Introduction
Chronic obstructive pulmonary disease (COPD) and tuberculosis (TB) are increasingly recognized as intersecting global health challenges, particularly in low- and middle-income countries and among aging populations. Beyond shared risk factors, prior pulmonary TB has emerged as an independent and robust determinant of COPD, even in never-smokers. This overlap creates a unique clinical scenario in which structural lung damage, persistent immune activation, and systemic inflammation interact to elevate cardiovascular disease (CVD) risk. Understanding COPD through a TB-aware lens is therefore essential for advancing both respiratory and cardiovascular outcomes in high-burden settings.
Epidemiology and Distinct COPD–Post-TB Phenotypes
Epidemiological evidence consistently demonstrates higher COPD prevalence among individuals with a history of pulmonary TB. This post-TB COPD phenotype is clinically distinct, characterized by mixed obstructive–restrictive ventilatory defects, reduced diffusing capacity (DLCO), and radiographic sequelae such as fibrosis and bronchiectasis. Patients frequently experience higher exacerbation rates, increased hospitalizations, and worse functional status, underscoring the need to recognize post-TB lung disease as more than conventional smoking-related COPD.
Pathobiological Mechanisms Linking TB, COPD, and Cardiovascular Risk
Mechanistic studies suggest that convergent biological pathways drive excess cardiopulmonary risk in COPD patients with prior TB. Chronic immune activation, endothelial dysfunction, prothrombotic remodeling, and dysregulated lipid metabolism contribute to a milieu that promotes atherosclerosis, venous thromboembolism, and pulmonary hypertension. Additional processes such as molecular mimicry and epigenetic reprogramming following TB infection provide biologic plausibility for long-term systemic effects extending well beyond pulmonary impairment.
Biomarkers, Multimarker Panels, and Risk Stratification
Single biomarkers inadequately capture the complex risk profile of COPD–TB overlap. Emerging evidence supports the use of multimarker panels integrating inflammatory markers, endothelial injury indicators, myocardial strain or fibrosis biomarkers, and coagulation factors. These panels offer incremental prognostic value beyond traditional clinical variables, potentially enabling earlier identification of patients at heightened cardiovascular risk and facilitating more precise, personalized management strategies.
Risk Prediction Models and Sleep-Disordered Breathing Considerations
While contemporary tools such as QRISK4 now include COPD as a cardiovascular risk factor, they do not explicitly account for prior TB or post-TB COPD phenotypes. This gap limits their accuracy in TB-endemic regions. Additionally, sleep-disordered breathing, which is prevalent in COPD and associated with adverse cardiovascular outcomes, remains underexplored in post-TB populations. Incorporating TB history and sleep-related variables into future prediction models could substantially improve risk estimation.
Clinical and Implementation Implications in Resource-Limited Settings
In resource-constrained environments, pragmatic approaches are essential. Integrated assessments combining clinical history, targeted biomarkers, spirometry with lung volumes, DLCO, six-minute walk testing, and focused imaging can guide individualized care. Prioritized access to positive airway pressure therapy, guideline-concordant pharmacotherapy, and task-shifting strategies are feasible adaptations. Ultimately, TB-aware cardiopulmonary risk models and implementation studies are urgently needed to translate mechanistic insights into equitable, real-world benefits.
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