Noninvasive Morphologic and Hemodynamic Evaluation of Type B Aortic Dissection: State of the Art and Future Perspectives

Abstract

Stanford type B aortic dissection (TBAD) is associated with relatively high rates of morbidity and mortality, and appropriate treatment selection is important for optimizing patient outcomes. Depending on individualized risk factors, clinical presentation, and imaging findings, patients are generally stratified to optimal medical therapy anchored by antihypertensives or thoracic endovascular aortic repair (TEVAR). Using standard anatomic imaging with CT or MRI, several high-risk features including aortic diameter, false lumen (FL) features, size of entry tears, involvement of major aortic branch vessels, or evidence of visceral malperfusion have been used to select patients likely to benefit from TEVAR. However, even with these measures, the number needed to treat for TEVAR remains, and improved risk stratification is needed. Increasingly, the relationship between FL hemodynamics and adverse aortic remodeling in TBAD has been studied, and evolving noninvasive techniques can measure numerous FL hemodynamic parameters that may improve risk stratification. In addition to summarizing the current clinical state of the art for morphologic TBAD evaluation, this review provides a detailed overview of noninvasive methods for TBAD hemodynamics characterization, including computational fluid dynamics and four-dimensional flow MRI.

Keywords: CT, Image Postprocessing, MRI, Cardiac, Vascular, Aorta, Dissection

© RSNA, 2021

Summary

This review provides an update on state-of-the-art imaging evaluation of type B aortic dissection, covering clinically applicable aortic morphologic features, as well as recent developments in the evaluation of in vivo and in silico blood flow hemodynamics.

Essentials

• ■ Morphologic findings derived from anatomic aortic imaging with either CT or MRI are critical for providing surgeons with information necessary to make treatment decisions in type B aortic dissection (TBAD). These features include descending aorta diameter, false lumen (FL) characteristics and thrombosis, and entry tear size and location.

• ■ While thoracic endovascular aortic repair has shown promise in the prophylactic treatment of uncomplicated TBAD, it remains challenging to identify which patients will develop complications and require repair using current imaging and clinical tools.

• ■ FL pressurization is associated with adverse aortic remodeling and risk of adverse outcomes, and though difficult to measure, could be central to the risk stratification of TBAD.

• ■ Computational fluid dynamics and four-dimensional flow MRI are uniquely suited for the assessment of TL and FL hemodynamics through measurement of parameters like wall shear stress, FL ejection fraction, and stasis.

Introduction

Aortic dissection occurs due to a tear in the intimal layer of the aorta, which results in separation within the medial layer and allows blood flow into a false lumen (FL), divided from the true lumen (TL) by the resultant intimomedial flap. Dissections are classified by their anatomic location: Type A aortic dissections (TAADs) involve the ascending aorta (defined as proximal to the first arch branch vessel), and type B aortic dissections (TBADs) do not involve the ascending aorta, though they may involve the aortic arch (1). Type A dissections are generally considered surgical emergencies due to their high rates of mortality. Following surgical repair, many patients with repaired type A aortic dissection will be left with residual dissection involving the arch and/or the descending thoracic aorta (rTAAD). While the initial insult and treatment paradigm is different, these patients with rTAAD are frequently studied, clinically followed, and risk stratified in a similar fashion to TBAD and thus are included in many studies throughout this review.

The yearly incidence of TBAD in the United States is approximately 20–30 cases per 1 million people (2). Once diagnosed, TBAD is categorized as complicated (cTBAD) or uncomplicated (uTBAD). cTBAD (defined as one or more of the following: aortic rupture, refractory pain, rapid aortic expansion, uncontrollable hypertension, or malperfusion of the renal, visceral, spinal, or lower extremity vasculature) is associated with a significantly higher early mortality rate than uTBAD (16.1% vs 2.6%) (3). Moreover, the treatment paradigms differ between the two. The standard treatment for cTBAD involves open surgical repair or, more commonly, thoracic endovascular aortic repair (TEVAR), while uTBAD is frequently managed with optimal medical therapy (OMT) centered around antihypertensive-based reduction of aortic wall stress and FL pressurization (4). The goal of both OMT and TEVAR is to decrease adverse aortic remodeling—specifically, aneurysmal dilatation—while promoting favorable remodeling, such as complete FL thrombosis.

However, complication rates remain high in uTBAD, with 25%–30% of uncomplicated cases progressing toward complication within the first 14 days (5). Long-term outcomes are similarly poor, as up to 30% of medically managed patients experience clinically significant aneurysmal degeneration in the first 4 years, only 27% remain free from aortic growth or aneurysm in the first 5 years, and nearly 40% will eventually require surgical intervention (6–8). With a 3-year mortality rate approaching 25%, there has been increasing interest in prophylactic management of uTBAD with TEVAR prior to complication onset (9).

There is evidence to suggest protective effects of TEVAR in uTBAD, as long-term results from the International Registry of Acute Aortic Dissection demonstrated a decreased 5-year mortality rate in patients treated with TEVAR compared with those treated with OMT (15.5% vs 29.0%) (8). The Investigation of Stent Grafts in Aortic Dissection trial, which randomized 140 patients with uTBAD to undergo TEVAR with OMT or OMT alone, noted similar results: The TEVAR with OMT cohort had an improved 5-year aorta-specific mortality rate (6.9% vs 19.3%) (10). A recent retrospective study analyzing 357 patients with uTBAD treated with either TEVAR or OMT also reported a decreased 5-year aorta-related mortality rate (5.9% vs 13.9%), as well as a decrease in 5-year all-cause mortality (8.1% vs 17.8%) in the TEVAR group (Fig 1) (11). Importantly, TEVAR itself carries risks such as retrograde TAAD, a rare but potentially lethal complication with an estimated incidence of 2.5% but a mortality rate of 37.1% (12). Other rare but potentially devastating procedural complications, such as stroke and paraplegia, further underscore the necessity for appropriate risk stratification in patients with uTBAD. Moreover, the reported number needed to treat with TEVAR to prevent one aorta-related fatality is 13, suggesting a substantial opportunity for improved risk stratification and cost-effective care in this cohort (10). Therefore, diagnostic tools are needed that can better discern which patients with uTBAD will eventually experience complications and thus require TEVAR, and which will have satisfactory outcomes with medical management alone.

Figure 1:

Kaplan-Meier survival analysis in the matched patients (with uncomplicated type B aortic dissection) who were treated with TEVAR or BMT. The differences between the two groups were assessed with log-rank test. (A) Freedom from all-cause death between the two groups. Freedom from all-cause death in the TEVAR group was significantly greater than that of the BMT group (P = .028). (B) Freedom from aortic-related death between the two groups. Freedom from aortic-related death in the TEVAR group was significantly greater than that of the BMT group (P = .044). (Reprinted, under a CC BY license, from reference 11). Note that best medical treatment (BMT) terminology is equivalent to optimal medical therapy. TEVAR = thoracic endovascular aortic repair.

Current and Emerging Morphologic Risk-Stratification Strategies

Noninvasive imaging is a key tool for diagnosis and risk stratification in TBAD. Generally, contrast material–enhanced CT angiography is the diagnostic modality of choice due to its widespread availability and rapid acquisition. MR angiography can also provide similar information without exposing the patient to ionizing radiation or iodinated contrast media, but studies are generally longer and less readily available in some centers. Numerous morphologic features, primarily derived from CT data, have been studied in an effort to better risk stratify patients with TBAD (Table 1). In general, these prognostic features can be broken into three key categories: aortic diameter, FL characteristics, and primary entry tear measurements.

Table 1:

High-Risk Imaging and Hemodynamic Features

Maximum Aortic Diameter

In TBAD, maximum aortic diameter is defined as the largest diameter of the dissected aorta segments and should include both TL and FL in the measurement. This measurement is acquired in a cross section that is perpendicular to the aortic centerline as assessed in double-oblique multiplanar reformations. The diameter should be measured from aortic outer wall to outer wall and pass through the aortic center (Fig 2). An increased maximum aortic diameter has been shown to predict aortic complications in numerous studies (13). In particular, a cutoff of greater than or equal to 40 mm was established in a 1995 analysis of 41 patients with TBAD, which found that a baseline aortic diameter greater than this cutoff was predictive of aortic enlargement (14). A 2018 analysis of 254 patients with uTBAD found the same cutoff value to predict the need for late aortic intervention (7). Several other studies have found an increased aortic diameter to be predictive of mortality as well, and because of these data and the relative ease of obtaining this measurement, maximal aortic diameter should be reported in all patients with TBAD.

Figure 2:

(A–D) Images from standard CT evaluation of rTAAD show multiple planar reformatted imaging with (D) double oblique measurement of descending aorta diameter. This patient has repaired TAAD and a large fenestration between the true lumen (TL) and the false lumen (FL) in the proximal aortic arch (red arrow). rTAAD = residual type B aortic dissection following repair of type A aortic dissection.

FL Characteristics

The cross-sectional size of the FL has been studied both in isolation and relative to the TL. In absolute terms, an initial FL diameter of greater than or equal to 22 mm was found to predict late aneurysmal degeneration in a 2007 study of 51 patients with rTAAD and 49 patients with TBAD (15). This cutoff value was obtained through receiver operating curve analysis with a sensitivity of 100% and a specificity of 76%. Similarly, a 2008 prospective analysis of 55 patients with TBAD found that an initial maximal FL area of greater than or equal to 922 mm2 was associated with a significantly higher incidence of in-hospital complications, including limb ischemia, progression of dissection, and aortic rupture (16).

Several other studies have attempted to identify high-risk FL characteristics by relating the size of the FL to the TL. For instance, in a 2012 study, TL compression—defined as the diameter ratio TL/(TL+FL) of less than 25%—was noted to predict dissection-related adverse events but was not predictive of mortality (17). In a similar approach, a 2015 retrospective study of 117 patients with TBAD quantified the ratio of the TL volume to the FL volume and, via receiver operating curve characteristic analysis, found that a ratio of less than 0.8 was highly predictive of requiring aortic intervention, while a ratio of more than 1.6 was highly predictive of freedom from delayed operation (18). A 2013 analysis of 62 conservatively managed patients with TBAD studied the effect of FL structure and location on aortic dilatation and found that both an FL location at the inner (vs outer) aortic curvature and an elliptic (vs circular) TL with a saccular FL were associated with increased aortic growth rate (19). Finally, a 2017 retrospective study of 83 patients with uTBAD measured the FL circumferential extent, defined as the angular distance in degrees between the two FL insertion points in the intimal flap (Fig 3). Unlike the FL diameters and volumes described above, the authors found this parameter to be unaffected by the variable position of the dissection membrane along the thoracic aorta. Moreover, they found an FL angular extent of more than 249° to be an independent predictor of adverse events such as aortic rupture, rapid aortic growth, and aneurysm formation (20).

Figure 3:

Representative MR angiographic image of a type B aortic dissection in cross section utilizing a respiratory navigator–gated, T2-prepared balanced steady-state free precession sequence. In this patient, the false lumen (FL) circumferential extent is approximately 215° of the total circumference of the aorta. According to Sailer et al, an FL angular extent greater than 249° is considered a high-risk feature predictive of adverse events (20). TL = true lumen.

Combining several of these risk factors, Sailer et al also attempted to derive a risk prediction model to identify patients with uTBAD most at risk for adverse outcomes on the basis of several clinical and CT-derived morphologic features (20). This work found that a model using clinical history of connective tissue disease (hazard ratio [HR], 2.94 [95% CI: 1.29, 6.72]), descending aorta maximal diameter (HR, 1.10 [95% CI: 1.01, 1.04]), circumferential cross-sectional extent of FL (HR, 1.03 [95% CI: 1.01, 1.04]), FL outflow volume (HR, 0.999 [95% CI: 0.998, 1.000]), and number of intercostals (HR, 0.89 [95% CI: 0.80, 0.98]) allowed for stratification of patients with TBAD into low, intermediate, and high-risk groups with respective risks of 7.4%, 20.6%, and 54.4% for adverse events at 2 years after imaging. Overall, this model resulted in a c-statistic of 73.8% for adverse events at 2 years. Notably, connective tissue disease, aortic diameter, and FL circumferential extent were all associated with increased risk, while FL outflow volume (estimated by number of large vessels arising from the FL) and number of intercostal arteries were “protective.” The fact that more outflow from the FL large vessels or intercostals was associated with decreased risk in this model supports the theory that decreased pressurization of the FL is important in reducing adverse aortic remodeling (20).

Evidence suggests that full patency of the FL is associated with higher morbidity and mortality than complete thrombosis, likely due to persistent FL pressurization with resultant adverse remodeling in the setting of a thinned outer FL wall (21). Alternatively, a completely thrombosed FL excludes blood entry, prevents FL pressurization, and has a protective effect. Partial thrombosis of the FL may reflect the highest risk state and has been associated with increased aortic growth rate, larger numbers of aorta-related adverse events, and worse patient outcomes than either a patent or completely thrombosed FL (22). Recent literature suggests that partial FL thrombosis is the consequence of decreased FL outflow that results in slower, stagnant blood flow and thus increased thrombus formation (23). While it is reasonable to hypothesize that unique flow states and/or dissection anatomy may predispose patients to FL partial thrombosis, it is not clear when partial thrombosis is part of a favorable remodeling process as opposed to a high-risk feature.

Primary Entry Tear Size and Location

Primary entry tear sites can be identified in most patients, and some authors have suggested that entry tear location and size may correlate with adverse outcomes in TBAD. In a 2012 study of 76 patients with TBAD and 108 patients with rTAAD, the authors found via multivariate analysis that the size of the primary entry tear was a predictor of dissection-related adverse events, as well as mortality (17). In particular, receiver operating characteristic analysis identified a cutoff value of greater than or equal to 10 mm with 85% sensitivity and 87% specificity. Moreover, proximal location of the primary entry tear was also found to be a significant predictor of aorta-related complications (17). A 2013 retrospective study of 60 patients with TBAD did not identify entry tear distance from the left subclavian artery to correlate with aortic growth rate, though the authors did find via subgroup analysis that patients whose entry tear was located within 5 cm of the left subclavian artery demonstrated significantly increased aortic growth rates compared with those with entry tears distal to this cutoff (24). This study also found that patients with a single entry tear had higher rates of aortic diameter increase compared with patients with either zero or multiple entry tears (24). Notably, in the multivariate model of morphologic predictors from Sailer et al, entry tear size and location were not associated with risk of late adverse events in TBAD (20).

In summary, numerous morphologic risk predictors have been studied. The evidence supporting maximum aortic diameter and complete FL thrombosis, in particular, is relatively strong, and both are reasonably straightforward metrics to incorporate in the standard clinical imaging assessments. There is relative paucity of quality evidence to support the regular use of additional morphologic parameters at this time (13).

Role of Hemodynamics in TBAD

Pressurization of the FL seems to be associated with adverse FL remodeling and the risk of aortic rupture and other complications. This hypothesis is supported by the primary treatment methods used in TBAD, antihypertensives, which reduce mean arterial pressure, and TEVAR, which limits flow into the FL. Overall, FL pressure is likely related to a complex interplay of numerous factors, including vessel wall mechanics, neurohormonal control, and medications. Relative TL and FL outflow resistances are also important contributing factors that can vary with the degree of FL thrombosis, the number of re-entry tears, and branch vessels arising from the FL (Fig 4) (20,25,26). While pressure is difficult to quantify noninvasively, FL flow features are easier to measure in vivo, and, because they are driven by relative pressures within the FL, may be useful for understanding risks of adverse remodeling.

Figure 4:

Boxplot shows the spatial variation and mean values of lumen pressure difference between the false lumen (FL) and the true lumen (TL) of an ex vivo porcine model after propagation with and without distal re-entry tear. Mean values are represented by diamond symbol within the boxplot. (Reprinted, under a CC BY license, from reference 26).

Methods of Hemodynamic Assessment and Measured Parameters

Computational Fluid Dynamics

Computational fluid dynamics is a branch of fluid mechanics that numerically solves the governing equations of fluid flow, producing quantitative estimations of velocity, pressure, and other velocity-derived metrics (27). Initial CT images are used to reconstruct three-dimensional models of patient-specific aortas with incorporated meshing to simulate in vivo blood flow dynamics. Blood flow through the aorta is modeled as a homogeneous, incompressible Newtonian fluid and assumed to be laminar (28). Between three and five cardiac cycles are used to establish the steady-state flow and damp out noisy velocity and pressure forms. Once a steady-state solution at the maximum flow rate is obtained, it can be used as the initial input condition for programs like ABAQUS/CFD (Simuleon) (29). Computational fluid dynamics has been used to study factors that contribute to varying degrees of FL outflow resistance and the aortic consequences of such factors (Table 2). A 2015 study, for instance, found that the key determinant of FL flow rate was the size of the primary entry tear (30). This conclusion was corroborated in a 2016 analysis, which determined that, in addition to a larger entry tear, increased FL pressure was associated with small and/or absent distal tears (31). Clinically, a greater percentage of total aortic flow passing through the FL has been linked to an increased risk of aneurysm formation and expansion (29). Computational fluid dynamics studies have also demonstrated that an elevated diastolic FL-to-TL transluminal pressure gradient increases the risk of malperfusion and tear propagation (28,32). Recent analysis has shown that this gradient increases as the exit tear shrinks and the entry tear enlarges (33).

Table 2:

Computational Fluid Dynamics: Hemodynamic Parameters and Key Findings

Wall shear stress, the friction force of blood flowing tangential to the vessel wall, is another hemodynamic parameter that has been explored using computational fluid dynamics (Fig 5). Computational fluid dynamics studies have demonstrated an association between high wall shear stress and rapid aortic growth rate, as well as increased risk of retrograde TAAD development (29,34). On the other hand, regions of stagnant flow that promote thrombus formation have been found to be associated with low wall shear stress (30,35).

Figure 5:

Left: Patient-specific TBAD reconstructed from CT image. Right: TAWSS shows areas of high wall shear stress proximally at entry tear (right). (Reprinted, under a CC BY license, from reference 27). TAWSS = time-averaged wall shear stress, TBAD = type B aortic dissection.

In summary, computational fluid dynamics offers extremely high spatial and temporal resolution and can precisely model complex fluid flow, though it remains an approximation of actual fluid flow and thus has several limitations. First, this technique relies on three-dimensional anatomic model inputs derived from CT or MRI data and thus requires precise segmentation to provide accurate, patient-specific models. Flow quantification is also highly dependent on user-supplied boundary conditions for inflow and outflow, fluid-structure interactions at tissue interfaces, and tissue-specific mechanical properties, which are all often difficult to measure and require multiple assumptions. Finally, computational fluid dynamics requires enormous computational power, particularly when employing a deformable model where the vessel wall and dissection membrane are allowed to move over the cardiac cycle (36). Taken together, these realities suggest that while computational fluid dynamics is a powerful research tool used to help understand the complicated hemodynamics involved in aortic dissection, it is unlikely to become a clinical tool in the near future.

4D Flow MRI

Four-dimensional (4D) flow is a phase-contrast MRI technique that uses time-resolved velocity encoding in all three spatial dimensions to noninvasively visualize and quantify in vivo blood flow and other advanced hemodynamic parameters (37). In general, sequence parameters can be adapted to individual anatomy and physiology to acquire a relatively high spatial (~ 2.5 mm³) and temporal (~ 40 msec) resolution with acquisition times on the order of 10 minutes. Data postprocessing generally includes corrections for Maxwell terms, eddy currents, and velocity aliasing, and it takes approximately 15–20 minutes to perform the postprocessing and generate velocity maximum intensity projections, streamlines, or particle traces for visualization with current commercially available postprocessing tools. These tools also allow for quantification of net flow, retrograde flow, peak velocity, FL stroke volume, and time-to-peak flow by placing two-dimensional analysis planes at regions of interest (37). In the context of TBAD, 4D flow has been used for quantitative and qualitative TL and FL hemodynamics (Fig 6), though most published studies are limited by relatively small sample sizes and heterogeneous cohorts (Table 3).

Figure 6:

Images in a 69-year-old man with repaired type A aortic dissection. Color-coded streamline visualizations during (A) midsystole, (B) late systole, and (C) early diastole show the differences in flow patterns in the TL (solid arrow) and FL. Open arrow indicates a local region of flow acceleration. (Reprinted, under a CC BY license, from reference 37). FL = false lumen, TL = true lumen.

Table 3:

4D Flow MRI Hemodynamic Parameters and Key Findings

TL and FL Flow Features

Qualitatively, 4D flow can identify flow vortices, regions in which fluid revolves around a given axis, and helical flow, which is the three-dimensional equivalent. Francois et al found helical flow was present in the FL of 11 of 13 patients with TBAD. In a 2019 study of fenestrated silicone models, flow vortices were noted to be most obvious at the primary exit tear (37,38).

Relative to the TL, the FL has been shown to have higher degrees of retrograde flow both in patients with chronic uTBAD and rTAAD (37,39). Another group employed a novel multivelocity encoding technique to analyze 10 patients with rTAAD and found the peak systolic flow rate to be lower in the FL than in the TL and reduced overall in both lumina when compared with healthy controls (Fig 7) (39). A 2017 analysis that used pulsatile flow through a silicone model calculated the FL reverse flow index, a quantitative measure of the percentage of blood volume flowing retrograde at a given aortic slice. The authors found that pulsatile flow resulted in passive deformation of the intimal flap, with predominantly forward flow during systole and an elevated reverse flow index at end diastole. Hemodynamically, the consequence of this flow reversal was a relatively low time-averaged FL wall shear stress, potentially signaling increased thrombosis via blood stagnation (40).

Figure 7:

Blood flow rate per aortic lumen area (mL/s/cm²) curves standardized by one cardiac cycle. (A–D) Control participants. (E–H) TL of patients with CDTAD. (I–K) FL of patients with CDTAD. * = P < .01 versus control (peak systole), † = P < .05 versus control (peak systole), ‡ = P < .05 versus CDTAD TL (peak systole). (Reprinted, with permission, from reference 39). CTDAD = chronic descending thoracic aortic dissection, FL = false lumen, TL = true lumen.

In a study of 12 patients with uTBAD, an elevated FL “stroke volume” (net flow) was associated with rapid aortic expansion (41). The group also analyzed areas of helical flow, a flow pattern that is perpendicular to the direction of total blood flow, and subsequently quantified the helicity by assessing the amount of flow rotation at the beginning and end of the cardiac cycle. The authors found that increased helicity was also associated with increased rates of aortic expansion (41).

A key limitation of many 4D flow studies is the use of qualitative flow pattern assessment or exclusively localized hemodynamic metric quantification. To broaden this analysis to global quantitative assessment, Jarvis et al developed 4D flow-derived voxel-wise parametric maps of potentially relevant hemodynamic variables, including flow stasis and kinetic energy, in both the TL and FL (Fig 8) (42). These maps enabled both regional and global flow characterization, as well as metric comparison across different TBAD subtypes. In particular, the authors analyzed the hemodynamic changes in six patients with chronic uTBAD as well as 14 patients with rTAAD and compared both sets to 21 age-matched controls. In this study, mean FL reverse flow was elevated in rTAAD relative to uTBAD and higher in both subgroups compared with controls. Moreover, mean flow stasis was elevated in uTBAD relative to rTAAD and again higher in both subgroups than controls. FL kinetic energy, meanwhile, was inversely related to flow stasis, as it was found to be highest in controls and lowest in patients with uTBAD (Fig 9) (42). Further studies exploring how these parameters correlate with adverse remodeling, FL thrombosis, and adverse outcomes are needed to understand the clinical applicability of these advanced parameters.

Figure 8:

Forward flow, reverse flow, kinetic energy (KE), and stasis maps in three example subjects. Top row: A 55-year-old medically managed patient with TBAD; middle row: a 63-year-old patient with rTAAD after open AAo replacement with aortic valve replacement; and bottom row: a 54-year-old control. Arrows show regions of elevated forward flow, reverse flow, and KE (patient with AAo repair), as well as elevated stasis (patient with TBAD). (Reprinted, under a CC BY license, from reference 42). AAo = ascending aorta, rTAAD = residual type B aortic dissection following repair of type A aortic dissection, TBAD = type B aortic dissection.

Figure 9:

Hemodynamic characterization of the FL in patients with TBAD. Boxplot is shown with red line = median, large box = interquartile range, 25%–75% of data. Each data point represents the average ROI value for one subject along the FL (for patients) or entire aorta (for controls). * = P < .05, ** = P< .001. (Reprinted, under a CC BY license, from reference 42). Red + indicates outliers, values that fall below the boxplot-defined minimum and above the maximum. AAo Repair = repaired type A (ascending aorta [AAo]) aortic dissection, ET = open elephant trunk repair, FL = false lumen, KE = kinetic energy, ROI = region of interest, TBAD = type B aortic dissection.

Entry Tears and Fenestrations

Similar to morphologic assessment, primary entry tears are relatively easily identified with 4D flow MRI.

A recent analysis of 16 patients with uTBAD found that changes in flow were related to the size of the intimal entry tear: A larger tear was negatively correlated with TL flow velocity and positively correlated with FL net flow, peak flow, and flow velocity (43).

The FL ejection fraction is an intuitive parameter recently proposed by Burris et al that may offer a simplified approach to quantifying FL pressurization. While FL retrograde flow describes the amount of backward flow throughout the entire FL, the FL ejection fraction describes only the proportion of FL flow exiting retrograde at the dominant entry tear and should increase as FL pressure increases relative to TL pressure (Fig 10) (44). A 2019 study of 12 patients with uTBAD found that the FL ejection fraction was significantly elevated among patients with a history of FL enlargement (45). One year later, the same group analyzed 18 patients with chronic uTBAD and found FL fraction to be an independent predictor of aortic growth rate, along with classically described factors like baseline aortic dimension and entry tear distance from the left subclavian artery (Fig 11) (44). Given the clinical availability of 4D flow postprocessing, visualization, and quantification software, this measurement is relatively straightforward and clinically feasible. Further assessment of interobserver variability of this technique and application in larger cohorts are needed.

Figure 10:

Four-dimensional (4D) flow hemodynamic assessment. (A) The FL EF was measured in the plane of the dominant entry tear and was defined as the proportion of retrograde flow (L/min) exiting the FL during diastole over the systolic antegrade flow volume (L/min) at the dominant entry tear. (B) Three-dimensional visualization of 4D flow MRI data in a patient with TBAD demonstrating the flow analysis plane for the entry tear FL EF measurement (red line) and the TL and FL analysis planes (gray line) measured 3 cm distal to the tear. Antegrade flow is depicted in the TL and FL during systole (black arrow), with retrograde flow being “ejected” from the FL during diastole (yellow arrow) in a representative case with measured FL EF of 49%. (Reprinted, under a CC BY license, from reference 44). FL EF = false lumen ejection fraction, LSC = left subclavian artery, TBAD = type B aortic dissection, TL = true lumen.

Figure 11:

Scatterplots demonstrate the correlations between aortic growth rate and (A) baseline maximal aortic diameter, (B) false lumen ejection fraction, (C) dominant entry tear size, and (D) distance from the LSC to the entry tear. (Reprinted, under a CC BY license, from reference 44). LSC = left subclavian artery.

4D flow has also been used to evaluate distal re-entry tears and fenestrations. Though the precise hemodynamic effects of these fenestrations have only recently begun to be investigated, surgically or endovascularly introducing small tears to equilibrate transluminal pressures and reduce pressure gradients has been performed with promising results (46,47). While difficult to detect with current imaging methods, computational fluid dynamics analyses suggest that these small fenestrations are hemodynamically active, as they have been found to equalize transluminal pressures, alter the risk of dissection progression and/or rupture, and impact the perfusion of visceral arteries (48). Notably, a recent analysis of 19 patients with uTBAD found that 4D flow detected hemodynamically active fenestrations better than combined traditional MRI and MR angiography and comparable to CT angiography, suggesting that a combination of imaging methods could yield the best results (Figs 12, 13) (49).

Figure 12:

(A) CTA, (B) 4D flow MRI velocity MIP overlaid on magnitude images in an oblique sagittal view, and (C) CEMRA. The CTA and MRA clearly demonstrate dissection anatomy (TL [yellow arrows] and FL), however, both are often limited by blurring artifact related to pulsatile flap motion. The 4D flow velocity MIP reveals four discrete fenestrations from their associated flow jets into the FL during systole (white arrows). (Reprinted, under CC BY 4.0 license, from reference 49). AAo = ascending aorta, CEMRA = contrast material–enhanced MR angiogram, CTA = CT angiogram, DAo = descending aorta, FL = false lumen, MIP = maximum intensity projection, TL = true lumen, 4D = four dimensional.

Figure 13:

(A) Image from CEMRA demonstrates a complex type B dissection. (B) Image from 4D flow MRI velocity MIP during systole reveals several large, relatively high-velocity jets entering an aneurysmal segment of the false lumen (*) at the proximal DAo (white arrows) and impinging on the false lumen wall. (C) In diastole, there is retrograde flow into the true lumen at these sites (white arrows), with an additional fenestration in the distal DAo seen only due to diastolic flow (red arrow). This fenestration was not seen at CT. (Reprinted, with permission, from reference 49). AAo = ascending aorta, CEMRA = contrast material–enhanced MR angiogram, DAo = descending aorta, MIP = maximum intensity projection, 4D = four dimensional.

A 2019 study of fenestrated silicone models showed that transluminal fluid shift at fenestration sites was found to contribute to vortex formation as a result of excess flow escaping the FL and dissipating into the TL, which may aid in fenestration visualization (38). Perhaps intuitively, the authors of this study suggest that the flow across these fenestrations will decrease diastolic pressure gradients between TL and FL (38). At present, it is not clear if fenestration hemodynamic quantification is feasible or would provide additional information relative to overall TL and FL flow features.

Treatment Response

4D flow has also demonstrated potential value in post-TEVAR flow assessment. A 2019 case report found that postoperatively, TL flow volumes increased while flow at re-entry tears fell, ultimately reducing FL volume (50). Recent analysis of silicone models after endograft deployment corroborated these results to a certain degree; endograft exclusion of the FL resulted in restoration of normal flow rates, but the effect was only observed in the region of the endograft at the primary entry tear. Distally, at re-entry sites, the FL remained canalized, suggesting that without complete endograft coverage, unfavorable hemodynamics may persist (51).

Conclusion

Noninvasive, imaging-based evaluation is crucial to the diagnosis and risk stratification of patients with uTBAD. Due to the relatively low incidence of cases and heterogeneity of TBAD subtypes, risk-stratification tools are difficult to study in this disease, but improved approaches for personalized and cost-effective treatment selection are needed. In this context, the potential roles of both morphologic and hemodynamic assessment are evolving rapidly, as is our understanding of the factors that drive complications. Current anatomic risk stratification techniques are the mainstay of TBAD assessment. However, due to the role of FL pressurization in adverse aortic remodeling, in vivo hemodynamic assessment may complement other clinical and morphologic parameters to improve TBAD risk stratification. As 4D flow MRI is becoming increasingly clinically feasible, there is an opportunity to further explore the complex hemodynamics at the entry tear and in the FL, which have shown early promise. Larger cohorts, multicenter collaboration, and streamlined analysis are required to fully assess the potential of these approaches.