Development of hyperdynamic circulation and response to [beta]-blockers in compensated cirrhosis with portal hypertension
Nonselective [beta]-blockers are useful to prevent bleeding in patients with cirrhosis and large varices but not to prevent the development of varices in those with compensated cirrhosis and portal hypertension (PHT). This suggests that the evolutionary stage of PHT may influence the response to [be...
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Veröffentlicht in: | Hepatology (Baltimore, Md.) Md.), 2016-01, Vol.63 (1), p.197 |
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creator | Villanueva, Càndid Albillos, Agustín Genesca, Joan Abraldes, Juan G Calleja, Jose L Aracil, Carles Banares, Rafael Morillas, Rosa Poca, María Penas, Beatriz Augustin, Salvador Garcia-Pagan, Joan Carles Pavel, Oana Bosch, Jaume |
description | Nonselective [beta]-blockers are useful to prevent bleeding in patients with cirrhosis and large varices but not to prevent the development of varices in those with compensated cirrhosis and portal hypertension (PHT). This suggests that the evolutionary stage of PHT may influence the response to [beta]-blockers. To characterize the hemodynamic profile of each stage of PHT in compensated cirrhosis and the response to [beta]-blockers according to stage, we performed a prospective, multicenter (tertiary care setting), cross-sectional study. Hepatic venous pressure gradient (HVPG) and systemic hemodynamic were measured in 273 patients with compensated cirrhosis before and after intravenous propranolol (0.15 mg/kg): 194 patients had an HVPG ≥10 mm Hg (clinically significant PHT [CSPH]), with either no varices (n = 80) or small varices (n = 114), and 79 had an HVPG >5 and |
doi_str_mv | 10.1002/hep.28264 |
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This suggests that the evolutionary stage of PHT may influence the response to [beta]-blockers. To characterize the hemodynamic profile of each stage of PHT in compensated cirrhosis and the response to [beta]-blockers according to stage, we performed a prospective, multicenter (tertiary care setting), cross-sectional study. Hepatic venous pressure gradient (HVPG) and systemic hemodynamic were measured in 273 patients with compensated cirrhosis before and after intravenous propranolol (0.15 mg/kg): 194 patients had an HVPG ≥10 mm Hg (clinically significant PHT [CSPH]), with either no varices (n = 80) or small varices (n = 114), and 79 had an HVPG >5 and <10 mm Hg (subclinical PHT). Patients with CSPH had higher liver stiffness (P < 0.001), worse Model for End-Stage Liver Disease score (P < 0.001), more portosystemic collaterals (P = 0.01) and splenomegaly (P = 0.01) on ultrasound, and lower platelet count (P < 0.001) than those with subclinical PHT. Patients with CSPH had lower systemic vascular resistance (1336 ± 423 versus 1469 ± 335 dyne · s · cm-5, P < 0.05) and higher cardiac index (3.3 ± 0.9 versus 2.8 ± 0.4 L/min/m2, P < 0.01). After propranolol, the HVPG decreased significantly in both groups, although the reduction was greater in those with CSPH (-16 ± 12% versus -8 ± 9%, P < 0.01). The HVPG decreased ≥10% from baseline in 69% of patients with CSPH versus 35% with subclinical PHT (P < 0.001) and decreased ≥20% in 40% versus 13%, respectively (P = 0.001). Conclusion: Patients with subclinical PHT have less hyperdynamic circulation and significantly lower portal pressure reduction after acute [beta]-blockade than those with CSPH, suggesting that [beta]-blockers are more suitable to prevent decompensation of cirrhosis in patients with CSPH than in earlier stages. (Hepatology 2016;63:197-206)]]></description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.28264</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>Hoboken: Wolters Kluwer Health, Inc</publisher><subject>Beta blockers ; Bleeding ; Cirrhosis ; Heart diseases ; Hemorrhage ; Hepatology ; Hypertension ; Intravenous administration ; Liver cirrhosis ; Liver diseases ; Propranolol ; Splenomegaly ; Ultrasound</subject><ispartof>Hepatology (Baltimore, Md.), 2016-01, Vol.63 (1), p.197</ispartof><rights>2016 by the American Association for the Study of Liver Diseases</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids></links><search><creatorcontrib>Villanueva, Càndid</creatorcontrib><creatorcontrib>Albillos, Agustín</creatorcontrib><creatorcontrib>Genesca, Joan</creatorcontrib><creatorcontrib>Abraldes, Juan G</creatorcontrib><creatorcontrib>Calleja, Jose L</creatorcontrib><creatorcontrib>Aracil, Carles</creatorcontrib><creatorcontrib>Banares, Rafael</creatorcontrib><creatorcontrib>Morillas, Rosa</creatorcontrib><creatorcontrib>Poca, María</creatorcontrib><creatorcontrib>Penas, Beatriz</creatorcontrib><creatorcontrib>Augustin, Salvador</creatorcontrib><creatorcontrib>Garcia-Pagan, Joan Carles</creatorcontrib><creatorcontrib>Pavel, Oana</creatorcontrib><creatorcontrib>Bosch, Jaume</creatorcontrib><title>Development of hyperdynamic circulation and response to [beta]-blockers in compensated cirrhosis with portal hypertension</title><title>Hepatology (Baltimore, Md.)</title><description><![CDATA[Nonselective [beta]-blockers are useful to prevent bleeding in patients with cirrhosis and large varices but not to prevent the development of varices in those with compensated cirrhosis and portal hypertension (PHT). This suggests that the evolutionary stage of PHT may influence the response to [beta]-blockers. To characterize the hemodynamic profile of each stage of PHT in compensated cirrhosis and the response to [beta]-blockers according to stage, we performed a prospective, multicenter (tertiary care setting), cross-sectional study. Hepatic venous pressure gradient (HVPG) and systemic hemodynamic were measured in 273 patients with compensated cirrhosis before and after intravenous propranolol (0.15 mg/kg): 194 patients had an HVPG ≥10 mm Hg (clinically significant PHT [CSPH]), with either no varices (n = 80) or small varices (n = 114), and 79 had an HVPG >5 and <10 mm Hg (subclinical PHT). Patients with CSPH had higher liver stiffness (P < 0.001), worse Model for End-Stage Liver Disease score (P < 0.001), more portosystemic collaterals (P = 0.01) and splenomegaly (P = 0.01) on ultrasound, and lower platelet count (P < 0.001) than those with subclinical PHT. Patients with CSPH had lower systemic vascular resistance (1336 ± 423 versus 1469 ± 335 dyne · s · cm-5, P < 0.05) and higher cardiac index (3.3 ± 0.9 versus 2.8 ± 0.4 L/min/m2, P < 0.01). After propranolol, the HVPG decreased significantly in both groups, although the reduction was greater in those with CSPH (-16 ± 12% versus -8 ± 9%, P < 0.01). The HVPG decreased ≥10% from baseline in 69% of patients with CSPH versus 35% with subclinical PHT (P < 0.001) and decreased ≥20% in 40% versus 13%, respectively (P = 0.001). Conclusion: Patients with subclinical PHT have less hyperdynamic circulation and significantly lower portal pressure reduction after acute [beta]-blockade than those with CSPH, suggesting that [beta]-blockers are more suitable to prevent decompensation of cirrhosis in patients with CSPH than in earlier stages. (Hepatology 2016;63:197-206)]]></description><subject>Beta blockers</subject><subject>Bleeding</subject><subject>Cirrhosis</subject><subject>Heart diseases</subject><subject>Hemorrhage</subject><subject>Hepatology</subject><subject>Hypertension</subject><subject>Intravenous administration</subject><subject>Liver cirrhosis</subject><subject>Liver diseases</subject><subject>Propranolol</subject><subject>Splenomegaly</subject><subject>Ultrasound</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNp9kEtLAzEYRYMoWKsL_0HA9dS8Jo-l1CcU3OhKpCQz3zBTp0lMUqX_3pG6dnU3554LF6FLShaUEHbdQ1wwzaQ4QjNaM1VxXpNjNCNMkcpQbk7RWc4bQogRTM_Q_ha-YAxxC77g0OF-HyG1e2-3Q4ObITW70ZYheGx9ixPkGHwGXAJ-c1Dse-XG0HxAynjwuAnbCD7bAu1vNfUhDxl_D6XHMaRix4O9TMxkPEcnnR0zXPzlHL3e370sH6vV88PT8mZVRSpoqZyRrRDaacsMkZoqQTlI2hFlZVdrITnX1kkFrG2FAt04sJZ34JigxjjL5-jq4I0pfO4gl_Um7JKfJtfU0OkFbmr5L6VqIqgmVPMfWDBs1A</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Villanueva, Càndid</creator><creator>Albillos, Agustín</creator><creator>Genesca, Joan</creator><creator>Abraldes, Juan G</creator><creator>Calleja, Jose L</creator><creator>Aracil, Carles</creator><creator>Banares, Rafael</creator><creator>Morillas, Rosa</creator><creator>Poca, María</creator><creator>Penas, Beatriz</creator><creator>Augustin, Salvador</creator><creator>Garcia-Pagan, Joan Carles</creator><creator>Pavel, Oana</creator><creator>Bosch, Jaume</creator><general>Wolters Kluwer Health, Inc</general><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope></search><sort><creationdate>20160101</creationdate><title>Development of hyperdynamic circulation and response to [beta]-blockers in compensated cirrhosis with portal hypertension</title><author>Villanueva, Càndid ; Albillos, Agustín ; Genesca, Joan ; Abraldes, Juan G ; Calleja, Jose L ; Aracil, Carles ; Banares, Rafael ; Morillas, Rosa ; Poca, María ; Penas, Beatriz ; Augustin, Salvador ; Garcia-Pagan, Joan Carles ; Pavel, Oana ; Bosch, Jaume</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p141t-b96d448b8a2906817413e61f07a6f5846338ab67e2dd47e8cbeaa3feb24199ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Beta blockers</topic><topic>Bleeding</topic><topic>Cirrhosis</topic><topic>Heart diseases</topic><topic>Hemorrhage</topic><topic>Hepatology</topic><topic>Hypertension</topic><topic>Intravenous administration</topic><topic>Liver cirrhosis</topic><topic>Liver diseases</topic><topic>Propranolol</topic><topic>Splenomegaly</topic><topic>Ultrasound</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Villanueva, Càndid</creatorcontrib><creatorcontrib>Albillos, Agustín</creatorcontrib><creatorcontrib>Genesca, Joan</creatorcontrib><creatorcontrib>Abraldes, Juan G</creatorcontrib><creatorcontrib>Calleja, Jose L</creatorcontrib><creatorcontrib>Aracil, Carles</creatorcontrib><creatorcontrib>Banares, Rafael</creatorcontrib><creatorcontrib>Morillas, Rosa</creatorcontrib><creatorcontrib>Poca, María</creatorcontrib><creatorcontrib>Penas, Beatriz</creatorcontrib><creatorcontrib>Augustin, Salvador</creatorcontrib><creatorcontrib>Garcia-Pagan, Joan Carles</creatorcontrib><creatorcontrib>Pavel, Oana</creatorcontrib><creatorcontrib>Bosch, Jaume</creatorcontrib><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Villanueva, Càndid</au><au>Albillos, Agustín</au><au>Genesca, Joan</au><au>Abraldes, Juan G</au><au>Calleja, Jose L</au><au>Aracil, Carles</au><au>Banares, Rafael</au><au>Morillas, Rosa</au><au>Poca, María</au><au>Penas, Beatriz</au><au>Augustin, Salvador</au><au>Garcia-Pagan, Joan Carles</au><au>Pavel, Oana</au><au>Bosch, Jaume</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Development of hyperdynamic circulation and response to [beta]-blockers in compensated cirrhosis with portal hypertension</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><date>2016-01-01</date><risdate>2016</risdate><volume>63</volume><issue>1</issue><spage>197</spage><pages>197-</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><coden>HPTLD9</coden><abstract><![CDATA[Nonselective [beta]-blockers are useful to prevent bleeding in patients with cirrhosis and large varices but not to prevent the development of varices in those with compensated cirrhosis and portal hypertension (PHT). This suggests that the evolutionary stage of PHT may influence the response to [beta]-blockers. To characterize the hemodynamic profile of each stage of PHT in compensated cirrhosis and the response to [beta]-blockers according to stage, we performed a prospective, multicenter (tertiary care setting), cross-sectional study. Hepatic venous pressure gradient (HVPG) and systemic hemodynamic were measured in 273 patients with compensated cirrhosis before and after intravenous propranolol (0.15 mg/kg): 194 patients had an HVPG ≥10 mm Hg (clinically significant PHT [CSPH]), with either no varices (n = 80) or small varices (n = 114), and 79 had an HVPG >5 and <10 mm Hg (subclinical PHT). Patients with CSPH had higher liver stiffness (P < 0.001), worse Model for End-Stage Liver Disease score (P < 0.001), more portosystemic collaterals (P = 0.01) and splenomegaly (P = 0.01) on ultrasound, and lower platelet count (P < 0.001) than those with subclinical PHT. Patients with CSPH had lower systemic vascular resistance (1336 ± 423 versus 1469 ± 335 dyne · s · cm-5, P < 0.05) and higher cardiac index (3.3 ± 0.9 versus 2.8 ± 0.4 L/min/m2, P < 0.01). After propranolol, the HVPG decreased significantly in both groups, although the reduction was greater in those with CSPH (-16 ± 12% versus -8 ± 9%, P < 0.01). The HVPG decreased ≥10% from baseline in 69% of patients with CSPH versus 35% with subclinical PHT (P < 0.001) and decreased ≥20% in 40% versus 13%, respectively (P = 0.001). Conclusion: Patients with subclinical PHT have less hyperdynamic circulation and significantly lower portal pressure reduction after acute [beta]-blockade than those with CSPH, suggesting that [beta]-blockers are more suitable to prevent decompensation of cirrhosis in patients with CSPH than in earlier stages. (Hepatology 2016;63:197-206)]]></abstract><cop>Hoboken</cop><pub>Wolters Kluwer Health, Inc</pub><doi>10.1002/hep.28264</doi></addata></record> |
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subjects | Beta blockers Bleeding Cirrhosis Heart diseases Hemorrhage Hepatology Hypertension Intravenous administration Liver cirrhosis Liver diseases Propranolol Splenomegaly Ultrasound |
title | Development of hyperdynamic circulation and response to [beta]-blockers in compensated cirrhosis with portal hypertension |
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