ArticleJACC. Basic to translational science2024
Reduced Stroke Volume and Brain Perfusion Drive Postural Hyperventilation in Postural Orthostatic Tachycardia Syndrome.
Article in JACC. Basic to translational science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mapping cerebral blood flow in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and orthostatic intolerance: insights from a systematic review.Journal of translational medicine · 2025Pooled it
- Frequency and characteristics of multi-domain autonomic dysfunction in patients with spontaneous intracranial hypotension.Headache · 2026Article
- Assessment of internal consistency reliability and concurrent validity of PROMISJournal of patient-reported outcomes · 2026Article
- Stroke volume reduction impairs cerebrovascular regulation through ETCOClinical autonomic research : official journal of the Clinical Autonomic Research Society · 2026Article
- Heart Rate Lowering With Ivabradine and Burden of Symptoms in Patients With Postural Orthostatic Tachycardia Syndrome.Journal of cardiovascular pharmacology · 2025Article
- Cerebral Blood Flow in Orthostatic Intolerance.Journal of the American Heart Association · 2025Review
- Novel brain SPECT imaging unravels abnormal cerebral perfusion in patients with postural orthostatic tachycardia syndrome and cognitive dysfunction.Scientific reports · 2025Article
- Hyperventilation during rest and exercise in orthostatic intolerance and Spiky-Leaky Syndrome.Frontiers in neurology · 2025Article
- Determinants of Exercise Intolerance in Postural Orthostatic Tachycardia Syndrome: A Systematic Review.Exercise, sport & movement · 2025Article
- Novel Mechanisms of Postural Hyperventilation in Postural Orthostatic Tachycardia Syndrome: Toward Discovery of Terra Incognita.JACC. Basic to translational science · 2024Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Postural hyperventilation has been implicated as a cause of postural orthostatic tachycardia syndrome (POTS), yet the precise mechanisms underlying the heightened breathing response remain unclear. This study challenges current hypotheses by revealing that exaggerated peripheral chemoreceptor activity is not the primary driver of postural hyperventilation. Instead, significant contributions from reduced stroke volume and compromised brain perfusion during orthostatic stress were identified. These findings shed light on our understanding of POTS pathophysiology, emphasizing the critical roles of systemic hemodynamic status. Further research should explore interventions targeting stroke volume and brain perfusion for more effective clinical management of POTS.
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