Factors associated with false lumen changes in patients with superior mesenteric artery dissection

Abstract

Background:

False lumen changes (FLCs) are the main reference for the prognosis judgment and treatment plan selection for type IIa superior mesenteric artery dissection (SMAD).

Methods:

For this retrospective study, 55 patients with symptomatic type IIa SMAD were included. Computational fluid dynamics (CFD) analysis was used to explore the hemodynamic basis of FLCs. Correlation and multiple linear regression analyses were performed to identify clinical, morphological and hemodynamic factors associated with FLCs.

Results:

The FLCs of patients with successful conservative treatment (n = 29) are significantly higher than those with failed conservative treatment (n = 26) (58.5 ± 21.1% vs 10.9 ± 17.4%, p < 0.0001). Positive correlations were seen between FLCs and the morphological parameters false lumen length (FLL)/dissection entrance length (DEL) and FLL. In terms of hemodynamic parameters, negative correlations were seen between FLCs and time-averaged wall shear stress (TAWSS), vorticity, and high areas of TAWSS and vorticity, whereas positive correlations were seen between FLCs and oscillatory shear index (OSI), relative residence time (RRT), and high areas of OSI and RRT. Multiple linear regression analysis identified symptom duration (odds ratio [OR], 0.93; 95% CI, 0.91–0.96; p < 0.0001), FLL/DEL (OR, 1.30; 95% CI, 1.01–1.67; p = 0.044), and high RRT area (OR, 2.03; 95% CI, 1.48–2.78; p < 0.0001) as predictors of FLCs.

Conclusion:

The clinical predictor symptom duration, morphological factor FLL/DEL, and the hemodynamic factor high RRT area can serve as predictors of FLCs in patients with symptomatic type IIa SMAD.

Keywords

computational fluid dynamics arterial dissection mesenteric artery

Background

As imaging techniques have continued to evolve, the number of cases of superior mesenteric artery dissection (SMAD) identified on imaging has increased.¹ Compared with other types of SMAD (type I: with both entry and re-entry site in true and false lumen, the morphological structure of dissection tends to be stable; type IIb: with thrombus in false lumen, most of this type recovers smoothly; type III: with the occlusion of SMA trunk, the risk of intestinal ischemic necrosis is high, early endovascular therapy and timely open surgery is proposed), type IIa with visible false lumen but no visible re-entry site (blind pouch of false lumen) has the most uncertain clinical prognosis, and the most effective treatment options for this condition are still under debate (Figure 1).^2–6 In cases of type IIa SMAD, instability related to the blood flow in the false lumen can lead to distal propagation, rupture, or the formation of a thrombus. The enlargement or delayed reduction of the false lumen will cause progressive or persistent compression of the true lumen, and even rupture of the dissection aneurysm, leading to continuous aggravating or unrelieved symptoms in patients, ultimately resulting in the failure of conservative treatment. In addition, patients with persistent false lumens are unable to complete the remodeling of SMA for a long time, and the probability of long-term recurrence is also higher. On the contrary, patients with false lumens which shrink or thrombosis in the short-term can achieve faster SMA remodeling and always have better prognosis. Therefore, false lumen changes (FLCs) are one of the main reference standards for treatment plan selection and prognosis judgment.^7–10 However, the prediction of FLCs has not been proposed.

Figure 1.

The classification of superior mesenteric artery dissection (SMAD) and the manifestation of false lumen changes in the type IIa SMAD.

In this retrospective study, morphological and hemodynamic factors in patients with type IIa SMAD were assessed using a computational fluid dynamics (CFD) simulation based on patient-specific superior mesenteric artery (SMA) geometries and individual blood flow conditions. Correlations between these factors and FLCs were identified, and potential predictors of FLCs were then determined based on these findings.

Methods

Study design

This retrospective study was approved by the participating institutional review boards with a waiver of informed consent. Yun’s classification of SMAD was applied in this study. Consecutive patients with symptomatic type Ⅱa SMAD diagnosed on computed tomography angiography (CTA) who underwent conservative therapy as first-line treatment between January 2010 and December 2022 were included in this study. Patients with other types of SMAD, those who underwent endovascular intervention or open surgery as first-line treatment, those who received anticoagulants or antiplatelet therapy during conservative treatment, those who were lost to follow up, and those with blurred CTA images were excluded from the analysis. Demographic and clinical information of enrolled patients was collected from the medical records system.

Management and follow-up

The course of therapy used in this study has been described previously.⁶ The conservative management included fasting, observation, blood pressure control, and pain control. Owing to the fact that anticoagulants or antiplatelet therapy cannot prevent distal propagation and are likely to delay false lumen thrombosis, more and more evidence has appeared to support not using them as routine treatment methods during conservative treatment.^11–16 The failure of conservative treatment was defined as the persistence or aggravation of symptoms and signs, continuous expansion of the false lumen, or a newly appeared dissecting aneurysm during treatment. CTA (Core 128; Philips, Rotterdam, The Netherlands) and Do-ppler sonography (Philips Ultrasound, Inc., Rotterdam, The Netherlands) were performed within 1 week after the diagnosis of SMAD, and the status of SMAD was assessed and related data were recorded. For follow up, CTA was performed at 1 month, 6 months, and 1 year after discharge.

Morphological measurements

Two radiologists and two interventional angiologists with more than 10 years of clinical experience independently determined the morphological measurements for each case. In cases of disagreement, differences were discussed until an agreement was reached.

The morphological parameters included in this study were as follows: (1) dissection entrance length (DEL), defined as the optimal diameter length of the cross-section of the false lumen entrance channel which was calculated by Mimics Research 19.0 (Materialise HQ, Louvain, Bel-gium) based on the automatically extracted centerline of the SMAD 3D model; (2) false lumen length (FLL) and diameter, defined as the long-axis diameter and the short-axis diameter of the false lumen based on the maximum cross-section of the false lumen in sagittal reconstruction of the CTA image, respectively^5,17; (3) aortomesenteric angle, defined as the angle between the abdominal aorta major axis and the SMA major axis based on the sagittal reconstruction of the CTA image¹⁸; (4) maximum curvature of the SMA, defined as the maximum curvature of the SMA central axis, which was automatically identified and calculated by using SOLIDWORKS 2017 (Dassault Systèmes, Paris, France)¹⁹; (5) distance from the SMA ostium to the dissection origin; (6) true lumen stenosis rate, defined as the cross-sectional area at the greatest stenosis site on the true lumen divided by the proximal normal artery (the greatest stenosis location and the normal lumen diameter location at the SMA was identified by two independent interventional angiologists); and (7) the number and average diameter of side branches in the involved segment of the SMAD, quantified and measured based on a SMA 3D model extracted by Mimics Research 19.0 (Materialise, Leuven, Belgium) (Figure S1).

The 3D models of the false lumens were extracted and segmented based on thin-slice CTA images (slice thickness: 1.0 mm) using Mimics Research 19.0. The false lumen models were then imported into Geomagic Wrap 2017 (Raindrop Geomagic, Research Triangle Park, NC, USA) in STL format, and the volume was automatically calculated (Figure 2A).^20–22 FLCs at 1 month were defined as (V₀ – V₁)/V₀, where V₀ is the false lumen volume at the time of SMAD diagnosis and V₁ is the false lumen volume at 1-month follow up (or at last follow up in cases of failed treatment).

Figure 2.

(A) Schematic diagram of the 3D model extraction process for the false lumen. The arrow heads point to the false lumen. V₀ indicates the volume of the false lumen at the time of superior mesenteric artery dissection (SMAD) diagnosis, and V₁ indicates the volume of the false lumen at 1-month follow up (or at the last follow up in cases of failed treatment). (B) Inlet pressure and outlet mass flow rate waveform applied in this computational fluid dynamics simulation.

The ultrasonic Doppler blood flow spectrums for the ostium of the celiac trunk and bilateral renal artery, the distal abdominal aorta and SMA at the umbilical level, and the ostium of main branches within the range of the SMAD were collected using the Philips EPIQ 7 system (Philips Ultrasound, Inc.), as described in previous studies.^23,24

Construction of SMAD geometries and computational fluid dynamics (CFD) simulation

To recreate the hemodynamic environment in the false lumen of each patient at the time of SMAD diagnosis, CFD simulations were carried out based on 55 patient-specific 3D models reconstructed from the patient’s first-time CTA data (slice thickness: 1.0 mm) by using Mimics Research 19.0 with automatic smoothing by Geomagic Wrap 2017. In addition to the trunk of the abdominal aorta and SMA (from 5 cm above the celiac trunk to the level of the umbilical cord), the ostium of the celiac trunk and bilateral renal artery, and the ostium of main branches within the range of the dissection were all preserved and reconstructed. The reconstructed geometry was then meshed in ICEM-CFD (Ansys, Canonsburg, PA, USA), and the prism layers were created. Sensitivity grid analysis was conducted for each case. When standard volume mesh (abdominal aorta mesh size: 0.5 mm; SMAD mesh size: 0.3 mm; 2.4–7.2 million tetrahedral elements) and refined volume mesh (abdominal aorta mesh size: 0.3 mm; SMAD mesh size: 0.1 mm; 11.2–17.8 million tetrahedral elements) were compared, the average difference in the time-averaged wall shear stress (TAWSS) distribution was found to be < 1%.²⁵

A transient simulation for each patient was performed using the CFD solver in CFX (Ansys) to solve the Navier–Stokes equations for incompressible steady flow. Blood was considered a homogeneous, incompressible Newtonian fluid with a dynamic viscosity of 0.0035 Pa·s and a density of 1045 kg/m³.²⁶ In terms of boundary conditions, the inlet condition used for simulations was the set of pressure wave points at the proximal end of the abdominal aorta corrected by the patient’s systolic and diastolic pressures and heart rate (the average values measured during their hospitalization).^27,28 All of the outlet conditions were based on the set of mass flow points extracted and converted from ultrasonic Doppler blood flow spectrums (first measured after the diagnosis of SMAD) and the cross-sectional area of each outlet in the patient-specific geometry models (Figure 2B). A rigid wall and no-slip boundary condition were set. The hemodynamic parameters assessed were as follows: TAWSS, oscillatory shear index (OSI), relative residence time (RRT), and vorticity (all defined as the average values of the false lumen wall), as well as high TAWSS area, high OSI area, high RRT area, and high vorticity (defined as the proportion of the false lumen wall in which these parameters were higher than average). The CFD simulation results were then imported and postprocessed using CFD-POST (Ansys) to determine the flow pattern, assess the hemodynamic parameter distribution, and extract data for quantitative analysis. Two radiologists and a bioengineer performed the geometries reconstruction and CFD simulations together.

Idealized univariate model reconstruction

To analyze the influence of each particular morphological feature on hemodynamics in the false lumen while eliminating the influence of other morphological parameters, specific SMAD models were manually deformed and modified using Geomagic Wrap 2017. The FLL/DEL values of the idealized geometric models were defined as the upper quartiles and lower quartiles of that for all included patients. For the boundary conditions of the idealized geometric models’ simulation, the median values of blood pressure and corresponding vessel mass flow for all patients were used (see the online supplemental material).

Statistical analysis

SPSS 26.0 (IBM Corp., Armonk, NY, USA) was used for statistical analysis. Normally distributed continuous variables were calculated as mean ± SD. Nonnormally distributed continuous variables were calculated as median (IQR). The chi-squared test was used for categorical variables. Correlations between clinical, morphological, and hemodynamic parameters and FLCs were assessed using Spearman (nonnormally distributed continuous variables) or Pearson (normally distributed continuous variables) correlation analysis. Multicollinearity tests of all independent variables were conducted (see the online supplemental material). Multiple linear regression analysis was used to identify the most likely predictors of FLCs, with results reported as odds ratios (ORs) and corresponding 95% CIs. Statistical significance was considered to be p < 0.05.

Results

Patients

Of the 287 patients diagnosed with symptomatic SMAD during the study period, 232 (80.8%) were excluded from the study because they did not meet the inclusion criteria. Figure 3 shows the detailed inclusion process of the study population. The remaining 55 patients (51 men, four women; mean age, 54.1 ± 7.6 years; range, 41–74 years) were included in the analysis. Table 1 summarizes the clinical manifestations, imaging characteristics, and hemodynamic variables in all the study patients. Conservative treatment was succeeded in 29 (52.7%) patients and failed in 26 (47.3%) patients. The characteristics of the FLCs of all patients are shown in Table 2. The false lumen volumes of all patients during the follow-up period are shown in Figure 4.

Figure 3.

Flow chart of inclusion and exclusion in enrolled patients.

Table 1.

Clinical characteristics, morphological parameters, and hemodynamic variables in study patients.

	Patients (n = 55)
Clinical characteristics
Age, years	54.1 ± 7.6
Male sex	51 (92.7)
Interval^a, hours	5 [3, 8]
Symptom duration, days
1–3	3 (5.5)
3–5	6 (10.9)
5–7	7 (12.7)
7–10	7 (12.7)
⩾ 10	6 (10.9)
Aggravation	26 (47.3)
Comorbidity
Hypertension	28 (50.9)
Hyperlipidemia	21 (38.2)
Diabetes mellitus	4 (7.3)
Smoking (current or ex-smoker)	31 (56.4)
Serum biomarkers
D-dimer, mg/L	0.34 [0.17, 0.70]
Neutrophil counts, ×10⁹/L	5.14 ± 2.26
Platelet counts, ×10⁹/L	194.39 ± 38.77
Triglyceride, mmol/L	1.34 ± 0.80
Low-density lipoprotein cholesterol, mmol/L	2.67 ± 0.96
High-density lipoprotein cholesterol, mmol/L	1.11 ± 0.27
Morphological parameters
Aortomesenteric angle, °	64.9 ± 22.3
Superior mesenteric artery maximum curvature, mm⁻¹	0.047 [0.023, 0.069]
Distance from ostium, mm	28.3 ± 12.7
Number of side branches	2 [1, 2]
Diameter of side branches, mm	3.3 ± 1.3
False lumen diameter, mm	6.5 ± 2.1
Dissection entrance length, mm	6.7 ± 2.7
False lumen length, mm	19.5 ± 9.44
False lumen diameter/dissection entrance length	1.1 ± 0.6
False lumen length/dissection entrance length	3.3 ± 2.0
True lumen stenosis rate, %	49.7 ± 21.8
False lumen changes rate, %	36.0 ± 30.8
Hemodynamic variables in false lumen
Time-averaged wall shear stress, Pa	0.57 [0.122, 1.450]
Oscillatory shear index	0.14 [0.100, 0.235]
Relative residence time, Pa⁻¹	42.21 [5.480, 510.540]
Vorticity, s⁻¹	105.53 [44.330, 188.480]
High time-averaged wall shear stress area, %	21.3 [0.8, 33.8]
High oscillatory shear index area, %	39.2 ± 22.8
High relative residence time area, %	29.8 ± 20.2
High vorticity area, %	34.9 ± 23.5

Data are presented as n (%), mean ± SD, or median [IQR].

Interval: time from onset of symptoms to time of first computed tomography angiography examination.

Table 2.

Clinical outcomes and false lumen changes (FLCs) in study patients.

	Conservative treatment success(n = 29)	Conservative treatment failure(n = 26)	p-value
FLCs, %, mean ± SD	58.5 ± 21.1	10.9 ± 17.4	< 0.0001
FLCs distribution, n			< 0.0001
< 0%	0	3
0–30%	0	23
30–50%	14	0
> 50%	15	0

Figure 4.

False lumen volume line charts. (A) False lumen volume of each patient and (B) the median and IQR of the false lumen volume of all patients during the follow-up period.

Correlations between morphological and hemodynamic factors and FLCs

One clinical factor was found to be negatively correlated with FLCs: symptom duration (r_s = −0.721; p < 0.0001). Two morphological factors were found to be positively correlated with FLCs: FLL/DEL (r = 0.618; p < 0.0001) and FLL (r = 0.498; p < 0.0001). Four hemodynamic factors were found to be negatively correlated with FLCs: TAWSS (r_s = −0.621; p < 0.0001), high TAWSS area (r_s = −0.408; p = 0.002), vorticity (r_s = −0.606; p < 0.0001), and high vorticity area (r = −0.568; p < 0.0001). Four hemodynamic factors were found to be positively correlated with FLCs: OSI (r_s = 0.720; p < 0.0001), high OSI area (r = 0.667; p < 0.0001), RRT (r_s = 0.773; p < 0.0001), and high RRT area (r = 0.805; p < 0.0001) (Table 3).

Table 3.

Correlations between morphological and hemodynamic factors and false lumen changes.

	Correlation
	r	p-value
Clinical factors
Age, years	0.086	0.53
Male sex	0.084^a	0.54
Interval^b, hours	−0.262^a	0.053
Symptom duration, days	−0.721^a	< 0.0001
Hypertension	−0.135^a	0.33
Hyperlipidemia	−0.125^a	0.36
Diabetes mellitus	−0.234^a	0.086
Smoking (current or ex-smoker)	0.097^a	0.48
D-dimer, mg/L	0.034^a	0.80
Neutrophil counts, ×10⁹/L	0.083	0.55
Platelet counts, ×10⁹/L	0.082	0.55
Triglyceride, mmol/L	0.196	0.15
Low-density lipoprotein cholesterol, mmol/L	−0.227	0.095
High-density lipoprotein cholesterol, mmol/L	−0.089	0.52
Morphological factors
Aortomesenteric angle	−0.04	0.77
Superior mesenteric artery maximum curvature	−0.136^a	0.32
Distance from ostium	−0.018	0.90
Number of side branches	−0.087^a	0.53
Diameter of side branches	0.110	0.43
False lumen diameter	0.074	0.59
Dissection entrance length	−0.252	0.063
False lumen length	0.498	< 0.0001
False lumen diameter/dissection entrance length	0.238	0.08
False lumen length/dissection entrance length	0.618	< 0.0001
True lumen stenosis rate	0.042	0.76
Hemodynamic factors
Time-averaged wall shear stress	−0.621^a	< 0.0001
Oscillatory shear index	0.720^a	< 0.0001
Relative residence time	0.773^a	< 0.0001
Vorticity	−0.606^a	< 0.0001
High time-averaged wall shear stress area	−0.408^a	0.002
High oscillatory shear index area	0.667	< 0.0001
High relative residence time area	0.805	< 0.0001
High vorticity area	−0.568	< 0.0001

Correlation calculated as r_s.

Interval: time from onset of symptoms to time of first computed tomography angiography examination.

Predictors of false lumen changes (FLCs)

Multiple linear regression analysis demonstrated that symptom duration (OR = 0.93; 95% CI: 0.91–0.96; p < 0.0001), FLL/DEL (OR = 1.30; 95% CI: 1.01–1.67; p = 0.044), and high RRT area (OR = 2.03; 95% CI: 1.48–2.78; p < 0.0001) were significant predictors of FLCs.

Hemodynamic analysis

Figure 5 shows the hemodynamic parameters TAWSS, OSI, RRT, vorticity, and the blood flow pattern in patients with the most FLCs (P1 and P2) and in patients with the least FLCs (P3 and P4). The higher TAWSS and vorticity regions all appeared around the dissection entrance in these patients, whereas the higher OSI and RRT regions were mostly distributed in one or two poles of the false lumen away from the dissection entrance. For P1 and P2, little or no blood flow could enter the false lumen, and the flow into the false lumen could not form a loop to re-enter the true lumen; however, for P3 and P4, a large amount of blood flow could enter the false lumen. Figure 6A shows the distribution of hemodynamic parameters and the blood flow pattern in conjunction with a follow-up CTA image.

Figure 5.

Hemodynamic parameter distribution and flow characteristics in the two patients demonstrating the most FLCs (100%; P1 and P2) and in the two patients demonstrating the least FLCs (−30.5% and −38.3%; P3 and P4). (A) TAWSS. (B) OSI. (C) RRT. (D) Vorticity. High OSI and high RRT regions in P1 and P2 are more widely distributed than in P3 and P4, whereas the distribution characteristics of TAWSS and vorticity are the opposite. (E) The blood flow volume and velocity in the false lumen of P3 and P4 were substantially higher than those in the false lumen of P1 and P2.

Figure 6.

(A) Image from computed tomography angiography performed at 1-month follow up and the corresponding computational fluid dynamics simulation. High RRT, high OSI, and low velocity distribution areas in the false lumen are highly consistent with the location of thrombus, whereas high TAWSS, vorticity, and velocity distribution areas are well matched with the residual portion of the false lumen. (B) Effect of FLL and FLL/DEL on hemodynamics and flow in the false lumen: (a) FLL/DEL = 4.0; FLL = 31.3 mm; (b) FLL/DEL = 2.0; FLL = 15.7 mm; (c) FLL/DEL = 2.0; FLL = 31.3 mm. Changes in FLL/DEL correspond with changes in the distribution of hemodynamic parameters in the false lumen.

Hemodynamic changes with different false lumen length (FLL)/ dissection entrance length (DEL)

The blood flow velocity and capacity in the false lumen of models ‘a’ and ‘b’ were significantly lower than those in the false lumen of model ‘c’. The high OSI and RRT areas, which were mainly distributed in the distal end of the false lumen, were larger in models ‘a’ and ‘b’ than in model ‘c’. In model ‘c’, the high TAWSS and vorticity areas, which were concentrated near the dissection entrance, were larger than in models ‘a’ and ‘b’ (Figure 6B). The fluid simulation results under another two different boundary conditions are shown in the online supplemental material (Figure S2).

Discussion

The ability to predict FLCs early in patients with type IIa SMAD is important, as this information can affect the choice of treatment. In this study, we found that the FLCs were the most obvious during the 1-month follow up after the diagnosis of SMAD. Besides, three novel predictors of FLCs were identified: symptom duration (clinical predictor), FLL/DEL (morphological predictor), and high RRT area (hemodynamic predictor). This study also demonstrated that FLL, OSI, RRT, and high OSI area were positively correlated with FLCs, whereas TAWSS, vorticity, high TAWSS area, and high vorticity area were negatively correlated with FLCs. The higher TAWSS and vorticity areas appeared around the dissection entrance; the higher OSI and RRT areas were mostly distributed in one or two poles of the false lumen, away from the entrance, findings highly consistent with the location of thrombosis in the false lumen.

Previous studies have shown that the outcomes of type IIa SMAD are the most difficult to predict among all SMAD types and that type IIa SMAD is often associated with the failure of conservative management and delay of SMA remodeling.^3,29 In cases of type I SMAD, the false lumen has both entry and re-entry sites, and blood can flow smoothly through the false lumen with a velocity similar to that seen in the true lumen. Therefore, most cases of type I SMAD tend to be stable.⁵ In cases of type IIb SMAD, absorption of the formed thrombus is common and usually leads to disappearance of the false lumen.^30,31 Conservative management is thus usually chosen for patients with type I or type IIb SMAD.³² In type III SMAD, occlusion of the SMA restricts the collateral blood supply, which puts the patient at high risk of intestinal necrosis; thus, early intervention is generally recommended.³³ Based on our results, patients with type IIa SMAD often have the most obvious FLCs within the 1-month follow up after diagnosis, so it is necessary to strictly follow up and manage all patients during this period. For patients with rapid reduction of false lumen within the 1-month follow up, we could appropriately prolong the follow-up interval and reduce unnecessary CTA examination. However, for patients with enlargement or delayed reduction of false lumen within the 1-month follow up, we should follow up closely and take interventional therapy when necessary. In addition, symptom duration is the only clinical predictor of FLCs we found, which is consistent with previous studies.²⁹ Therefore, in clinical practice, shorter symptom duration is an important basis for evaluating FLCs and the outcomes of type IIa SMAD patients during conservative treatment.

Vorticity describes the size or speed of a vortex; TAWSS describes the time average value of blood flow-induced friction stress acting on the vascular wall; OSI reflects the oscillatory degree of WSS on the vascular wall; RRT describes the residence time of the particle, which combines the effects of TAWSS and OSI to provide more comprehensive information about the near-wall hemodynamics.³⁴ Based on the CFD simulation findings in this study, schematic diagrams of blood flow in three different kinds of false lumen were created (online supplemental material Figure S3). In model A, the blood flow can re-enter the true lumen; therefore, the blood flow in the false lumen forms the circulation, leading to lower OSI and RRT and higher TAWSS and vorticity. This type of local hemodynamic environment has been found to be unfavorable to the formation of thrombus, and the blood pressure gradient between the true and false lumens limi-ts the ability to shrink or stop expansion of the false lumen.^35,36 In model B, which has the same FLL as model A but lower DEL, the blood flow of the false lumen cannot re-enter the true lumen, leading to formation of a local vortex zone in the false lumen. This chaotic low-speed blood flow results in higher OSI and RRT and lower TAWSS and vorticity,³⁷ which encourages mixing of coagulation proteins and creates a procoagulant microenvironment for platelet aggregation and fibrin formation at the false lumen wall.³⁸ In model C, thrombus is less likely to form in the initial and middle parts of the false lumen than in the lower pole of the false lumen, which may increase the risk of symptoms and lead to the failure of conservative management.³⁰

The local hemodynamic state in the false lumen therefore plays a crucial role in the occurrence of FLCs. Higher OSI and RRT regions are accompanied by the formation of thrombus in the false lumen, whereas higher TAWSS and vorticity regions probably indicate expansion of the false lumen. These findings suggest that a false lumen with lower FLL/DEL but higher FLL (model A) tends to be stable for a long time but at risk of enlargement. In these cases, conservative management and close observation are preferred. A false lumen with higher FLL/DEL (model B) can form thrombus quickly, and so these cases should be managed conservatively. In a false lumen with lower FLL/DEL and higher FLL (model C), remodeling is less likely to occur and the false lumen is more likely to expand; thus, these cases should be closely followed and endovascular therapy should be considered.

Study limitations

The main limitation of this study was its retrospective nature. Because of the rarity of SMAD, this study was also limited by its small sample size; nevertheless, this remains one of the largest patient cohorts to be reported to date in this subtype and is the first study to analyze factors associated with FLCs in patients with type IIa SMAD. Calculations of morphological parameters were performed manually, not automatically, and the reference vessel diameter was difficult to determine precisely because of the small diameter of the mesenteric artery; these factors may have biased the results. The computational prediction model of FLC was not created because of technical reasons and because the dynamic viscosity of the blood is not patient-specific. Finally, there are intrinsic relationships between various hemodynamic parameters, so they are not completely independent variables in multiple linear regression. In future studies, we hope to apply more comprehensive parameters to compensate for the interdependence of basic hemodynamic parameters and better explore the combined effects of basic hemodynamic parameters on FLCs.

Conclusion

This study suggests that symptom duration (clinical predictor), FLL/DEL (morphological factor), and high RRT area (hemodynamic factor) can serve as early predictors of FLCs in patients with symptomatic type IIa SMAD. These findings suggest that patients with type IIa SMAD with shorter symptom duration, higher FLL/DEL, and larger high RRT area tend to complete the disappearance of false lumen quickly and recovery after conservative management, whereas patients with longer symptom duration, lower FLL/DEL, and smaller high RRT area have a higher risk of false lumen enlargement and disease deterioration. Therefore, close follow up is recommended to detect any progression in SMAD and to intervene when necessary.

Supplemental Material

sj-docx-1-vmj-10.1177_1358863X231220624 – Supplemental material for Factors associated with false lumen changes in patients with superior mesenteric artery dissection

Supplemental material, sj-docx-1-vmj-10.1177_1358863X231220624 for Factors associated with false lumen changes in patients with superior mesenteric artery dissection by Junhao Mei, Yuan Yuan, Hui Yan, Xi Zhao, Tongqing Xue, Haobo Su and Zhongzhi Jia in Vascular Medicine

Footnotes

Acknowledgements

We thank Liulan Qian, biostatistician, Department of Scientific Research and Education, the Affiliated Changzhou Second People’s Hospital of Nanjing Medical University, Changzhou, China, for her help with data analysis and Megan Griffiths, scientific writer, Cleveland, Ohio, USA, for her help with revising the manuscript.

Data availability statement

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

Declaration of conflicting interests

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

Funding

This study was supported by the Changzhou Sci & Tech Program (CZ20220029), China Postdoctoral Science Foundation (2023M730371), Clinical Research Project of Changzhou Medical Center of Nanjing Medical University (CMCC202206), and the Natural Science Foundation of China (81401498). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

ORCID iDs

Junhao Mei

Zhongzhi Jia

Supplementary material

The supplementary material is available online with the article.

References

Luan

Guan

, et al. Isolated superior mesenteric artery dissection in China. J Vasc Surg 2016; 63: 530–536.

Liu

Shu

, et al. Long-term outcome of spontaneous isolated superior mesenteric artery dissection in different angiographic types. Vascular 2023; 31: 668–677.

Sun

Wang

Que

, et al. Management of patients with uncomplicated symptomatic isolated mesenteric artery dissection: a multicentre experience. Eur J Vasc Endovasc Surg 2022; 64: 507–514.

Acosta

Gonçalves

. Management of spontaneous isolated mesenteric artery dissection: A systematic review. Scand J Surg 2021; 110: 130–138.

Yuan

Sheng

, et al. Management strategy and radiologic outcomes of symptomatic spontaneous isolated superior mesenteric artery dissection based on angiographic classification: The follow-up experience in a single center. J Endovasc Ther. Published online Nov 8, 2022. DOI: 15266028221133700.

Björck

Koelemay

Acosta

, et al. Editor’s Choice – Management of the diseases of mesenteric arteries and veins: Clinical practice guidelines of the European Society of Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg 2017; 53: 460–510.

Tomita

Obara

Sekimoto

, et al. Evolution of computed tomographic characteristics of spontaneous isolated superior mesenteric artery dissection during conservative management. Circ J 2016; 80: 1452–1459.

Kimura

Kato

Nagao

, et al. Outcomes and radiographic findings of isolated spontaneous superior mesenteric artery dissection. Eur J Vasc Endovasc Surg 2017; 53: 276–281.

Ichiba

Hara

Yunoki

, et al. Serial follow-up evaluation with computed tomography after conservative medical treatment in patients with symptomatic spontaneous isolated superior mesenteric artery dissection. Vasc Endovascular Surg 2017; 51: 538–544.

10.

Yoshida

Yoshizako

Maruyama

, et al. The value of CT findings for prognostic prediction of spontaneous superior mesenteric artery dissection. Acta Radiol 2019; 60: 542–548.

11.

Yoo

Choi

SJN

Lee

. Antithrombotic therapy has no beneficial effect in conservative treatment of spontaneous isolated superior mesenteric arterial dissection. Ann Surg Treat Res 2021; 100: 166–174.

12.

Loeffler

Obara

Fujimura

, et al. Medical therapy and intervention do not improve uncomplicated isolated mesenteric artery dissection outcomes over observation alone. J Vasc Surg 2017; 66: 202–208.

13.

Kim

Park

, et al. Outcomes of spontaneous isolated superior mesenteric artery dissection without antithrombotic use. Eur J Vasc Endovasc Surg 2018; 55: 132–137.

14.

Wang

Zhao

, et al. Systematic review and meta-analysis of current evidence in spontaneous isolated celiac and superior mesenteric artery dissection. J Vasc Surg 2018; 68: 1228–1240.

15.

Heo

Kim

Woo

, et al. Treatment strategy based on the natural course for patients with spontaneous isolated superior mesenteric artery dissection. J Vasc Surg 2017; 65: 1142–1151.

16.

Chen

Shi

Wang

, et al. Primary conservative therapy for symptomatic isolated mesenteric artery dissection with severely compressed true lumen or large dissecting aneurysm. J Vasc Interv Radiol 2021; 32: 49–55.

17.

Yun

Kim

Park

, et al. Clinical and angiographic follow-up of spontaneous isolated superior mesenteric artery dissection. Eur J Vasc Endovasc Surg 2009; 37: 572–577.

18.

, et al. The significance of the angle between superior mesenteric artery and aorta in spontaneous isolated superior mesenteric artery dissection. Ann Vasc Surg 2017; 45: 117–126.

19.

Jia

Mei

Ding

, et al. The pathogenesis of superior mesenteric artery dissection: An in-depth study based on fluid–structure interaction and histology analysis. Comput Methods Programs Biomed 2022; 226: 107187.

20.

Sobocinski

Lombardi

Dias

, et al. Volume analysis of true and false lumens in acute complicated type B aortic dissections after thoracic endovascular aortic repair with stent grafts alone or with a composite device design. J Vasc Surg 2016; 63: 1216–1224.

21.

Yoo

Baek

Park

, et al. Thrombus volume as a predictor of nonrecanalization after intravenous thrombolysis in acute stroke. Stroke 2018; 49: 2108–2115.

22.

Harbaugh

Raghavan

. Three-dimensional geometrical characterization of cerebral aneurysms. Ann Biomed Eng 2004; 32: 264–273.

23.

Wang

, et al. Combination of colour dupl-ex and contrast enhanced ultrasound as an alternative to computed tomography angiography in superior mesenteric artery dissection surveillance. Eur J Vasc Endovasc Surg 2019; 58: 884–889.

24.

Dong

, et al. Hemodynamic parameters that may predict false-lumen growth in type-B aortic dissection after endovascular repair: A preliminary study on long-term multiple follow-ups. Med Eng Phys 2017; 50: 12–21.

25.

Qiu

Wang

Zhao

, et al. Association between blood flow pattern and rupture risk of abdominal aortic aneurysm based on computational fluid dynamics. Eur J Vasc Endovasc Surg 2022; 64: 155–164.

26.

Qiu

Wang

Fan

, et al. Role of intraluminal thrombus in abdominal aortic aneurysm ruptures: A hemodynamic point of view. Med Phys 2019; 46: 4263–4275.

27.

Benim

Nahavandi

Assmann

, et al. Simulation of blood flow in human aorta with emphasis on outlet boundary conditions. Appl Math Model 2011; 35: 3175–3188.

28.

Zhang

Liu

Zhang

, et al. CTA-based non-invasive estimation of pressure gradients across a CoA: A validation against cardiac catheterisation. J Cardiovasc Transl Res 2021; 14: 873–882.

29.

Wang

Chen

Shi

, et al. Mesenteric artery remodeling after conservative management in patients with superior mesenteric artery dissection. J Vasc Interv Radiol 2019; 30: 1964–1971.

30.

Hau

Chan

Cheung

, et al. Risk factor analysis and treatment outcome of patients with spontaneous superior celiac axis or superior mesenteric artery dissection. J Vasc Surg 2023; 77: 150–157.

31.

Kim

Jung

Cho

, et al. Clinical and radiologic course of symptomatic spontaneous superior dissection of the superior mesenteric artery treated with conservative management. J Vasc Surg 2014; 59: 465–472.

32.

Heo

Kim

Woo

, et al. Treatment strategy based on the natural course for patients with spontaneous isolated superior mesenteric artery dissection. J Vasc Surg 2017; 65: 1142–1151.

33.

Huang

Zhang

, et al. Natural course and treatment of symptomatic spontaneous isolated superior mesenteric artery dissection with total true lumen occlusion. Vasc Endovascular Surg 2023; 57: 41–47.

34.

Mutlu

Salman

Al-Thani

, et al. How does hemodynamics affect rupture tissue mechanics in abdominal aortic aneurysm: Focus on wall shear stress derived parameters, time-averaged wall shear stress, oscillatory shear index, endothelial cell activation potential, and relative residence time. Comput Biol Med 2023; 154: 106609.

35.

Armour

Menichini

Hanna

, et al. Computational modeling of flow and thrombus formation in type B aortic dissection: The influence of false lumen perfused side branches. In: Sommer

Haspinger

Ogden

(eds) Solid (bio)mechanics: challenges of the next decade: a book dedicated to Professor Gerhard A Holzapfel. Cham: Springer International Publishing, 2022, pp.53–72.

36.

Jafarinia

Armour

Gibbs

RGJ

, et al. Shear-driven modelling of thrombus formation in type B aortic dissection. Front Bioeng Biotechnol 2022; 10: 1033450.

37.

Ribeiro de Sousa

Vallecilla

Chodzynski

, et al. Determination of a shear rate threshold for thrombus formation in intracranial aneurysms. J Neurointerv Surg 2016; 8: 853–858.

38.

Wilson

Virag

Di Achille

, et al. Biochemomechanics of intraluminal thrombus in abdominal aortic aneurysms. J Biomech Eng 2013; 135: 021011.

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