{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T14:23:14Z","timestamp":1787840594579,"version":"build-2784847793"},"reference-count":10,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","license":[{"start":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T00:00:00Z","timestamp":1761955200000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,11]]},"abstract":"<jats:p>Despite advancements in the diagnosis and management of atrial septal defect (ASD), key hemodynamic aspects remain poorly understood. This review explores limitations of the pulmonary-to-systemic flow ratio (Qp:Qs), the impact of exercise on shunt volume, and predictors of pulmonary arterial hypertension. We highlight that Qp:Qs may not reflect true pulmonary blood flow, particularly during exertion, and that exercise-induced augmentation of shunt flow could predispose to right heart overload. Future studies integrating advanced imaging and hemodynamic measures are essential to refine risk stratification and management in patients with ASD.<\/jats:p>","DOI":"10.4103\/apc.apc_164_25","type":"journal-article","created":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T12:00:10Z","timestamp":1773662410000},"page":"594-597","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Unresolved questions in atrial septal defect pathophysiology: Shunt dynamics, exercise physiology, and pulmonary vascular disease risk"],"prefix":"10.4103","volume":"18","author":[{"given":"Ashish H.","family":"Shah","sequence":"first","affiliation":[{"name":"Section of Cardiology, Department of Internal Medicine, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, 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