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Telmisartan improves vascular function independently of metabolic and antihypertensive effects in hypertensive subjects with impaired glucose tolerance

Abstract Background Hypertensive patients with IGT have increased risk for cardiovascular disease and progression to diabetes mellitus. Clinical trials suggest that the ARB telmisartan uniquely possesses PPARγ agonistic properties and improves insulin resistance as well as vascular endothelial dysfu...

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Published in:International journal of cardiology 2010-03, Vol.139 (3), p.289-296
Main Authors: Perl, Sabine, Schmölzer, Isabella, Sourij, Harald, Pressl, Helga, Eder, Michaela, Zweiker, Robert, Wascher, Thomas C
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container_title International journal of cardiology
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creator Perl, Sabine
Schmölzer, Isabella
Sourij, Harald
Pressl, Helga
Eder, Michaela
Zweiker, Robert
Wascher, Thomas C
description Abstract Background Hypertensive patients with IGT have increased risk for cardiovascular disease and progression to diabetes mellitus. Clinical trials suggest that the ARB telmisartan uniquely possesses PPARγ agonistic properties and improves insulin resistance as well as vascular endothelial dysfunction. The aim of the present study was to compare vascular effects of telmisartan and losartan in relation to their metabolic and antihypertensive effects in hypertensive patients with IGT. Materials and methods 24 patients were randomised in a double-blind, prospective, cross-over trial. At baseline and after 12 weeks of either treatment an oGTT, and endothelial function testing was performed. Results Endothelial function improved significantly by telmisartan treatment but not by losartan treatment (FMD; T : 7.9 ± 0.7%, vs B : 6.4 ± 0.8, p < 0.01; vs L : 6.4 ± 0.6, p < 0.001) at almost identical antihypertensive effect of both agents. Insulin resistance assessed by HOMA ( T : 2.20 ± 0.47 vs B : 3.04 ± 0.60, p < 0.01; vs L : 3.38 ± 0.84, T vs L p < 0.05) and ISI120 ( T : 0.114 ± 0.003 vs B : 0.092 ± 0.002, p < 0.001; vs L : 0.090 ± 0.006, T vs L p < 0.01) improved significantly after telmisartan only, as did glucose tolerance ( p < 0.01). The improvement of the endothelial function observed, significantly depended on pretreatment insulin resistance but was independent of improvements of insulin resistance, blood pressure or glucose tolerance. Conclusion In hypertensive patients with IGT telmisartan compared to losartan improved endothelial function and insulin resistance independently, supporting the hypothesis that glucometabolic and vascular insulin resistance are differentially regulated.
doi_str_mv 10.1016/j.ijcard.2008.10.048
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Clinical trials suggest that the ARB telmisartan uniquely possesses PPARγ agonistic properties and improves insulin resistance as well as vascular endothelial dysfunction. The aim of the present study was to compare vascular effects of telmisartan and losartan in relation to their metabolic and antihypertensive effects in hypertensive patients with IGT. Materials and methods 24 patients were randomised in a double-blind, prospective, cross-over trial. At baseline and after 12 weeks of either treatment an oGTT, and endothelial function testing was performed. Results Endothelial function improved significantly by telmisartan treatment but not by losartan treatment (FMD; T : 7.9 ± 0.7%, vs B : 6.4 ± 0.8, p < 0.01; vs L : 6.4 ± 0.6, p < 0.001) at almost identical antihypertensive effect of both agents. Insulin resistance assessed by HOMA ( T : 2.20 ± 0.47 vs B : 3.04 ± 0.60, p < 0.01; vs L : 3.38 ± 0.84, T vs L p < 0.05) and ISI120 ( T : 0.114 ± 0.003 vs B : 0.092 ± 0.002, p < 0.001; vs L : 0.090 ± 0.006, T vs L p < 0.01) improved significantly after telmisartan only, as did glucose tolerance ( p < 0.01). The improvement of the endothelial function observed, significantly depended on pretreatment insulin resistance but was independent of improvements of insulin resistance, blood pressure or glucose tolerance. Conclusion In hypertensive patients with IGT telmisartan compared to losartan improved endothelial function and insulin resistance independently, supporting the hypothesis that glucometabolic and vascular insulin resistance are differentially regulated.]]></description><identifier>ISSN: 0167-5273</identifier><identifier>EISSN: 1874-1754</identifier><identifier>DOI: 10.1016/j.ijcard.2008.10.048</identifier><identifier>PMID: 19118910</identifier><identifier>CODEN: IJCDD5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Adult ; Aged ; Antihypertensive Agents - pharmacology ; Antihypertensive Agents - therapeutic use ; Arterial hypertension. Arterial hypotension ; Benzimidazoles - therapeutic use ; Benzoates - therapeutic use ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cardiovascular ; Cross-Over Studies ; Diabetes. Impaired glucose tolerance ; Double-Blind Method ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Endothelial function ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Glucose Intolerance - blood ; Glucose Intolerance - drug therapy ; Glucose Intolerance - physiopathology ; Humans ; Hypertension ; Hypertension - drug therapy ; Hypertension - metabolism ; Hypertension - physiopathology ; Hypoglycemic Agents - therapeutic use ; Impaired glucose tolerance ; Male ; Medical sciences ; Middle Aged ; Prospective Studies ; Telmisartan ; Vascular Diseases - drug therapy ; Vascular Diseases - metabolism ; Vascular Diseases - physiopathology</subject><ispartof>International journal of cardiology, 2010-03, Vol.139 (3), p.289-296</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2008 Elsevier Ireland Ltd</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2008 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c446t-ad2ee96ab5bd06c205e5469cc3950e8f05c2ad5bbd2d6397c7c5cd9c837b1f4a3</citedby><cites>FETCH-LOGICAL-c446t-ad2ee96ab5bd06c205e5469cc3950e8f05c2ad5bbd2d6397c7c5cd9c837b1f4a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=22570858$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19118910$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Perl, Sabine</creatorcontrib><creatorcontrib>Schmölzer, Isabella</creatorcontrib><creatorcontrib>Sourij, Harald</creatorcontrib><creatorcontrib>Pressl, Helga</creatorcontrib><creatorcontrib>Eder, Michaela</creatorcontrib><creatorcontrib>Zweiker, Robert</creatorcontrib><creatorcontrib>Wascher, Thomas C</creatorcontrib><title>Telmisartan improves vascular function independently of metabolic and antihypertensive effects in hypertensive subjects with impaired glucose tolerance</title><title>International journal of cardiology</title><addtitle>Int J Cardiol</addtitle><description><![CDATA[Abstract Background Hypertensive patients with IGT have increased risk for cardiovascular disease and progression to diabetes mellitus. Clinical trials suggest that the ARB telmisartan uniquely possesses PPARγ agonistic properties and improves insulin resistance as well as vascular endothelial dysfunction. The aim of the present study was to compare vascular effects of telmisartan and losartan in relation to their metabolic and antihypertensive effects in hypertensive patients with IGT. Materials and methods 24 patients were randomised in a double-blind, prospective, cross-over trial. At baseline and after 12 weeks of either treatment an oGTT, and endothelial function testing was performed. Results Endothelial function improved significantly by telmisartan treatment but not by losartan treatment (FMD; T : 7.9 ± 0.7%, vs B : 6.4 ± 0.8, p < 0.01; vs L : 6.4 ± 0.6, p < 0.001) at almost identical antihypertensive effect of both agents. Insulin resistance assessed by HOMA ( T : 2.20 ± 0.47 vs B : 3.04 ± 0.60, p < 0.01; vs L : 3.38 ± 0.84, T vs L p < 0.05) and ISI120 ( T : 0.114 ± 0.003 vs B : 0.092 ± 0.002, p < 0.001; vs L : 0.090 ± 0.006, T vs L p < 0.01) improved significantly after telmisartan only, as did glucose tolerance ( p < 0.01). The improvement of the endothelial function observed, significantly depended on pretreatment insulin resistance but was independent of improvements of insulin resistance, blood pressure or glucose tolerance. Conclusion In hypertensive patients with IGT telmisartan compared to losartan improved endothelial function and insulin resistance independently, supporting the hypothesis that glucometabolic and vascular insulin resistance are differentially regulated.]]></description><subject>Adult</subject><subject>Aged</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>Antihypertensive Agents - therapeutic use</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Benzimidazoles - therapeutic use</subject><subject>Benzoates - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular</subject><subject>Cross-Over Studies</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Double-Blind Method</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Endothelial function</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Glucose Intolerance - blood</subject><subject>Glucose Intolerance - drug therapy</subject><subject>Glucose Intolerance - physiopathology</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - physiopathology</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Impaired glucose tolerance</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Prospective Studies</subject><subject>Telmisartan</subject><subject>Vascular Diseases - drug therapy</subject><subject>Vascular Diseases - metabolism</subject><subject>Vascular Diseases - physiopathology</subject><issn>0167-5273</issn><issn>1874-1754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNqFUsGOFCEQJUbjzq7-gTFcjKceobtpmouJ2ahrsokH1zOhi2qXlqFHoMfMl_i70s5EoxcPQFL16hX1XhHyjLMtZ7x7NW3dBCbabc1YX0Jb1vYPyIb3sq24FO1DsikwWYlaNhfkMqWJMdYq1T8mF1xx3ivONuTHHfqdSyZmE6jb7eN8wEQPJsHiTaTjEiC7uaSCxT2WK2R_pPNId5jNMHsH1ARbTnb3xz3GjCG5A1IcR4ScSh39K56WYfqV-O7y_drQuIiWfvELzAlpnj1GEwCfkEej8Qmfnt8r8vnd27vrm-r24_sP129uK2jbLlfG1oiqM4MYLOugZgJF2ymARgmG_cgE1MaKYbC17RolQYIAq6Bv5MDH1jRX5OWJt0z-bcGUdVED0HsTcF6Sll3d9qyTvCDbExLinFLEUe-j25l41Jzp1RE96ZMjenVkjRZHStnzc4Nl2KH9U3S2oABenAFFdOPHdXyXfuPqWkjWi5Xo9QmHRY6Dw6gTOCxS2aIgZG1n97-f_EsA3gVXen7FI6ZpXmIoUmuuU62Z_rRuz7o8rGecM8Wbn0Q1xjE</recordid><startdate>20100318</startdate><enddate>20100318</enddate><creator>Perl, Sabine</creator><creator>Schmölzer, Isabella</creator><creator>Sourij, Harald</creator><creator>Pressl, Helga</creator><creator>Eder, Michaela</creator><creator>Zweiker, Robert</creator><creator>Wascher, Thomas C</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20100318</creationdate><title>Telmisartan improves vascular function independently of metabolic and antihypertensive effects in hypertensive subjects with impaired glucose tolerance</title><author>Perl, Sabine ; Schmölzer, Isabella ; Sourij, Harald ; Pressl, Helga ; Eder, Michaela ; Zweiker, Robert ; Wascher, Thomas C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c446t-ad2ee96ab5bd06c205e5469cc3950e8f05c2ad5bbd2d6397c7c5cd9c837b1f4a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Antihypertensive Agents - pharmacology</topic><topic>Antihypertensive Agents - therapeutic use</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Benzimidazoles - therapeutic use</topic><topic>Benzoates - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular</topic><topic>Cross-Over Studies</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Double-Blind Method</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Endothelial function</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>Glucose Intolerance - blood</topic><topic>Glucose Intolerance - drug therapy</topic><topic>Glucose Intolerance - physiopathology</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - physiopathology</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>Impaired glucose tolerance</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Prospective Studies</topic><topic>Telmisartan</topic><topic>Vascular Diseases - drug therapy</topic><topic>Vascular Diseases - metabolism</topic><topic>Vascular Diseases - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Perl, Sabine</creatorcontrib><creatorcontrib>Schmölzer, Isabella</creatorcontrib><creatorcontrib>Sourij, Harald</creatorcontrib><creatorcontrib>Pressl, Helga</creatorcontrib><creatorcontrib>Eder, Michaela</creatorcontrib><creatorcontrib>Zweiker, Robert</creatorcontrib><creatorcontrib>Wascher, Thomas C</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Perl, Sabine</au><au>Schmölzer, Isabella</au><au>Sourij, Harald</au><au>Pressl, Helga</au><au>Eder, Michaela</au><au>Zweiker, Robert</au><au>Wascher, Thomas C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Telmisartan improves vascular function independently of metabolic and antihypertensive effects in hypertensive subjects with impaired glucose tolerance</atitle><jtitle>International journal of cardiology</jtitle><addtitle>Int J Cardiol</addtitle><date>2010-03-18</date><risdate>2010</risdate><volume>139</volume><issue>3</issue><spage>289</spage><epage>296</epage><pages>289-296</pages><issn>0167-5273</issn><eissn>1874-1754</eissn><coden>IJCDD5</coden><abstract><![CDATA[Abstract Background Hypertensive patients with IGT have increased risk for cardiovascular disease and progression to diabetes mellitus. Clinical trials suggest that the ARB telmisartan uniquely possesses PPARγ agonistic properties and improves insulin resistance as well as vascular endothelial dysfunction. The aim of the present study was to compare vascular effects of telmisartan and losartan in relation to their metabolic and antihypertensive effects in hypertensive patients with IGT. Materials and methods 24 patients were randomised in a double-blind, prospective, cross-over trial. At baseline and after 12 weeks of either treatment an oGTT, and endothelial function testing was performed. Results Endothelial function improved significantly by telmisartan treatment but not by losartan treatment (FMD; T : 7.9 ± 0.7%, vs B : 6.4 ± 0.8, p < 0.01; vs L : 6.4 ± 0.6, p < 0.001) at almost identical antihypertensive effect of both agents. Insulin resistance assessed by HOMA ( T : 2.20 ± 0.47 vs B : 3.04 ± 0.60, p < 0.01; vs L : 3.38 ± 0.84, T vs L p < 0.05) and ISI120 ( T : 0.114 ± 0.003 vs B : 0.092 ± 0.002, p < 0.001; vs L : 0.090 ± 0.006, T vs L p < 0.01) improved significantly after telmisartan only, as did glucose tolerance ( p < 0.01). The improvement of the endothelial function observed, significantly depended on pretreatment insulin resistance but was independent of improvements of insulin resistance, blood pressure or glucose tolerance. Conclusion In hypertensive patients with IGT telmisartan compared to losartan improved endothelial function and insulin resistance independently, supporting the hypothesis that glucometabolic and vascular insulin resistance are differentially regulated.]]></abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>19118910</pmid><doi>10.1016/j.ijcard.2008.10.048</doi><tpages>8</tpages></addata></record>
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identifier ISSN: 0167-5273
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subjects Adult
Aged
Antihypertensive Agents - pharmacology
Antihypertensive Agents - therapeutic use
Arterial hypertension. Arterial hypotension
Benzimidazoles - therapeutic use
Benzoates - therapeutic use
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Cardiovascular
Cross-Over Studies
Diabetes. Impaired glucose tolerance
Double-Blind Method
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Endothelial function
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Female
Glucose Intolerance - blood
Glucose Intolerance - drug therapy
Glucose Intolerance - physiopathology
Humans
Hypertension
Hypertension - drug therapy
Hypertension - metabolism
Hypertension - physiopathology
Hypoglycemic Agents - therapeutic use
Impaired glucose tolerance
Male
Medical sciences
Middle Aged
Prospective Studies
Telmisartan
Vascular Diseases - drug therapy
Vascular Diseases - metabolism
Vascular Diseases - physiopathology
title Telmisartan improves vascular function independently of metabolic and antihypertensive effects in hypertensive subjects with impaired glucose tolerance
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