Impact of telmisartan on the inflammatory state in patients with coronary atherosclerosis – Influence on IP-10, TNF-α and MCP-1
► Hypertension is a prominent cause for coronary artery disease and associated with inflammation. ► Telmisartan has well-known antihypertensive and less-known anti-inflammatory effects. ► In hypertensive patients telmisartan only selectively affects cytokines/chemokines. ► We detected a hypothetic b...
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Veröffentlicht in: | Cytokine (Philadelphia, Pa.) Pa.), 2013-05, Vol.62 (2), p.290-296 |
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description | ► Hypertension is a prominent cause for coronary artery disease and associated with inflammation. ► Telmisartan has well-known antihypertensive and less-known anti-inflammatory effects. ► In hypertensive patients telmisartan only selectively affects cytokines/chemokines. ► We detected a hypothetic biphasic association between coronary artery calcification and MCP-1. ► TNF-α, IP-10 and MCP-1 could play a role in the progression of atherosclerosis.
Hypertension is one of the most prominent risk factors for coronary artery disease (CAD). Treatment of hypertension is therefore important for reducing cardiovascular events and the progression of atherosclerosis. Several treatment strategies are common in clinical practice for example the use of ACE-blockers or angiotensin receptor II blockers (ARBs), so called sartans. Telmisartan, belonging to the class of ARBs, was shown to exert anti-inflammatory effects besides the blood pressure lowering.
In this work, two separate substudy groups of hypertensives were compared. 16 patients with arterial hypertension have been treated with telmisartan (initial 40mg Kinzalmono®) for 7.3±4.4months. The telmisartan group was compared to a matched control group including 31 hypertensive patients without telmisartan treatment with a follow up period of 1.9±0.5years. Serum samples from the beginning and the end of follow up were analyzed with Luminex® technology for 26 cytokines and chemokines. The baseline scores of coronary artery calcification (CAC) were gathered by multislice detector computer tomography.
After 7months of telmisartan treatment and 2years in control patients most of the measured analytes did not change significantly. MCP-1 (P=0.001; P |
doi_str_mv | 10.1016/j.cyto.2013.02.001 |
format | Article |
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Hypertension is one of the most prominent risk factors for coronary artery disease (CAD). Treatment of hypertension is therefore important for reducing cardiovascular events and the progression of atherosclerosis. Several treatment strategies are common in clinical practice for example the use of ACE-blockers or angiotensin receptor II blockers (ARBs), so called sartans. Telmisartan, belonging to the class of ARBs, was shown to exert anti-inflammatory effects besides the blood pressure lowering.
In this work, two separate substudy groups of hypertensives were compared. 16 patients with arterial hypertension have been treated with telmisartan (initial 40mg Kinzalmono®) for 7.3±4.4months. The telmisartan group was compared to a matched control group including 31 hypertensive patients without telmisartan treatment with a follow up period of 1.9±0.5years. Serum samples from the beginning and the end of follow up were analyzed with Luminex® technology for 26 cytokines and chemokines. The baseline scores of coronary artery calcification (CAC) were gathered by multislice detector computer tomography.
After 7months of telmisartan treatment and 2years in control patients most of the measured analytes did not change significantly. MCP-1 (P=0.001; P<0.001) was increased significantly in both telmisartan and control group. The relative decrease in IP-10 and TNF-α levels was observed in telmisartan group, as opposed to the increase in control (telmisartan vs. control P=0.048; P=0.01). No linear rank-correlation between measured analytes and the initial CAC was found.
Telmisartan reduced blood pressure in patients with atherosclerosis and arterial hypertension within a short time period, whereas the inflammatory status of these patients remained largely unchanged. An involvement of telmisartan in the regulation of inflammatory and anti-inflammatory mediators in the context of CAD and CAC is possible, but cannot clearly be assumed based on the present findings.</description><identifier>ISSN: 1043-4666</identifier><identifier>EISSN: 1096-0023</identifier><identifier>DOI: 10.1016/j.cyto.2013.02.001</identifier><identifier>PMID: 23541900</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Angiotensin II Type 1 Receptor Blockers - therapeutic use ; Angiotensin-Converting Enzyme Inhibitors - therapeutic use ; anti-inflammatory activity ; Atherosclerosis ; Atherosclerosis - drug therapy ; Benzimidazoles - therapeutic use ; Benzoates - therapeutic use ; blood pressure ; Blood Pressure - drug effects ; blood serum ; calcification ; Chemokine CCL2 - blood ; Chemokine CXCL10 - blood ; Chemokines ; computed tomography ; coronary artery disease ; Coronary Artery Disease - drug therapy ; coronary vessels ; Cytokines ; Female ; Humans ; hypertension ; Hypertension - drug therapy ; Inflammation - drug therapy ; Interleukin-6 - blood ; Male ; Middle Aged ; patients ; Risk factors ; Telmisartan ; Tumor Necrosis Factor-alpha - blood</subject><ispartof>Cytokine (Philadelphia, Pa.), 2013-05, Vol.62 (2), p.290-296</ispartof><rights>2013</rights><rights>Copyright © 2013. Published by Elsevier Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c380t-89eab48487c50569cb17dfc5ffe3bde5ea57c92d5221220ec49c12bd4b0821373</citedby><cites>FETCH-LOGICAL-c380t-89eab48487c50569cb17dfc5ffe3bde5ea57c92d5221220ec49c12bd4b0821373</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1043466613000513$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23541900$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Klinghammer, Lutz</creatorcontrib><creatorcontrib>Urschel, Katharina</creatorcontrib><creatorcontrib>Cicha, Iwona</creatorcontrib><creatorcontrib>Lewczuk, Piotr</creatorcontrib><creatorcontrib>Raaz-Schrauder, Dorette</creatorcontrib><creatorcontrib>Achenbach, Stephan</creatorcontrib><creatorcontrib>Garlichs, Christoph D.</creatorcontrib><title>Impact of telmisartan on the inflammatory state in patients with coronary atherosclerosis – Influence on IP-10, TNF-α and MCP-1</title><title>Cytokine (Philadelphia, Pa.)</title><addtitle>Cytokine</addtitle><description>► Hypertension is a prominent cause for coronary artery disease and associated with inflammation. ► Telmisartan has well-known antihypertensive and less-known anti-inflammatory effects. ► In hypertensive patients telmisartan only selectively affects cytokines/chemokines. ► We detected a hypothetic biphasic association between coronary artery calcification and MCP-1. ► TNF-α, IP-10 and MCP-1 could play a role in the progression of atherosclerosis.
Hypertension is one of the most prominent risk factors for coronary artery disease (CAD). Treatment of hypertension is therefore important for reducing cardiovascular events and the progression of atherosclerosis. Several treatment strategies are common in clinical practice for example the use of ACE-blockers or angiotensin receptor II blockers (ARBs), so called sartans. Telmisartan, belonging to the class of ARBs, was shown to exert anti-inflammatory effects besides the blood pressure lowering.
In this work, two separate substudy groups of hypertensives were compared. 16 patients with arterial hypertension have been treated with telmisartan (initial 40mg Kinzalmono®) for 7.3±4.4months. The telmisartan group was compared to a matched control group including 31 hypertensive patients without telmisartan treatment with a follow up period of 1.9±0.5years. Serum samples from the beginning and the end of follow up were analyzed with Luminex® technology for 26 cytokines and chemokines. The baseline scores of coronary artery calcification (CAC) were gathered by multislice detector computer tomography.
After 7months of telmisartan treatment and 2years in control patients most of the measured analytes did not change significantly. MCP-1 (P=0.001; P<0.001) was increased significantly in both telmisartan and control group. The relative decrease in IP-10 and TNF-α levels was observed in telmisartan group, as opposed to the increase in control (telmisartan vs. control P=0.048; P=0.01). No linear rank-correlation between measured analytes and the initial CAC was found.
Telmisartan reduced blood pressure in patients with atherosclerosis and arterial hypertension within a short time period, whereas the inflammatory status of these patients remained largely unchanged. An involvement of telmisartan in the regulation of inflammatory and anti-inflammatory mediators in the context of CAD and CAC is possible, but cannot clearly be assumed based on the present findings.</description><subject>Angiotensin II Type 1 Receptor Blockers - therapeutic use</subject><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</subject><subject>anti-inflammatory activity</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - drug therapy</subject><subject>Benzimidazoles - therapeutic use</subject><subject>Benzoates - therapeutic use</subject><subject>blood pressure</subject><subject>Blood Pressure - drug effects</subject><subject>blood serum</subject><subject>calcification</subject><subject>Chemokine CCL2 - blood</subject><subject>Chemokine CXCL10 - blood</subject><subject>Chemokines</subject><subject>computed tomography</subject><subject>coronary artery disease</subject><subject>Coronary Artery Disease - drug therapy</subject><subject>coronary vessels</subject><subject>Cytokines</subject><subject>Female</subject><subject>Humans</subject><subject>hypertension</subject><subject>Hypertension - drug therapy</subject><subject>Inflammation - drug therapy</subject><subject>Interleukin-6 - blood</subject><subject>Male</subject><subject>Middle Aged</subject><subject>patients</subject><subject>Risk factors</subject><subject>Telmisartan</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><issn>1043-4666</issn><issn>1096-0023</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1O3TAUha2qqPyUDXTQetgBSa_tOD9SJ-gJ2icBrQSMLce5KX5K4lfbr4gZYgtdCRthEV0Jjh7tsBPbuj7nyOczIe8Y5AxY-WmVm7vocg5M5MBzAPaK7DFoygyAi9fzuRBZUZblLtkPYQUAjaiqN2SXC1mwBmCPPCzHtTaRup5GHEYbtI96om6i8QapnfpBj6OOzt_REHWcR3Sto8UpBnpr4w01zrtJp3udHN4FM8yrDfTP_W-6TAEbnAzOicvvGYMjenVxmj09Uj119HyRRm_JTq-HgIcv-wG5Pj25WnzNzr59WS6OzzIjaohZ3aBui7qoKyNBlo1pWdX1RvY9irZDiVpWpuGd5JxxDmiKxjDedkULNWeiEgfk4zZ37d3PDYaoUl2Dw6AndJugmCgqLiWIMkn5VmpSleCxV2tvx1RSMVAze7VSM3s1s1fAVWKfTO9f8jftiN0_y1_YSfBhK-i1U_qHt0FdX6YEmT6mlqKSSfF5q8DE4ZdFr4KxM77OejRRdc7-7wXPwSOgDQ</recordid><startdate>20130501</startdate><enddate>20130501</enddate><creator>Klinghammer, Lutz</creator><creator>Urschel, Katharina</creator><creator>Cicha, Iwona</creator><creator>Lewczuk, Piotr</creator><creator>Raaz-Schrauder, Dorette</creator><creator>Achenbach, Stephan</creator><creator>Garlichs, Christoph D.</creator><general>Elsevier Ltd</general><scope>FBQ</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>20130501</creationdate><title>Impact of telmisartan on the inflammatory state in patients with coronary atherosclerosis – Influence on IP-10, TNF-α and MCP-1</title><author>Klinghammer, Lutz ; Urschel, Katharina ; Cicha, Iwona ; Lewczuk, Piotr ; Raaz-Schrauder, Dorette ; Achenbach, Stephan ; Garlichs, Christoph D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c380t-89eab48487c50569cb17dfc5ffe3bde5ea57c92d5221220ec49c12bd4b0821373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Angiotensin II Type 1 Receptor Blockers - therapeutic use</topic><topic>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</topic><topic>anti-inflammatory activity</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - drug therapy</topic><topic>Benzimidazoles - therapeutic use</topic><topic>Benzoates - therapeutic use</topic><topic>blood pressure</topic><topic>Blood Pressure - drug effects</topic><topic>blood serum</topic><topic>calcification</topic><topic>Chemokine CCL2 - blood</topic><topic>Chemokine CXCL10 - blood</topic><topic>Chemokines</topic><topic>computed tomography</topic><topic>coronary artery disease</topic><topic>Coronary Artery Disease - drug therapy</topic><topic>coronary vessels</topic><topic>Cytokines</topic><topic>Female</topic><topic>Humans</topic><topic>hypertension</topic><topic>Hypertension - drug therapy</topic><topic>Inflammation - drug therapy</topic><topic>Interleukin-6 - blood</topic><topic>Male</topic><topic>Middle Aged</topic><topic>patients</topic><topic>Risk factors</topic><topic>Telmisartan</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Klinghammer, Lutz</creatorcontrib><creatorcontrib>Urschel, Katharina</creatorcontrib><creatorcontrib>Cicha, Iwona</creatorcontrib><creatorcontrib>Lewczuk, Piotr</creatorcontrib><creatorcontrib>Raaz-Schrauder, Dorette</creatorcontrib><creatorcontrib>Achenbach, Stephan</creatorcontrib><creatorcontrib>Garlichs, Christoph D.</creatorcontrib><collection>AGRIS</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>Cytokine (Philadelphia, Pa.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Klinghammer, Lutz</au><au>Urschel, Katharina</au><au>Cicha, Iwona</au><au>Lewczuk, Piotr</au><au>Raaz-Schrauder, Dorette</au><au>Achenbach, Stephan</au><au>Garlichs, Christoph D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of telmisartan on the inflammatory state in patients with coronary atherosclerosis – Influence on IP-10, TNF-α and MCP-1</atitle><jtitle>Cytokine (Philadelphia, Pa.)</jtitle><addtitle>Cytokine</addtitle><date>2013-05-01</date><risdate>2013</risdate><volume>62</volume><issue>2</issue><spage>290</spage><epage>296</epage><pages>290-296</pages><issn>1043-4666</issn><eissn>1096-0023</eissn><abstract>► Hypertension is a prominent cause for coronary artery disease and associated with inflammation. ► Telmisartan has well-known antihypertensive and less-known anti-inflammatory effects. ► In hypertensive patients telmisartan only selectively affects cytokines/chemokines. ► We detected a hypothetic biphasic association between coronary artery calcification and MCP-1. ► TNF-α, IP-10 and MCP-1 could play a role in the progression of atherosclerosis.
Hypertension is one of the most prominent risk factors for coronary artery disease (CAD). Treatment of hypertension is therefore important for reducing cardiovascular events and the progression of atherosclerosis. Several treatment strategies are common in clinical practice for example the use of ACE-blockers or angiotensin receptor II blockers (ARBs), so called sartans. Telmisartan, belonging to the class of ARBs, was shown to exert anti-inflammatory effects besides the blood pressure lowering.
In this work, two separate substudy groups of hypertensives were compared. 16 patients with arterial hypertension have been treated with telmisartan (initial 40mg Kinzalmono®) for 7.3±4.4months. The telmisartan group was compared to a matched control group including 31 hypertensive patients without telmisartan treatment with a follow up period of 1.9±0.5years. Serum samples from the beginning and the end of follow up were analyzed with Luminex® technology for 26 cytokines and chemokines. The baseline scores of coronary artery calcification (CAC) were gathered by multislice detector computer tomography.
After 7months of telmisartan treatment and 2years in control patients most of the measured analytes did not change significantly. MCP-1 (P=0.001; P<0.001) was increased significantly in both telmisartan and control group. The relative decrease in IP-10 and TNF-α levels was observed in telmisartan group, as opposed to the increase in control (telmisartan vs. control P=0.048; P=0.01). No linear rank-correlation between measured analytes and the initial CAC was found.
Telmisartan reduced blood pressure in patients with atherosclerosis and arterial hypertension within a short time period, whereas the inflammatory status of these patients remained largely unchanged. An involvement of telmisartan in the regulation of inflammatory and anti-inflammatory mediators in the context of CAD and CAC is possible, but cannot clearly be assumed based on the present findings.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>23541900</pmid><doi>10.1016/j.cyto.2013.02.001</doi><tpages>7</tpages></addata></record> |
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subjects | Angiotensin II Type 1 Receptor Blockers - therapeutic use Angiotensin-Converting Enzyme Inhibitors - therapeutic use anti-inflammatory activity Atherosclerosis Atherosclerosis - drug therapy Benzimidazoles - therapeutic use Benzoates - therapeutic use blood pressure Blood Pressure - drug effects blood serum calcification Chemokine CCL2 - blood Chemokine CXCL10 - blood Chemokines computed tomography coronary artery disease Coronary Artery Disease - drug therapy coronary vessels Cytokines Female Humans hypertension Hypertension - drug therapy Inflammation - drug therapy Interleukin-6 - blood Male Middle Aged patients Risk factors Telmisartan Tumor Necrosis Factor-alpha - blood |
title | Impact of telmisartan on the inflammatory state in patients with coronary atherosclerosis – Influence on IP-10, TNF-α and MCP-1 |
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