AB0758 Subclinical Atherosclerosis is not Accelerated in Well-Controlled Ankylosing Spondylitis: Original Data and Meta-Analysis of Published Studies
BackgroundChronic inflammatory rheumatic diseases associate with increased risk of cardiovascular disease (CVD) in part due to accelerated atherosclerosis. While this is well established for rheumatoid arthritis (1), data on ankylosing spondylitis (AS) is limited and the relative contribution of inf...
Gespeichert in:
| Veröffentlicht in: | Annals of the rheumatic diseases 2015-06, Vol.74 (Suppl 2), p.1152 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | Suppl 2 |
| container_start_page | 1152 |
| container_title | Annals of the rheumatic diseases |
| container_volume | 74 |
| creator | Arida, A. Protogerou, A.D. Konstantonis, G. Konsta, M. Delicha, E. Kitas, G.D. Sfikakis, P.P. |
| description | BackgroundChronic inflammatory rheumatic diseases associate with increased risk of cardiovascular disease (CVD) in part due to accelerated atherosclerosis. While this is well established for rheumatoid arthritis (1), data on ankylosing spondylitis (AS) is limited and the relative contribution of inflammation versus classical cardiovascular risk factors remains a matter of controversy (2).ObjectivesTo address this controversy in an original, carefully designed study of subclinical atherosclerosis in AS patients, as well as in a meta-analysis of previous studies.MethodsAtheromatic plaques in carotid and femoral arteries, carotid hypertrophy (intima-media thickness-IMT; cross sectional area) and carotid stiffness by ultrasound, as well as aortic stiffness by pulse wave velocity were examined in consecutive non-diabetic CVD-free, AS patients. Apparently healthy individuals carefully matched 1:1 with patients for age, gender, smoking, dyslipidemia and hypertension served as controls. A meta-analysis of those studies that examined subclinical atherosclerosis in AS patients versus controls with comparable CVD risk factors, published up to June 2014, was also performed. Studies were subsequently stratified according to the mean level of disease activity (BASDAI> or or |
| doi_str_mv | 10.1136/annrheumdis-2015-eular.2937 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_1901767017</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4322500159</sourcerecordid><originalsourceid>FETCH-LOGICAL-b1277-6fd3c7414104bc2064b676a6a561e4d7fe85789502ab33f1da78108650bacfd53</originalsourceid><addsrcrecordid>eNqVkc9OwyAcx4nRxDl9B5KdO2FtodNTnX-TGU2m8Ugo0I3J6AR66M2Lz-D7-SRS58GrCfkRvvl-vwE-AIwwGmOcklNurVupdiO1TyYI54lqDXfjyTSle2CAM1JEmaB9MEAIpUk2JfQQHHm_jkdU4GIAPssLRPPi6_1j0VbCaKsFN7AMK-UaL0w_tYdx2SbAUggVJR6UhNrCF2VMMmtscI0xUSrta2ei3y7hYttY2RkdtD-DD04vtY21lzxwyK2E9yrwpIxS17c3NXxsK6P9KpYsQiu18sfgoObGq5PffQier6-eZrfJ_OHmblbOkwpPKE1ILVNBM5xhlFUivjWrCCWc8JxglUlaqyKnxTRHE16laY0lpwVGBclRxUUt83QIRrverWveWuUDWzetizfzDE8RpoTGEV3nO5eI_-GdqtnW6Q13HcOI9STYHxKsJ8F-SLCeREyTXbrarP8V_AaPGJdV</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1901767017</pqid></control><display><type>article</type><title>AB0758 Subclinical Atherosclerosis is not Accelerated in Well-Controlled Ankylosing Spondylitis: Original Data and Meta-Analysis of Published Studies</title><source>BMJ Journals - NESLi2</source><creator>Arida, A. ; Protogerou, A.D. ; Konstantonis, G. ; Konsta, M. ; Delicha, E. ; Kitas, G.D. ; Sfikakis, P.P.</creator><creatorcontrib>Arida, A. ; Protogerou, A.D. ; Konstantonis, G. ; Konsta, M. ; Delicha, E. ; Kitas, G.D. ; Sfikakis, P.P.</creatorcontrib><description>BackgroundChronic inflammatory rheumatic diseases associate with increased risk of cardiovascular disease (CVD) in part due to accelerated atherosclerosis. While this is well established for rheumatoid arthritis (1), data on ankylosing spondylitis (AS) is limited and the relative contribution of inflammation versus classical cardiovascular risk factors remains a matter of controversy (2).ObjectivesTo address this controversy in an original, carefully designed study of subclinical atherosclerosis in AS patients, as well as in a meta-analysis of previous studies.MethodsAtheromatic plaques in carotid and femoral arteries, carotid hypertrophy (intima-media thickness-IMT; cross sectional area) and carotid stiffness by ultrasound, as well as aortic stiffness by pulse wave velocity were examined in consecutive non-diabetic CVD-free, AS patients. Apparently healthy individuals carefully matched 1:1 with patients for age, gender, smoking, dyslipidemia and hypertension served as controls. A meta-analysis of those studies that examined subclinical atherosclerosis in AS patients versus controls with comparable CVD risk factors, published up to June 2014, was also performed. Studies were subsequently stratified according to the mean level of disease activity (BASDAI> or <4), and the proportion of patients receiving anti-TNF biological therapy (> or <50%).ResultsIn this contemporary cohort comprising of 67 AS patients (82% men), aged 47.5+12.5 years (mean ± SD), with median disease duration of 12 years and BASDAI of 1.8 (IQR 0.4-3.6), of whom 66% were receiving anti-TNF treatment, atheromatic plaques were slightly less prevalent compared to controls. Moreover, carotid hypertrophy and stiffness, as well as aortic stiffness, were comparable between patients and their matched controls. Meta-analysis and meta-regression analysis of 14 studies, including the present study, revealed that carotid IMT is significantly increased in AS patients versus controls. On the other hand, analysis of those studies examining also the presence of carotid plaques revealed no statistical difference in the relative risk of the presence of carotid plaques between AS patients and their matched controls. Interestingly, however, increased IMT was not evident in studies involving well-controlled patients (mean BASDAI <4) or in those studies which included >50% of anti-TNF-treated patients.ConclusionsSubclinical atherosclerosis is not accelerated in well-controlled AS patients.ReferencesPeters MJ, et al. EULAR evidence-based recommendations for cardiovascular risk management in patients with rheumatoid arthritis and other forms of inflammatory arthritis. Ann Rheum Dis 2010;69:325-31.Mathieu S, et al. Cardiovascular profile in ankylosing spondylitis: a systematic review and meta-analysis. Arthritis Care Res 2011;4:557-63.Disclosure of InterestNone declared</description><identifier>ISSN: 0003-4967</identifier><identifier>EISSN: 1468-2060</identifier><identifier>DOI: 10.1136/annrheumdis-2015-eular.2937</identifier><identifier>CODEN: ARDIAO</identifier><language>eng</language><publisher>Kidlington: Elsevier Limited</publisher><ispartof>Annals of the rheumatic diseases, 2015-06, Vol.74 (Suppl 2), p.1152</ispartof><rights>2015, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><rights>Copyright: 2015 (c) 2015, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://ard.bmj.com/content/74/Suppl_2/1152.1.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://ard.bmj.com/content/74/Suppl_2/1152.1.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,776,780,3183,23550,27901,27902,77569,77600</link.rule.ids></links><search><creatorcontrib>Arida, A.</creatorcontrib><creatorcontrib>Protogerou, A.D.</creatorcontrib><creatorcontrib>Konstantonis, G.</creatorcontrib><creatorcontrib>Konsta, M.</creatorcontrib><creatorcontrib>Delicha, E.</creatorcontrib><creatorcontrib>Kitas, G.D.</creatorcontrib><creatorcontrib>Sfikakis, P.P.</creatorcontrib><title>AB0758 Subclinical Atherosclerosis is not Accelerated in Well-Controlled Ankylosing Spondylitis: Original Data and Meta-Analysis of Published Studies</title><title>Annals of the rheumatic diseases</title><description>BackgroundChronic inflammatory rheumatic diseases associate with increased risk of cardiovascular disease (CVD) in part due to accelerated atherosclerosis. While this is well established for rheumatoid arthritis (1), data on ankylosing spondylitis (AS) is limited and the relative contribution of inflammation versus classical cardiovascular risk factors remains a matter of controversy (2).ObjectivesTo address this controversy in an original, carefully designed study of subclinical atherosclerosis in AS patients, as well as in a meta-analysis of previous studies.MethodsAtheromatic plaques in carotid and femoral arteries, carotid hypertrophy (intima-media thickness-IMT; cross sectional area) and carotid stiffness by ultrasound, as well as aortic stiffness by pulse wave velocity were examined in consecutive non-diabetic CVD-free, AS patients. Apparently healthy individuals carefully matched 1:1 with patients for age, gender, smoking, dyslipidemia and hypertension served as controls. A meta-analysis of those studies that examined subclinical atherosclerosis in AS patients versus controls with comparable CVD risk factors, published up to June 2014, was also performed. Studies were subsequently stratified according to the mean level of disease activity (BASDAI> or <4), and the proportion of patients receiving anti-TNF biological therapy (> or <50%).ResultsIn this contemporary cohort comprising of 67 AS patients (82% men), aged 47.5+12.5 years (mean ± SD), with median disease duration of 12 years and BASDAI of 1.8 (IQR 0.4-3.6), of whom 66% were receiving anti-TNF treatment, atheromatic plaques were slightly less prevalent compared to controls. Moreover, carotid hypertrophy and stiffness, as well as aortic stiffness, were comparable between patients and their matched controls. Meta-analysis and meta-regression analysis of 14 studies, including the present study, revealed that carotid IMT is significantly increased in AS patients versus controls. On the other hand, analysis of those studies examining also the presence of carotid plaques revealed no statistical difference in the relative risk of the presence of carotid plaques between AS patients and their matched controls. Interestingly, however, increased IMT was not evident in studies involving well-controlled patients (mean BASDAI <4) or in those studies which included >50% of anti-TNF-treated patients.ConclusionsSubclinical atherosclerosis is not accelerated in well-controlled AS patients.ReferencesPeters MJ, et al. EULAR evidence-based recommendations for cardiovascular risk management in patients with rheumatoid arthritis and other forms of inflammatory arthritis. Ann Rheum Dis 2010;69:325-31.Mathieu S, et al. Cardiovascular profile in ankylosing spondylitis: a systematic review and meta-analysis. Arthritis Care Res 2011;4:557-63.Disclosure of InterestNone declared</description><issn>0003-4967</issn><issn>1468-2060</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNqVkc9OwyAcx4nRxDl9B5KdO2FtodNTnX-TGU2m8Ugo0I3J6AR66M2Lz-D7-SRS58GrCfkRvvl-vwE-AIwwGmOcklNurVupdiO1TyYI54lqDXfjyTSle2CAM1JEmaB9MEAIpUk2JfQQHHm_jkdU4GIAPssLRPPi6_1j0VbCaKsFN7AMK-UaL0w_tYdx2SbAUggVJR6UhNrCF2VMMmtscI0xUSrta2ei3y7hYttY2RkdtD-DD04vtY21lzxwyK2E9yrwpIxS17c3NXxsK6P9KpYsQiu18sfgoObGq5PffQier6-eZrfJ_OHmblbOkwpPKE1ILVNBM5xhlFUivjWrCCWc8JxglUlaqyKnxTRHE16laY0lpwVGBclRxUUt83QIRrverWveWuUDWzetizfzDE8RpoTGEV3nO5eI_-GdqtnW6Q13HcOI9STYHxKsJ8F-SLCeREyTXbrarP8V_AaPGJdV</recordid><startdate>201506</startdate><enddate>201506</enddate><creator>Arida, A.</creator><creator>Protogerou, A.D.</creator><creator>Konstantonis, G.</creator><creator>Konsta, M.</creator><creator>Delicha, E.</creator><creator>Kitas, G.D.</creator><creator>Sfikakis, P.P.</creator><general>Elsevier Limited</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope></search><sort><creationdate>201506</creationdate><title>AB0758 Subclinical Atherosclerosis is not Accelerated in Well-Controlled Ankylosing Spondylitis: Original Data and Meta-Analysis of Published Studies</title><author>Arida, A. ; Protogerou, A.D. ; Konstantonis, G. ; Konsta, M. ; Delicha, E. ; Kitas, G.D. ; Sfikakis, P.P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b1277-6fd3c7414104bc2064b676a6a561e4d7fe85789502ab33f1da78108650bacfd53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arida, A.</creatorcontrib><creatorcontrib>Protogerou, A.D.</creatorcontrib><creatorcontrib>Konstantonis, G.</creatorcontrib><creatorcontrib>Konsta, M.</creatorcontrib><creatorcontrib>Delicha, E.</creatorcontrib><creatorcontrib>Kitas, G.D.</creatorcontrib><creatorcontrib>Sfikakis, P.P.</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><jtitle>Annals of the rheumatic diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Arida, A.</au><au>Protogerou, A.D.</au><au>Konstantonis, G.</au><au>Konsta, M.</au><au>Delicha, E.</au><au>Kitas, G.D.</au><au>Sfikakis, P.P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>AB0758 Subclinical Atherosclerosis is not Accelerated in Well-Controlled Ankylosing Spondylitis: Original Data and Meta-Analysis of Published Studies</atitle><jtitle>Annals of the rheumatic diseases</jtitle><date>2015-06</date><risdate>2015</risdate><volume>74</volume><issue>Suppl 2</issue><spage>1152</spage><pages>1152-</pages><issn>0003-4967</issn><eissn>1468-2060</eissn><coden>ARDIAO</coden><abstract>BackgroundChronic inflammatory rheumatic diseases associate with increased risk of cardiovascular disease (CVD) in part due to accelerated atherosclerosis. While this is well established for rheumatoid arthritis (1), data on ankylosing spondylitis (AS) is limited and the relative contribution of inflammation versus classical cardiovascular risk factors remains a matter of controversy (2).ObjectivesTo address this controversy in an original, carefully designed study of subclinical atherosclerosis in AS patients, as well as in a meta-analysis of previous studies.MethodsAtheromatic plaques in carotid and femoral arteries, carotid hypertrophy (intima-media thickness-IMT; cross sectional area) and carotid stiffness by ultrasound, as well as aortic stiffness by pulse wave velocity were examined in consecutive non-diabetic CVD-free, AS patients. Apparently healthy individuals carefully matched 1:1 with patients for age, gender, smoking, dyslipidemia and hypertension served as controls. A meta-analysis of those studies that examined subclinical atherosclerosis in AS patients versus controls with comparable CVD risk factors, published up to June 2014, was also performed. Studies were subsequently stratified according to the mean level of disease activity (BASDAI> or <4), and the proportion of patients receiving anti-TNF biological therapy (> or <50%).ResultsIn this contemporary cohort comprising of 67 AS patients (82% men), aged 47.5+12.5 years (mean ± SD), with median disease duration of 12 years and BASDAI of 1.8 (IQR 0.4-3.6), of whom 66% were receiving anti-TNF treatment, atheromatic plaques were slightly less prevalent compared to controls. Moreover, carotid hypertrophy and stiffness, as well as aortic stiffness, were comparable between patients and their matched controls. Meta-analysis and meta-regression analysis of 14 studies, including the present study, revealed that carotid IMT is significantly increased in AS patients versus controls. On the other hand, analysis of those studies examining also the presence of carotid plaques revealed no statistical difference in the relative risk of the presence of carotid plaques between AS patients and their matched controls. Interestingly, however, increased IMT was not evident in studies involving well-controlled patients (mean BASDAI <4) or in those studies which included >50% of anti-TNF-treated patients.ConclusionsSubclinical atherosclerosis is not accelerated in well-controlled AS patients.ReferencesPeters MJ, et al. EULAR evidence-based recommendations for cardiovascular risk management in patients with rheumatoid arthritis and other forms of inflammatory arthritis. Ann Rheum Dis 2010;69:325-31.Mathieu S, et al. Cardiovascular profile in ankylosing spondylitis: a systematic review and meta-analysis. Arthritis Care Res 2011;4:557-63.Disclosure of InterestNone declared</abstract><cop>Kidlington</cop><pub>Elsevier Limited</pub><doi>10.1136/annrheumdis-2015-eular.2937</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0003-4967 |
| ispartof | Annals of the rheumatic diseases, 2015-06, Vol.74 (Suppl 2), p.1152 |
| issn | 0003-4967 1468-2060 |
| language | eng |
| recordid | cdi_proquest_journals_1901767017 |
| source | BMJ Journals - NESLi2 |
| title | AB0758 Subclinical Atherosclerosis is not Accelerated in Well-Controlled Ankylosing Spondylitis: Original Data and Meta-Analysis of Published Studies |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-19T00%3A35%3A18IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=AB0758%E2%80%85Subclinical%20Atherosclerosis%20is%20not%20Accelerated%20in%20Well-Controlled%20Ankylosing%20Spondylitis:%20Original%20Data%20and%20Meta-Analysis%20of%20Published%20Studies&rft.jtitle=Annals%20of%20the%20rheumatic%20diseases&rft.au=Arida,%20A.&rft.date=2015-06&rft.volume=74&rft.issue=Suppl%202&rft.spage=1152&rft.pages=1152-&rft.issn=0003-4967&rft.eissn=1468-2060&rft.coden=ARDIAO&rft_id=info:doi/10.1136/annrheumdis-2015-eular.2937&rft_dat=%3Cproquest_cross%3E4322500159%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1901767017&rft_id=info:pmid/&rfr_iscdi=true |