122 AJTCCM VOL. 29 NO. 3 2023
RESEARCH
Background. Pulmonary hypertension (PH) aer tuberculosis (TB) is typically not included among the chronic lung diseases causing PH
(group 3 PH), with few data available to support the inclusion.
Objectives. To determine the prevalence of PH in an adult population completing TB treatment.
Methods. is single-centre, cross-sectional study only included patients with their rst documented episode of TB, and who were in the
second half of treatment or had recently completed treatment. PH was assessed using transthoracic echocardiography. Questionnaires were
completed, and spirometry and a 6-minute walk test were performed.
Results. One hundred patients were enrolled, with a mean age of 37.1 years, of whom 58% were male and 46% HIV positive. e median
time since initiation of TB treatment was 22 weeks. e mean (standard deviation) measured right ventricular systolic pressure (RVSP)
was 23.6 (6.24) mmHg. One participant had PH (dened as RVSP ≥40 mmHg; 95% condence interval (CI) 0.0 - 3.0) and a further 3 had
possible PH (RVSP ≥35 and <40 mmHg), with a combined PH prevalence of 4% (95% CI 0.2 - 7.8). Airow obstruction on spirometry was
found in 13.3% of 98 patients, while 25.5% had a reduced forced vital capacity. ere was no association between RVSP or PH/possible PH
and sex, age, HIV status, systemic hypertension, spirometry measurements or 6-minute walking distance. Smoking status was associated
with RVSP, but not with the presence of PH/possible PH.
Conclusion. ere was a signicant prevalence of PH in this preliminary study of predominantly young patients completing treatment for
a rst episode of TB. Larger and more detailed studies are warranted.
Keywords. Post-tuberculosis, pulmonary hypertension, echocardiography, tuberculosis, cor pulmonale.
Afr J Thoracic Crit Care Med 2023;29(3):e676. https://doi.org/10.7196/AJTCCM.2023.v29i3.676
Pulmonary hypertension in adults completing
tuberculosistreatment
B W Allwood,1 MB BCh, FCP (SA), MPH, Cert Pulmonology (SA) Phys, PhD ; S Manie,2 BSc, MSc, PhD ;
M Stolbrink,1,3 BM BCh, MSc, MA, DTM&H ; L Hunter,4 MB ChB, PhD ; S Matthee,5 BSc (Med), MB ChB, MMed (Fam Med);
G Meintjes,6 MB ChB, FCP (SA), FRCP, MPH, PhD ; S L Amosun,2 PhD, PGDip ;
A Pecoraro,4 MB ChB, MMed (Int Med), FCP (SA), Cert Cardiology (SA), PhD ;
G Walzl,7 MB ChB, MMed (Int Med), FCP (SA), PhD ; E Irusen,1 MB ChB, FCP (SA), PhD, FCCP
1 Division of Pulmonology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University and Tygerberg Hospital, Cape Town,
SouthAfrica
2 Department of Health and Rehabilitation Sciences, Faculty of Health Sciences, University of Cape Town, South Africa
3 Clinical Sciences, Liverpool School of Tropical Medicine, Liverpool, UK
4 Division of Cardiology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University and Tygerberg Hospital, Cape Town,
SouthAfrica
5 Site B Khayelitsha Community Health Centre, Western Cape Department of Health, Cape Town, South Africa
6 Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa; Wellcome Centre for Infectious Diseases Research in Africa,
Institute f Infectious Disease and Molecular Medicine, University of Cape Town, South Africa
7 DST-NRF Centre of Excellence for Biomedical Tuberculosis Research and South African Medical Research Council Centre for Tuberculosis Research, Division
of Molecular Biology and Human Genetics, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town,
SouthAfrica
Corresponding author: B W Allwood (brianallwood@sun.ac.za)
Study synopsis
What the study adds. Of 100 adult patients with their rst episode of tuberculosis (TB) who underwent echocardiograms near the end of
treatment completion to determine the prevalence of pulmonary hypertension (PH), 1 (1%) had PH and a further 3 (3%) had possible PH.
ere was no association between sex, age, HIV status, lung function or 6-minute walking distance and the presence of PH. e study adds
to the growing awareness of the association of TB with pulmonary vascular disease. It shows that even in a young population with a rst
episode of TB treated in an ambulatory setting, there is a signicant prevalence of PH on treatment completion.
Implications of the ndings. Given that 10.6 million people acquire TB annually, the absolute global burden of cases with PH is likely to
be high, but is underappreciated to date. Further work is urgently needed in this eld.
AJTCCM VOL. 29 NO. 3 2023 123
RESEARCH
Pulmonary hypertension (PH), now dened as a mean pulmonary
artery pressure (PAP) >20 mmHg, is estimated to aect ~1% of the
global population.[1] PH occurring in the context of chronic lung
diseases (CLDs) is classied as group 3 PH or CLD-associated PH
(CLD-PH), and is the second most common cause of PH aer le
heart disease, accounting for ~8% of all PH cases.[2,3] e most recent
guidelines cite chronic obstructive pulmonary disease (COPD) and
interstitial lung disease (ILD) as common causes of CLD-PH, yet omit
post-tuberculosis (TB) lung disease as a cause.[1,2,4]
ere are an estimated 155 million survivors of TB alive today,[5]
mainly living in low- and middle-income countries, and pulmonary
vascular complications aer TB have been named as one of the post-
TB clinical syndromes.[6] However, very little is known about PH
either occurring during active TB or developing aer TB treatment
completion, and the pathogenesis thereof. e development of right
ventricular (RV) failure following TB was documented in the 1950s,
yet disappeared from the literature for almost 5 decades.[7,8] More
recently, a study from China estimated that 39% of CLD-PH cases
could be attributed to previous TB,[9] and it has been our anecdotal
clinical experience that the majority of cases of CLD-PH in South
Africa (SA) are due to previous TB.[10] One study described elevated
PAP in 9.5% of 777 recently diagnosed hospitalised patients with
pulmonary TB,[11] and another found PH in 72 of 76 post-TB patients
who presented with chronic symptoms.[12] However, both studies
had signicant selection bias, thereby limiting extrapolation of the
ndings to TB patients in general.
Raised PAP in the context of other CLD (e.g. COPD and ILD)
heralds a poor prognosis, prompting a shift in the PH literature
towards early diagnosis of CLD-PH.[2] Whether this poor prognosis
is true of post-TB PH is not known. However, limited data suggest
that this may indeed be the case, with a small single-centre study
concluding that the median survival following an episode of TB was
10 months, if the echocardiographic estimates of PAP were raised.[13]
Previous TB may yet prove to be one of the most important causes
of CLD-PH globally, given the high burden of TB in low- and middle-
income countries, but many important questions remain unanswered.
The aim of this study was to determine the prevalence of PH,
assessed using echocardiography, in an adult population completing
ambulatory TB treatment, and to assess associated risk factors.
Methods
is was a single-centre, cross-sectional study of adults attending
an outpatient community TB clinic in Khayelitsha, Cape Town, SA.
All participants were at least 18 years old and had their rst episode
of microbiologically conrmed pulmonary TB. ey attended for a
single study visit near treatment completion, aer at least 5 months
of anti-TB therapy and not longer than 3 months aer treatment
cessation. Patients were excluded if they had any known pre-existing
heart disease.
e primary outcome was the presence of PH on echocardiography.
The secondary outcomes were the association of PH with
spirometric measurements, 6-minute walking distance (6MWD) and
comorbidities.
All participants completed symptom questionnaires, did a 6-minute
walk test and underwent spirometry according to the American oracic
Society/European Respiratory Society guideline.[14] Transthoracic
echocardiograms were conducted by a single trained echocardiographer
and reviewed by a single cardiology consultant following the British
Society of Transthoracic Echocardiography guideline.[15] e RV systolic
pressure (RVSP) was estimated using the maximum velocity (Vmax)
of tricuspid regurgitation (TR) and applying the modied Bernoulli
equation to determine the pressure dierence between the right-sided
chambers and adding the estimated right atrial pressure (RAP). e
RAP was estimated using the diameter changes of the inferior vena
cava during sning.[15] e tricuspid annular plane systolic excursion
(TAPSE) and RV wall motion were recorded. PH was diagnosed if
the RVSP was ≥40 mmHg in the absence of RV outow obstruction
(including pulmonary stenosis), and when the other features
suggesting PH were present (reduced TAPSE, RV dilation, septal wall
motion abnormality). ‘Possible PH’ was dened as an RVSP ≥35 and
<40mmHg. An RVSP <35 mmHg was considered normal. In patients
without TR, pulmonary regurgitation (PR) was used to estimated RVSP.
In the absence of both TR and PR, the RVSP was considered normal if
the RAP was not elevated, the right atrium was not dilated and the RV
Tei index was <0.4.
Sample size calculations estimated that 42 participants were
required to detect a 10% proportion of participants with PH with
a power of 0.9 and a significance level of 0.05 on a presumed
population prevalence of 1%. To detect a prevalence <10%, we
aimed to recruit 100 participants. Statistical analysis was performed
for the outcome variables (RVSP and presence of PH and possible
PH) using standard parametric and non-parametric measures of
comparison. Fisher’s exact test was used to explore the eect of
predictor variables on the presence of denite and possible PH.
Associations of echocardiography ndings and predictor variables
were initially assessed visually and then by median regression
analysis. Signicance was determined at a p-value <0.05. Analysis
was conducted using Stata 15 (2017) (StataCorp, USA).
Ethical approval to conduct the study was obtained from the
Stellenbosch University Human Ethics Research Committee (ref. no.
N16/01/11). All participants provided written informed consent.
Results
Demographics
A total of 100 patients were recruited between April and November
2016. e mean age was 37.1 years (range 18 - 73), and 58% were male;
46% were HIV positive, with a median (interquartile range) CD4
count of 142 (56 - 253) cells/µL for the 30 participants whose count
was known. e time from initiation of TB treatment to recruitment
was a median of 22 weeks (14 - 37 weeks minimum to maximum). All
the participants were black Africans. Two participants had systemic
hypertension and one had diabetes, no participant reported a history
of underlying heart disease or venous thromboembolism, and 54% of
participants were never smokers (Table1).
Echocardiography results
It was possible to estimate the RVSP in 72 participants. e remainder
did not have a TR or PR jet, and the RVSP was assumed to be normal.
e mean (standard deviation (SD)) RVSP was 23.6 (6.24) mmHg.
RAP was estimated in 99 participants: in 92 (92.9%) it was <5 mmHg,
in 5 (5.1%) 5 - 10 mmHg, and in 2 (2.0%) >10 mmHg. TAPSE of
<17mm was found in 3 of 98 participants (3.1%) (Fig.1).
124 AJTCCM VOL. 29 NO. 3 2023
RESEARCH
One participant was found to have PH,
with an estimated RVSP of ≥40mmHg (95%
confidence interval (CI) 0.0 - 3.0), while a
further 3 had possible PH with an estimated
RVSP between ≥35 and <40mmHg, giving
a combined PH prevalence (possible and
probable) of 4% (95% CI 0.2 - 7.8). One of
the participants with possible PH was found
to have a restrictive muscular ventriculoseptal
defect, and a second a secundum atrioseptal
defect without haemodynamic eect.
Additional unexpected echocardiography
findings were concentric left ventricular
hypertrophy secondary to hypertension (n=1
participant) and a congenital abnormality of
the mitral and aortic valves (n=1).
Spirometry and 6MWD results
Acceptable spirometry was performed by
98patients. e mean (SD) forced expiratory
volume in 1 second (FEV1) and forced vital
capacity (FVC) were 87.8% (20.8%) predicted
and 93.4% (18.9%) predicted, respectively.
e mean (SD) FEV1/FVC ratio was 78.5 (9.3).
irteen participants (13.3%) had an FEV1/
FVC ratio <0.7 and would be considered to
have airow obstruction, while 29 (29.6%)
and 4 (4.1%) had an FEV1 <80% predicted
and <50% predicted, respectively. A reduced
FVC (<80% predicted) was found in 25
(25.5%) participants, with 4 (4.1%) having an
FVC <60% predicted. e mean (SD) 6MWD
was 499.5 (97.4) m for the 96participants
who completed the test (Table2).
Univariate and multivariate
analysis
There were no associations between the
presence of PH or possible PH and sex,
age, smoking status, HIV status or systemic
hypertension (p>0.05 for all) (Supplementary
Table 1, available online at https://www.
samedical.org/file/2067). Multivariate
regression was therefore not undertaken.
ere was no association visually between
RVSP and time since initiating TB treatment,
sex, age, BMI, 6MWD or lung function
parameters (Supplementary Fig.1, https://
www.samedical.org/file/2067). Visual
analysis revealed that ever smoking may
have inuenced RVSP (Supplementary Fig.2,
https://www.samedical.org/le/2067). Owing
to the skewed data, median regression was
used. irty participants had missing values
on some of the covariates. In the developed
model, ever smoking was statistically
Table1. Demographics and clinical characteristics of the study participants (N=100)
Variabl e n (%)*
Age (years), mean (SD) 37.1 (12.4)
Male sex 58 (58)
Black African 100 (100)
Comorbidities
HIV
Negative 53 (53)
Unknown 1 (1)
Positive 46 (46)
On ART 46
CD4 count known 30
Nadir CD4 count (cells/µL), median (IQR) 142 (56 - 253)
Hypertension 2 (2)
Diabetes mellitus 1 (1)
Previous venous thromboembolism 0
Known heart disease†0
Previous episode of TB†0
BMI (kg/m2), mean (SD) 24.3 (5.2)
Smoking status
Never 54 (54)
Ex-smoker 31 (31)
Current 15 (15)
SD = standard deviation; ART = antiretroviral therapy; IQR = interquartile range;
TB = tuberculosis.
*Except where otherwise indicated.
†An exclusion criterion.
Patients undergoing echocardiography,
N=100
RAP estimated,
n=99
TAPSE measured,
n=98
≥17 mm,
n=95 (96.9%)
<17 mm,
n=3 (3.1%)
TR jet measured,
n=100
Present,
n=72 (72%)
Not present,
n=28 (28%)
Possible PH,
n=3
PH,
n=1
5 - 10 mmHg,
n=5 (5.1%)
>10 mmHg,
n=2 (2.0%)
<5 mmHg,
n=92 (92.9%)
Fig.1. Overview of echocardiography ndings (N=100). (TR = tricuspid regurgitation; TAPSE
= tricuspid annular plane systolic excursion; PH = pulmonary hypertension; RAP = right atrial
pressure.)
AJTCCM VOL. 29 NO. 3 2023 125
RESEARCH
signicantly associated with RVSP (coecient 4.14; 95% CI 0.39 -
7.90) when adjusted for age, time since initiating of TB treatment,
percentage of predicted FEV1, percentage of predicted FVC, and body
mass index (Table3).
Discussion
e prevalence of PH in 100 patients who were currently receiving
or had recently completed TB treatment was signicant (1 conrmed
and 3 possible cases) aer a median of 22 weeks of treatment. Almost
half of the patients were HIV positive (n=46), and 46 were current
or ex-smokers. Other comorbidities were rare. Pulmonary function
was generally preserved in this group, with the mean FEV1 and FVC
percentage of predicted being 88% and 93%, respectively. ere were
no associations between estimated pulmonary pressures (RVSP) or
PH/possible PH and sex, age, BMI, 6MWD or lung function, although
smoking status was signicantly associated with RVSP.
ese ndings dier from two previous studies, where PH was
present in from 10% up to 95% of TB patients,[11,12] and our clinical
experience, where anecdotally the prevalence of PH aer TB is high.
However, the study from Iran[11] had a high prevalence of participants
with opium addiction (18.7%), and both this and the study from
India[12] suered from signicant selection bias. e prevalence of
PH in the present study is particularly interesting given the high
proportion of patients with HIV. HIV is a well described cause of
group 1 PH (pulmonary arterial hypertension), with a cross-sectional
study from a referral HIV centre in Ethiopia estimating the prevalence
of PH to be 14%,[16] yet in our study the prevalence of PH was lower,
and showed no associations with HIV status.
On face value, our findings support the possibility that the
prevalence of PH may have been overestimated in previous studies
for the majority of ambulatory patients with TB. However, when
extrapolating from both the local and global incidence of TB, even this
lower-than-expected prevalence rate may suggest impressive numbers
of new cases of PH. is is supported by the nding that in 39% of
patients with CLD-PH from China, TB was named as the cause.[9] It is
plausible that this study, and our own clinical experience, may reect
referral bias. However, it is also possible that the development of PH
may be delayed until long aer completion of TB treatment and was
therefore not detected by our study design. Certainly, we know that
in a proportion of patients, lung function changes evolve during the
year aer treatment completion.[17] For example, 1 year aer treatment
completion, 1 in 5 of 305 patients in Malawi demonstrated a decline in
FEV1, and 1 in 3 reported residual symptoms.[18] Although our study
showed no association between time since initiation of treatment and
pulmonary pressures, it is possible that this time interval would be
too short to detect these changes. Another SA study of 20 patients,
evaluated at a median of 30 months aer TB diagnosis, demonstrated
declining TAPSE and RV function with increased time from diagnosis,
supporting the hypothesis that PH may evolve with increasing time
following TB treatment completion.[19]
It is also possible that co-factors may increase the likelihood of PH
aer TB. We demonstrated a signicant association between smoking
status and RVSP, but not PH. Given that PH may evolve over time,
and that PAP is a continuous variable, this nding should be explored
further. e contribution of smoking to PH in the context of COPD
is poorly understood, but may be related to vascular dysfunction.[20,21]
In contrast, however, the previously mentioned Iranian study found
no signicant dierence in smoking status between those with PH
and those without.[11] Further work is needed to determine whether
smoking is indeed an independent risk factor or eect modier in the
context of TB.
We excluded patients with previous TB, which may be an important
risk factor for the development of PH. Certainly, recurrent TB is an
important risk factor for post-TB lung disease.[22] e importance of
signicant structural lung damage in the development of PH aer
TB is not yet known, but was suggested by Ahmed etal.,[23] who
found abnormal chest radiographs in all of 14 patients with PH and
previously treated TB, implying that signicant structural diseases
may be a prerequisite for subsequent development of PH.
Our study benefited from the recruitment of a patient cohort
who were currently completing or had completed ambulatory
TB treatment, which was representative of the local TB patient
population, with a high prevalence of HIV and few comorbidities. By
only including participants with their rst episode of TB, the possible
eects of previous TB were minimised. Other common causes of PH
were excluded; however, radiographic imaging was not included as
part of this study.
Table2. Spirometry and 6MWD results (N=98)
Variabl e n (%)*
FEV1 (L), mean (SD) 2.46 (0.70)
FEV1 (% predicted), mean (SD) 87.8 (20.8)
FEV1 <80% predicted 29 (29.6)
FEV1 <50% predicted 4 (4.1)
FVC (L), mean (SD) 3.14 (0.80)
FVC (% predicted), mean (SD) 93.4 (18.9)
FVC <80% predicted 25 (25.5)
FVC <60% predicted 4 (4.1)
FEV1/FVC ratio, mean (SD) 78.5 (9.3)
FEV1/FVC <0.7 13 (13.3)
6MWD (m), mean (SD) 499.5 (97.4)
Missing 2 (2.0)
6MWD = 6-minute walking distance; FEV1 = forced expiratory volume in 1 second;
SD = standard deviation; FVC = forced vital capacity.
*Except where otherwise indicated.
Table3. Results of median regression for predictor variables
associated with RVSP
Variabl e
Adjusted coecient estimate
(95% CI) p-value
Ever smoker 4.14 (0.39 - 7.90) 0.03*
Age 0.09 (–0.03 - 0.22) 0.15
Time since TB
treatment initiation
0.04 (–0.01 - 0.09) 0.10
Female sex 0.61 (–3.21 - 4.43) 0.75
FVC (% predicted) –0.04 (–0.22 - 0.15) 0.71
FEV1 (% predicted) 0.04 (–0.15 - 0.22) 0.69
BMI 0.27 (–0.08 - 0.61) 0.13
RVSP = right ventricular systolic pressure; CI = condence interval; TB = tuberculosis;
FVC = forced vital capacity; FEV1 = forced expiratory volume in 1 second;
BMI = body mass index.
*Signicant result (p<0.05).
126 AJTCCM VOL. 29 NO. 3 2023
RESEARCH
e study was limited by being a single-centre study with a small
sample size and a small number of identied PH cases, although
the calculated sample size was exceeded. We estimated pulmonary
pressures using echocardiography, which is an eective tool for this
purpose; however, we did not perform the gold-standard right heart
catheterisation, and our estimates may have been inuenced by the
well-described measurement errors of echocardiography.[24] To limit
some of these errors, including between-operator variability, a single
echocardiographer performed all scans in this study. It is, however,
also possible that our study suffered from random or unknown
selection biases, for example with more symptomatic patients less
likely to agree to participate.
e prevalence of PH in our study ndings must also be interpreted
against the prevalence of other causes of PH, where the prevalence
of group 1 PH (pulmonary arterial hypertension) is estimated at
48- 55 cases per million population (~0.005%), while for advanced
COPD with chronic respiratory failure or referred for transplant,
PH is reported in between 1% and 5% of cases, similar rates to our
young population.[4] ese prevalence data suggest that a gure of
~4% for individuals newly ill with TB is not insubstantial. To date
there have been no prospective studies on the long-term eects of
TB causing PH in high-prevalence settings. It is therefore important
to replicate this study in other high-prevalence settings and develop
prospective cohorts to study the progression of post-TB lung, PH
and other cardiovascular diseases over time following completion of
TBtreatment.
Conclusion
In this preliminary study that recruited a young population completing
treatment for the rst episode of TB with a high HIV co-infection rate,
there was a signicant prevalence of PH, which must be interpreted
against the backdrop of the very high TB burden in southern Africa
(meaning that the absolute burden of cases with PH is likely to be
high). Further work to conrm these ndings in other populations is
needed, as well as prospective cohort studies to assess the evolution
of PH over time aer TB treatment, and potential inuences of other
factors, most importantly smoking and recurrent TB.
Declaration. BWA and EI are members of the editorial board.
Acknowledgements. We would like to thank the patients and sta at
Site B Khayelitsha Community Health Centre and the study team, who
contributed and made this research possible.
Author contributions. BWA, EI, GW: conceptualised the study. SMan,
SMat, SLA, GM: assisted with patient recruitment, lung function and
other tests, and data quality. LH: performed all echocardiograms. AP:
quality controlled all echocardiograms. MS: data analysis and statistics.
All authors: manuscript preparation.
Funding.is study was funded in part through a GlaxoSmithKline/
South African oracic Society Research Scholarship Award (BA). MS
was funded by a Wellcome Trust Clinical PhD fellowship (grant no.
203919/Z/16/Z). e Wellcome Trust had no role in study design, data
analysis and interpretation or writing of this manuscript. The views
expressed are those of the author(s) and not necessarily those of the
Wellcome Trust.
Conicts of interest.None.
1. Hoeper MM, Humbert M, Souza R, etal. A global view of pulmonary hypertension.
Lancet Respir Med 2016;4(4):306-322. https://doi.org/10.1016/S2213-2600(15)00543-3
2. Nathan SD, Barbera JA, Gaine SP, et al. Pulmonary hypertension in chronic
lung disease and hypoxia. Eur Respir J 2019;53(1):1801914. https://doi.
org/10.1183/13993003.01914-2018
3. Enea I, Ghio S, Bongarzoni A, etal. [Echocardiographic alterations suggestive of
pulmonary hypertension in the Italian ultrasonography laboratories. Epidemiological
data from the INCIPIT study (INCidence of Pulmonary Hypertension in Italian
ulTrasonography laboratories)]. G Ital Cardiol (Rome) 2010;11(5):402-407.
4. Humbert M, Kovacs G, Hoeper MM, etal. 2022 ESC/ERS guidelines for the diagnosis
and treatment of pulmonary hypertension. Eur Heart J 2022;43(38):3618-3731.
https://doi.org/10.1093/eurheartj/ehac237
5. Dodd PJ, Yuen CM, Jayasooriya SM, van der Zalm MM, Seddon JA. Quantifying
the global number of tuberculosis survivors: A modelling study. Lancet Infect Dis
2021;21(7):984-992. https://doi.org/10.1016/S1473-3099(20)30919-1
6. Allwood BW, van der Zalm MM, Amaral AFS, etal. Post-tuberculosis lung health:
Perspectives from the First International Symposium. Int J Tuberc Lung Dis
2020;24(8):820-828. https://doi.org/10.5588/ijtld.20.0067
7. Samuelsson S. Chronic cor pulmonale in pulmonary tuberculosis. Acta Med Scand
1952;142(5):315-324. https://doi.org/10.1111/j.0954-6820.1952.tb13871.x
8. Walzer I, Frost T. Cor pulmonale: A consideration of clinical and autopsy ndings.
Dis Chest 1954;26(2):192-198.
9. Chen Y, Liu C, Lu W, etal. Clinical characteristics and risk factors of pulmonary
hypertension associated with chronic respiratory diseases: A retrospective study.
Jorac Dis 2016;8(3):350-358. https://doi.org/10.21037/jtd.2016.02.58
10. Allwood BW, Maarman GJ, Kyriakakis CG, Doubell AF. Post-pulmonary tuberculosis
complications in South Africa and a potential link with pulmonary hypertension:
Premise for clinical and scientic investigations. S Afr Med J 2018;108(7):529. https://
doi.org/10.7196/SAMJ.2018.v108i7.13359
11. Marjani M, Baghaei P, Malekmohammad M, etal. Eect of pulmonary hypertension
on outcome of pulmonary tuberculosis. Braz J Infect Dis 2014;18(5):487-490. https://
doi.org/10.1016/j.bjid.2014.02.006
12. Akkara AS, Shah AD, Adalja M, Akkara AG, Rathi A, Shah DN. Pulmonary
tuberculosis: e day aer. Int J Tuberc Lung Dis 2013;17(6):810-813. https://doi.
org/10.5588/ijtld.12.0317
13. Vyslouzil Z, Polak J, Widimsky J, Sukova M. Pathogenesis of pulmonary hypertension
in tuberculosis. Czech Med 1980;3(2):123-131.
14. Graham BL, Steenbruggen I, Miller MR, etal. Standardisation of spirometry 2019
update. An ocial American oracic Society and European Respiratory Society
technical statement. Am J Respir Crit Care Med 2019;200(8):e70-e88. https://doi.
org/10.1164/rccm.201908-1590ST
15. Zaidi A, Knight DS, Augustine DX, etal.; British Society for Echocardiography.
Echocardiographic assessment of the right heart in adults: A practical guideline from
the British Society of Echocardiography. Echo Res Pract 2020;7(1):G19-G41. https://
doi.org/10.1530/ERP-19-0051
16. Huluka DK, Mekonnen D, Abebe S, etal. Prevalence and risk factors of pulmonary
hypertension among adult patients with HIV infection in Ethiopia. Pulm Circ
2020;10(4):2045894020971518. https://doi.org/10.1177/2045894020971518
17. Allwood BW, Maasdorp E, Kim GJ, etal. Transition from restrictive to obstructive lung
function impairment during treatment and follow-up of active tuberculosis. Int J Chron
Obstruct Pulmon Dis 2020;15:1039-1047. https://doi.org/10.2147/COPD.S219731
18. Meghji J, Lesosky M, Joekes E, etal. Patient outcomes associated with post-tuberculosis
lung damage in Malawi: A prospective cohort study. orax 2020;75(3):269-278.
https://doi.org/10.1136/thoraxjnl-2019-213808
19. Kalla IS, Miri A, Seedat F. Occult pulmonary arterial hypertension in patients with
previous pulmonary tuberculosis. Afr J orac Crit Care Med 2020;26(4):133-137.
https://doi.org/10.7196/AJTCCM.2020.v26i4.110
20. Keusch S, Hildenbrand FF, Bollmann T, etal. Tobacco smoke exposure in pulmonary
arterial and thromboembolic pulmonary hypertension. Respiration 2014;88(1):38-45.
https://doi.org/10.1159/000359972
21. Huang SK. Knocking out smoking and pulmonary hypertension with a K. Am J Respir
Crit Care Med 2021;203(10):1216-1218. https://doi.org/10.1164/rccm.202011-4121ED
22. Allwood BW, Byrne A, Meghji J, Rachow A, van der Zalm MM, Schoch OD. Post-
tuberculosis lung disease: Clinical review of an under-recognised global challenge.
Respiration 2021;100(8):751-763. https://doi.org/10.1159/000512531
23. Ahmed AEH, Ibrahim AS, Elshae SM. Pulmonary hypertension in patients with
treated pulmonary tuberculosis: Analysis of 14 consecutive cases. Clin Med Insights
Circ Respir Pulm Med 2011;5:1-5. https://doi.org/10.4137/CCRPM.S6437
24. Rich JD, Shah SJ, Swamy RS, Kamp A, Rich S. Inaccuracy of Doppler echocardiographic
estimates of pulmonary artery pressures in patients with pulmonary hypertension:
Implications for clinical practice. Chest 2011;139(5):988-993. https://doi.org/10.1378/
chest.10-1269
Submitted 13 January 2023. Accepted 23 July 2023. Published 19 September 2023.
