{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T02:07:26Z","timestamp":1790820446891,"version":"4.1.0"},"reference-count":125,"publisher":"Cambridge University Press (CUP)","issue":"7","license":[{"start":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T00:00:00Z","timestamp":1783296000000},"content-version":"unspecified","delay-in-days":5,"URL":"https:\/\/www.cambridge.org\/core\/terms"}],"content-domain":{"domain":["cambridge.org"],"crossmark-restriction":true},"short-container-title":["Cardiol Young"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Paediatric dysautonomia has become increasingly recognised in children and adolescents, particularly in the post-COVID era. Affected patients commonly present with dizziness, palpitations, exercise intolerance, fatigue, and syncope, although reported prevalence varies widely because of evolving definitions and heterogeneous referral patterns. Contemporary evidence suggests that post-COVID dysautonomia arises from complex interactions among central autonomic network dysfunction, neurovascular dysregulation, impaired venous return, endothelial injury, hypovolemia, and altered cerebral perfusion, with tachycardia often representing a compensatory physiological response rather than a primary cardiac abnormality. Clinical phenotypes include postural orthostatic tachycardia syndrome, neurocardiogenic syncope, orthostatic hypotension, inappropriate sinus tachycardia, and undifferentiated orthostatic intolerance, frequently accompanied by fatigue, cognitive dysfunction, gastrointestinal symptoms, sleep disturbances, and post-exertional symptom exacerbation. Paediatric dysautonomia is best conceptualised as a distributed brain\u2013heart\u2013vascular network disorder that requires mechanistic understanding, standardised orthostatic assessment, and careful exclusion of structural heart disease and arrhythmia. The rapid expansion of specialised dysautonomia programmes and direct-to-consumer diagnostic pathways has also contributed to broader, and occasionally premature, application of autonomic diagnoses. Management should follow a stepwise, mechanism-guided approach emphasising patient education, trigger avoidance, hydration and salt optimisation, lower-body compression, individualised exercise rehabilitation, pacing strategies when post-exertional symptom exacerbation is present, school accommodations, and phenotype-directed pharmacotherapy for persistent functional impairment. Although post-COVID dysautonomia shares features with established paediatric autonomic disorders, important gaps remain in disease definitions, mechanistic understanding, and evidence-based treatment, underscoring the need for multidisciplinary care, standardised diagnostic frameworks, and prospective paediatric research.<\/jats:p>","DOI":"10.1017\/s1047951126113900","type":"journal-article","created":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T09:19:36Z","timestamp":1783329576000},"page":"1329-1339","update-policy":"https:\/\/doi.org\/10.1017\/policypage","source":"Crossref","is-referenced-by-count":0,"title":["Post-COVID paediatric dysautonomia: never the heart, always the brain\u2014myth or 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