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\begin{document}

\title{Ascending Aortic Length and Type A Dissection: A Propensity
Score-Matched Cohort Analysis}



\author[1]{Gregory Boyajian}%
\author[1]{Nikhil K. Prasad}%
\author[1]{Bryan Nixon}%
\author[1]{Zachary Bolten}%
\author[1]{Irina Kolesnik}%
\author[1]{Chetan Pasrija}%
\author[1]{Aakash Shah}%
\author[1]{Shahab Toursavadkohi}%
\author[1]{Sari D. Holmes}%
\author[2]{Jean Jeudy}%
\author[1]{Bradley Taylor}%
\author[1]{Mehrdad Ghoreishi}%
\affil[1]{University of Maryland Department of Surgery}%
\affil[2]{University of Maryland School of Medicine Division of Radiology}%


\vspace{-1em}



  
  \date{May 29, 2024}


\begingroup
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\selectlanguage{english}
\begin{abstract}
\textbf{Background:} Little information is available regarding the
relationship between ascending aortic length and acute aortic events. We
aim to evaluate whether patients with acute type A aortic dissection
(ATAAD) exhibit differential aortic measurements compared to control
patients. \textbf{Methods:} Data were collected on patients with ATAAD
and control patients who received imaging for unrelated conditions.
Propensity score matching was conducted using age, sex, race, body
surface area, and hypertension in the logistic model. After matching, 67
patients remained in each group. Aortic morphometry was assessed via
computed tomographic angiography. Ascending aortic length was defined as
the centerline distance between the sinotubular junction (STJ) and the
origin of the brachiocephalic trunk. \textbf{Results:} The mean
ascending aortic length was 76.9 \selectlanguage{ngerman}± 15.7 mm (range 36.8 to 115.0 mm) for
patients with ATAAD and was 62.0 ± 10.7 mm (range 34.0 to 87.8 mm) for
control patients, which was a significant difference (t=-6.4,
P\textless{}0.001). ATAAD patients had greater diameter at STJ (median:
41.6 vs 30.2 mm, z=7.5, P\textless{}0.001) and diameter at PAB (median:
42.3 vs 32.2 mm, z=6.8, P\textless{}0.001) compared with controls. A
maximum ascending aortic diameter \textgreater{}5.5 cm (at either the
PAB or STJ) was present in 12 of 67 cases (18\%) and 0 of 67 controls
(P\textless{}0.001). \textbf{Conclusions:} Ascending aortic length is
significantly greater in patients who experienced ATAAD compared to
matched controls. Elongation of the aorta may play a role in the
pathogenesis of ATAAD, and assessment of ascending aortic length may be
valuable as a predictive marker for aortic events.%
\end{abstract}\selectlanguage{ngerman}%



\sloppy


\textbf{Title:} Ascending Aortic Length and Type A Dissection: A
Propensity Score-Matched Cohort Analysis

\textbf{Authors:} Gregory P. Boyajian MD\textsuperscript{1}, Nikhil K.
Prasad MBChB\textsuperscript{1}, Bryan Nixon MD\textsuperscript{1},
Zachary Bolten MD\textsuperscript{1}, Irina Kolesnik
BS\textsuperscript{1}, Chetan Pasrija MD\textsuperscript{1}, Aakash Shah
MD\textsuperscript{1}, Shahab Toursavadkohi MD\textsuperscript{3}, Sari
D. Holmes PhD\textsuperscript{1}, Jean Jeudy MD\textsuperscript{2},
Bradley Taylor MD\textsuperscript{1}, Mehrdad Ghoreishi
MD\textsuperscript{1}

\emph{First Author ORCID: 0000-0002-1295-7307}

\textbf{Affiliations:}

1 University of Maryland School of Medicine, Division of Cardiac Surgery

2 University of Maryland School of Medicine, Division of Radiology

3 University of Maryland School of Medicine, Division of Vascular
Surgery

\textbf{Data Availability Statement:} The dataset used and analyzed
during the current study was generated from medical records at the
affiliated institution, and is available from the corresponding author
on reasonable request.

\textbf{Funding Statement:} No specific funding was associated with the
research or publication of this work.

\textbf{Disclosures:} No authors disclose any conflicts of interest
related to this work.

\textbf{Institutional Review Board:} Exempt from IRB approval under
Category (4): Secondary research for which consent is not required

\textbf{ABSTRACT}

\textbf{Background:} Little information is available regarding the
relationship between ascending aortic length and acute aortic events. We
aim to evaluate whether patients with acute type A aortic dissection
(ATAAD) exhibit differential aortic measurements compared to control
patients.

\textbf{Methods:} Data were collected on patients with ATAAD and control
patients who received imaging for unrelated conditions. Propensity score
matching was conducted using age, sex, race, body surface area, and
hypertension in the logistic model. After matching, 67 patients remained
in each group. Aortic morphometry was assessed via computed tomographic
angiography. Ascending aortic length was defined as the centerline
distance between the sinotubular junction (STJ) and the origin of the
brachiocephalic trunk.

\textbf{Results:} The mean ascending aortic length was 76.9 \selectlanguage{ngerman}± 15.7 mm
(range 36.8 to 115.0 mm) for patients with ATAAD and was 62.0 ± 10.7 mm
(range 34.0 to 87.8 mm) for control patients, which was a significant
difference (t=-6.4, P\textless{}0.001). ATAAD patients had greater
diameter at STJ (median: 41.6 vs 30.2 mm, z=7.5, P\textless{}0.001) and
diameter at PAB (median: 42.3 vs 32.2 mm, z=6.8, P\textless{}0.001)
compared with controls. A maximum ascending aortic diameter
\textgreater{}5.5 cm (at either the PAB or STJ) was present in 12 of 67
cases (18\%) and 0 of 67 controls (P\textless{}0.001).

\textbf{Conclusions:} Ascending aortic length is significantly greater
in patients who experienced ATAAD compared to matched controls.
Elongation of the aorta may play a role in the pathogenesis of ATAAD,
and assessment of ascending aortic length may be valuable as a
predictive marker for aortic events.

\textbf{Keywords:} Aorta, Ascending, Dissection, Anatomy

\textbf{TEXT}

INTRODUCTION

Acute type A aortic dissection (ATAAD) is a life-threatening emergency
that is increasing in both prevalence and
incidence\textsuperscript{1,2}. There is well-documented correlation
between aortic dilation and risk of aortic dissection, and current
guidelines for preventative surgical intervention are based on
measurements of aortic diameter\textsuperscript{3--7}. As our
understanding of thoracic aortic disease expands, it has become clear
that many patients experience aortic dissection at an aortic diameter
less than the current intervention guideline of 5.5
cm\textsuperscript{8--10}. Therefore, supplementation of the current
diameter-based guidelines with an additional predictor of aortic
dissection is warranted. Little information is known about the
relationship between length of the ascending thoracic aorta and risk of
aortic dissection. In recent years, ascending aortic length has been
identified as a ``neglected dimension'' that may predict risk for
ATAAD\textsuperscript{11--13}. However, no study has compared aortic
length in patients with ATAAD to aortic length in a population of
matched controls. We aim to evaluate whether patients who present with
ATAAD exhibit differential aortic length compared to control patients.

PATIENTS AND METHODS

\emph{Patient selection and data collection}

This study was performed at a single institution. There was no specific
funding provided for this study. This study was exempt from
Institutional Review Board approval under Category (4): Secondary
research for which consent is not required. We retrospectively compared
two groups of patients who had computed tomography angiograms (CTA) of
their thoracic aorta performed either at UMMC or a referral center prior
to transfer to UMMC. We first identified 71 patients treated for ATAAD
at UMMC between November 2015 and February 2020 who had thin-slice
(\textless{}2mm) electrocardiogram-gated CTAs of the thoracic aorta
available. To identify controls, we queried our imaging database for
thin-slice ECG-gated CTA of the thoracic aorta conducted for reasons
other than aortic pathology (such as evaluation of suspected pulmonary
embolism). Potential controls were identified (\emph{n} =205).
Propensity score matching was conducted to determine the final study
sample. The propensity score was calculated with a logistic model
including age, sex, race, body surface area (at time of imaging), and
hypertension and matched using a caliper of 0.5 and exact matching on
sex, race, and hypertension. Body surface area was calculated using the
Mosteller Formula. After matching, 67 patients remained in each group
with balance on the factors in the model (Table 1).

\emph{Selection of landmarks}

The ascending thoracic aorta is defined by international guidelines as
``the tubular portion of the ascending aorta beginning at the
sinotubular junction and extending to the brachiocephalic artery
origin''\textsuperscript{6,14}. Study landmarks were selected based on
these guidelines. We considered selecting the aortic valve annulus as
our proximal landmark but decided that the sinotubular junction would be
a more consistently reproducible landmark due to the technical
difficulty involved in orienting the aortic valve cusps to identify the
annulus.

\emph{Image analysis}

Image analysis was conducted according to a standardized protocol. CTA
analysis was conducted by manually demarcating an aortic centerline
extending from the level of the aortic valve anulus through the origin
of the left subclavian artery. Curved planar reformatted images were
generated using the aortic centerline as the reference point (Figure 1).
The sinotubular junction (STJ) and the origin of the innominate artery
(IA) were then identified and labeled (Figure 2). The STJ was defined as
the earliest point that the ascending aorta becomes tube-like. The
origin of the IA was defined as the most proximal point at which the
wall of the IA touches the ascending aorta (rather than at the middle of
the IA lumen). The path length, distance, and tortuosity between the STJ
and IA were recorded. The pulmonary artery bifurcation was identified in
transverse plane and measured at the widest point of both the left and
right branches of the PA (Figure 2). Cross-sectional area, average
diameter, maximum diameter, and minimum diameter were measured at the
levels of the STJ, IA, and PA bifurcation.

\emph{Statistical analysis}

All analyses were conducted with SPSS Statistics, Version 27 (IBM Corp.,
Armonk, NY) and R version 3.6.1 (The R Foundation for Statistical
Computing, Vienna, Austria). Continuous variables are reported as mean ±
standard deviation or median (interquartile range {[}IQR{]}), depending
on normality, and categorical variables are reported as frequency
(percent). Group comparisons were conducted with independent
samples\emph{t} -tests or Mann-Whitney U tests for continuous variables
and Chi-Squared or Fisher's Exact tests for categorical variables, as
appropriate. Wilcoxon signed-rank tests were used to compare related
samples. Spearman correlations were used to compare two continuous
variables. Double-robust linear regression analyses were conducted to
compare cases and controls on the aortic measurement variables with
adjustment for the factors in the propensity score model (age, sex,
race, body surface area, and hypertension) to account for any residual
confounding that may have been present. A subset of 10 patients (5 cases
and 5 controls) were measured by all three personnel who conducted the
image analysis to evaluate inter-rater reliability using intraclass
correlation coefficients (ICC) based on a single-measurement,
absolute-agreement, and 2-way mixed-effects model.

RESULTS

\emph{Demographic differences in aortic dimensions}

In the matched sample (\emph{N} =134), female sex was associated with
lower values on all measurements. Age was not associated with aortic
measurements. Body surface area was associated with greater tortuosity
(\emph{r\textsubscript{s}} =0.26, \emph{P} =0.002) and greater diameter
at the STJ (\emph{r\textsubscript{s}} =0.30, \emph{P} \textless{}0.001)
and PAB (\emph{r\textsubscript{s}} =0.19, \emph{P} =0.029). Hypertension
was associated with greater tortuosity (\emph{P} =0.044). However, all
factors in the propensity score model were well-balanced between the
cases and controls. Across the entire cohort, aortic diameter at PAB was
significantly greater than aortic diameter at STJ (median: 34.6 vs
33.4,\emph{P} \textless{}0.001).

In control patients, age was not associated with aortic measurements,
such as aortic length (\emph{r\textsubscript{s}} =0.05, \emph{P}
=0.674), average aortic diameter at PAB (\emph{r\textsubscript{s}}
=0.24,\emph{P} =0.055), and average aortic diameter at STJ
(\emph{r\textsubscript{s}} =0.12, \emph{P} =0.337). In ATAAD patients,
older age was associated with lower average (\emph{r\textsubscript{s}}
=-0.34, \emph{P} =0.004) and max (\emph{r\textsubscript{s}}
=-0.34\emph{, P} =0.005) aortic diameter at STJ, but not related to
other measurements, such as aortic length (\emph{r\textsubscript{s}}
=0.15, \emph{P} =0.220; Figure 3). In the control group, BSA was not
related to aortic measurements, but in the ATAAD group, greater BSA was
associated with greater tortuosity (\emph{r\textsubscript{s}} =0.30,
\emph{P} =0.015) and greater average aortic diameter at STJ
(\emph{r\textsubscript{s}} =0.43,\emph{P} \textless{}0.001). BSA was not
associated with aortic length in either group (Figure 4). In patients
with ATAAD, hypertension was only associated with greater tortuosity
(1.11 vs 1.08, \emph{P} =0.011) and no measurements were associated with
hypertension within the control patients.

\emph{Differences in aortic dimensions between cases and controls}

The mean AB length was 76.9 ± 15.7 mm (range 36.8 to 115.0 mm) for
patients with ATAAD and was 62.0 ± 10.7 mm (range 34.0 to 87.8 mm) for
control patients, which was a significant difference (\emph{t}
=-6.4,\emph{P} \textless{}0.001; Figure 5A). ATAAD patients had greater
diameter at STJ (median: 41.6 vs 30.2 mm, \emph{z} =7.5,\emph{P}
\textless{}0.001; Figure 5B) and diameter at PAB (median: 42.3 vs 32.2
mm, \emph{z} =6.8, \emph{P} \textless{}0.001; Figure 5C) compared with
controls. There was no difference between ATAAD and control patients in
median tortuosity (1.13 vs 1.11, \emph{z} =1.4,\emph{P} =0.170; Table
2). Multivariable analyses found that aortic length (\selectlanguage{greek}β\selectlanguage{english}=0.48, \emph{P}
\textless{}0.001), aortic diameter at STJ (\selectlanguage{greek}β\selectlanguage{english}=0.62, \emph{P}
\textless{}0.001), and aortic diameter at PAB (\selectlanguage{greek}β\selectlanguage{english}=0.56,\emph{P}
\textless{}0.001) were significantly greater for the ATAAD group
compared with the control group. No difference between cases and
controls was found for tortuosity in the multivariable analysis
(\selectlanguage{greek}β\selectlanguage{english}=0.14,\emph{P} =0.083).

A maximum ascending aortic diameter \textgreater{}5.5 cm (at either the
PAB or STJ) was present in 12 of 67 cases (18\%) and 0 of 67 controls
(\emph{P} \textless{}0.001). A maximum ascending aortic diameter
\textgreater{}5.0 cm (at either the PAB or STJ) was present in 22 of 67
cases (33\%) and 0 of 67 controls (\emph{P} \textless{}0.001).

\emph{Inter-rater reliability}

In the subset of 10 patients used to evaluate inter-rater reliability,
most aortic measurements were found to have acceptable to excellent
inter-rater reliability, including average aortic diameter at PAB
(ICC=0.74, 95\% CI: 0.42--0.92, \emph{P} \textless{}0.001), max aortic
diameter at PAB (ICC=0.93, 95\% CI: 0.70--0.99,\emph{P}
\textless{}0.001), average aortic diameter at STJ (ICC=0.75, 95\% CI:
0.46--0.92, \emph{P} \textless{}0.001), and max aortic diameter at STJ
(ICC=0.71, 95\% CI: 0.49--0.93, \emph{P} \textless{}0.001). Although the
inter-rater reliability was low for tortuosity (ICC=0.36, 95\% CI:
-0.001--0.75, \emph{P} =0.029), this measurement had reduced
variability, which can greatly impact these ICC analyses.

COMMENT

Ascending aortic length was significantly higher among patients who
presented with ATAAD. However, more than 80\% of patients who presented
with ATAAD in this cohort had an aortic diameter less than the cut-off
value for an elective ascending aortic replacement. Assessment of
ascending aortic length may be valuable as a predictive marker for
aortic events.

\emph{Ascending Aortic Length}

Several studies have investigated the relationship between ascending
aortic length and aortic dissection. Dr. Tobias Kruger was among the
first to draw attention to this topic in his paper ``Ascending aortic
elongation and the risk of dissection.'' Kruger et al. retrospectively
studied CTAs of ATAAD patients and compared measurements to CTAs of
healthy controls. They observed that hypertensive patients exhibited
greater aortic diameter and length than non-hypertensive
patients\textsuperscript{11}. However, they concluded that the patients
in their sample with hypertension were significantly older than
non-hypertensive patients, therefore, definitive judgments on the impact
of hypertension on aortic morphology could not be made. In our matched
sample, we determined that hypertension was associated with greater
tortuosity (\emph{P} =0.044), but not with greater aortic length
(\emph{P} =0.266\emph{)} or diameter at the STJ (\emph{P} =0.655) and
PAB (\emph{P} =0.367). Kruger et al. also found that ATAAD patients had
elongated ascending aortas when compared to healthy
controls\textsuperscript{11}. It is important to note that while Kruger
et al. measured two-dimensional projections in the sagittal and frontal
planes, therefore, length measurement values are not directly comparable
with our data.

In 2018, Heuts et al. published a retrospective analysis of aortic
morphometrics in ATAAD and propensity-score matched to healthy controls.
They utilized CT scans to construct and measure a three-dimensional
modelled aortic centerline. The results showed that the ATAAD group had
an almost 1-cm greater average ascending aortic length, even after
adjusting for dissection-induced morphologic changes by reducing length
measurements 10\%\textsuperscript{15}. Our data show the ATAAD group had
a 1.49-cm greater average ascending aortic length without adjusting
length measurements, and a 0.72-cm greater average length when reducing
ATAAD length measurements by 10\%.

More recently, Wu et al. characterized the association between ascending
aortic elongation and aortic adverse events (including aortic
dissection). They utilized gated CT scans and a three-dimensional image
analysis technique to measure the ascending aorta from the aortic
annulus to the origin of the innominate artery. Their analysis showed
that aortic elongation is strongly associated with increased risk for
adverse aortic events---patients with very elongated aortas
(\(\geq\)13 cm) had an almost 5-fold higher average yearly
rate of adverse aortic events when compared with patients with shorter
ascending aortas (\textless{}9 cm)\textsuperscript{16}. The authors
emphasized the importance of two distinct ``hinge points'' in ascending
aortic length that were correlated with increased probability of adverse
aortic events, ultimately proposing an ascending aortic length of 11 cm
(measured from aortic annulus to origin of the IA) as a threshold for
elective aneurysm repair. Our study parameters differed in that we
defined ascending aortic length as the distance from the STJ to the
origin of the innominate. The distance from aortic valve annulus to
sinotubular junction is approximately 2 cm, so we can infer that any
patients in our cohort with an ascending aortic length of 9 cm would
meet or come close to meeting the threshold proposed by Wu et
al.\textsuperscript{17} In our cohort, 13 of 67 cases (19.4\%) and 0 of
67 controls had an ascending aortic length of 9 cm or greater. When
length measurements in ATAAD patients were decreased by 10\% as an
inexact adjustment for dissection-induced morphologic changes (similar
to the Heuts et al. paper), this number falls to just 6 of 67 cases
(9.0\%). As Wu et al. noted, the proposed 11-cm threshold for
intervention is a ``conservative'' threshold, but it may identify
patients who do not meet the diameter-based intervention standard. They
observed that 70.4\% of the patients in their cohort who experienced
dissection at a diameter less than 5.5 cm exhibited an aortic length
greater than 11 cm\textsuperscript{13}. In our cohort, 16\% of the
patients who experienced dissection at a diameter less than 5.5 cm
exhibited an aortic length greater than 9 cm. Of the six patients in our
cohort who were estimated to have an ascending aortic length that would
meet the Wu et al. length-based intervention standard, 5 of the 6
(83.3\%) had a maximum ascending aortic diameter less than 5.5 cm. Out
of 67 cases in our cohort, only 21 patients (31\%) would have met either
the length-based or current diameter-based intervention guidelines based
on unadjusted post-dissection measurements (which are certainly greater
than pre-dissection measurements).

Dissection pathology changes the normal anatomy of the ascending
thoracic aorta. Rylski et al. noted a 5.4\% average increase in
ascending aortic centerline length after aortic dissection even when the
ascending aorta was primarily nondissected, although results were not
statistically significant\textsuperscript{9}. Similarly, Wu et al. found
an average ascending aortic length increase of 2.7\% in 10 patients with
pre-dissection CT scans\textsuperscript{16}. In the absence of a CT scan
conducted immediately prior to dissection, it is impossible to know the
truest pre-dissection dimensions of the ascending thoracic aorta. Given
the incredible obstacles to a prospective study design on this topic, we
believe that an appropriately powered, matched retrospective analysis is
sufficient for drawing some conclusions about ascending aortic length
differences in ATAAD and control patients.

Our findings demonstrate that patients with ATAAD have greater path
length of the thoracic aorta from the STJ to the origin of the IA when
compared to matched controls. The proposed mechanism linking aortic
length to aortic dissection investigates longitudinal forces on the
aortic intima and the effect of aortic lengthening on tissue stress.
Aortic dissections most frequently result in an intimal tear in the
transverse (circumferential) direction, which indicates a pathologic
stress in the longitudinal axis\textsuperscript{18,19}. Tissue
elasticity is critical in the ascending aorta, where pulsatile blood
flow is transformed to a waveform through the damping effect of aortic
distension and recoil. Since aortic elongation results in a loss of
elasticity and a subsequent increase in wall stress on the intima, it
seems likely that the increased degree of longitudinal stress in
elongated aortas predispose patients to aortic
dissection\textsuperscript{11,20,21}. Regardless of the exact tissue
mechanisms that link ascending aortic length and aortic dissection,
establishing that this relationship exists is an important step toward
developing better screening criteria.

\emph{Ascending Aortic Diameter}

Several papers have investigated geometric changes induced by aortic
dissection, mostly focusing on measurements of aortic diameter. In a
multi-center retrospective study, Rylski et al. characterized the
morphologic changes induced by aortic dissection by comparing
pre-dissection CTAs with post-dissection CTAs in 63 non-Marfans,
non-bicuspid aortic valve patients. They determined that aortic
dissection changes aortic geometry, noting significant increases in
diameter, ellipticity, volume, and tortuosity after aortic dissection.
Interestingly, they determined that post-dissection increases in aortic
diameter were most pronounced in the mid-ascending aorta, where average
maximum diameter was 32\% larger after aortic
dissection\textsuperscript{9}. In his study on ascending aortic length,
Wu et al. found 10 patients with pre-dissection CT scans and noted an
average aortic diameter increase of 0.8 cm\textsuperscript{13}.
Therefore, it is not surprising that in our study ATAAD patients had
significantly greater ascending aortic diameter compared with controls.
We evaluated diameter at the STJ and PAB and found that the diameter of
the ascending aorta was greater at the PAB. Additionally, we found that
a cutoff of 5.5 cm diameter at either site along the ascending aorta was
highly specific for ATAAD and was not present in any of the controls.
However, only 18\% of cases had a maximum ascending aortic diameter
\textgreater{}5.5 cm, which further reinforces the need for more
sensitive screening criteria.

\emph{Ascending Aortic Tortuosity}

Tortuosity is the ratio of path length to linear distance between two
endpoints (in this case, the centerline endpoints at the STJ and IA).
This measure may be of some clinical significance in understanding the
natural history and pathophysiology of connective tissue disease and
aortic dissection. However, in our study we did not appreciate any
significant differences between the case and control groups.

\emph{Limitations}

This is a retrospectively designed study and is therefore prone to bias.
We attempted to reduce bias by matching based on age, sex, race, body
surface area, and hypertension. We also found no significant difference
between cases and controls in many relevant areas, including smoking
status (\emph{P} =0.121), connective tissue disease (\emph{P} =0.619),
and bicuspid aortic valve (\emph{P} \textgreater{}0.999). However, the
two groups were not entirely similar, as there was a significantly
greater prevalence of both diabetes and active malignancy in the control
group. In a sensitivity analyses, adjusting for these two variables did
not eliminate any of the significant effects we reported.

Blinding the researchers to case/control status was impractical since
dissection pathology was obviously apparent in image analysis. In some
cases, the dissection pathology contributed to greater difficulty in
identifying landmarks and conducting measurements. This was particularly
problematic in cases where root dilation resulted in an ambiguous STJ,
which was noted in seven cases (10.4\%). However, we did not eliminate
these cases from analysis because it would complicate the case-control
matching process and likely introduce a selection bias.

The major limitation of this study is the effect of dissection pathology
on aortic length. Pre-dissection CT scans were not available for
patients in our study, thus, it should be understood that the
measurements reported here likely differ from the actual pre-dissection
values.

\emph{Conclusion}

The central finding of this study is that ascending aortic length is
significantly greater in patients who experienced thoracic aortic
dissection compared to matched controls. This observation supports the
hypothesis that elongation of the aorta contributes to the pathogenesis
of thoracic aortic dissection. Therefore, measurement of the ascending
aortic length may be a useful tool for identifying patients at high risk
of aortic dissection.

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\textbf{Table 1.} Patient Characteristics\selectlanguage{english}
\begin{longtable}[]{@{}llll@{}}
\toprule
& \textbf{Controls (\emph{n}=67)} & \textbf{Cases (\emph{n}=67)} &
\emph{P} \textbf{value}\tabularnewline
\midrule
\endhead
Age & 63 (55--71) & 60 (50--72) & 0.892\tabularnewline
Female & 25 (37) & 25 (37) & \textgreater{}0.999\tabularnewline
Race & & & \textgreater{}0.999\tabularnewline
White & 26 (39) & 26 (39) &\tabularnewline
Black & 34 (51) & 34 (51) &\tabularnewline
Asian & 3 (5) & 3 (5) &\tabularnewline
Other & 4 (6) & 4 (6) &\tabularnewline
Body surface area & 2.0 (1.8--2.1) & 2.0 (1.8--2.2) &
0.340\tabularnewline
\emph{MEDICAL HISTORY} & & &\tabularnewline
Diabetes & 22 (33) & 8 (12) & 0.004\tabularnewline
Hypertension & 60 (90) & 60 (90) & \textgreater{}0.999\tabularnewline
Chronic pulmonary disease & 12 (18) & 10 (15) & 0.641\tabularnewline
Chronic liver disease & 1 (2) & 2 (3) &
\textgreater{}0.999\tabularnewline
Peripheral artery disease & 0 & 1 (2) &
\textgreater{}0.999\tabularnewline
Previous stroke & 6 (9) & 4 (6) & 0.511\tabularnewline
Active malignancy & 14 (21) & 3 (5) & 0.004\tabularnewline
Past malignancy & 1 (2) & 3 (5) & 0.619\tabularnewline
Connective tissue disease & 1 (2) & 3 (5) & 0.619\tabularnewline
Smoking status & & {[}\emph{n}=61{]} & 0.121\tabularnewline
Current/former smoker & 41 (61) & 29 (48) &\tabularnewline
Never smoker & 26 (39) & 32 (53) &\tabularnewline
\emph{CARDIAC HISTORY} & & &\tabularnewline
Arrhythmia & 6 (9) & 5 (8) & 0.753\tabularnewline
Aortic aneurysm & 2 (3) & 7 (10) & 0.165\tabularnewline
Prior endovascular cardiac procedure & 0 & 5 (8) & 0.058\tabularnewline
Prior open cardiac surgery & 4 (6) & 6 (9) & 0.511\tabularnewline
Coronary artery disease & 12 (18) & 6 (9) & 0.129\tabularnewline
Valvular disease & 6 (9) & 5 (8) & 0.753\tabularnewline
Mitral regurgitation & 3 (5) & 1 (2) & 0.619\tabularnewline
Aortic regurgitation & 0 & 2 (3) & 0.496\tabularnewline
Aortic stenosis & 3 (5) & 2 (3) & \textgreater{}0.999\tabularnewline
Pacemaker/implantable cardioverter defibrillator & 3 (5) & 2 (3) &
\textgreater{}0.999\tabularnewline
Bovine arch & 0 & 2 (3) & 0.496\tabularnewline
Bicuspid aortic valve & 2 (3) & 2 (3) &
\textgreater{}0.999\tabularnewline
\bottomrule
\end{longtable}

\textbf{Table 2.} Aortic Measurements\selectlanguage{english}
\begin{longtable}[]{@{}llll@{}}
\toprule
& \textbf{Controls (\emph{n}=67)} & \textbf{Cases (\emph{n}=67)} &
\emph{P} \textbf{value}\tabularnewline
\midrule
\endhead
AB path length & 62.0 \selectlanguage{ngerman}± 10.7 & 76.9 \selectlanguage{ngerman}± 15.7 &
\textless{}0.001\tabularnewline
Tortuosity & 1.11 (1.08--1.15) & 1.13 (1.09--1.17) &
0.170\tabularnewline
Average aortic diameter at PAB & 32.2 (30.2--34.5) & 42.3 (35.8--46.7) &
\textless{}0.001\tabularnewline
Average aortic diameter at STJ & 30.2 (27.9--33.1) & 41.6 (34.7--47.2) &
\textless{}0.001\tabularnewline
\bottomrule
\end{longtable}

Data presented as mean \selectlanguage{ngerman}± SD or median (IQR) Abbreviations: PAB,
pulmonary artery bifurcation; STJ, sinotubular junction.

\textbf{Figures}

Figure 1a\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

Figure 1b\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

Figure 1c\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

Figure 1d\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image4/image4}

\end{center}
\end{figure}

Figure 2a\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image5/image5}

\end{center}
\end{figure}

Figure 2b\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image6/image6}

\end{center}
\end{figure}

Figure 2c\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image7/image7}

\end{center}
\end{figure}

Figure 2d\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image8/image8}

\end{center}
\end{figure}

Figure 2e\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image9/image9}

\end{center}
\end{figure}

Figure 3\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image10/image10}

\end{center}
\end{figure}

Figure 4\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image11/image11}

\end{center}
\end{figure}

Figure 5a\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image12/image12}

\end{center}
\end{figure}

Figure 5b\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image13/image13}

\end{center}
\end{figure}

Figure 5c\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image14/image14}

\end{center}
\end{figure}

\textbf{Figure Legends}

Figure 1. Aortic centerline creation in TeraRecon: (A) Aortic centerline
points (sagittal plane), (B) Aortic centerline points (transverse
plane), (C \& D) CPR-generated aortic centerline and manual correction
of a misaligned point.

Figure 2. TeraRecon image captures illustrating: (A) Centerline
extending from the Aortic valve beyond the origin of the innominate
artery, (B) STJ and IA labeled, (C) Cross-section of the PA bifurcation,
(D) Cross-section of the Aorta at the origin of the innominate, and (E)
Cross-section of the aorta at the level of the STJ.

Figure 3. Scatterplot of age and aortic length separated by ATAAD and
control patients.

Figure 4. Scatterplot of BSA and aortic length separated by ATAAD and
control patients.

Figure 5. Histograms demonstrating the distribution of (A) aortic
length, (B) aortic diameter at STJ, and (C) aortic diameter at PAB for
the ATAAD and control groups.

\selectlanguage{english}
\FloatBarrier
\end{document}

