Triple therapy comprising an inhaled corticosteroid (ICS), a long-acting β₂-agonist (LABA), and a long-acting muscarinic antagonist (LAMA) has become an important treatment option for chronic obstructive pulmonary disease (COPD). Major randomized controlled trials have demonstrated reductions in exacerbations, improvements in lung function, and better health-related quality of life in selected patients. However, uncertainty remains regarding whether triple therapy should be prescribed universally as first-line treatment for symptomatic COPD or reserved for patients most likely to benefit from ICS. This narrative review evaluates contemporary GOLD recommendations, major clinical trials, blood eosinophils as a treatment-response biomarker, mortality outcomes, and ICS-associated pneumonia risk. Evidence from IMPACT, ETHOS, TRIBUTE, FULFIL, TRILOGY, and other studies supports triple therapy in appropriately selected patients with established COPD, particularly those with previous exacerbations. However, most pivotal trials enrolled patients receiving maintenance inhalers, limiting direct extrapolation to treatment-naïve patients. Blood eosinophil counts, exacerbation history, concomitant asthma, and infection susceptibility should guide treatment selection. Indian publications additionally highlight challenges involving COPD awareness, diagnostic practices, inhaler access, and rational prescribing. LABA/LAMA remains the preferred initial treatment for most symptomatic patients without a compelling indication for ICS, whereas initial triple therapy may be considered in selected high-risk patients, particularly those with blood eosinophils ≥300 cells/µL. A phenotype-directed approach offers the most rational balance between exacerbation prevention, symptom control, and treatment-related harm.

Post-COVID-19 condition, commonly called Long COVID, has shifted the clinical question from whether a patient survived the acute infection to whether normal health and function have returned. For some, recovery is straightforward; for others, symptoms persist, fluctuate or appear after an interval, affecting several organ systems at once. This narrative review examines rheumatological, hematological and vascular, immunological and infectious, neuropsychiatric, and cardiovascular sequelae, including sudden cardiac death (SCD). Proposed mechanisms include immune dysregulation, persistent antigenic stimulation in subsets of patients, endothelial injury, altered coagulation, autonomic dysfunction, neuroinflammation, residual tissue damage and the consequences of critical illness. These mechanisms are neither mutually exclusive nor universal. The practical challenge is to recognize meaningful patterns without assuming that every symptom is caused by COVID-19. Joint pain does not automatically indicate autoimmune disease; an elevated D-dimer does not diagnose thrombosis; urticaria does not establish generalized immune deficiency; and “brain fog” should prompt a thoughtful assessment rather than dismissal or premature attribution. Observational evidence suggests increased risks of selected cardiovascular outcomes after infection, but SCD is a separate endpoint and must be evaluated with specific evidence. A phenotype-led approach—targeted investigation, attention to alternative diagnoses, clear communication and individualized rehabilitation—offers the most defensible current strategy. Indian clinical publications add useful regional context, particularly for inflammatory markers, radiological outcomes, tuberculosis and post-COVID symptoms, but should be interpreted according to study design and limitations.