Role of Re-entry Tears on the Dynamics of Type B Dissection Flap
Role of Re-entry Tears on the Dynamics of Type B Dissection Flap
JOSHUA KRIEGER 0 1 3
BLAYNE ROEDER 0 1 3
STEPHAN HAULON 1 3 5
SEAN CHAMBERS 0 1 3
GHASSAN S. KASSAB 1 3 4
0 Cook Medical Inc , Bloomington, IN , USA
1 Medical Innovations Institute , 11107 Roselle St., Rm. 211, San Diego, CA 92121 , USA. Electronic mail:
2 3DT holdings LLC , San Diego, CA , USA
3 FDR , Lumen pressure, Dilation, Strain
4 California Medical Innovations Institute , 11107 Roselle St., Rm. 211, San Diego, CA 92121 , USA
5 Aortic Center, Hoˆ pital Cardiologique , CHU de Lille, Lille , France
-Mortality during follow-up after acute Type B aortic dissection is substantial with aortic expansion observed in over 59% of the patients. Lumen pressure differential is considered a prime contributing factor for aortic dilation after propagation. The objective of the study was to evaluate the relationship between changes in vessel geometry with and without lumen pressure differential post propagation in an ex vivo porcine model with comparison with patient clinical data. A pulse duplicator system was utilized to propagate the dissection within descending thoracic porcine aortic vessels for set proximal (%circumference of the entry tear: 40%, axial length: 2 cm) and re-entry (50% of distal vessel circumference) tear geometry. Measurements of lumen pressure differential were made along with quantification of vessel geometry (n = 16). The magnitude of mean lumen pressure difference measured after propagation was low (~ 5 mmHg) with higher pressures measured in false lumen and as anticipated the pressure difference approached zero after the creation of distal re-entry tear. False lumen Dissection Ratio (FDR) defined as arc length of dissected wall divided by arc length of dissection flap, had mean value of 1.59 ± 0.01 at pressure of 120/80 mmHg post propagation with increasing values with increase in pulse pressure that was not rescued with the creation of distal re-entry tear (p < 0.01). An average FDR of 1.87 ± 0.27 was measured in patients with acute Type B dissection. Higher FDR value (FDR = 1 implies zero dissection) in the presence of distal re-entry tear demonstrates an acute change in vessel morphology in response to the dissection independent of local pressure changes challenges the re-apposition of the aortic wall.
Acute aortic dissection; Ex vivo model; Clinical
The current treatment for Type B dissection which
always includes best medical, treatment, and
eventually endovascular or surgical intervention or a
combination of both, aims to stabilize the hemodynamics
and restore blood flow to end organs, and reduce the
risk of rupture. Early mortality from Type B aortic
dissection is substantial, varying between 10 and
29%24,29,32 with follow-up mortality rates approaching
1 in every 4 patients at 3 years.34 Aortic expansion
during follow-up was reported in 59% of patients with
average rate of 1.7 ± 0.7 mm/year.5,13 Computed
tomography show the acute enlargement of dissected
aorta of almost 25% from its baseline.23
Currently, the risk factor to predict aortic dissection
dilation is the aortic diameter. The criteria for repair of
aneurysmal dissection are a diameter > 5.0 to 6.0 cm,
or rapid expansion in a chronic aneurysmal dissection
> 1 cm/year.8,30 In a clinical study27 performed across
101 patients with Type B acute dissection without
complications, a maximum aortic diameter of > 4 cm
and a patent false lumen during the acute phase served
as important predictors for aortic enlargement in the
Although several in vivo and ex vivo studies have
been reported describing the patterns of dissection and
the associated characteristics of hemodynamic
parameters, flow and velocity,2,3,6,9,21,31 few studies
have examined the lumen pressure differential and the
risk for aortic dilation. Phantom ex vivo models using
polymer tubes (which have different physiological
properties than biological tissue and a rigid flap) have
been used to show the relationship between tear
configuration (size, number, location) and false lumen
pressure.1,25,35 The shape of the pressure waveforms in
2017 The Author(s). This article is an open access publication
both the lumens were shown to be identical in an
artificially created dissection in an ex vivo porcine
model.21 An in vivo study using a swine model of
retrograde endovascular aortic dissection with re-entry
tear report aortic dilation at the dissection portion.19
The depth of the dissection plain was, however,
unpredictable, inconsistent and technique dependent.
To systematically understand the spontaneous
antegrade Type B dissection, we have recently shown
the relationship between initial tear geometry and
pulse pressure magnitude for initiation and
propagation of dissection.20 Using an ex vivo porcine model for
spontaneous Type B dissection we reproduce the
lumen pressure characteristics with and without distal
reentry tear, evaluate the changes in the dissected vessel
geometry and compare against measurements made in
aortae of patients with acute Type B dissection.
Tissue Sample Preparation
The descending thoracic porcine aortas were
obtained from local slaughterhouse (Sierra for medical
science, Whittier, CA, USA) and cut to 20 cm in length
from the arch. Fresh samples were stored in 0.9%
saline solution followed by preparation and testing
within 24 h of tissue arrival at the facility. The aortae
were prepared for testing by removing any loose
adventitial tissue and ligating the major branches using
silk suture (Henry Schien, Melville, NJ, USA), as
Initial Entry Tear
All initial entry tears were manually created inside
the vessel, at ~ 5 cm from the arch using a surgical
blade. The %circumferential length of the entry tear
defined previously in Peelukhana et al.20 was created
along the vessel circumference and was set at 40%. The
dissection plane was set in the media layer at 1/3rd the
vessel wall thickness. The layers were separated and
advanced using fine-tip forceps to the desired axial
length of 2 cm (measured along the length of the
vessel) and later confirmed using ultrasound (US)
measurements. This created the true lumen (TL) and false
lumen (FL) within the vessel.
The aorta was flipped inside out after exposure to
the pulsatile flow. The final tear circumference at
proximal end and the axial length of the propagated
flap were measured using a suture and a ruler
respectively. A re-entry tear was created at the distal end of
the propagated flap by using a surgical blade. The
%circumferential length of the re-entry tear was set at
50% of distal vessel circumference.
Pulse Duplicator Test System
A pulse duplicator [PD] (PD; BDC laboratories,
Wheat Ridge, CO, USA) reproduced the physiological
flow and pressures in the porcine aorta vessel
integrated within the test system (Fig. 1). Detailed
description of the setup can be found in Peelukhana
et al.20 Inlet flow rate was measured using an inline
flow probe (ME13PXN; Transonics Inc., Ithaca, NY,
USA) was set to 2 L/min for all tested aorta samples.
The pump parameters were set constant for each
experiment (HR: 72 bpm, Systole/diastole ratio =
35/65%). Based on previous porcine in vivo length
measurement of the aorta, an average stretch ratio of
30% was incorporated for all the vessels prior to
testing by adjusting the distance between the inlet and
CIRS blood mimicking fluid was used as blood
analog, with a q = 1050 kg/m3, and dynamic viscosity
of l = 4 cP or 0.004 Pa.s (Model 046, Computerized
Imaging Reference Systems, Incorporated (CIRS),
Norfolk, VA, USA). The container tank was filled with
0.9% saline solution such that the test vessel was
The inlet pressure was set at 120/80 mmHg. The
pulse pressure was subsequently increased in steps of
20 mmHg. The test vessel was subjected to each
pressure step for 3 min before the next pressure increment.
This stepwise increase continued till propagation
occurred and/or the limit of the PD system was reached
which was set at 300 mmHg. Any dissection that
propagated above pulse pressure of ~ 200 mmHg was
not included for data analysis.
To obtain the local pressures within the FL and TL,
7 Fr. catheters were enabled within the inlet and outlet
ports, respectively. The pressure and flow data was
obtained for 5 s at 5000 Hz frequency using Statys PD
integrated data-acquisition system. A L15-i70
ultrasound (US) transducer connected to IE33 ultrasound
machine (Phillips Ultrasound, Bothell, WA, USA) was
used for visualization. The PD pump output trigger
was connected US ECG leads to synchronize the
pressure from the Statys PD software with the flap
Prior to start of the experiment, the TL and FL
pressure catheters were adjusted in the proximal end of
the entry tear and confirmed using the Echo imaging.
The catheters were held for 3 min at each location
prior to measurement to allow for the pressure to
equilibrate. The velocities were measured in the pulse
wave Doppler mode while flap and lumen geometric
characteristics were imaged in B-mode.
Ten porcine aorta vessels were used to obtain the
lumen pressure differential. The methodology without
the catheters was replicated to obtain geometric
relationship between false lumen and flap (n = 6). The
delta lumen pressure difference was calculated by
subtracting the TL from the FL pressures after
propagation with and without a single distal re-entry tear.
For a given test vessel, the average time of exposure to
the pulsatile flow was 1.5 ± 0.3 h.
To characterize the lumen cross sectional area
changes post-propagation and with distal re-entry tear,
the %TL CSA at peak systole and diastole pressures
were assessed as described in Peelukhana et al.20 To
identify the extent of the false lumen expansion post
propagation and with creation of a distal re-entry tear,
we defined the ratio of the arc length of false lumen
(dissected wall) to arc length of flap as False lumen
Dissection Ratio (FDR) as shown in Fig. 2. FDR of
value 1 implies no dissection (i.e., intact wall) while
FDR >1 implies dissection of greater degrees with
increasing value of FDR. Using Fiji image processing
software,26 the arc length of the false and true lumen
along with the flap length were measured at all
locations (proximal, middle and distal) for each pulse
pressure (120/80, 140/80, 160/80 mmHg). For a given
location and pulse pressure, the FDR was averaged
over the peak systolic and diastolic pressure. At the
proximal end for a given pulse pressure, the
%undissected wall was defined as the ratio of TL arc length to
arc length at 0% dissection (baseline). The
circumferential Green strain on the flap was quantified as:
1 ðFlap Arc Length2Peak SystoleÞ
ðFlap Arc Length2DiastoleÞ
ðFlap Arc Length2DiastoleÞ!
The thicknesses of the flap along with FL and TL at
proximal and distal ends were measured using a
micrometer caliper (Mitutoyo America Corporation,
Aurora, Il, USA) before and after the creation of a
distal re-entry tear. The average of three readings was
used to obtain the final value. The %change in the
thickness was calculated as:
False Lumen þ Flap True lumen thickness
True lumen thickness
The data were assessed for normality (skewness and
kurtosis). Descriptive statistics were calculated for all
the variables. Statistical analysis was two-tailed and
was carried out at an alpha level of 0.05. Variables
were logarithmically transformed in case of deviation
from normality. Chi square and t-tests were used to
assess significance for categorical and continuous
variables respectively. Linear mixed-effects regression
models were used to assess the effect of percent of
undissected wall circumference and pulse pressure at a
fixed location (proximal end) on FDR for porcine
aortae and the effect of demographic (age, gender) and
clinical variables (hypertension, systole and diastolic
pressure) on patient FDR values. Repeated measures
ANOVA was used to evaluate the relationship between
location within the dissected portion, pulse pressure
and presence of re-entry tear on the FDR values.
Spearman’s rank correlation was utilized to test the
strength of relationship between FDR values and
gender for patient data. All data are expressed as mean
Clinical FDR Data
Clinical data was gathered from the Cook Medical
STABLE I clinical trial which evaluated the Zenith
Dissection Endovascular System in the treatment of
Type B aortic dissections for comparative analysis of
FDR between the in vitro test setup and the in vivo
conditions. In accordance with current legislative
recommendation, the interventions were performed with
approval of the Institutional Review Board. All
patients were informed in detail about the
endovascular intervention and gave written consent. While the
trial evaluated both acute and chronic aortic
dissections, only those patients treated for acute,
complicated Type B aortic dissection were included in the
analysis. Additionally, patients who had poor or no
pre-operative imaging from the trial were excluded
from this analysis. For each case, non-gated computed
tomography (CT) images were utilized to first identify
the primary entry tear. Measurements of the dissection
flap length and false lumen arc length were performed
at the first slice distal to entry tear. The measured FDR
per patients represents the cycle average value. An
example is this measurement is depicted in Fig. 2c.
Lumen Pressure Characteristics of Type B Dissection
The mean proximal circumferential propagation
was 72.8 (
)% and the average axial length after
propagation was 12.6 (1.2) cm.
The magnitude of the lumen pressure difference
after propagation was consistent across the three
spatial locations with mean value of 4.6 (2.1) mmHg with
higher pressure measured within the FL (Fig. 3). As
expected, the mean pressure difference approached
zero with the creation of the distal re-entry tear [0.24
(1.4) mmHg]. The longitudinal profile of the lumen
pressure difference, however, indicated a gradient
along the length of the dissected portion with
maximum difference at the distal end [% re-entry
circumference = 45.7 (6.8)].
Interestingly, the absolute magnitude of the
measured pressure increased in both the lumens while the
pressure difference across did not vary significantly
before and after propagation. A mean percent
increase in pressure magnitude of 27.9 (
measured in the FL compared to 33.3 (
)% in TL. In
addition to the alleviation in the lumen pressure
differential, the creation of the re-entry tear also
restored the pressure magnitude to that measured prior
Position and configuration of the intimal flap has
been shown to correlate with dynamic obstruction10 in
aortic dissection. The flap dynamics were assessed by
quantifying the flap configuration and the TL cross
sectional area over peak systole and diastole phase of
the cardiac cycle at the proximal and distal locations
within the dissected portion of the vessel. The flap
configuration at the proximal end of the vessel was
curved towards FL during systole phase in 37.5% of
samples and doubled to 75% with re-entry tear.
Similar trend was observed at the distal end of the vessel
with the flap curvature towards FL in 12.5% of
samples post propagation to 75% with re-entry tear.
Similar to pre-propagation,20 the flap curvature was
towards FL in diastole and was identical for proximal
and distal ends increasing from 75% and 25%
respectively to 100% with re-entry tear (Fig. 2). The
gain in %TL CSA with the creation of the distal
reentry was significant at both proximal [t(
) = 12.67,
p = 2.034e209] and distal end [t(
) = 5.85,
p = 3.164e205] as shown in Fig. 4.
In two of the aortic vessels post propagation
(excluded from analysis), the flap collapsed onto the true
lumen with near complete occlusion both at proximal
and distal ends. Consequently, large pressure
differentials were measured between the lumens after
propagation [76 (
) mmHg]. The creation of the distal
reentry tear, however, eliminated the pressure difference
between the lumens.
False Lumen Dilation Ratio (FDR) and Vessel
Ratio of TL to flap arc length was calculated to
account for contribution of elastic recoil and
shortening of the flap to the FDR values and was consistent
across samples [1.01 (0.17)]. The depth of the dissection
plane within the media which also influence the FDR
and dilation, measured 35.74 (1.7)% at proximal
dissection increasing to 51.26 (5.8)% at distal end of the
dissection. The %change in wall thickness which assess
the lateral expansion in the vessels within the
experimental period, was not significant at proximal [t(
1.65, p = 0.15] and distal [t(
) = 1.46, p = 0.20]
portions of the dissected vessel with the creation of the
By using random effects for sample, depth of
dissection plane and the percent circumference of TL
wall, we controlled for different mean ratings
associated with these variables. For a fixed location
(proximal end), pulse pressure influenced FDR [v(
19.81, p = 0.00005] by increasing it by 0.026 (0.005)
for every pulse pressure increase of 20 mmHg.
Presence of re-entry tear increased the FDR when
compared to post-propagation values by 0.008(0.004) and
was significant (p = 0.0003). However, the percent of
original wall circumference was not significant on
FDR values (Fig. 5).
Presence of distal re-entry tear [F(
) = 13.89,
p = 0.002] and location within the dissected portion of
the vessel [F(
) = 5.382, p = 0.01] significantly
influenced the FDR values, while the effect of
increasing pulse pressure was not significant (Fig. 6).
FDR was higher with the presence of large distal
reentry tear [1.62 (0.083)] when compared to
postpropagated values [1.60 (0.085)]; a significant increase
of 0.017 [95% CI, 0.008–0.026, t(53) = 3.848,
p = 0.0003]. FDR values also increased by 0.072 [95%
CI, 0.048–0.095, t(
) = 6.19, p = 4.3e207] in the
middle [1.64 (0.06)] and by 0.068 [95% CI, 0.03–0.107,
) = 3.66, p = 0.0008] in the distal portion [1.63
(0.11)] when compared to proximal [1.56 (0.06)] end of
the dissected portion of the aortic vessel.
No new dissections were observed within any of the
aortic specimens and arterial branches were not
Similar to FDR, presence of distal re-entry tear
) = 5.34, p = 0.035] and location within the
dissected portion of the vessel [F(
) = 6.23,
p = 0.005] significantly influenced the circumferential
flap strain (Fig. 7). The increasing pulse pressure did
not influence the flap strain values. Lower values of
flap strain were associated with the creation of distal
reentry tear [t(53) = 2.72, p = 0.008]. The
circumferential flap strain increased significantly along the
length of the vessel with maximum values at distal end
when compared to proximal [t(
) = 2.67, p = 0.011]
and middle [t(
) = 3.21, p = 0.003] portions.
Demographic Summary and Clinical FDR
Thirty patients [21 men (70%) and 9 women (30%)]
with average age of 57.9 (11.9) years were included in
this study. Twenty-five (83.3%) of the patients
presented as hypertensive at the time of diagnosis, with
average pressures 141.5 (42.6) mmHg and 75.5 (26.6)
mmHg for systolic and diastolic respectively and none
were diabetic. Amongst this patient set, 20 (58%) had
multiple entry tears and 18 (52%) had more than two
re-entry tears. Detailed clinical summary is listed in
The FDR for the entire dissection cohort measured
1.87 ± 0.27, with no statistical differences between
men and women. Hypertension significantly influenced
FDR values after controlling for age and gender
) = 8.11, p = 0.0044) with decrease by 0.36 (0.12)
when compared to subjects without hypertension.
Systolic and diastolic pressure values did not influence
the measured FDR values for these subjects.
Significant correlation was observed between sex
and the flap length at first communication
(q = 2 0.43, p = 0.023) with higher values measured
for males when compared to females. The minimum
FDR for the entire cohort was 1.43 and the maximum
FDR was 2.59, thus showing that in all acute
dissection patients contraction of the dissection flap occurs
in combination with expansion of the separated false
vessel wall and significant extension is needed to
reappose the dissection flap to the false lumen wall.
Endovascular treatment using stent-graft to treat
aortic Type B dissection has produced acceptable
outcome.7,8,18 The relatively high incidence of increasing
aortic diameter, however, require subsequent
intervention. These considerations make it important to
understand the physical properties of the aortic wall
and the influence of these properties on aortic wall
behavior after acute aortic dissection. In this
reproducible ex vivo model of Type B acute aortic dissection,
the magnitude of the lumen pressure difference was
minimal post propagation, dependent on flap
movement, and was restored to equilibrium with the
creation of distal re-entry tear. Large dilation of the false
lumen (FDR >1.6) was measured post-propagation
that was dependent on regional biomechanical
properties of the aorta, independent of pulse pressure and
local lumen pressure differences, and was not restored
with the creation of distal re-entry tear. Interestingly
patients with acute Type B dissection had overall
higher mean FDR values (~ 1.88) with higher values
for normotensive patients independent of age and sex.
These results highlight the requisite for significant
extension required to re-appose the flap against the
false lumen wall as well as consideration for the
mechanical properties of the aortic wall for successful
The true lumen compression was attributed to
greater pressure in false lumen and due to pulsatile
dynamics of the flap. As evident from the changes in
true lumen cross sectional area, a discrepancy in lumen
sizes did not imply the existence of a pressure gradient.
The transmural pressure showed dependence on local
anatomical biomechanical properties evident from the
longitudinal lumen pressure distribution along the
length of the dissection and was more pronounced with
the presence of re-entry tear. Although the gain in the
cross-sectional area of the true lumen along the
dissection length was significant with the creation of the
distal re-entry tear, it did not re-expand to baseline due
to the elastic recoil of the dissection flap. Clinically,
intravascular stents are deployed to expand the true
lumen and may result in tearing or rupture to the flap
since the deployment of stent does not alter the
pressure gradient across the flap. Although the measured
magnitude of the pressure difference post-propagation
was small (~ 5 mmHg), the difference was positive over
the entire cardiac cycle (peak systolic, diastolic and
mean pressure). Previous in vitro models of aortic
dissection using phantom materials showed decreased
systolic pressure instead of significant increase in the
diastolic pressure within the false lumen in the absence
of an exit tear as compared to the true lumen.1,25,35
This could be attributed to a mismatch between the
shear modulus and the tensile strength of the polymer
phantom compared to aortic tissue along with presence
of a rigid flap.
Relevance of an ex vivo model of dissection is
related to reproducibility of the characteristics of human
Type B dissection. Following dissection, the overall
aortic dilation was due to the false lumen expansion
(increasing FDR values). The true lumen
circumference which is flanked by dissection flap at negligible
transmural pressure and original elastic rich wall
remained relatively unchanged before and after creation
of the re-entry tear. Patency of the false lumen is
identified as an independent clinical risk factor to
predict aortic dilation15,28,33 with increased false lumen
pressure due to outflow restrictions (partial thrombosis
or uneven tear size) as explanation for aortic
dilation.1,35 In the absence of trans dissection flap pressure
gradient it is important to evaluate the load on the flap
and the FL wall considering current treatment options
i.e., stent graft or septectomy. The uneven distribution
of the elastin layers in the false lumen after the partial
separation of the media layers reduces the compliance
of the aortic wall. Subsequently the circumferential
stress in the vessel wall which is uniform under
physiological conditions will be altered.12 In addition
regional anatomy dictates variation in nonlinear
biomechanical response due to changes in wall
thickness and collagen content with blood pressure.11,14,37
For a fixed location within the dissection length,
increasing pulse pressure and patent false lumen led to
increased FDR values for a consistent depth of
dissection. Pulse pressure was however not a critical
factor for the increased dilation of the false lumen along
the entire length of the dissection. Local regional
properties evident from changes in FDR values
between the proximal to distal end of the aorta and the
presence of a large distal tear were overall significant
factors influencing false lumen dilation. These results
suggest a dissociation between pressure gradient and
risk for dilation. The false lumen dilation increases
relative to flap i.e., increase in FDR but the flap
dimensions in the circumferential and lateral directions
do not change significantly with increase in pulse
pressure indicating a structural limitation to
expansion. Significant stiffness of the aged human aorta
when compared to porcine aorta or lack of completely
developed distal tears could explain the higher
measured values of FDR in human patients with Type B
dissection.16,33 While the significant effect of
hypertension on FDR values was anticipated; association of
higher FDR values with normotensive patients was
surprising and is not readily explainable. This may
have resulted due to the small sample size, inclusion of
younger patients in the cohort or variation in the
initiation of the entry tear between subjects. Although we
did not observe any compensating change in both true
and false wall thickness over the short (~h)
experimental timeline, long term in vivo remodeling may
influence the stress distribution and further
remodeling.7,17,18 It is also important to note that current
endovascular treatments that target re-apposition of
the aortic wall are not designed for complete
compensation of the initial dilation of the wall.18 This
results in a patent false lumen (below the level of thoracic
stent graft) which over time increases the need for
Some limitations of the current study should be
acknowledged. First the effect of aortic arch anatomy
was not accounted for during the experiments.
Second, the results of this study pertain only to acute
dissections in the absence of false lumen remodeling.
Third, neo-intimal thickening of the flap has been
reported clinically during follow-up, which might
restrict the flap movement. Fourth, we replicated
dissections with two tears while multiple tears are
regularly observed during clinical imaging.22 Fifth,
the tears were perpendicular to the flow which may
not represent the biologically relevant orientation;
i.e., spiral tears have been reported.4 Sixth, the FDR
and static pressure measured likely depend on size of
the tear. Finally, effects of patent side branches which
has been shown to increase the false lumen cross
sectional area36 were not accounted and warrant
Higher FDR values (FDR = 1 implies zero
dissection) in the presence of distal re-entry tear demonstrate
an acute change in vessel morphology in response to
the dissection independent of local pressure. This
retraction of the flap is likely a result of residual strain
in the wall and makes re-apposition of the aortic wall
No competing financial interests exist.
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