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.