Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes
Objective: To assess the relation between markers of inflammation and the presence of multiple vulnerable plaques in patients with non-ST segment elevation acute coronary syndromes. Design: Prospective cohort study of 55 patients with non-ST segment elevation acute coronary syndromes and angiographi...
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| Veröffentlicht in: | Heart (British Cardiac Society) 2004-08, Vol.90 (8), p.847-852 |
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| description | Objective: To assess the relation between markers of inflammation and the presence of multiple vulnerable plaques in patients with non-ST segment elevation acute coronary syndromes. Design: Prospective cohort study of 55 patients with non-ST segment elevation acute coronary syndromes and angiographically documented coronary disease. Blood samples were obtained at study entry for the assessment of high sensitivity C reactive protein (CRP), neopterin, and neutrophil count. Coronary stenoses were assessed by quantitative computerised angiography and classified as “complex” (irregular borders, ulceration, or filling defects) or “smooth” (absence of complex features). Extent of disease was also assessed by a validated angiographic score. Results: Neutrophil count (r = 0.36, p = 0.007), CRP concentration (r = 0.33, p = 0.02), and neopterin concentration (r = 0.45, p < 0.001) correlated with the number of complex stenoses. Patients with multiple (three or more) complex stenoses, but not patients with multiple smooth lesions, had a higher neutrophil count (5.9 (1.4) × 109/l v 4.8 (1.4) × 109/l, p = 0.02), CRP concentration (log transformed) (1.08 (0.63) v 0.6 (0.6), p = 0.03), and neopterin concentration (log transformed) (0.94 (0.18) v 0.79 (0.15), p = 0.002). Multiple regression analysis showed that neopterin concentration (B = 4.8, 95% confidence interval (CI) 1.9 to 7.7, p = 0.002) and extent of coronary artery disease (B = 0.6, 95% CI 0.03 to 1.2, p = 0.04) were independently associated with the number of complex stenoses. Conclusions: Acute inflammatory markers such as high neutrophil count, CRP concentration, and neopterin concentration correlate with the presence of multiple angiographically complex coronary stenoses. Neopterin concentration was a stronger predictor of multiple complex plaques than were neutrophil count and CRP concentration. These findings suggest that a relation exists between inflammation and pancoronary plaque vulnerability. |
| doi_str_mv | 10.1136/hrt.2003.015826 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1768348</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4020640641</sourcerecordid><originalsourceid>FETCH-LOGICAL-b452t-d66cbb669800f90ec937f4a3f99c99840de67faa8acf0b211861b48623c024c83</originalsourceid><addsrcrecordid>eNqFkl2P1CAUhhujcT_02jtDYjRq0lkolMKNiZnoalw_ouu6d4QydIdZCl1ox53f4p-Vps26emO4OITz8J5zeMmyRwguEML0aB36RQEhXkBUsoLeyfYRoSwvIDq_m_a4LHMKcbWXHcS4gRASzuj9bA-VRYk54fvZr48yXOoQgW-AcY2VbSt74x2QbgXawfamsxoo36ZwDWKvnY86gueddMoH72TYgc7Kq0GD7WCdDrI21vS7F0kNdElKuz6Cn6ZfA-dd_u0URH3RpkOgrd7OpdTQjzVmubhzq-BbHR9k9xppo344x8Ps-9s3p8t3-cnn4_fL1yd5Tcqiz1eUqrqmlDMIGw614rhqiMQN54pzRuBK06qRkknVwLpAiFFUE0YLrGBBFMOH2atJtxvqVq9U6i5IK7pg2tSP8NKIvzPOrMWF3wpUUYbJKPBsFgg-vUTsRWui0tZKp_0QBaUVHFcCn_wDbvwQXBouaTFICSkQT9TRRKngYwy6uWkFQTHaLpLtYrRdTLanG49vT_CHn31OwNMZkFFJ24Rkn4m3OM5pgUahfOJMsvr6Jp_-iKAVrkrx6Wwpvpwd8x_w67n4kPiXE1-3m_92-RtRcNc6</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1780644219</pqid></control><display><type>article</type><title>Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Avanzas, P ; Arroyo-Espliguero, R ; Cosín-Sales, J ; Aldama, G ; Pizzi, C ; Quiles, J ; Kaski, J C</creator><creatorcontrib>Avanzas, P ; Arroyo-Espliguero, R ; Cosín-Sales, J ; Aldama, G ; Pizzi, C ; Quiles, J ; Kaski, J C</creatorcontrib><description>Objective: To assess the relation between markers of inflammation and the presence of multiple vulnerable plaques in patients with non-ST segment elevation acute coronary syndromes. Design: Prospective cohort study of 55 patients with non-ST segment elevation acute coronary syndromes and angiographically documented coronary disease. Blood samples were obtained at study entry for the assessment of high sensitivity C reactive protein (CRP), neopterin, and neutrophil count. Coronary stenoses were assessed by quantitative computerised angiography and classified as “complex” (irregular borders, ulceration, or filling defects) or “smooth” (absence of complex features). Extent of disease was also assessed by a validated angiographic score. Results: Neutrophil count (r = 0.36, p = 0.007), CRP concentration (r = 0.33, p = 0.02), and neopterin concentration (r = 0.45, p < 0.001) correlated with the number of complex stenoses. Patients with multiple (three or more) complex stenoses, but not patients with multiple smooth lesions, had a higher neutrophil count (5.9 (1.4) × 109/l v 4.8 (1.4) × 109/l, p = 0.02), CRP concentration (log transformed) (1.08 (0.63) v 0.6 (0.6), p = 0.03), and neopterin concentration (log transformed) (0.94 (0.18) v 0.79 (0.15), p = 0.002). Multiple regression analysis showed that neopterin concentration (B = 4.8, 95% confidence interval (CI) 1.9 to 7.7, p = 0.002) and extent of coronary artery disease (B = 0.6, 95% CI 0.03 to 1.2, p = 0.04) were independently associated with the number of complex stenoses. Conclusions: Acute inflammatory markers such as high neutrophil count, CRP concentration, and neopterin concentration correlate with the presence of multiple angiographically complex coronary stenoses. Neopterin concentration was a stronger predictor of multiple complex plaques than were neutrophil count and CRP concentration. These findings suggest that a relation exists between inflammation and pancoronary plaque vulnerability.</description><identifier>ISSN: 1355-6037</identifier><identifier>EISSN: 1468-201X</identifier><identifier>DOI: 10.1136/hrt.2003.015826</identifier><identifier>PMID: 15253949</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Cardiovascular Society</publisher><subject>Acute coronary syndromes ; Agreements ; Angina pectoris ; Angina, Unstable - blood ; Angina, Unstable - pathology ; Biological and medical sciences ; Biomarkers - blood ; Blood ; C reactive protein ; C-Reactive Protein - metabolism ; Cardiology ; Cardiology. Vascular system ; Cardiovascular disease ; Cardiovascular Medicine ; Classification ; Cohort Studies ; Coronary Artery Disease - blood ; Coronary Artery Disease - pathology ; Coronary Disease - blood ; Coronary Disease - pathology ; Coronary heart disease ; Coronary Stenosis - blood ; Coronary Stenosis - pathology ; Coronary vessels ; Female ; Heart ; Heart attacks ; Hospitals ; Humans ; Inflammation ; Leukocyte Count ; Macrophages - metabolism ; Male ; Medical imaging ; Medical sciences ; Middle Aged ; Morphology ; neopterin ; Neopterin - metabolism ; Neutrophils ; plaque complexity ; Prospective Studies ; Studies ; Syndrome</subject><ispartof>Heart (British Cardiac Society), 2004-08, Vol.90 (8), p.847-852</ispartof><rights>Copyright 2004 by Heart</rights><rights>2004 INIST-CNRS</rights><rights>Copyright: 2004 Copyright 2004 by Heart</rights><rights>Copyright © Copyright 2004 by Heart 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b452t-d66cbb669800f90ec937f4a3f99c99840de67faa8acf0b211861b48623c024c83</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768348/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768348/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15996216$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15253949$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Avanzas, P</creatorcontrib><creatorcontrib>Arroyo-Espliguero, R</creatorcontrib><creatorcontrib>Cosín-Sales, J</creatorcontrib><creatorcontrib>Aldama, G</creatorcontrib><creatorcontrib>Pizzi, C</creatorcontrib><creatorcontrib>Quiles, J</creatorcontrib><creatorcontrib>Kaski, J C</creatorcontrib><title>Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes</title><title>Heart (British Cardiac Society)</title><addtitle>Heart</addtitle><description>Objective: To assess the relation between markers of inflammation and the presence of multiple vulnerable plaques in patients with non-ST segment elevation acute coronary syndromes. Design: Prospective cohort study of 55 patients with non-ST segment elevation acute coronary syndromes and angiographically documented coronary disease. Blood samples were obtained at study entry for the assessment of high sensitivity C reactive protein (CRP), neopterin, and neutrophil count. Coronary stenoses were assessed by quantitative computerised angiography and classified as “complex” (irregular borders, ulceration, or filling defects) or “smooth” (absence of complex features). Extent of disease was also assessed by a validated angiographic score. Results: Neutrophil count (r = 0.36, p = 0.007), CRP concentration (r = 0.33, p = 0.02), and neopterin concentration (r = 0.45, p < 0.001) correlated with the number of complex stenoses. Patients with multiple (three or more) complex stenoses, but not patients with multiple smooth lesions, had a higher neutrophil count (5.9 (1.4) × 109/l v 4.8 (1.4) × 109/l, p = 0.02), CRP concentration (log transformed) (1.08 (0.63) v 0.6 (0.6), p = 0.03), and neopterin concentration (log transformed) (0.94 (0.18) v 0.79 (0.15), p = 0.002). Multiple regression analysis showed that neopterin concentration (B = 4.8, 95% confidence interval (CI) 1.9 to 7.7, p = 0.002) and extent of coronary artery disease (B = 0.6, 95% CI 0.03 to 1.2, p = 0.04) were independently associated with the number of complex stenoses. Conclusions: Acute inflammatory markers such as high neutrophil count, CRP concentration, and neopterin concentration correlate with the presence of multiple angiographically complex coronary stenoses. Neopterin concentration was a stronger predictor of multiple complex plaques than were neutrophil count and CRP concentration. These findings suggest that a relation exists between inflammation and pancoronary plaque vulnerability.</description><subject>Acute coronary syndromes</subject><subject>Agreements</subject><subject>Angina pectoris</subject><subject>Angina, Unstable - blood</subject><subject>Angina, Unstable - pathology</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - blood</subject><subject>Blood</subject><subject>C reactive protein</subject><subject>C-Reactive Protein - metabolism</subject><subject>Cardiology</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular Medicine</subject><subject>Classification</subject><subject>Cohort Studies</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - pathology</subject><subject>Coronary Disease - blood</subject><subject>Coronary Disease - pathology</subject><subject>Coronary heart disease</subject><subject>Coronary Stenosis - blood</subject><subject>Coronary Stenosis - pathology</subject><subject>Coronary vessels</subject><subject>Female</subject><subject>Heart</subject><subject>Heart attacks</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Leukocyte Count</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Medical imaging</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Morphology</subject><subject>neopterin</subject><subject>Neopterin - metabolism</subject><subject>Neutrophils</subject><subject>plaque complexity</subject><subject>Prospective Studies</subject><subject>Studies</subject><subject>Syndrome</subject><issn>1355-6037</issn><issn>1468-201X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkl2P1CAUhhujcT_02jtDYjRq0lkolMKNiZnoalw_ouu6d4QydIdZCl1ox53f4p-Vps26emO4OITz8J5zeMmyRwguEML0aB36RQEhXkBUsoLeyfYRoSwvIDq_m_a4LHMKcbWXHcS4gRASzuj9bA-VRYk54fvZr48yXOoQgW-AcY2VbSt74x2QbgXawfamsxoo36ZwDWKvnY86gueddMoH72TYgc7Kq0GD7WCdDrI21vS7F0kNdElKuz6Cn6ZfA-dd_u0URH3RpkOgrd7OpdTQjzVmubhzq-BbHR9k9xppo344x8Ps-9s3p8t3-cnn4_fL1yd5Tcqiz1eUqrqmlDMIGw614rhqiMQN54pzRuBK06qRkknVwLpAiFFUE0YLrGBBFMOH2atJtxvqVq9U6i5IK7pg2tSP8NKIvzPOrMWF3wpUUYbJKPBsFgg-vUTsRWui0tZKp_0QBaUVHFcCn_wDbvwQXBouaTFICSkQT9TRRKngYwy6uWkFQTHaLpLtYrRdTLanG49vT_CHn31OwNMZkFFJ24Rkn4m3OM5pgUahfOJMsvr6Jp_-iKAVrkrx6Wwpvpwd8x_w67n4kPiXE1-3m_92-RtRcNc6</recordid><startdate>20040801</startdate><enddate>20040801</enddate><creator>Avanzas, P</creator><creator>Arroyo-Espliguero, R</creator><creator>Cosín-Sales, J</creator><creator>Aldama, G</creator><creator>Pizzi, C</creator><creator>Quiles, J</creator><creator>Kaski, J C</creator><general>BMJ Publishing Group Ltd and British Cardiovascular Society</general><general>BMJ</general><general>BMJ Publishing Group LTD</general><general>Copyright 2004 by Heart</general><scope>BSCLL</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</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>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20040801</creationdate><title>Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes</title><author>Avanzas, P ; Arroyo-Espliguero, R ; Cosín-Sales, J ; Aldama, G ; Pizzi, C ; Quiles, J ; Kaski, J C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b452t-d66cbb669800f90ec937f4a3f99c99840de67faa8acf0b211861b48623c024c83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Acute coronary syndromes</topic><topic>Agreements</topic><topic>Angina pectoris</topic><topic>Angina, Unstable - blood</topic><topic>Angina, Unstable - pathology</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - blood</topic><topic>Blood</topic><topic>C reactive protein</topic><topic>C-Reactive Protein - metabolism</topic><topic>Cardiology</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular Medicine</topic><topic>Classification</topic><topic>Cohort Studies</topic><topic>Coronary Artery Disease - blood</topic><topic>Coronary Artery Disease - pathology</topic><topic>Coronary Disease - blood</topic><topic>Coronary Disease - pathology</topic><topic>Coronary heart disease</topic><topic>Coronary Stenosis - blood</topic><topic>Coronary Stenosis - pathology</topic><topic>Coronary vessels</topic><topic>Female</topic><topic>Heart</topic><topic>Heart attacks</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Leukocyte Count</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Medical imaging</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Morphology</topic><topic>neopterin</topic><topic>Neopterin - metabolism</topic><topic>Neutrophils</topic><topic>plaque complexity</topic><topic>Prospective Studies</topic><topic>Studies</topic><topic>Syndrome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Avanzas, P</creatorcontrib><creatorcontrib>Arroyo-Espliguero, R</creatorcontrib><creatorcontrib>Cosín-Sales, J</creatorcontrib><creatorcontrib>Aldama, G</creatorcontrib><creatorcontrib>Pizzi, C</creatorcontrib><creatorcontrib>Quiles, J</creatorcontrib><creatorcontrib>Kaski, J C</creatorcontrib><collection>Istex</collection><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>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>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>ProQuest Central</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>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 Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Heart (British Cardiac Society)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Avanzas, P</au><au>Arroyo-Espliguero, R</au><au>Cosín-Sales, J</au><au>Aldama, G</au><au>Pizzi, C</au><au>Quiles, J</au><au>Kaski, J C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes</atitle><jtitle>Heart (British Cardiac Society)</jtitle><addtitle>Heart</addtitle><date>2004-08-01</date><risdate>2004</risdate><volume>90</volume><issue>8</issue><spage>847</spage><epage>852</epage><pages>847-852</pages><issn>1355-6037</issn><eissn>1468-201X</eissn><abstract>Objective: To assess the relation between markers of inflammation and the presence of multiple vulnerable plaques in patients with non-ST segment elevation acute coronary syndromes. Design: Prospective cohort study of 55 patients with non-ST segment elevation acute coronary syndromes and angiographically documented coronary disease. Blood samples were obtained at study entry for the assessment of high sensitivity C reactive protein (CRP), neopterin, and neutrophil count. Coronary stenoses were assessed by quantitative computerised angiography and classified as “complex” (irregular borders, ulceration, or filling defects) or “smooth” (absence of complex features). Extent of disease was also assessed by a validated angiographic score. Results: Neutrophil count (r = 0.36, p = 0.007), CRP concentration (r = 0.33, p = 0.02), and neopterin concentration (r = 0.45, p < 0.001) correlated with the number of complex stenoses. Patients with multiple (three or more) complex stenoses, but not patients with multiple smooth lesions, had a higher neutrophil count (5.9 (1.4) × 109/l v 4.8 (1.4) × 109/l, p = 0.02), CRP concentration (log transformed) (1.08 (0.63) v 0.6 (0.6), p = 0.03), and neopterin concentration (log transformed) (0.94 (0.18) v 0.79 (0.15), p = 0.002). Multiple regression analysis showed that neopterin concentration (B = 4.8, 95% confidence interval (CI) 1.9 to 7.7, p = 0.002) and extent of coronary artery disease (B = 0.6, 95% CI 0.03 to 1.2, p = 0.04) were independently associated with the number of complex stenoses. Conclusions: Acute inflammatory markers such as high neutrophil count, CRP concentration, and neopterin concentration correlate with the presence of multiple angiographically complex coronary stenoses. Neopterin concentration was a stronger predictor of multiple complex plaques than were neutrophil count and CRP concentration. These findings suggest that a relation exists between inflammation and pancoronary plaque vulnerability.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Cardiovascular Society</pub><pmid>15253949</pmid><doi>10.1136/hrt.2003.015826</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute coronary syndromes Agreements Angina pectoris Angina, Unstable - blood Angina, Unstable - pathology Biological and medical sciences Biomarkers - blood Blood C reactive protein C-Reactive Protein - metabolism Cardiology Cardiology. Vascular system Cardiovascular disease Cardiovascular Medicine Classification Cohort Studies Coronary Artery Disease - blood Coronary Artery Disease - pathology Coronary Disease - blood Coronary Disease - pathology Coronary heart disease Coronary Stenosis - blood Coronary Stenosis - pathology Coronary vessels Female Heart Heart attacks Hospitals Humans Inflammation Leukocyte Count Macrophages - metabolism Male Medical imaging Medical sciences Middle Aged Morphology neopterin Neopterin - metabolism Neutrophils plaque complexity Prospective Studies Studies Syndrome |
| title | Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes |
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