Ankylosing spondylitis is a chronic inflammatory
disease that leads to characteristic spinal deformities,
such as flattening of lumbar lordosis and kyphosis,
mainly as a result of axial involvement.[
16] The
inflammatory condition in the thoracic vertebrae and
costovertebral joints gradually leads to fusion and
ossification of the spine, resulting in increased dorsal
kyphosis and thoracic stiffness.[
17] Severe spinal
kyphosis causes fatigue in the diaphragm and other
muscles, intra-abdominal discomfort, and decreased
lung function.[
18] Decreased chest expansion and lung
parenchymal abnormalities are significant factors
linked to pulmonary dysfunction.[
19]
Pulmonary arterial hypertension is more
common in connective tissue autoimmune disorders
such as systemic sclerosis, mixed connective tissue
disease, and Sjögren’s syndrome; however, there
are limited studies on the association between
ankylosing spondylitis and PAH. Inflammation
and interstitial lung disease in connective tissue
diseases are important mechanisms that play a role
in the formation and progression of PAH. The risk
of right heart failure and death is increased in these
patients due to elevated pulmonary artery pressure.
Pulmonary arterial hypertension symptoms in
autoimmune diseases are nonspecific. Clinical
evaluation, physical examination, respiratory
function tests, echocardiographic measurements, and
right heart catheterization are used in the diagnosis
of PAH. In the study conducted by Colalillo et
al.,[20] they reported that decreased TAPSE and TAPSE/systolic pulmonary artery pressure ratio
in echocardiographic measurements in systemic
sclerosis patients had predictive importance for the
diagnosis of PAH and mortality.[21]
Studies have found a higher prevalence of death
from cardiovascular disease in AS patients than the
general population, particularly from congestive
heart failure and ischemic heart disease.[22,23] In
echocardiographic studies in AS, the prevalence of
aortic valve insufficiency and diastolic left ventricular
dysfunction was increased.[23,24] It has been suggested
that the cause of left ventricular dysfunction may be
impaired filling and relaxation of the left ventricle
due to inflammation or fibrosis in the myocardium
due to disease activity in AS patients.[22,23] While
previous studies have examined left ventricular
functions in AS patients, there is limited research
on RV function in this population. In a study
conducted by Karoli et al.,[25] echocardiography
of 56 AS patients revealed PAH in 60.7%, RV
dilatation in 30.4%, RV hypertrophy, and thickening
of the interventricular symptoms in 37.5%. In this
study, they found PAH to be common in AS
patients. These changes were found to be correlated
with thoracic spinal lesions and long disease
duration. In another study on 55 AS patients with
predominant spinal lesions, grade 3 sacroiliitis on
plain radiographs, and long disease duration, PAH,
RV hypertrophy, and RV dilatation were detected
in 70.96%, 47.3%, and 34.5%, respectively.[26] There
are cases in the literature describing the relationship
between AS and PAH.[7,27] In our study, similar to
previous literature, Group 2, which exhibited lower
TAPSE values, had longer disease duration and
higher disease activity scores. The longer duration
of disease in Group 2, in which TAPSE was lower,
may have caused changes in the myocardium over
time. Excessive contraction of the myocardium
may have caused a decrease in myocardial fibers
over time and eventually led to the development of
fibrosis. Myocardial fibrosis may also have caused a
decrease in TAPSE. It has been demonstrated that
RV fibrosis strongly correlates with RV function.[28]
The value of RV fibrosis is still debated. Fibrotic
remodeling may be a protective adaptation to some
extent to preserve ventricular shape and function
against increased pressures.[29] In AS, which is a
chronic inflammatory disease, inflammation can
increase myofibroblast activation, which may result
in fibrosis.[30] Since patients who did not develop pulmonary hypertension were included in this study,
the increased TAPSE in patients with sacroiliitis
might reflect an adaptive change that occurred in
these patients in the early period.
In the lung, AS causes ankylosis in the thoracic
vertebrae, fusion in the costovertebral joints,
sternoclavicular joint, enthesitis in the manubrium,
chest wall restriction, pleural thickening, apical
fibrosis, and chest pain, causing difficulty in
breathing and a decrease in respiratory functions.
Additionally, obstructive sleep apnea syndrome is
increased in these patients compared to the normal
population. Pain in the waist and hips due to
sacroiliitis and lumbar involvement are factors that
affect lumbar flattening and breathing. Due to these
changes, pressure increases in the pulmonary artery
and RV functions are affected.[31] In our study, we
found that TAPSE was increased in the group with
sacroiliitis. It may suggest that there may be an
increase in RV functions in patients with sacroiliitis
to compensate for the decrease in lung capacity
caused by pain or that it may be a finding due to
pericardial involvement.
There are some limitations to this study. This
single-center study involved a relatively small number
of patients, which may limit the applicability of the
results to a broader population. The limitations of
the study include not using additional parameters and
advanced imaging methods to assess the RV structure
and functions in AS patients.
In conclusion, this is the first study to explore the
correlation between sacroiliitis and TAPSE values
in AS patients. This study found an independent
relationship between sacroiliitis and TAPSE in
patients with AS. Changes in cardiac function may
occur in patients with AS without clinically significant
myocardial damage. Transthoracic echocardiography,
which is a noninvasive procedure to detect these
functions at an early stage, can be used more frequently
in daily practice.
Data Sharing Statement: The data that support the
findings of this study are available from the corresponding
author upon reasonable request.
Author Contributions: Development of study concept and
design: O.C.; Acquisition, analysis and interpretation of the
data: E.E., O.C.; Statistical analysis: M.C.; Writing: O.C., K.I.
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.
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