables . Overall cohort . PSM cohort . TBAD (n = 173) . Controls (n = 185) . P-value . Standardized differencea . TBAD (n = 127) . Controls (n = 127) . P-value . Standardized differencea . Age (years) 52.7 ± 11.4 57.8 ± 10.5 <0.001 −46.5 53.8 ± 10.8 56.3 ± 10.9 0.06 −23.0 Male gender 152 (87.9) 106 (57.3) <0.001 72.7 107 (84.3) 106 (83.5) 1 2.2 BMI (kg/m2) 25.5 ± 3.9 25.4 ± 3.3 0.88 2.8 25.5 ± 3.8 25.9 ± 3.3 0.4 −11.2 BSA 1.8 ± 0.2 1.8 ± 0.2 0.005 31.5 1.8 ± 0.2 1.8 ± 0.2 0.48 −5.25 Hypertension 100 (57.8) 98 (53.0) 0.36 9.7 77 (60.6) 68 (53.5) 0.31 14.3 Variables . Overall cohort . PSM cohort . TBAD (n = 173) . Controls (n = 185) . P-value . Standardized differencea . TBAD (n = 127) . Controls (n = 127) . P-value . Standardized differencea . Age (years) 52.7 ± 11.4 57.8 ± 10.5 <0.001 −46.5 53.8 ± 10.8 56.3 ± 10.9 0.06 −23.0 Male gender 152 (87.9) 106 (57.3) <0.001 72.7 107 (84.3) 106 (83.5) 1 2.2 BMI (kg/m2) 25.5 ± 3.9 25.4 ± 3.3 0.88 2.8 25.5 ± 3.8 25.9 ± 3.3 0.4 −11.2 BSA 1.8 ± 0.2 1.8 ± 0.2 0.005 31.5 1.8 ± 0.2 1.8 ± 0.2 0.48 −5.25 Hypertension 100 (57.8) 98 (53.0) 0.36 9.7 77 (60.6) 68 (53.5) 0.31 14.3 Data are presented as mean ± standard deviation and n (%). a Standardized difference is the mean difference divided by the pooled standard deviation, expressed as a percentage. BMI: body mass index; BSA: body surface area; PSM: propensity-score matching; TBAD: type B aortic dissection. Open in new tab Propensity score matching cohort Age, sex, BSA, BMI and hypertension significantly influenced the proximal aorta dimensions [18–20]; therefore, we included these variables in the model to calculate propensity scores. The propensity scores pre- and postmatching as well as their distribution are presented in Supplementary Material, Fig. S1. Finally, 127 pairs underwent further measurements and comparisons. Aortic diameters In the TBAD group, the ascending aorta was much larger than in controls. Likewise, the aortic arch and the total proximal aorta had larger aortic diameters (all P < 0.05, Table 2). Except for ‘point F’, the aortic diameter of the proximal aorta was ∼10% larger in the TBAD group versus controls. Table 2: Anatomical variables of TBAD patients and controls in the PSM cohort . TBAD (n = 127) . Controls (n = 127) . Mean difference (TBAD-controls) . Mean variance ratio (mean difference/controls × 100%) . P-value . Diameter (cm)  STJ, point A 3.0 ± 0.5 2.7 ± 0.3 0.3 11.1 <0.001  Mid-ascending aorta, point B 3.5 ± 0.6 3.2 ± 0.4 0.3 9.4 <0.001  End-ascending aorta, point C 3.3 ± 0.5 3.0 ± 0.3 0.3 10.0 <0.001  End-INA, point D 3.1 ± 0.5 2.8 ± 0.3 0.3 10.1 <0.001  End-LCCA, point E 2.8 ± 0.5 2.5 ± 0.2 0.3 10.7 <0.001  End-LSA, point F 2.4 ± 0.4 2.3 ± 0.2 0.1 4.3 0.012 Length (cm)  Ascending aorta 7.3 ± 1.1 6.5 ± 0.8 0.8 12.3 <0.001  Aortic arch 3.9 ± 0.7 3.6 ± 0.6 0.3 8.3 <0.001  Total proximal aorta 11.3 ± 1.3 10.2 ± 1.0 1.1 10.7 <0.001 Tortuosity index (%)  Ascending aorta 113.1 ± 4.9 112.2 ± 3.9 NA NA 0.11  Aortic arch 104.2 ± 2.4 102.3 ± 1.3 1.9 1.9 <0.001  Total proximal aorta 126.7 ± 7.3 123.0 ± 4.9 3.7 3.0 <0.001 Angulation (°)  Ascending aorta 83.6 ± 13.2 79.7 ± 10.8 3.9 4.9 0.01  Aortic arch 53.4 ± 13.0 41.7 ± 11.1 11.7 28.1 <0.001  Total proximal aorta 114.8 ± 12.3 103.8 ± 10.0 11.0 10.6 <0.001 . TBAD (n = 127) . Controls (n = 127) . Mean difference (TBAD-controls) . Mean variance ratio (mean difference/controls × 100%) . P-value . Diameter (cm)  STJ, point A 3.0 ± 0.5 2.7 ± 0.3 0.3 11.1 <0.001  Mid-ascending aorta, point B 3.5 ± 0.6 3.2 ± 0.4 0.3 9.4 <0.001  End-ascending aorta, point C 3.3 ± 0.5 3.0 ± 0.3 0.3 10.0 <0.001  End-INA, point D 3.1 ± 0.5 2.8 ± 0.3 0.3 10.1 <0.001  End-LCCA, point E 2.8 ± 0.5 2.5 ± 0.2 0.3 10.7 <0.001  End-LSA, point F 2.4 ± 0.4 2.3 ± 0.2 0.1 4.3 0.012 Length (cm)  Ascending aorta 7.3 ± 1.1 6.5 ± 0.8 0.8 12.3 <0.001  Aortic arch 3.9 ± 0.7 3.6 ± 0.6 0.3 8.3 <0.001  Total proximal aorta 11.3 ± 1.3 10.2 ± 1.0 1.1 10.7 <0.001 Tortuosity index (%)  Ascending aorta 113.1 ± 4.9 112.2 ± 3.9 NA NA 0.11  Aortic arch 104.2 ± 2.4 102.3 ± 1.3 1.9 1.9 <0.001  Total proximal aorta 126.7 ± 7.3 123.0 ± 4.9 3.7 3.0 <0.001 Angulation (°)  Ascending aorta 83.6 ± 13.2 79.7 ± 10.8 3.9 4.9 0.01  Aortic arch 53.4 ± 13.0 41.7 ± 11.1 11.7 28.1 <0.001  Total proximal aorta 114.8 ± 12.3 103.8 ± 10.0 11.0 10.6 <0.001 Values are presented as mean ± standard deviation. Points A–F are illustrated in Fig. 2. INA: innominate artery; LCCA: left common carotid artery; LSA: left subclavian artery; NA: not applicable; PSM: propensity-score matching; STJ: sinotubular junction; TBAD: type B aortic dissection. Open in new tab Table 2: Anatomical variables of TBAD patients and controls in the PSM cohort . TBAD (n = 127) . Controls (n = 127) . Mean difference (TBAD-controls) . Mean variance ratio (mean difference/controls × 100%) . P-value . Diameter (cm)  STJ, point A 3.0 ± 0.5 2.7 ± 0.3 0.3 11.1 <0.001  Mid-ascending aorta, point B 3.5 ± 0.6 3.2 ± 0.4 0.3 9.4 <0.001  End-ascending aorta, point C 3.3 ± 0.5 3.0 ± 0.3 0.3 10.0 <0.001  End-INA, point D 3.1 ± 0.5 2.8 ± 0.3 0.3 10.1 <0.001  End-LCCA, point E 2.8 ± 0.5 2.5 ± 0.2 0.3 10.7 <0.001  End-LSA, point F 2.4 ± 0.4 2.3 ± 0.2 0.1 4.3 0.012 Length (cm)  Ascending aorta 7.3 ± 1.1 6.5 ± 0.8 0.8 12.3 <0.001  Aortic arch 3.9 ± 0.7 3.6 ± 0.6 0.3 8.3 <0.001  Total proximal aorta 11.3 ± 1.3 10.2 ± 1.0 1.1 10.7 <0.001 Tortuosity index (%)  Ascending aorta 113.1 ± 4.9 112.2 ± 3.9 NA NA 0.11  Aortic arch 104.2 ± 2.4 102.3 ± 1.3 1.9 1.9 <0.001  Total proximal aorta 126.7 ± 7.3 123.0 ± 4.9 3.7 3.0 <0.001 Angulation (°)  Ascending aorta 83.6 ± 13.2 79.7 ± 10.8 3.9 4.9 0.01  Aortic arch 53.4 ± 13.0 41.7 ± 11.1 11.7 28.1 <0.001  Total proximal aorta 114.8 ± 12.3 103.8 ± 10.0 11.0 10.6 <0.001 . TBAD (n = 127) . Controls (n = 127) . Mean difference (TBAD-controls) . Mean variance ratio (mean difference/controls × 100%) . P-value . Diameter (cm)  STJ, point A 3.0 ± 0.5 2.7 ± 0.3 0.3 11.1 <0.001  Mid-ascending aorta, point B 3.5 ± 0.6 3.2 ± 0.4 0.3 9.4 <0.001  End-ascending aorta, point C 3.3 ± 0.5 3.0 ± 0.3 0.3 10.0 <0.001  End-INA, point D 3.1 ± 0.5 2.8 ± 0.3 0.3 10.1 <0.001  End-LCCA, point E 2.8 ± 0.5 2.5 ± 0.2 0.3 10.7 <0.001  End-LSA, point F 2.4 ± 0.4 2.3 ± 0.2 0.1 4.3 0.012 Length (cm)  Ascending aorta 7.3 ± 1.1 6.5 ± 0.8 0.8 12.3 <0.001  Aortic arch 3.9 ± 0.7 3.6 ± 0.6 0.3 8.3 <0.001  Total proximal aorta 11.3 ± 1.3 10.2 ± 1.0 1.1 10.7 <0.001 Tortuosity index (%)  Ascending aorta 113.1 ± 4.9 112.2 ± 3.9 NA NA 0.11  Aortic arch 104.2 ± 2.4 102.3 ± 1.3 1.9 1.9 <0.001  Total proximal aorta 126.7 ± 7.3 123.0 ± 4.9 3.7 3.0 <0.001 Angulation (°)  Ascending aorta 83.6 ± 13.2 79.7 ± 10.8 3.9 4.9 0.01  Aortic arch 53.4 ± 13.0 41.7 ± 11.1 11.7 28.1 <0.001  Total proximal aorta 114.8 ± 12.3 103.8 ± 10.0 11.0 10.6 <0.001 Values are presented as mean ± standard deviation. Points A–F are illustrated in Fig. 2. INA: innominate artery; LCCA: left common carotid artery; LSA: left subclavian artery; NA: not applicable; PSM: propensity-score matching; STJ: sinotubular junction; TBAD: type B aortic dissection. Open in new tab Aortic length Compared with controls, the lengths of the ascending aorta, aortic arch and total proximal aorta were significantly longer in the TBAD group, with mean comparative increases of 0.8, 0.3 and 1.1 cm, respectively (all P < 0.001, Fig. 3A and Table 2). Figure 3: Open in new tabDownload slide Morphological and geometrical differences in the proximal aorta between patients with TBAD and controls. (A) Length comparison within different aortic segments. (B) Tortuosity index (%) of the different aortic segments for the control and TBAD groups. (C) Comparison of angulation within different aortic segments. TBAD: type B aortic dissection. Figure 3: Open in new tabDownload slide Morphological and geometrical differences in the proximal aorta between patients with TBAD and controls. (A) Length comparison within different aortic segments. (B) Tortuosity index (%) of the different aortic segments for the control and TBAD groups. (C) Comparison of angulation within different aortic segments. TBAD: type B aortic dissection. Tortuosity index No significant differences were observed between groups for the tortuosity index of the ascending aorta (P = 0.11; Table 2 and Fig. 3B). The tortuosity index values for the aortic arch and total proximal aorta in the TBAD group were significantly higher versus controls (both P < 0.001), with a mean increase in ratio of 1.9% and 3.0%, respectively (Table 2). Angulation Compared with controls, the angulations of the ascending aorta, aortic arch and total proximal aorta were significantly higher in the TBAD group (P = 0.01, P < 0.001 and P < 0.001, respectively), with mean comparative increases of 4.9%, 28.1% and 10.6%, respectively (Fig. 3C and Table 2). Geometric features associated with type B aortic dissection We used binary logistic regression analysis to identify the geometric features that remained independently associated with TBAD. Model 1 identified aortic arch diameter (point D level), ascending aorta length and aortic arch tortuosity index (%) as variables with strong associations with TBAD (Table 3). In addition to aortic arch diameter, both ascending aorta length and aortic arch tortuosity index (%) were independently related to TBAD (OR 3.49, CI 2.01–6.08; P < 0.001 and OR 1.91, CI 1.40–2.59; P < 0.001, respectively). Table 3: Binary logistic regression analysis for the occurrence of TBAD: model 1 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 1 Ascending aorta length (cm) 1.25 0.28 3.49 2.01 6.08 <0.001 Aortic arch tortuosity index (%) 0.64 0.15 1.91 1.40 2.59 <0.001 Aorta diameter in end-INA (point D) (cm) 1.41 0.52 4.12 1.49 11.38 0.006 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 1 Ascending aorta length (cm) 1.25 0.28 3.49 2.01 6.08 <0.001 Aortic arch tortuosity index (%) 0.64 0.15 1.91 1.40 2.59 <0.001 Aorta diameter in end-INA (point D) (cm) 1.41 0.52 4.12 1.49 11.38 0.006 P-value: forwards stepwise method. Initial covariates: ascending aorta and arch length; tortuosity index (%) of the ascending aorta, arch and total proximal aorta (from STJ to LSA); aorta diameter at each point (A–F). Points A–F are illustrated in Fig. 2. INA: innominate artery; LSA: left subclavian artery; STJ: sinotubular junction; TBAD: type B aortic dissection. Open in new tab Table 3: Binary logistic regression analysis for the occurrence of TBAD: model 1 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 1 Ascending aorta length (cm) 1.25 0.28 3.49 2.01 6.08 <0.001 Aortic arch tortuosity index (%) 0.64 0.15 1.91 1.40 2.59 <0.001 Aorta diameter in end-INA (point D) (cm) 1.41 0.52 4.12 1.49 11.38 0.006 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 1 Ascending aorta length (cm) 1.25 0.28 3.49 2.01 6.08 <0.001 Aortic arch tortuosity index (%) 0.64 0.15 1.91 1.40 2.59 <0.001 Aorta diameter in end-INA (point D) (cm) 1.41 0.52 4.12 1.49 11.38 0.006 P-value: forwards stepwise method. Initial covariates: ascending aorta and arch length; tortuosity index (%) of the ascending aorta, arch and total proximal aorta (from STJ to LSA); aorta diameter at each point (A–F). Points A–F are illustrated in Fig. 2. INA: innominate artery; LSA: left subclavian artery; STJ: sinotubular junction; TBAD: type B aortic dissection. Open in new tab When investigating the angulation-related predictors using model 2 (Table 4), in addition to aortic arch diameter and ascending aorta length, aortic arch angulation was independently related to TBAD (OR 1.08, CI 1.04–1.12; P < 0.001). Table 4: Binary logistic regression analysis for the occurrence of TBAD: model 2 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 2 Ascending aorta length (cm) 1.16 0.29 3.18 1.79 5.63 <0.001 Aortic arch angulation (°) 0.07 0.02 1.08 1.04 1.12 <0.001 Aorta diameter in end-INA (point D) (cm) 1.83 0.56 6.22 2.07 18.70 0.001 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 2 Ascending aorta length (cm) 1.16 0.29 3.18 1.79 5.63 <0.001 Aortic arch angulation (°) 0.07 0.02 1.08 1.04 1.12 <0.001 Aorta diameter in end-INA (point D) (cm) 1.83 0.56 6.22 2.07 18.70 0.001 P-value: forward stepwise method. Initial covariates: ascending aorta and aortic arch length; angulation of the ascending aorta and aortic arch; aorta diameter at each point (A–F). Points A–F are illustrated in Fig. 2. INA: innominate artery; LSA: left subclavian artery; STJ: sinotubular junction; TBAD: type B aortic dissection. Open in new tab Table 4: Binary logistic regression analysis for the occurrence of TBAD: model 2 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 2 Ascending aorta length (cm) 1.16 0.29 3.18 1.79 5.63 <0.001 Aortic arch angulation (°) 0.07 0.02 1.08 1.04 1.12 <0.001 Aorta diameter in end-INA (point D) (cm) 1.83 0.56 6.22 2.07 18.70 0.001 Model . Anatomical variable . B-coefficient . Standard error . Odds ratio . 95% confidence interval for odds ratio . P-value . Lower . Upper . 2 Ascending aorta length (cm) 1.16 0.29 3.18 1.79 5.63 <0.001 Aortic arch angulation (°) 0.07 0.02 1.08 1.04 1.12 <0.001 Aorta diameter in end-INA (point D) (cm) 1.83 0.56 6.22 2.07 18.70 0.001 P-value: forward stepwise method. Initial covariates: ascending aorta and aortic arch length; angulation of the ascending aorta and aortic arch; aorta diameter at each point (A–F). Points A–F are illustrated in Fig. 2. INA: innominate artery; LSA: left subclavian artery; STJ: sinotubular junction; TBAD: type B aortic dissection. Open in new tab DISCUSSION Previous studies demonstrated that the diameter of the descending aorta is insufficient to adequately predict the risk of developing TBAD [21]. The presence of a dilated proximal aorta was also not sufficiently effective and specific [9] because this is also a crucial risk factor predicting TAAD [3, 22]. These findings highlight the need to develop other anatomical and specific factors to identify patients at risk for TBAD. For this purpose, first, we identified the significant dilation, elongation, increased tortuosity and angulation within the proximal aorta in TBAD patients. Second, we demonstrated that the increased tortuosity and angulation of the aortic arch may play independent and specific roles in the development of TBAD. Considering previous studies, several different findings require special attention. Lescan et al. [10] reported significant aortic elongation only in the aortic arch and no significant change in the ascending aorta, whereas Shirali et al. [9] described increased aortic length in the total proximal aorta and ascending aorta, but did not indicate changes in the aortic arch. However, in our study, we saw elongation in both the aortic arch and ascending aorta in TBAD patients. This may be reasonable based on the recognized loss of longitudinal elasticity in the aorta media [23]. Regarding the geometric alteration in the proximal aorta, Shirali et al. [9] investigated the tortuosity of the total proximal aorta between normotensive patients without AD, hypertensive patients without AD and a TBAD group, but reported no significant specific tortuosity differences. However, in our study, we identified greater tortuosity and angulation in the proximal aorta, especially in the aortic arch, in patients with TBAD. This is a reasonable finding that can be explained by the elongated aortic arch in TBAD. Because the aortic arch segment is relatively fixed by the innominate artery and LSA, this may result in increased tortuosity and angulation. Identifying these significant anatomical differences also permits investigating the detailed and specific anatomical predictors of TBAD. Previously, in addition to increased aortic arch diameter, Shirali et al. [9] demonstrated that total aortic length and tortuosity were independent risk factors, but the authors failed to interpret the function of specific segment-related predictors. Lescan et al. [10] reported significant elongation in the aortic arch and not in the ascending aorta, but did not investigate the related predictive value. In our study, significant aortic elongation was observed in both the ascending aorta and aortic arch, with a mean increase of 0.8 and 0.3 cm, respectively. However, only the elongated ascending aorta, not the aortic arch, remained independently associated with TBAD in the multivariate analysis, which validated the hypothesis by Shirali et al. [9] that the elongated ascending aorta may be used as a predictor of AD risk. However, considering the similar role that ascending aorta elongation plays in the development of TAAD [2, 3], other specific geometric features should be considered to predict TBAD risk. Differing from previous studies, in addition to aortic length and diameter, we evaluated detailed aortic segment geometrical comparisons of tortuosity and angulation. Our results showed significantly increased tortuosity and angulation in the aortic arch segment in the TBAD group, with a mean increase in ratio of 1.9% and 28.1%, respectively, which were independent predictors of TBAD in the multivariate analysis. These findings may indicate that severe or greater aortic arch tortuosity and angulation are associated with TBAD independently and specifically. Interestingly, our findings were in accordance with the conclusions of a recent study stating that type III arch configuration is associated with TBAD [7] because type III arch presents peculiar geometric features, namely, a more tortuous and angulated aortic arch [14]. Besides, increased aortic arch tortuosity and angulation better explain the mechanism of TBAD development. Generally, any conditions that increase wall shear stress (WSS) and decrease aorta media degeneration are potential risk factors for TBAD [24]. According to a study by Nathan et al. [25], there were peaks in WSS above the sinotubular junction and distally to the LSA ostium in the normal thoracic aorta. Previous studies demonstrated that greater tortuosity of the proximal aorta leads to stronger helical flow through the distal arch, which increases WSS [11, 26]. According to our results, the area with increased tortuosity was in the aortic arch, not in the ascending aorta, which indicates that increased WSS was present in the segment distally to the aortic arch, following the principles of haemodynamics. Previous studies have confirmed that the magnitude of the haemodynamic forces applied on the aortic wall of Ishimaru zone 3 increased gradually from type I to type III arch configuration [14, 27]. This may suggest that increased aortic arch angulation is accompanied by increased WSS on the zone 3 aortic wall. Under increased WSS, apoptosis in the local smooth muscle cells is accelerated [28], which triggers the formation of tears and the development of TBAD when blood pressure increases suddenly. To some extent, this also explains why entry tears are most often located just distally to the origin of the LSA [29]. However, the specific relationship between altered aortic arch geometry and TBAD requires validation using computer-aided fluid dynamics research. Limitations We recognize that the major limitation in our study was the retrospective design. To confirm a clear causal relationship between altered aorta geometry and dissection, a prospective and longitudinal study is needed; however, given the low incidence rate of TBAD, this would be a challenge. Therefore, we consider our study design combined with modelling of the dimensions to be the best achievable alternative. Second, although we considered that age and other demographic data were homogenous, and we excluded patients with a bovine arch, which is associated with an increased incidence of dissection [8], there may still have been unavoidable selection bias from unknown factors affecting proximal aorta dimensions, such as antihypertensive drug therapy. Third, all the CTA images we used were not electrocardiogram (ECG)-gated, and the CTA maximum slice thickness of 3 mm may impact the measurement accuracy. To minimize measurement error as much as possible, ECG-gated and only thin-slice (1.0 or 1.5 mm) CTA images should be included in future studies. Fourth, patients with TBAD were not enrolled from multicentre studies. Our findings must be validated in multicentre studies involving ethnically diverse populations. CONCLUSION In addition to proximal aorta dilation, significant elongation was seen in both the ascending aorta and aortic arch in TBAD patients. Using advanced tortuosity and angulation measurement approaches based on aorta CLL analysis, we found significant geometric alteration in the proximal aorta in TBAD patients. Increased aortic arch tortuosity and angulation could be independent and specific predictors of TBAD. Further investigations are needed to assess the pathophysiological role and diagnostic value of aortic arch tortuosity and angulation. Conflict of interest: none declared. Author contributions Long Cao: Conceptualization; Data curation; Formal analysis; Investigation; Methodology; Resources; Software; Visualization; Writing—original draft; Writing—review & editing. Weihang Lu: Conceptualization; Data curation; Investigation; Methodology; Resources; Software; Validation; Writing—original draft. Yangyang Ge: Data curation; Formal analysis; Investigation; Methodology; Resources; Validation; Visualization; Writing—original draft. Xinhao Wang: Formal analysis; Investigation; Resources; Software; Validation; Visualization. Yuan He: Data curation; Formal analysis; Investigation; Resources; Supervision. Guoyi Sun: Investigation; Methodology; Resources; Software; Visualization. Jie Liu: Data curation; Formal analysis; Investigation; Methodology; Resources. 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Google Scholar Crossref Search ADS PubMed WorldCat Abbreviations AD Aortic dissection BMI Body mass index BSA Body surface area CI Confidence interval CLL Centre lumen line CTA Computed tomography angiography LSA Left subclavian artery OR Odds ratio TAAD Type A aortic dissection TBAD Type B aortic dissection WSS Wall shear stress Author notes † Long Cao, Weihang Lu and Yangyang Ge authors contributed equally to this study. © The Author(s) 2020. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

Journal

European Journal of Cardio-Thoracic Surgery – Oxford University Press

Published: Oct 1, 2020

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