The goal of the present study was to elucidate
the effects of TEVAR-induced aortic stiffening on
LVEF and other cardiac remodeling parameters. It
is known that from the origin of the left subclavian
artery, mobility and compliance decrease towards
the descending aorta and infrarenal aorta. Therefore,
in patients with TAA, cases in which the proximal
landing zone was zone 3 were selected, and this zone was thought to be the most influencing area for aortic
stiffness as it is the closest zone to the aortic arch.
The elastic structure of the aorta plays a critical
role in hemodynamic adaptation.[5] However, the
elastic properties of the aorta diminish with age or the
presence of risk factors, such as smoking, hypertension,
hyperlipidemia, and atherosclerosis. Apart from these
factors, stiffening of the aortic wall after TEVAR due
to the endograft structure affects cardiac remodeling.
Some studies involving animal experiments have
indicated clinical conditions such as tachycardia,
hypertension, and reduced coronary perfusion in the
early period after TEVAR.[9] However, in our patient
group, these clinical findings were not observed in the
early period. No early cardiac or adverse hemodynamic
events were detected in any of the patients. In a
report published by Kreibich et al.,[13] the impact of
TEVAR on cardiac remodeling for aortic aneurysms
was investigated in a cohort of 31 patients, revealing
a decline in biventricular functions. Additionally, the
research highlighted a decrease in TAPSE (tricuspid
annular plane systolic excursion) and LVEF within
the study group. In our study, we evaluated the
left ventricular functions using LVEF measurements,
and similarly, we observed a statistically significant
reduction in LVEF (p=0.01) during the postoperative
follow-up period. Furthermore, a notable increase in
IVS thickness, a parameter utilized for assessing left
ventricular mass (p=0.041), was also evident. This
situation may indicate a subclinical coronary perfusion
reduction that manifested as an effect over time.
Sincos et al.[14] reported in a histologic and
immunohistochemical study the structural deterioration
of the aortic wall after implantation of an endograft,
with decreased amounts of muscle and elastic fibers.
Halloran et al.[15] demonstrated that collagen and elastin
content relative to the luminal surface area decrease with
distance from the heart. Therefore, we may conclude
that TEVAR procedures pose a higher risk of arterial
stiffness compared to infrarenal abdominal aortic cases.
These differences likely affect the compliance and
structural integrity of the aorta.
Not only the decrease of mobility of the aortic
arch but the oversizing of the endograft is one of the
factors influencing the arterial stiffness. In patients
with blunt thoracic aortic injury, particularly those
who are younger and nonatherosclerotic aortas with
smaller diameters, it is recommended that oversizing
should not exceed 10%, as do the type B aortic dissections. Notably, after endovascular repair, there
is an observed loss of elasticity in the aortic wall
regardless of the degree of oversizing. Based on
the best available evidence, the current standard of
10 to 20% of oversizing, depending on the aortic
pathology, appears to be safe and preferable.[16,17]
In 2018, van Bakel et al.[18] examined cardiac
remodeling based on preoperative and postoperative
data of eight patients who underwent TEVAR for
TAAs. A significant increase in left ventricular mass
index due to afterload increase was observed. In
the same study, the preoperative and postoperative
antihypertensive drug regimens of the patients were
evaluated. Prior to TEVAR, 25 patients were receiving
antihypertensive treatment, while after the procedure,
antihypertensive drugs were prescribed to all
31 patients. Patients were administered dual (p=0.75)
or triple (p=0.33) antihypertensive drug therapy after
TEVAR. Beta-blockers and calcium channel blockers
were the most commonly used medications.[18] During
the follow-up, dual antihypertensive medication was
initiated for treatment in our study cohort. Among
those not achieving the target blood pressure range
during follow-ups, triple antihypertensive therapy
was prescribed for eight (25%) patients. In dual
therapy, beta-blockers and angiotensin-converting
enzyme inhibitors/angiotensin receptor blockers
were preferred. For patients requiring triple therapy,
calcium channel blockers were added to the treatment
regimen.
Reducing aortic stiffness will contribute to the
long-term preservation of the left ventricle and
a decrease in hypertensive-related adverse cardiac
effects. With an appropriate antihypertensive
treatment plan aiming to lower afterload, it is
likely that the heart can be protected through
this mechanism in the long term. According to
our research, medical device producers ought to
create more compliant endografts to mitigate the
mismatch between the device and aorta. To further
manage blood pressure following TEVAR, extensive
antihypertensive medication is required.
There are some limitations to this study.
The number of patients included in this study is
relatively small, as the majority of patients who
were treated at our center were excluded. Due to
the retrospective design of the study, we could only
compare routine measurements, such as LVEF,
LVEDD, and IVS diameter, during preoperative preparation and postoperative follow-up. However,
more valuable parameters, such as left ventricular
mass index, LVPWd (left ventricular posterior wall
end-diastole), and TAPSE, could be investigated to
assess cardiac remodeling. Since echocardiogram
dates were randomly determined, we could not
provide information about the change processes.
However, at the end of the follow-up period, there
was a statistical change in both LVEF and IVS.
In conclusion, endovascular aortic procedures
increase aortic stiffness, while open surgical repair
does not. Therefore, lifelong follow-up should be
mandatory to evaluate the aortic disease progression
or endovascular complications, as well as related
cardiovascular outcomes. For more accurate results,
prospective studies involving large cohorts are
necessary. Despite our evaluation being conducted
in a limited patient population, our findings suggest
that the stiffening of the aortic structure after
TEVAR has a negative impact on cardiac remodeling.
Consequently, it is imperative to explore new and
more flexible designs for thoracic endograft structures.
Careful adjustment of medical treatment may warrant
the addition of medications that reduce afterload for
patients.
Ethics Committee Approval: The study protocol was
approved by the Ankara Bilkent City Hospital Ethics
Committee (date: 01.12.2021, no: E1-21-2184). The study
was conducted in accordance with the principles of the
Declaration of Helsinki.
Patient Consent for Publication: A written informed
consent was obtained from each patient.
Data Sharing Statement: The data that support the
findings of this study are available from the corresponding
author upon reasonable request.
Author Contributions: All authors contributed equally
to the article.
Conflict of Interest: The authors declared no conflicts
of interest with respect to the authorship and/or publication
of this article.
Funding: The authors received no financial support for
the research and/or authorship of this article.