{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T19:46:51Z","timestamp":1779997611094,"version":"3.53.1"},"reference-count":24,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2024,7,24]],"date-time":"2024-07-24T00:00:00Z","timestamp":1721779200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Liver International"],"published-print":{"date-parts":[[2024,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background and Aims<\/jats:title><jats:p>Nonselective beta\u2010blockers (NSBB) are the mainstay for treatment of portal hypertension (PH), but require caution in decompensated cirrhosis (DC) or acute\u2010on\u2010chronic liver failure (ACLF) with hypotension, hyponatremia, acute kidney injury (AKI) or type 2 hepatorenal syndrome (HRS). Midodrine is oral, rapidly acting, \u03b11\u2010adrenergic agonist. We evaluated acute effects of midodrine on hepatic venous pressure gradient (HVPG) in DC and ACLF with contraindications to NSBB.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Patients of DC (<jats:italic>n<\/jats:italic>\u2009=\u200930) with grade III ascites and serum sodium (Na) &lt;130\/systolic blood pressure (SBP) &lt;90\/type II HRS (group I) and ACLF patients (<jats:italic>n<\/jats:italic>\u2009=\u200930) with Na &lt;130\/SBP &lt;90\/AKI (group II) were included. HVPG was done at baseline and repeated 3\u2009h after 10\u2009mg midodrine. Primary outcome was HVPG response (reduction by &gt;20% or to &lt;12\u2009mmHg).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In group I, midodrine significantly reduced HVPG (19.2\u2009\u00b1\u20094.6 to 17.8\u2009\u00b1\u20094.2, <jats:italic>p<\/jats:italic>\u2009=\u2009.02) and heart rate (HR) (86.3\u2009\u00b1\u200911.6 to 77.9\u2009\u00b1\u200913.1, <jats:italic>p<\/jats:italic>\u2009&lt;\u2009.01) and increased mean arterial pressure (MAP) (74.1\u2009\u00b1\u20096.9 to 81.9\u2009\u00b1\u20096.6\u2009mmHg, <jats:italic>p<\/jats:italic>\u2009&lt;\u2009.01). In group II also, midodrine reduced HVPG (19.1\u2009\u00b1\u20094.1 to 17.0\u2009\u00b1\u20094.2) and HR (92.4\u2009\u00b1\u200913.7 to 84.6\u2009\u00b1\u200914.1) and increased MAP (85.4\u2009\u00b1\u20097.3 to 91.2\u2009\u00b1\u20097.6\u2009mmHg), <jats:italic>p<\/jats:italic>\u2009&lt;\u2009.01 for all. HVPG response was achieved in 3\/30 (10%) in group I and 8\/30 (26.7%) in group II. On logistic regression analysis, prerenal AKI (OR 11.04, 95% CI 1.83\u201366.18, <jats:italic>p<\/jats:italic>\u2009&lt;\u2009.01) and increase in MAP (OR 1.22, 95% CI 1.03\u20131.43, <jats:italic>p<\/jats:italic>\u2009=\u2009.02) were independent predictors of response. Increase in MAP by 8.5\u2009mmHg with midodrine had best cut\u2010off with AUROC of .76 for response.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>In decompensated cirrhosis and ACLF patients with contraindications to NSBB, midodrine is useful in decreasing HVPG. Dose of midodrine should be titrated to increase MAP atleast by 8.5\u2009mmHg.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.16033","type":"journal-article","created":{"date-parts":[[2024,7,24]],"date-time":"2024-07-24T10:22:34Z","timestamp":1721816554000},"page":"2714-2723","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Effect of midodrine on <scp>HVPG<\/scp> in advanced chronic liver disease and acute\u2010on\u2010chronic liver failure\u2014A pilot study"],"prefix":"10.1111","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5531-3608","authenticated-orcid":false,"given":"Chitranshu","family":"Vashishtha","sequence":"first","affiliation":[{"name":"Department of Hepatology Institute of Liver and Biliary Sciences  New Delhi India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ankit","family":"Bhardwaj","sequence":"additional","affiliation":[{"name":"Department of Epidemiology and Public Health Institute of Liver and Biliary Sciences  New Delhi India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5582-7759","authenticated-orcid":false,"given":"Ankur","family":"Jindal","sequence":"additional","affiliation":[{"name":"Department of Hepatology Institute of Liver and Biliary Sciences  New Delhi India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3448-8334","authenticated-orcid":false,"given":"Manoj","family":"Kumar","sequence":"additional","affiliation":[{"name":"Department of Hepatology Institute of Liver and Biliary Sciences  New Delhi India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0544-5610","authenticated-orcid":false,"given":"Shiv Kumar","family":"Sarin","sequence":"additional","affiliation":[{"name":"Department of Hepatology Institute of Liver and Biliary Sciences  New Delhi 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