{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T04:22:41Z","timestamp":1775535761181,"version":"3.50.1"},"reference-count":38,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2025,1,17]],"date-time":"2025-01-17T00:00:00Z","timestamp":1737072000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Swedish Heart Lung Foundation","award":["20220319"],"award-info":[{"award-number":["20220319"]}]},{"name":"Region Stockholm","award":["ALF FoUI 988024"],"award-info":[{"award-number":["ALF FoUI 988024"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,5,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Orthostatic hypotension (OH) is an important differential diagnosis in unexplained syncope. Neurogenic OH (nOH) has been postulated to differ from non-neurogenic OH (non-nOH), yet pathophysiological differences are largely unexplored. We aimed to investigate aetiology and tilt table test (TTT)-induced haemodynamic responses in symptomatic OH patients.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>We performed a retrospective study analysing patients referred for unexplained syncope or highly symptomatic orthostatic intolerance with TTT-verified classical OH (cOH). Medical records were analysed for the presumptive aetiology of cOH. Fifty-two patients (mean age 73 \u00b1 9 years, 46% women) with good quality TTT recordings were divided into three groups on clinical grounds: nOH, non-nOH, and mixed OH. The log-ratio (LR) method was applied to compare the decrease in mean arterial pressure (MAPLR) and corresponding contributions of heart rate (HRLR), stroke volume (SVLR), and total peripheral resistance (TPRLR) during the upright phase of TTT. The prevalence of cOH was 12 (23%) nOH, 14 (27%) non-nOH, and 26 (50%) mixed OH. No difference in MAPLR was observed among the three groups during the 4th upright minute of TTT (nOH: \u22120.10 \u00b1 0.04 vs. non-nOH: \u22120.07 \u00b1 0.05 and vs. mixed OH: \u22120.06 \u00b1 0.05, P = 0.10). The contributions of HRLR, SVLR, and TPRLR to the drop in MAPLR did not differ between groups (all P &amp;gt; 0.05).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>One-half of highly symptomatic OH patients had mixed OH, whereas one-quarter had either pure neurogenic or non-neurogenic OH, respectively. Different forms of OH were indifferentiable based on haemodynamic responses during TTT, questioning the clinical utility of such classification. Larger studies are needed to confirm these findings.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/europace\/euaf017","type":"journal-article","created":{"date-parts":[[2025,1,17]],"date-time":"2025-01-17T08:35:22Z","timestamp":1737102922000},"source":"Crossref","is-referenced-by-count":4,"title":["Aetiology and haemodynamic patterns of orthostatic hypotension in a tertiary syncope unit"],"prefix":"10.1093","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9057-9148","authenticated-orcid":false,"given":"Madeleine","family":"Johansson","sequence":"first","affiliation":[{"name":"Department of Clinical Sciences, Lund University , Jan Waldenstr\u00f6ms gata 35, 214 28 Malm\u00f6 ,","place":["Sweden"]},{"name":"Department of Cardiology, Sk\u00e5ne University Hospital , 214 28 Malm\u00f6 ,","place":["Sweden"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3219-1548","authenticated-orcid":false,"given":"Boriana S","family":"Gagaouzova","sequence":"additional","affiliation":[{"name":"Department of Neurology and Clinical Neurophysiology, Leiden University Medical Centre , PO Box 9600, 2300 RC Leiden ,","place":["Netherlands"]},{"name":"Polikliniek Stichting Epilepsie Instellingen Nederland (SEIN) , 2103 SW Heemstede ,","place":["Netherlands"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0999-7156","authenticated-orcid":false,"given":"Ineke A","family":"van Rossum","sequence":"additional","affiliation":[{"name":"Department of Neurology and Clinical Neurophysiology, Leiden University Medical Centre , PO Box 9600, 2300 RC Leiden ,","place":["Netherlands"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1435-8970","authenticated-orcid":false,"given":"Roland D","family":"Thijs","sequence":"additional","affiliation":[{"name":"Department of Neurology and Clinical Neurophysiology, Leiden University Medical Centre , PO Box 9600, 2300 RC Leiden ,","place":["Netherlands"]},{"name":"Polikliniek Stichting Epilepsie Instellingen Nederland (SEIN) , 2103 SW Heemstede ,","place":["Netherlands"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8475-0866","authenticated-orcid":false,"given":"Viktor","family":"Hamrefors","sequence":"additional","affiliation":[{"name":"Department of Clinical Sciences, Lund University , Jan Waldenstr\u00f6ms gata 35, 214 28 Malm\u00f6 ,","place":["Sweden"]},{"name":"Department of Cardiology, Sk\u00e5ne University Hospital , 214 28 Malm\u00f6 ,","place":["Sweden"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6953-7573","authenticated-orcid":false,"given":"J Gert","family":"van Dijk","sequence":"additional","affiliation":[{"name":"Department of Neurology and Clinical Neurophysiology, Leiden University Medical Centre , PO Box 9600, 2300 RC Leiden 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