Tuberculosis (TB) is a significant global health concern, causing substantial morbidity and mortality each year^1-2. In 2014, approximately 9.6 million new TB cases were reported globally, with India accounting for the highest burden, contributing an estimated 2.2 million cases. Around 40% of India’s population is believed to harbour latent TB infection. The Revised National Tuberculosis Control Program (RNTCP), which implements the WHO-recommended DOTS strategy, has successfully treated millions of TB patients, achieving a treatment success rate exceeding 85%³.

Patients who have completed a course of treatment for Pulmonary Tuberculosis (PTB) are frequently left with respiratory disability due to impairment in pulmonary function caused primarily by various thoracic sequelae. Some patients experience significant hypoxemia with pulmonary hypertension and ventilatory defects.^4-9 High prevalence of obstructive lung disease is seen in cured pulmonary TB patients. Studies that assessed the impact of treated PTB as a cause of disability have focused on impairment of lung function. A study done by Patil S et.al.¹⁰ concluded that lung function impairment is known to occur post-TB irrespective of duration of treatment and outcome of disease and obstructive lung disease is the predominant lung function impairment in post‑TB cases.¹⁰ It is known that persisting physiological impairment leads to gas exchange abnormalities and development of pulmonary hypertension, which is a cause of severe disability and reduced longevity.^11-14

However, despite these successes, TB treatment often leaves behind pulmonary sequelae, including airway, vascular, and parenchymal damage, leading to chronic complications such as pulmonary hypertension (PH). PH, a condition characterized by a mean pulmonary arterial pressure of more than 25 mm Hg, is associated with significant morbidity. Symptoms such as dyspnoea-, fatigue, and syncope can delay its diagnosis, highlighting the need for effective screening^15-17.

Studies have demonstrated an increased prevalence of obstructive lung diseases and PH among individuals treated for TB. For example, Ahmed et al. observed varying grades of pulmonary artery hypertension in 14 treated TB patients, with most showing elevated pulmonary artery systolic pressures¹⁸. These findings underscore the potential relationship between TB and PH, emphasizing the importance of targeted research to identify risk factors and the incidence of PH among TB survivors. A study done by Bhattacharyya P et al. have shown that a group of 40 patients having PH had history of pulmonary tuberculosis.¹⁹ But this study was not able to signify that pulmonary tuberculosis is a risk factor in causing PH. 

This study aims to investigate the association between treated pulmonary TB and PH, providing valuable insights for early detection and management strategies.

• AIM:
• To estimate incidence of pulmonary arterial hypertension (PAH) in patients treated for pulmonary tuberculosis having residual lesions.
• To assess risk factors of pulmonary arterial hypertension in patients treated for pulmonary tuberculosis having residual lesions.
• OBJECTIVES:
• To study clinical profile of patients treated for pulmonary tuberculosis with residual lesions.
• To find out the impact of smoking on the incidence of PAH in treated patients of pulmonary tuberculosis with residual lesions.

Source of Data Collection:

This observational clinical study was conducted in the Department of Respiratory Medicine at Geetanjali Medical College and Hospital (GMCH), Udaipur, Rajasthan, after obtaining ethical clearance from the Institutional Ethics Committee. A total of 75 patients were enrolled from the Outpatient Department (OPD) and Inpatient Department (IPD) of the Respiratory Medicine Department.

Inclusion Criteria:

1. Patients with a history of treated pulmonary tuberculosis (new or retreatment cases) who had completed the prescribed antitubercular treatment (ATT) regimen at the time of study enrolment.
2. Sputum smear-negative for acid-fast bacilli (AFB) (two samples) at the time of study inclusion.
3. Both male and female patients.
4. Adults aged 18 years and above.

Exclusion Criteria:

1. Patients with active pulmonary tuberculosis and sputum smear-positive status.
2. Pre-diagnosed cases of pulmonary arterial hypertension (PAH).
3. Patients with other cardiovascular conditions that could increase PAH.
4. Paediatric patients (age <18 years).
5. Immunocompromised individuals.

Methodology:
Patients attending the OPD/IPD were screened for eligibility based on the inclusion and exclusion criteria. Eligible participants underwent a detailed clinical evaluation, including symptom assessment, past TB history, smoking history, and prior ATT use. Sputum smear microscopy for AFB (two samples) was performed using Ziehl-Neelsen staining in the Department of Microbiology. Patients with negative sputum results provided written informed consent before study enrollment.

All participants underwent the following investigations:

1. Chest X-ray:
   A posteroanterior (PA) view was performed to identify residual lesions. Observed findings included fibrosis, fibrosis with bronchiectasis, fibro-cavitary lesions, calcified lesions, lymphadenopathy, and pleural thickening.
2. 2D Echocardiography:
   Transthoracic echocardiography was conducted using a Philips HD IE33 (matrix) machine in the Department of Cardiology. Pulmonary hypertension was evaluated by estimating pulmonary artery systolic pressure (PASP) using continuous wave Doppler to measure the tricuspid regurgitation gradient. The simplified Bernoulli equation (PASP = RA/RV PG + right atrial pressure) was used, where RA/RV PG is the right atrium/right ventricle pressure gradient, and right atrial pressure was determined using the inferior vena cava (IVC) collapsibility index. PH was defined as PASP >40 mm Hg.
3. Pulmonary Function Tests (PFT):
   Spirometry was performed using the RMS Helios 401 Spirometer to assess lung function. Tests were conducted before and 15 minutes after inhalation of 200 μg salbutamol, following ATS/ERS task force recommendations. Spirometry results were categorized as follows:
• Normal: FEV1/FVC >70% and FVC >80% predicted.
• Obstructive: FEV1/FVC <70% and FVC >80% predicted.
• Restrictive: FEV1/FVC >70% and FVC <80% predicted.
• Mixed: FEV1/FVC <70% and FVC <80% predicted.

Data Analysis:

Data were analysed using Microsoft Excel and Microsoft Access. Statistical significance was assessed using Chi-square and proportion tests with the assistance of a statistician.

This methodological approach ensured comprehensive evaluation of residual pulmonary complications and the incidence of pulmonary hypertension in treated pulmonary tuberculosis patients.

TABLE 1: Age wise distribution of patients

Majority of patients were in the age group of 51-60 years of age (61.3%). Around 15% were of age 20-30 years and 11% of age group 41-50 years of age.

Mean age of patients was 55.41years with standard deviation of 17.72.

TABLE 2: Gender wise distribution of patients

Out of total 75 patients, majority were Males (68%) followed by 32% Females.

TABLE 3: Distribution of patients according to Clinical Manifestations

Among total 75 patients, 85.33% were found with cough, 82.67% were with Sputum, 80% had complain of shortness of breath and 66.67% with loss of appetite. Whereas only 13.33% had fever and weight loss.

Thus, it was found that majority of patients were having cough, sputum, shortness of breath and loss of appetite.

TABLE 4: Distribution of patients according to history of Smoking

Among total 53.33% were non- smokers and 46.67% were smokers.

Figure 1: Distribution of patients according findings of X-Ray.

It was observed that fibrosis (24%), calcified lesions (22.67%), fibrocavitary (18.67%) and fibrotic bends (10.67%) were most common findings. Other radiological abnormalities were bronchiectasis (6.68%), calcified lymph nodes (2.67%), destroyed lung (2.67%), others (9.33%). Normal chest x-ray was found in 2.67% patients.

FIGURE 2: Distribution of patients according transthoracic echocardiography findings.

Out of 75 patients screened by transthoracic echocardiography, 38 patients (50.67%) had PAH, whereas 37 patients (49.33%) had no PAH. 

FIGURE 3: Distribution of patients according to interpretation of Spirometry

According to Spirometric interpretation, majority of the patients had obstructive pattern (84%), followed by restrictive pattern seen in 6.67% and mixed pattern seen in 2.70%. Normal spirometric interpretation were found in rest of the 6.67% patients.

TABLE 5: Distribution of patients according X-ray Findings and history of smoking.

It has been observed in table 6 that among total 18 (24%) patients having fibrosis on x-ray, 14(10%) were found having past history of smoking with p value of 0.002.  Similarly, smoking history were also commonly found in 5 (14.29%), 5 (14.29%), 3 (8.57%) patients having x-ray finding of fibrocavitary lesion, bronchiectasis, calcified lesions respectively with chi square value= 24.74.  This suggest statistical significance of history of smoking was more common in patients having x-ray finding of fibrosis, followed by fibrocavitary lesion, bronchiectasis, calcified lesions. 

TABLE 6: Distribution of patients according X ray findings and PAH

It has been observed in table 7 that PAH is most commonly found in patients having fibrosis on x-ray, i.e.  out of 75 patients, 11 (28.95%) patients were encountered with x-ray finding of   fibrosis & PAH which is statistically significant with p value of 0.003. similarly, 6 (15.79%), 5(13.16%) patients having x-ray findings of fibrocavitary, bronchiectasis respectively, had PAH with chi square value=16.73. This suggests close relationship of x-ray findings of fibrosis, fibrocavitary & bronchiectasis with PAH.  

TABLE 7: Distribution of patients according to PAH and history of smoking.

It has been observed in table 10 that patients who have history of smoking are more prone to have PAH, i.e. out of 75 patients, 22 (62.86%) patients have history of smoking and PAH as well with p value= 0.04 and chi square value=12.39.

This suggest that there is statistical significance between history of smoking and PAH.

Table 8: Distribution of patients according to interpretation of spirometry and PAH.

It has been observed in table 9 that PAH is most commonly found in patients having obstructive pattern on spirometry, i.e. out of 75 patients, 37 patients were having PAH and obstructive pattern on spirometry. This is statistically significant with p valve= 0.001. Similarly, PAH was also observed in 1 patient having mixed pattern on spirometry with chi square valve= 11.90. This suggest that there is strong association between airflow obstruction on spirometry with PAH.

This study was conducted in the Department of Respiratory Medicine at Geetanjali Medical College and Hospital over 12 months (March 2017 to April 2018). From the 100 patients initially screened, 25 were excluded due to positive sputum AFB smear. The remaining 75 patients underwent demographic and clinical evaluations, including smoking history, chest X-rays, pulmonary function tests (PFTs), and echocardiographic assessments for pulmonary arterial hypertension (PAH). Data were analysed using SPSS software.

Age and sex according distribution is given in table 1 & 2,

The age and sex distribution of the study population is summarized in Tables 1 and 2. Among the 75 patients analysed, the majority (61.3%) were within the age group of 51–80 years, followed by 15% in the 20–30 years range and 11% in the 41–50 years range. The mean age of the participants was 55.41 ± 17.72 years. Regarding gender distribution, 68% of the patients were male, and 32% were female. These findings align closely with those reported by Bhattacharyya P et al.¹⁹ and are comparable to the demographic characteristics observed in the study conducted by Ahmed AE et al.¹⁸ which reported a mean age of 43.7 years.

Distribution of patients according to clinical manifestation are given in table 3,

Among the 75 participants, the majority presented with respiratory symptoms, including cough (n = 64, 85%), sputum expectoration (n = 62, 82%), and breathlessness (n = 60, 80%). Systemic symptoms were less common, with fever (n = 10, 13%) and weight loss (n = 10, 13%) reported infrequently. These observations align closely with findings from the study by S.A. Akkara et al.²⁰, where 85% of patients (n = 224) reported respiratory complaints such as cough, sputum production, or breathlessness, with 42% experiencing fever due to secondary infections. Similarly, N. Singla et al.²¹ identified breathlessness (53%), cough with expectoration (43%), and a combination of cough and breathlessness (31%) as the most common symptoms of post-tubercular sequelae. In their study, 11 out of 51 patients (22%) were asymptomatic.

Further analysis of dyspnoea severity, using the MRC grading scale among 51 patients, revealed Grade 1 dyspnoea in 22%, Grade 2 in 18%, Grade 3 in 14%, and Grade 4 in 9%. No patients were categorized as having Grade 5 dyspnoea.

The Six-Minute Walk Test (6MWT) was completed by 47 patients, while 4 could not participate due to lack of cooperation. The walking distance ranged from 80 to 300 meters, with a mean ± SD distance of 217 ± 51 meters in 27 males and 187 ± 30 meters in 20 females, ranging from 160 to 248 meters.

Distribution of patients according to history of smoking are given in table 4:

Out of 75 patients, 40 (53.33%) were non-smokers, while 35 (46.67%) were smokers. These results are consistent with findings from Ahmed AE et al.^18, who reported that 11 out of 14 patients (79%) were non-smokers. Similarly, Bhattacharyya P et al.¹⁹ observed that 19 out of 40 patients (47.5%) were non-smokers. These observations warrant further correlation with additional variables for a more comprehensive analysis.

Distribution of patients according to x-ray findings are given in Figure 1:

A range of residual lesions and complications were observed in both treated and untreated cases of pulmonary tuberculosis. Chest X-ray (posteroanterior view) was performed on all 75 patients, revealing fibrosis (24%), calcified lesions (22.67%), fibrocavitary lesions (18.67%), and fibrotic bands (10.67%) as the most common findings. Additional radiological abnormalities included bronchiectasis (6.68%), calcified lymph nodes (2.67%), destroyed lung (2.67%), and normal chest X-ray in 2.67% of patients.

These findings align with a study by S. A. Akkara et al.^20, which classified radiological changes using Wilcox grading. In their study, 50% of patients (n = 119) had minimal fibrotic lesions, 38% (n = 100) exhibited involvement of more than two lobes (Wilcox Grade II), and 17% (n = 45) had Grade III chest X-ray changes. Similarly, Bhattacharyya P et al.¹⁹ identified fibrosis as the most prevalent finding, while Ahmed AE et al.¹⁸ reported fibrocavitary lesions as the most frequent abnormality (50%). Menon B et al.²² also observed that fibrosis (38%) was the most common pulmonary lesion in treated cases of pulmonary tuberculosis. These results are consistent with the current study.

Distribution of patients according to transthoracic echocardiographic finding are given in Figure 2:

Pulmonary arterial hypertension (PAH) was evaluated using echocardiography, a reliable non-invasive tool for assessing cardiac status (97). In this study, PAH was identified in 50% of patients.

A study by Bhattacharyya P et al.¹⁹ suggested a potential causal relationship between pulmonary tuberculosis and pulmonary hypertension (PH). Their findings showed that 40 patients diagnosed with PAH had a history of pulmonary tuberculosis. Similarly, Ahmed AE et al.¹⁸ observed varying grades of PAH in their cohort of 14 treated pulmonary tuberculosis patients, with an average follow-up duration of nine years post-cure. Their study reported that 64.3% of patients had an estimated pulmonary artery systolic pressure (PASP) of 51 to 80 mmHg, 28.6% had PASP of 40 to 50 mmHg, and one patient exhibited PASP greater than 80 mmHg.

Additionally, S. A. Akkara et al.²⁰ documented the presence of PAH in treated pulmonary tuberculosis patients. In their study, ECG and 2D echocardiography were performed on 76 patients, primarily those presenting with clinical signs of right-sided heart failure, such as pedal oedema or raised jugular venous pressure. Among these, four patients had normal findings, while the remaining cases displayed tall P waves on ECG and elevated right ventricular systolic pressure (RVSP) exceeding 30 mmHg. These findings are consistent with the observations in this study.

Distribution of patients according to interpretation of spirometry are given in figure 3:

In our study, pulmonary function abnormalities were identified in 93.37% of patients. Among these, the predominant pattern observed was obstructive (84%) on pulmonary function tests (PFT), followed by restrictive (6.67%), and mixed patterns (2.70%), while normal PFTs were noted in 6.67% of patients. Pulmonary function impairments are common among individuals treated for pulmonary tuberculosis (PTB). Previous studies have reported variable patterns and degrees of pulmonary dysfunction post-PTB treatment.

Manji et al.²³ reported abnormal lung function in 74% of cases, while Agarwala et al.²⁴ found that 52.7% of treated PTB patients exhibited an obstructive ventilatory defect. Pasipanodya et al.¹¹ highlighted that 59% of treated TB cases demonstrated impaired pulmonary function, with a significant proportion showing severe dysfunction, indicating that pulmonary impairment is a major sequela of PTB. Anno and Tomashefski et al.²⁵ documented respiratory function impairment in treated PTB patients, noting increased residual volume (RV), a higher RV/total lung capacity ratio, and reduced maximal breathing capacity in a selected group.

Similarly, Giuliani et al.²⁶ observed spirometric abnormalities in 62% of asymptomatic post-TB cases, suggesting that even those without symptoms are at risk of pulmonary function deficits. Snider et al.²⁷ found that restrictive (24%), obstructive (23%), and mixed (19%) dysfunctions were evenly distributed. Manji et al.²³ identified obstructive (42%), restrictive (13%), and mixed (19%) patterns, whereas Pasipanodya et al.¹¹ reported obstructive (15%), restrictive (31%), and mixed (13%) subtypes. Verma et al.²⁸ found restrictive (n=37) and mixed (n=21) patterns in 92 post-tubercular patients.

Other studies, including those by Long et al.²⁹, Willcox and Ferguson et al.⁹, Plit et al.³⁰, and Lee and Chang et al.³¹, reported comparable abnormalities in lung function. Ramos et al.³², Di Naso et al.³³, and N. Singla et al.²¹ attributed the high prevalence of mixed patterns to extensive fibrosis combined with airflow obstruction. Chushkin and Ots et al.³⁴ observed that 50% of treated PTB patients exhibited pulmonary impairments, including obstructive (34.6%), restrictive (8.4%), and mixed (3.7%) patterns.

The PLATINO study¹³, conducted across five Latin American countries, established a link between a history of tuberculosis and airflow obstruction, with a prevalence of 30.7%. Gaensler and Lindgren et al.³⁵ reported airflow obstruction in 61% of cases, while Brashier et al. (128) documented a 46% prevalence of airflow obstruction, which increased with the duration post-treatment. Baig et al.³⁶ found that 55.3% of treated PTB cases had an obstructive ventilatory defect, and Akkara et al.²⁰ reported obstructive airway disease in 86.8% of 257 treated PTB patients. Lastly, Zhou et al.³⁷ noted a 68% prevalence of obstructive disorders in treated TB cases.

Distribution of patients according to X-ray findings with history of smoking are given in table 5: The data presented in Table 5 indicates that among 18 patients (24%) with fibrosis observed on chest X-rays, 14 (10%) had a documented history of smoking, with a statistically significant p-value of 0.002. Similarly, smoking history was prevalent in patients with other radiographic findings, including fibrocavitary lesions (5 patients, 14.29%), bronchiectasis (5 patients, 14.29%), and calcified lesions (3 patients, 8.57%), with a chi-square value of 24.74. These findings highlight a statistically significant association between a history of smoking and the presence of specific chest X-ray abnormalities, particularly fibrosis, followed by fibrocavitary lesions, bronchiectasis, and calcified lesions.

Distribution of patients according to findings of X-ray with PAH are given in table 6:

The data in Table 6 reveals that pulmonary arterial hypertension (PAH) is most frequently associated with chest X-ray findings of fibrosis. Among 75 patients, 11 (28.95%) exhibited fibrosis and PAH, a statistically significant relationship with a p-value of 0.003. Additionally, PAH was observed in 6 patients (15.79%) with fibrocavitary lesions and 5 patients (13.16%) with bronchiectasis, with a chi-square value of 16.73. These results suggest a strong correlation between PAH and specific radiological findings, particularly fibrosis, followed by fibrocavitary lesions and bronchiectasis.

Ahmed AE et al.¹⁸ studied 14 patients treated for pulmonary tuberculosis (PTB) who developed pulmonary hypertension (PHT). All patients were sputum smear-negative at the time of the study. The mean age was 43.1 years, and half were male. Fibrocavitary lesions were the most common radiological abnormality, present in 50% of cases. Pulmonary artery systolic pressure (PASP) ranged from 51–80 mmHg in 64.3% (n=9), 40–50 mmHg in 28.6% (n=4), and >80 mmHg in 1 patient.

Richards and Fishman³⁹ identified several factors contributing to the development of Cor Pulmonale, including:

1. Reduced parenchymal elasticity due to chronic inflammation, impairing gas exchange and pulmonary vascular capacity.
2. Restricted pulmonary vascular bed, limiting its cross-section, extent, and distensibility.
3. Bronchospasm and exudates causing airflow obstruction.

These factors lead to hypoxia and hypercapnia, increasing cardiac output. The less distensible pulmonary vasculature struggles to accommodate the elevated output, resulting in pulmonary hypertension. Concurrent infections exacerbate oxygen demand and alveolar gas exchange impairment, further accentuating these mechanisms.

S.C. Kapoor et al.⁴⁰ observed diffuse fibrosis radiologically in one-third of PTB cases and broncho-stenosis in over half. Jain et al.⁴¹ reported poor arterial oxygen saturation in Cor Pulmonale cases and highlighted that even radiologically clear lungs may harbour small, scattered tubercular lesions. These lesions can lead to widespread pulmonary vascular sclerosis, significantly raising vascular pressure and increasing the incidence of Cor Pulmonale.

It is suggested that modern chemotherapy, while effective against active tuberculosis, contributes to sequelae such as fibrosis, hyalinization, and vascular sclerosis. These changes allow right heart hypertrophy under chronic pulmonary hypertension. Although concurrent emphysema is implicated in Cor Pulmonale development, S.C. Kapoor et al.⁴⁰ noted that clinical features of emphysema were absent in the majority of their cases, suggesting alternative mechanisms. Bronchospasm was present in half of their patients, further complicating the clinical picture.

Distribution of patients according to PAH and history of smoking are given in table 7:

Table 10 highlights that a history of smoking is significantly associated with pulmonary arterial hypertension (PAH). Among 75 patients, 22 (62.86%) had both a history of smoking and PAH, with a p-value of 0.04 and a chi-square value of 12.39, indicating statistical significance. This suggests that smoking history is an important risk factor for the development of PAH. Additionally, PAH was observed in 16 patients (40%) who were non-smokers in the study.

J.L. Wright et al.⁴² described structural changes in the vasculature of patients with moderate to severe obstructive diseases. These changes include intimal alterations with longitudinal muscle proliferation and focal fibro-elastic thickening. Increased intimal thickness is attributed to smooth muscle cell proliferation, elastin accumulation, and collagen deposition. Furthermore, the overall wall thickness (including the intima and muscular media) of pulmonary vessels (100–200 mm in external diameter) has been shown to correlate with pulmonary arterial pressure during exercise or with the pressure difference between rest and exercise. This remodelling reduces the distensibility of pulmonary vessels, contributing to the pathogenesis of PAH.

Distribution of patients according to interpretation of spirometry and PAH are given in table 8:

Table 8 demonstrates that pulmonary arterial hypertension (PAH) is most frequently associated with an obstructive pattern on spirometry. Among 75 patients, 37 exhibited both PAH and an obstructive pattern, a statistically significant finding with a p-value of 0.001. Additionally, PAH was observed in one patient with a mixed spirometric pattern, with a chi-square value of 11.90. These findings suggest a strong correlation between airflow obstruction on spirometry and the presence of PAH.

O’Hagen Spiekerkoetter et al⁴⁴AR et al.⁴³, and Meyer FJ et al.⁴⁵ have reported peripheral airflow obstruction in patients with PAH. Peacock AJ et al.⁴⁶ proposed that this obstruction may result from increased production of cytokines and growth mediators in the pulmonary vasculature, which stimulate proliferation in adjacent small airways. This process reduces the endothelial synthesis of the vasodilator nitric oxide (NO) and increases levels of the vasoconstrictor endothelin-1 (ET-1). These changes could impair peripheral airway function, as both mediators similarly affect vascular and airway smooth muscle. Furthermore, structural coupling between airways and pulmonary blood vessels may amplify mechanical forces due to shared structural alterations or vascular rigidity, leading to decreased lung elastic recoil.

Zhi-Cheng Jing et al.⁴⁷, in their study of 190 PAH patients, identified peripheral airway obstruction as a hallmark of pulmonary function impairment in PAH, with mid-expiratory flow at 50% of forced vital capacity (MEF50) being the most sensitive indicator of obstruction severity.

This study included 75 patients aged 20–90 years, comprising 51 males (68%) and 24 females (32%), with the majority (24%) belonging to the 51–60-year age group. The mean age was 55.41 ± 17.72 years.

1. Clinical Manifestations:
   Cough (85.33%), sputum expectoration (82.67%), shortness of breath (80%), and loss of appetite (66.67%) were the most prevalent symptoms.
2. Smoking History:
   A history of smoking was noted in 53.33% of patients, while 46.67% were non-smokers.
3. Radiological Findings:
   The most common radiological abnormalities were fibrosis (24%), calcified lesions (22.67%), fibrocavitary lesions (18.67%), and fibrotic bands (10.67%). Additional findings included bronchiectasis (6.68%), calcified lymph nodes (2.67%), destroyed lung (2.67%), and other lesions (9.33%). Normal chest X-rays were observed in 2.67% of patients.
4. Pulmonary Arterial Hypertension (PAH):
   Transthoracic echocardiography revealed PAH in 38 patients (50.67%), while 37 patients (49.33%) showed no evidence of PAH.
5. Spirometry Patterns:
   Most patients exhibited an obstructive spirometry pattern (84%), followed by restrictive (6.67%) and mixed patterns (2.70%). Normal spirometry findings were reported in 6.67% of cases.
6. PAH and Smoking History:
   PAH incidence was higher in smokers (22 patients, 62.86%) compared to non-smokers (16 patients, 40%).
7. PAH and Spirometry:
   PAH was exclusively associated with obstructive or mixed spirometry patterns, with no cases observed in patients with restrictive defects.

Conclusion

• In this study, age and sex were not identified as significant risk factors for PAH development. However, smoking and an obstructive pattern on spirometry were strong risk factors.
• PAH was notably prevalent among treated pulmonary tuberculosis patients with obstructive or mixed spirometry patterns and in smokers.
• To enhance early detection, spirometry is recommended for all treated pulmonary tuberculosis patients with residual lesions. If obstructive or mixed patterns are detected, 2D echocardiography should be performed to evaluate the presence of PAH

1. World health organization. Global tuberculosis report 2015. WHO report: Introduction; pg. 5
2. Brennan MJ, Thole J. Tuberculosis vaccines: a strategic blueprint for the next decade. Tuberculosis. 2012 Mar 1;92:S6-13.
3. India TB. Annual status report. Ministry of Health and Family Welfare, New Delhi: Government of India. 2016 Mar.
4. Singh B, Chaudhary O. trends of pulmonary impairment in persons with treated pulmonary tuberculosis. Int J Med Res Prof. 2015;1(1):8-11.
5. Anno H, Tomashefski JF. Studies on the impairment of respiratory function in pulmonary tuberculosis. American review of tuberculosis. 1955 Mar;71(3, Part 1):333-48.
6. Bobrowitz ID, Rodescu D, Marcus H, Abeles H. The destroyed tuberculous lung. Scandinavian journal of respiratory diseases. 1973 Dec;55(1):82-8.
7. Birath G, Caro J, Malmberg R, Simonsson BG. Airways obstruction in pulmonary tuberculosis. Scandinavian journal of respiratory diseases. 1966;47(1):27-36.
8. Malmberg R. Gas exchange in pulmonary tuberculosis. II. Review of literature, clinical significance and conclusions. Scandinavian journal of respiratory diseases. 1965 Dec;47(4):277-305.
9. Willcox PA, Ferguson AD. Chronic obstructive airways disease following treated pulmonary tuberculosis. Respiratory medicine. 1989 May 31;83(3):195-8.
10. Patil S, Patil R, Jadhav A. Pulmonary functions' assessment in post-tuberculosis cases by spirometry: Obstructive pattern is predominant and needs cautious evaluation in all treated cases irrespective of symptoms. International journal of mycobacteriology. 2018 Apr 1;7(2):128.
11. Pasipanodya JG, Miller TL, Vecino M, Munguia G, Garmon R, Bae S, Drewyer G, Weis SE. Pulmonary impairment after tuberculosis. CHEST Journal. 2007 Jun 1;131(6):1817-24.
12. Maguire GP, Anstey NM, Ardian M, Waramori G, Tjitra E, Kenangalem E, Handojo T, Kelly PM. Pulmonary tuberculosis, impaired lung function, disability and quality of life in a high-burden setting. The International Journal of Tuberculosis and Lung Disease. 2009 Dec 1;13(12):1500-6.
13. Menezes AM, Hallal PC, Perez-Padilla R, Jardim JR, Muino A, Lopez MV, Valdivia G, de Oca MM, Talamo C, Pertuze J, Victora CG. Latin American Project for the Investigation of Obstructive Lung Disease (PLATINO) Team. Tuberculosis and airflow obstruction: evidence from the PLATINO study in Latin America. Eur Respir J. 2007;30(6):1180-5.
14. Naeije R. Pulmonary hypertension and right heart failure in chronic obstructive pulmonary disease. Proceedings of the American Thoracic Society. 2005 Apr;2(1):20-2.
15. Naeije R. Pulmonary hypertension and right heart failure in chronic obstructive pulmonary disease. Proceedings of the American Thoracic Society. 2005 Apr;2(1):20-2.
16. Marjani M, Tabarsi P, Baghaei P, Moniri A, Malekmohammad M. Effect of pulmonary hypertension on outcome of pulmonary tuberculosis. International Journal of Mycobacteriology. 2015 Mar 31;4:158.
17. Schannwell CM, Steiner S, Strauer B. Diagnostics in pulmonary hypertension. Journal of physiology and pharmacology. 2007 Nov 1;58(5):591-602.
18. Ahmed AE, Ibrahim AS, Elshafie SM. Pulmonary hypertension in patients with treated pulmonary tuberculosis: analysis of 14 consecutive cases. Clinical medicine insights. Circulatory, respiratory and pulmonary medicine. 2011;5:1.
19. Bhattacharyya P, Saha D, Bhattacherjee PD, Das SK, Bhattacharyya PP, Dey R. Tuberculosis associated pulmonary hypertension: The revelation of a clinical observation. Lung India: official organ of Indian Chest Society. 2016 Mar;33(2):135.
20. Akkara SA, Shah AD, Adalja M, Akkara AG, Rathi A, Shah DN. Pulmonary tuberculosis: the day after. The International Journal of Tuberculosis and Lung Disease. 2013 Jun 1;17(6):810-3.
21. Singla N, Singla R, Fernandes S, Behera D. Post treatment sequelae of multi-drug resistant tuberculosis patients. Indian J Tuberc. 2009 Oct;56(4):206-12.
22. Menon B, Nima G, Dogra V, Jha S. Evaluation of the radiological sequelae after treatment completion in new cases of pulmonary, pleural, and mediastinal tuberculosis. Lung India: official organ of Indian Chest Society. 2015 May;32(3):241.
23. Manji M, Shayo G, Mamuya S, Mpembeni R, Jusabani A, Mugusi F. Lung functions among patients with pulmonary tuberculosis in Dar es Salaam–a cross-sectional study. BMC pulmonary medicine. 2016 Dec;16(1):58.
24. Agarwala A, Maikap MK, Panchadhyayee P, Mandal P, Roy PP. Chronic airway obstruction in post tubercular fibrosis cases: a serious lung function changes. International Journal of Research in Medical Sciences. 2016 Dec 16;4(12):5294-6.
25. Anno H, Tomashefski JF. Studies on the impairment of respiratory function in pulmonary tuberculosis. American review of tuberculosis. 1955 Mar;71(3, Part 1):333.
26. Guliani A, Bhalotra B, Parakh U, Jain N. Even asymptomatic patients may have serious lung function impairment after successful Tb treatment. InB52. TUBERCULOSIS: TREATMENT 2014 May (pp. A3203-A3203). American Thoracic Society.
27. Snider GL, Doctor L, Demas TA, Shaw AR. Obstructive airway disease in patients with treated pulmonary tuberculosis. American review of respiratory disease. 1971 May;103(5):625-40.
28. Verma SK, Narayan KV, Kumar S. A study on prevalence of obstructive airway disease among post pulmonary tuberculosis patients. Pulmon. 2009;11(1):4-7.
29. Long R, Maycher B, Dhar A, Manfreda J, Hershfield E, Anthonisen N. Pulmonary tuberculosis treated with directly observed therapy: serial changes in lung structure and function. Chest. 1998 Apr 1; 113(4):933-43
30. Plit ML, Anderson R, Van Rensburg CE, Page-Shipp L, Blott JA, Fresen JL, Feldman C. Influence of antimicrobial chemotherapy on spirometric parameters and pro-inflammatory indices in severe pulmonary tuberculosis. European respiratory journal. 1998 Aug 1;12(2):351-6.
31. Lee JH, Chang JH. Lung function in patients with chronic airflow obstruction due to tuberculous destroyed lung. Respiratory medicine. 2003 Nov 1;97(11):1237-42.
32. Ramos LM, Sulmonett N, Ferreira CS, Henriques JF, Miranda SS. Functional profile of patients with tuberculosis sequelae in a university hospital. Jornal Brasileiro de Pneumologia. 2006 Feb;32(1):43-7.
33. Di Naso FC, Pereira JS, Schuh SJ, Unis G. Functional evaluation in patients with pulmonary tuberculosis sequelae. Revista Portuguesa de Pneumologia (English Edition). 2011 Sep 1;17(5):216-21.
34. Chushkin MI, Ots ON. Impaired pulmonary function after treatment for tuberculosis: the end of the disease? Jornal Brasileiro de Pneumologia. 2017 Feb;43(1):38-43.
35. Gaensler EA, Lindgren I. Chronic bronchitis as an etiologic factor in obstructive emphysema: preliminary report. American Review of Respiratory Disease. 1959 Jul;80(1P2):185-93.
36. Baig IM, Saeed W, Khalil KF. Post-tuberculous chronic obstructive pulmonary disease. J Coll Physicians Surg Pak. 2010 Aug 1;20(8):542-4.
37. Zhou C, Nagayama N, Ohtsuka Y, Nagai H, Kawabe Y, Machida K, Sato K, Sagara Y. Long-term Study of Patients with Sequelae of Pulmonary Tuberculosis after Pneumonectomy-Obstructive Impairment and its Causes. The Japanese journal of thoracic diseases. 1995 Apr 25;33(4):416-21.
38. Ahmed AE, Ibrahim AS, Elshafie SM. Pulmonary hypertension in patients with treated pulmonary tuberculosis: analysis of 14 consecutive cases. Clinical medicine insights. Circulatory, respiratory and pulmonary medicine. 2011;5:1.
39. Richards DW, Fishman AP. Cor Pulmonale in Chronic Pulmonary Emphysema. Barach, A. L., and Bickerman, HA: Pulmonary Emphysema, Baltimore, Williams & Wilkins Company. 1956.
40. Kapoor SC. Cor pulmonale in pulmonary tuberculosis: A preliminary report on 66 patients.
41. Jain, S. K. (1956). Personal communication.
42. Wright JL, Levy RD, Churg A. Pulmonary hypertension in chronic obstructive pulmonary disease: current theories of pathogenesis and their implications for treatment. Thorax. 2005 Jul 1;60(7):605-9.
43. O'Hagan AR, Stillwell PC, Arroliga A. Airway Responsiveness to Inhaled Albuterol in Patients wit Pulmonary Hypertension. Clinical pediatrics. 1999 Jan;38(1):27-33.
44. Spiekerkoetter E, Fabel H, Hoeper MM. Effects of inhaled salbutamol in primary pulmonary hypertension. European Respiratory Journal. 2002 Sep 1;20(3):524-8.
45. Meyer FJ, Ewert R, Hoeper MM, Olschewski H, Behr J, Winkler J, Wilkens H, Breuer C, Kübler W, Borst MM. Peripheral airway obstruction in primary pulmonary hypertension. Thorax. 2002 Jun 1;57(6):473-6.
46. Peacock AJ. Primary pulmonary hypertension. Thorax. 1999 Dec 1;54(12):1107-18.
47. Jing ZC, Xu XQ, Badesch DB, Jiang X, Wu Y, Liu JM, Wang Y, Pan L, Li HP, Pu JL, Zhang ZL. Pulmonary function testing in patients with pulmonary arterial hypertension. Respiratory medicine. 2009 Aug 1;103(8):1136-42.