Inflammation and carotid artery : Risk for atherosclerosis study (ICARAS)
Compelling evidence suggests that inflammation is fundamentally involved in the pathogenesis of atherosclerosis; however, temporal correlation between inflammation and morphological features of atherosclerosis progression has not been demonstrated unequivocally. We prospectively studied 1268 consecu...
Gespeichert in:
Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2005-05, Vol.111 (17), p.2203-2209 |
---|---|
Hauptverfasser: | , , , , , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 2209 |
---|---|
container_issue | 17 |
container_start_page | 2203 |
container_title | Circulation (New York, N.Y.) |
container_volume | 111 |
creator | SCHILLINGER, Martin EXNER, Markus LALOUSCHEK, Wolfgang RUMPOLD, Helmut MAURER, Gerald WAGNER, Oswald MINAR, Erich MLEKUSCH, Wolfgang SABETI, Schila AMIGHI, Jasmin NIKOWITSCH, Robert TIMMEL, Ewald KICKINGER, Bernhard MINAR, Christoph PONES, Matthias |
description | Compelling evidence suggests that inflammation is fundamentally involved in the pathogenesis of atherosclerosis; however, temporal correlation between inflammation and morphological features of atherosclerosis progression has not been demonstrated unequivocally.
We prospectively studied 1268 consecutive patients who were initially asymptomatic with respect to carotid artery disease. Patients underwent serial carotid ultrasound investigations at baseline and after a follow-up interval of a median of 7.5 months (range 6 to 9 months), with measurement of carotid flow velocities and categorization of carotid arteries as 0% to 29%, 30% to 49%, 50% to 69%, 70% to 89%, or 90% to 99% stenosed or occluded. High-sensitivity C-reactive protein (hs-CRP) and serum amyloid A (SAA) were measured at baseline and follow-up. Progression of carotid atherosclerosis was found in 103 (8.1%) of 1268 patients. Hs-CRP and SAA, respectively, at baseline (P=0.004 and P=0.014) and follow-up (P |
doi_str_mv | 10.1161/01.CIR.0000163569.97918.C0 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67786715</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67786715</sourcerecordid><originalsourceid>FETCH-LOGICAL-c508t-e6823726fef544cf0561882d68900659f280ab6164550067b4903d5372ce63df3</originalsourceid><addsrcrecordid>eNpFkFtLwzAYhoMobk7_ggRB0YvWpGlOuxvFQ2EgTL0OWZpgtYeZtBf792ZusFwkJDzvl5cHgBuMUowZfkQ4LcpViuLCjFAmU8klFmmBTsAU0yxPckrkKZhGQCacZNkEXITwHa-McHoOJpgKiqkkU1CWnWt02-qh7juouwoa7fuhrqD2g_VbOIerOvxA13uohy_r-2Ca3V4HGIax2sL7slisFu8Pl-DM6SbYq8M5A5_PTx_Fa7J8e4nIMjEUiSGxTGSEZ8xZR_PcOEQZFiKrmJCxHpUuE0ivGWY5pfGBr3OJSEVjxFhGKkdm4G4_d-P739GGQbV1MLZpdGf7MSjGuWAc0wjO96CJdYO3Tm183Wq_VRipnUiFsIoi1VGk-hepChTD14dfxnVrq2P0YC4CtwdAB6Mb53Vn6nDkdjU4JeQPrOZ5lQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67786715</pqid></control><display><type>article</type><title>Inflammation and carotid artery : Risk for atherosclerosis study (ICARAS)</title><source>MEDLINE</source><source>American Heart Association Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Journals@Ovid Complete</source><creator>SCHILLINGER, Martin ; EXNER, Markus ; LALOUSCHEK, Wolfgang ; RUMPOLD, Helmut ; MAURER, Gerald ; WAGNER, Oswald ; MINAR, Erich ; MLEKUSCH, Wolfgang ; SABETI, Schila ; AMIGHI, Jasmin ; NIKOWITSCH, Robert ; TIMMEL, Ewald ; KICKINGER, Bernhard ; MINAR, Christoph ; PONES, Matthias</creator><creatorcontrib>SCHILLINGER, Martin ; EXNER, Markus ; LALOUSCHEK, Wolfgang ; RUMPOLD, Helmut ; MAURER, Gerald ; WAGNER, Oswald ; MINAR, Erich ; MLEKUSCH, Wolfgang ; SABETI, Schila ; AMIGHI, Jasmin ; NIKOWITSCH, Robert ; TIMMEL, Ewald ; KICKINGER, Bernhard ; MINAR, Christoph ; PONES, Matthias</creatorcontrib><description>Compelling evidence suggests that inflammation is fundamentally involved in the pathogenesis of atherosclerosis; however, temporal correlation between inflammation and morphological features of atherosclerosis progression has not been demonstrated unequivocally.
We prospectively studied 1268 consecutive patients who were initially asymptomatic with respect to carotid artery disease. Patients underwent serial carotid ultrasound investigations at baseline and after a follow-up interval of a median of 7.5 months (range 6 to 9 months), with measurement of carotid flow velocities and categorization of carotid arteries as 0% to 29%, 30% to 49%, 50% to 69%, 70% to 89%, or 90% to 99% stenosed or occluded. High-sensitivity C-reactive protein (hs-CRP) and serum amyloid A (SAA) were measured at baseline and follow-up. Progression of carotid atherosclerosis was found in 103 (8.1%) of 1268 patients. Hs-CRP and SAA, respectively, at baseline (P=0.004 and P=0.014) and follow-up (P<0.001 and P<0.001) and the change from baseline to follow-up (P<0.001 and P<0.001) were significantly associated with progressive atherosclerosis. Adjusted ORs (95% CI) for atherosclerosis progression with increasing quintiles of baseline hs-CRP were 1.65 (0.71 to 3.84), 1.87 (0.8 to 4.37), 3.32 (1.49 to 7.39), and 3.65 (1.65 to 8.08), and with increasing quintiles of baseline SAA, they were 0.86 (0.38 to 1.92), 0.99 (0.49 to 1.99), 1.72 (0.91 to 3.28), and 2.28 (1.24 to 4.20), respectively, compared with the lowest quintiles.
These findings supply evidence for a close temporal correlation between inflammation and morphological features of rapidly progressive carotid atherosclerosis, which suggests that elevation or increase of the inflammatory biomarkers hs-CRP and SAA identifies the presence of active atherosclerotic disease.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.0000163569.97918.C0</identifier><identifier>PMID: 15851593</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Aged ; Atherosclerosis (general aspects, experimental research) ; Atherosclerosis - diagnostic imaging ; Atherosclerosis - etiology ; Biological and medical sciences ; Blood and lymphatic vessels ; C-Reactive Protein - analysis ; Cardiology. Vascular system ; Carotid Artery Diseases - diagnostic imaging ; Carotid Artery Diseases - etiology ; Carotid Artery Diseases - pathology ; Carotid Stenosis ; Coronary heart disease ; Disease Progression ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Female ; Heart ; Humans ; Inflammation - complications ; Inflammation - diagnostic imaging ; Logistic Models ; Male ; Medical sciences ; Middle Aged ; Prospective Studies ; Risk Factors ; Serum Amyloid A Protein - analysis ; Ultrasonography</subject><ispartof>Circulation (New York, N.Y.), 2005-05, Vol.111 (17), p.2203-2209</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-e6823726fef544cf0561882d68900659f280ab6164550067b4903d5372ce63df3</citedby><cites>FETCH-LOGICAL-c508t-e6823726fef544cf0561882d68900659f280ab6164550067b4903d5372ce63df3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16778753$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15851593$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SCHILLINGER, Martin</creatorcontrib><creatorcontrib>EXNER, Markus</creatorcontrib><creatorcontrib>LALOUSCHEK, Wolfgang</creatorcontrib><creatorcontrib>RUMPOLD, Helmut</creatorcontrib><creatorcontrib>MAURER, Gerald</creatorcontrib><creatorcontrib>WAGNER, Oswald</creatorcontrib><creatorcontrib>MINAR, Erich</creatorcontrib><creatorcontrib>MLEKUSCH, Wolfgang</creatorcontrib><creatorcontrib>SABETI, Schila</creatorcontrib><creatorcontrib>AMIGHI, Jasmin</creatorcontrib><creatorcontrib>NIKOWITSCH, Robert</creatorcontrib><creatorcontrib>TIMMEL, Ewald</creatorcontrib><creatorcontrib>KICKINGER, Bernhard</creatorcontrib><creatorcontrib>MINAR, Christoph</creatorcontrib><creatorcontrib>PONES, Matthias</creatorcontrib><title>Inflammation and carotid artery : Risk for atherosclerosis study (ICARAS)</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Compelling evidence suggests that inflammation is fundamentally involved in the pathogenesis of atherosclerosis; however, temporal correlation between inflammation and morphological features of atherosclerosis progression has not been demonstrated unequivocally.
We prospectively studied 1268 consecutive patients who were initially asymptomatic with respect to carotid artery disease. Patients underwent serial carotid ultrasound investigations at baseline and after a follow-up interval of a median of 7.5 months (range 6 to 9 months), with measurement of carotid flow velocities and categorization of carotid arteries as 0% to 29%, 30% to 49%, 50% to 69%, 70% to 89%, or 90% to 99% stenosed or occluded. High-sensitivity C-reactive protein (hs-CRP) and serum amyloid A (SAA) were measured at baseline and follow-up. Progression of carotid atherosclerosis was found in 103 (8.1%) of 1268 patients. Hs-CRP and SAA, respectively, at baseline (P=0.004 and P=0.014) and follow-up (P<0.001 and P<0.001) and the change from baseline to follow-up (P<0.001 and P<0.001) were significantly associated with progressive atherosclerosis. Adjusted ORs (95% CI) for atherosclerosis progression with increasing quintiles of baseline hs-CRP were 1.65 (0.71 to 3.84), 1.87 (0.8 to 4.37), 3.32 (1.49 to 7.39), and 3.65 (1.65 to 8.08), and with increasing quintiles of baseline SAA, they were 0.86 (0.38 to 1.92), 0.99 (0.49 to 1.99), 1.72 (0.91 to 3.28), and 2.28 (1.24 to 4.20), respectively, compared with the lowest quintiles.
These findings supply evidence for a close temporal correlation between inflammation and morphological features of rapidly progressive carotid atherosclerosis, which suggests that elevation or increase of the inflammatory biomarkers hs-CRP and SAA identifies the presence of active atherosclerotic disease.</description><subject>Aged</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Atherosclerosis - diagnostic imaging</subject><subject>Atherosclerosis - etiology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>C-Reactive Protein - analysis</subject><subject>Cardiology. Vascular system</subject><subject>Carotid Artery Diseases - diagnostic imaging</subject><subject>Carotid Artery Diseases - etiology</subject><subject>Carotid Artery Diseases - pathology</subject><subject>Carotid Stenosis</subject><subject>Coronary heart disease</subject><subject>Disease Progression</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Female</subject><subject>Heart</subject><subject>Humans</subject><subject>Inflammation - complications</subject><subject>Inflammation - diagnostic imaging</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Prospective Studies</subject><subject>Risk Factors</subject><subject>Serum Amyloid A Protein - analysis</subject><subject>Ultrasonography</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkFtLwzAYhoMobk7_ggRB0YvWpGlOuxvFQ2EgTL0OWZpgtYeZtBf792ZusFwkJDzvl5cHgBuMUowZfkQ4LcpViuLCjFAmU8klFmmBTsAU0yxPckrkKZhGQCacZNkEXITwHa-McHoOJpgKiqkkU1CWnWt02-qh7juouwoa7fuhrqD2g_VbOIerOvxA13uohy_r-2Ca3V4HGIax2sL7slisFu8Pl-DM6SbYq8M5A5_PTx_Fa7J8e4nIMjEUiSGxTGSEZ8xZR_PcOEQZFiKrmJCxHpUuE0ivGWY5pfGBr3OJSEVjxFhGKkdm4G4_d-P739GGQbV1MLZpdGf7MSjGuWAc0wjO96CJdYO3Tm183Wq_VRipnUiFsIoi1VGk-hepChTD14dfxnVrq2P0YC4CtwdAB6Mb53Vn6nDkdjU4JeQPrOZ5lQ</recordid><startdate>20050503</startdate><enddate>20050503</enddate><creator>SCHILLINGER, Martin</creator><creator>EXNER, Markus</creator><creator>LALOUSCHEK, Wolfgang</creator><creator>RUMPOLD, Helmut</creator><creator>MAURER, Gerald</creator><creator>WAGNER, Oswald</creator><creator>MINAR, Erich</creator><creator>MLEKUSCH, Wolfgang</creator><creator>SABETI, Schila</creator><creator>AMIGHI, Jasmin</creator><creator>NIKOWITSCH, Robert</creator><creator>TIMMEL, Ewald</creator><creator>KICKINGER, Bernhard</creator><creator>MINAR, Christoph</creator><creator>PONES, Matthias</creator><general>Lippincott Williams & Wilkins</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>20050503</creationdate><title>Inflammation and carotid artery : Risk for atherosclerosis study (ICARAS)</title><author>SCHILLINGER, Martin ; EXNER, Markus ; LALOUSCHEK, Wolfgang ; RUMPOLD, Helmut ; MAURER, Gerald ; WAGNER, Oswald ; MINAR, Erich ; MLEKUSCH, Wolfgang ; SABETI, Schila ; AMIGHI, Jasmin ; NIKOWITSCH, Robert ; TIMMEL, Ewald ; KICKINGER, Bernhard ; MINAR, Christoph ; PONES, Matthias</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c508t-e6823726fef544cf0561882d68900659f280ab6164550067b4903d5372ce63df3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Aged</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Atherosclerosis - diagnostic imaging</topic><topic>Atherosclerosis - etiology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>C-Reactive Protein - analysis</topic><topic>Cardiology. Vascular system</topic><topic>Carotid Artery Diseases - diagnostic imaging</topic><topic>Carotid Artery Diseases - etiology</topic><topic>Carotid Artery Diseases - pathology</topic><topic>Carotid Stenosis</topic><topic>Coronary heart disease</topic><topic>Disease Progression</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Female</topic><topic>Heart</topic><topic>Humans</topic><topic>Inflammation - complications</topic><topic>Inflammation - diagnostic imaging</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Prospective Studies</topic><topic>Risk Factors</topic><topic>Serum Amyloid A Protein - analysis</topic><topic>Ultrasonography</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SCHILLINGER, Martin</creatorcontrib><creatorcontrib>EXNER, Markus</creatorcontrib><creatorcontrib>LALOUSCHEK, Wolfgang</creatorcontrib><creatorcontrib>RUMPOLD, Helmut</creatorcontrib><creatorcontrib>MAURER, Gerald</creatorcontrib><creatorcontrib>WAGNER, Oswald</creatorcontrib><creatorcontrib>MINAR, Erich</creatorcontrib><creatorcontrib>MLEKUSCH, Wolfgang</creatorcontrib><creatorcontrib>SABETI, Schila</creatorcontrib><creatorcontrib>AMIGHI, Jasmin</creatorcontrib><creatorcontrib>NIKOWITSCH, Robert</creatorcontrib><creatorcontrib>TIMMEL, Ewald</creatorcontrib><creatorcontrib>KICKINGER, Bernhard</creatorcontrib><creatorcontrib>MINAR, Christoph</creatorcontrib><creatorcontrib>PONES, Matthias</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>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SCHILLINGER, Martin</au><au>EXNER, Markus</au><au>LALOUSCHEK, Wolfgang</au><au>RUMPOLD, Helmut</au><au>MAURER, Gerald</au><au>WAGNER, Oswald</au><au>MINAR, Erich</au><au>MLEKUSCH, Wolfgang</au><au>SABETI, Schila</au><au>AMIGHI, Jasmin</au><au>NIKOWITSCH, Robert</au><au>TIMMEL, Ewald</au><au>KICKINGER, Bernhard</au><au>MINAR, Christoph</au><au>PONES, Matthias</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inflammation and carotid artery : Risk for atherosclerosis study (ICARAS)</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2005-05-03</date><risdate>2005</risdate><volume>111</volume><issue>17</issue><spage>2203</spage><epage>2209</epage><pages>2203-2209</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Compelling evidence suggests that inflammation is fundamentally involved in the pathogenesis of atherosclerosis; however, temporal correlation between inflammation and morphological features of atherosclerosis progression has not been demonstrated unequivocally.
We prospectively studied 1268 consecutive patients who were initially asymptomatic with respect to carotid artery disease. Patients underwent serial carotid ultrasound investigations at baseline and after a follow-up interval of a median of 7.5 months (range 6 to 9 months), with measurement of carotid flow velocities and categorization of carotid arteries as 0% to 29%, 30% to 49%, 50% to 69%, 70% to 89%, or 90% to 99% stenosed or occluded. High-sensitivity C-reactive protein (hs-CRP) and serum amyloid A (SAA) were measured at baseline and follow-up. Progression of carotid atherosclerosis was found in 103 (8.1%) of 1268 patients. Hs-CRP and SAA, respectively, at baseline (P=0.004 and P=0.014) and follow-up (P<0.001 and P<0.001) and the change from baseline to follow-up (P<0.001 and P<0.001) were significantly associated with progressive atherosclerosis. Adjusted ORs (95% CI) for atherosclerosis progression with increasing quintiles of baseline hs-CRP were 1.65 (0.71 to 3.84), 1.87 (0.8 to 4.37), 3.32 (1.49 to 7.39), and 3.65 (1.65 to 8.08), and with increasing quintiles of baseline SAA, they were 0.86 (0.38 to 1.92), 0.99 (0.49 to 1.99), 1.72 (0.91 to 3.28), and 2.28 (1.24 to 4.20), respectively, compared with the lowest quintiles.
These findings supply evidence for a close temporal correlation between inflammation and morphological features of rapidly progressive carotid atherosclerosis, which suggests that elevation or increase of the inflammatory biomarkers hs-CRP and SAA identifies the presence of active atherosclerotic disease.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>15851593</pmid><doi>10.1161/01.CIR.0000163569.97918.C0</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0009-7322 |
ispartof | Circulation (New York, N.Y.), 2005-05, Vol.111 (17), p.2203-2209 |
issn | 0009-7322 1524-4539 |
language | eng |
recordid | cdi_proquest_miscellaneous_67786715 |
source | MEDLINE; American Heart Association Journals; EZB-FREE-00999 freely available EZB journals; Journals@Ovid Complete |
subjects | Aged Atherosclerosis (general aspects, experimental research) Atherosclerosis - diagnostic imaging Atherosclerosis - etiology Biological and medical sciences Blood and lymphatic vessels C-Reactive Protein - analysis Cardiology. Vascular system Carotid Artery Diseases - diagnostic imaging Carotid Artery Diseases - etiology Carotid Artery Diseases - pathology Carotid Stenosis Coronary heart disease Disease Progression Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Female Heart Humans Inflammation - complications Inflammation - diagnostic imaging Logistic Models Male Medical sciences Middle Aged Prospective Studies Risk Factors Serum Amyloid A Protein - analysis Ultrasonography |
title | Inflammation and carotid artery : Risk for atherosclerosis study (ICARAS) |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-07T03%3A39%3A55IST&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=Inflammation%20and%20carotid%20artery%20:%20Risk%20for%20atherosclerosis%20study%20(ICARAS)&rft.jtitle=Circulation%20(New%20York,%20N.Y.)&rft.au=SCHILLINGER,%20Martin&rft.date=2005-05-03&rft.volume=111&rft.issue=17&rft.spage=2203&rft.epage=2209&rft.pages=2203-2209&rft.issn=0009-7322&rft.eissn=1524-4539&rft.coden=CIRCAZ&rft_id=info:doi/10.1161/01.CIR.0000163569.97918.C0&rft_dat=%3Cproquest_cross%3E67786715%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=67786715&rft_id=info:pmid/15851593&rfr_iscdi=true |