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Calprotectin and platelet aggregation in patients with stable coronary artery disease
Recent studies suggest that the inflammation-associated protein calprotectin may be implicated in the pathogenesis of coronary artery disease (CAD). However, the impact of calprotectin levels on platelet aggregation in CAD patients has never been investigated. We investigated the association between...
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Published in: | PloS one 2015-05, Vol.10 (5), p.e0125992-e0125992 |
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description | Recent studies suggest that the inflammation-associated protein calprotectin may be implicated in the pathogenesis of coronary artery disease (CAD). However, the impact of calprotectin levels on platelet aggregation in CAD patients has never been investigated.
We investigated the association between calprotectin levels and platelet aggregation in stable, high-risk CAD patients receiving aspirin as mono antiplatelet therapy. Furthermore, we aimed to investigate independent clinical and laboratory determinants of calprotectin levels.
We performed a cross-sectional study including 581 stable, high-risk CAD patients. All patients received 75 mg aspirin daily as mono antiplatelet therapy. Platelet aggregation was assessed by 1) impedance aggregometry (Multiplate Analyzer) using arachidonic acid (AA) and collagen as agonists and by 2) the VerifyNow Aspirin Assay. Low-grade inflammation was evaluated by calprotectin, high-sensitive C-reactive-protein (hs-CRP) and interleukin-6. Platelet activation was assessed by soluble P-selectin, and cyclooxygenase-1 inhibition was evaluated by serum thromboxane B2, both measured by ELISA.
Calprotectin levels correlated positively with platelet aggregation according to Multiplate Analyzer (r=0.12, p=0.01). Additionally, calprotectin was positively associated with leukocytes (r=0.33, p |
doi_str_mv | 10.1371/journal.pone.0125992 |
format | article |
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We investigated the association between calprotectin levels and platelet aggregation in stable, high-risk CAD patients receiving aspirin as mono antiplatelet therapy. Furthermore, we aimed to investigate independent clinical and laboratory determinants of calprotectin levels.
We performed a cross-sectional study including 581 stable, high-risk CAD patients. All patients received 75 mg aspirin daily as mono antiplatelet therapy. Platelet aggregation was assessed by 1) impedance aggregometry (Multiplate Analyzer) using arachidonic acid (AA) and collagen as agonists and by 2) the VerifyNow Aspirin Assay. Low-grade inflammation was evaluated by calprotectin, high-sensitive C-reactive-protein (hs-CRP) and interleukin-6. Platelet activation was assessed by soluble P-selectin, and cyclooxygenase-1 inhibition was evaluated by serum thromboxane B2, both measured by ELISA.
Calprotectin levels correlated positively with platelet aggregation according to Multiplate Analyzer (r=0.12, p=0.01). Additionally, calprotectin was positively associated with leukocytes (r=0.33, p<0.0001), hs-CRP (r=0.31, p<0.0001), interleukin-6 (r=0.28, p<0.0001), soluble P-selectin (r=0.10, p=0.02) and serum thromboxane B2 (r=0.10, p=0.02). Type 2 diabetes mellitus was an independent predictor of increased calprotectin levels (p=0.004), and trends were seen for body mass index (p=0.06) and smoking (p=0.07). Compliance with aspirin was confirmed by low serum thromboxane B2 levels in all patients (median [25%;75%]: 1.07 [0.52;1.87] ng/mL).
Calprotectin levels correlated positively, though weakly, with platelet aggregation and activation as well as serum thromboxane B2 in high-risk, stable CAD patients treated with aspirin.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0125992</identifier><identifier>PMID: 25970343</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Aged ; Agglomeration ; Arachidonic acid ; Aspirin ; Aspirin - therapeutic use ; Atherosclerosis ; Blood platelets ; Body mass ; Body mass index ; Body size ; C-Reactive Protein - metabolism ; Cardiology ; Cardiovascular disease ; Care and treatment ; Collagen ; Coronary artery ; Coronary artery disease ; Coronary Artery Disease - blood ; Coronary Artery Disease - drug therapy ; Coronary Artery Disease - physiopathology ; Coronary heart disease ; Coronary vessels ; Cross-Sectional Studies ; Cyclooxygenase-1 ; Diabetes ; Diabetes mellitus ; Diagnosis ; Dosage and administration ; Enzyme-linked immunosorbent assay ; Female ; Health sciences ; Heart attacks ; Heart diseases ; Heart surgery ; Hematology ; Hospitals ; Humans ; Inflammation ; Interleukin ; Interleukin 6 ; Interleukin-6 - blood ; Laboratories ; Leukocyte L1 Antigen Complex - blood ; Leukocytes ; Male ; Medication Adherence ; Middle Aged ; P-selectin ; Pathogenesis ; Patients ; Platelet Aggregation ; Platelet Aggregation Inhibitors - therapeutic use ; Proteins ; Quality ; Risk ; Risk factors ; Smoking ; Studies ; Therapy ; Thromboxane B2 - blood ; Type 2 diabetes ; Unsaturated fatty acids ; Weight control</subject><ispartof>PloS one, 2015-05, Vol.10 (5), p.e0125992-e0125992</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Larsen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Larsen et al 2015 Larsen et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-7e4eb5b367d89608f9d179fa0bec7acc92eccfdf25d33d288c2ec9c2c85470743</citedby><cites>FETCH-LOGICAL-c692t-7e4eb5b367d89608f9d179fa0bec7acc92eccfdf25d33d288c2ec9c2c85470743</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1683763950/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1683763950?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25970343$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Freson, Kathleen</contributor><creatorcontrib>Larsen, Sanne Bøjet</creatorcontrib><creatorcontrib>Grove, Erik Lerkevang</creatorcontrib><creatorcontrib>Pareek, Manan</creatorcontrib><creatorcontrib>Kristensen, Steen Dalby</creatorcontrib><creatorcontrib>Hvas, Anne-Mette</creatorcontrib><title>Calprotectin and platelet aggregation in patients with stable coronary artery disease</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Recent studies suggest that the inflammation-associated protein calprotectin may be implicated in the pathogenesis of coronary artery disease (CAD). However, the impact of calprotectin levels on platelet aggregation in CAD patients has never been investigated.
We investigated the association between calprotectin levels and platelet aggregation in stable, high-risk CAD patients receiving aspirin as mono antiplatelet therapy. Furthermore, we aimed to investigate independent clinical and laboratory determinants of calprotectin levels.
We performed a cross-sectional study including 581 stable, high-risk CAD patients. All patients received 75 mg aspirin daily as mono antiplatelet therapy. Platelet aggregation was assessed by 1) impedance aggregometry (Multiplate Analyzer) using arachidonic acid (AA) and collagen as agonists and by 2) the VerifyNow Aspirin Assay. Low-grade inflammation was evaluated by calprotectin, high-sensitive C-reactive-protein (hs-CRP) and interleukin-6. Platelet activation was assessed by soluble P-selectin, and cyclooxygenase-1 inhibition was evaluated by serum thromboxane B2, both measured by ELISA.
Calprotectin levels correlated positively with platelet aggregation according to Multiplate Analyzer (r=0.12, p=0.01). Additionally, calprotectin was positively associated with leukocytes (r=0.33, p<0.0001), hs-CRP (r=0.31, p<0.0001), interleukin-6 (r=0.28, p<0.0001), soluble P-selectin (r=0.10, p=0.02) and serum thromboxane B2 (r=0.10, p=0.02). Type 2 diabetes mellitus was an independent predictor of increased calprotectin levels (p=0.004), and trends were seen for body mass index (p=0.06) and smoking (p=0.07). Compliance with aspirin was confirmed by low serum thromboxane B2 levels in all patients (median [25%;75%]: 1.07 [0.52;1.87] ng/mL).
Calprotectin levels correlated positively, though weakly, with platelet aggregation and activation as well as serum thromboxane B2 in high-risk, stable CAD patients treated with aspirin.</description><subject>Activation</subject><subject>Aged</subject><subject>Agglomeration</subject><subject>Arachidonic acid</subject><subject>Aspirin</subject><subject>Aspirin - therapeutic use</subject><subject>Atherosclerosis</subject><subject>Blood platelets</subject><subject>Body mass</subject><subject>Body mass index</subject><subject>Body size</subject><subject>C-Reactive Protein - metabolism</subject><subject>Cardiology</subject><subject>Cardiovascular disease</subject><subject>Care and treatment</subject><subject>Collagen</subject><subject>Coronary artery</subject><subject>Coronary artery disease</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - drug therapy</subject><subject>Coronary Artery Disease - physiopathology</subject><subject>Coronary heart disease</subject><subject>Coronary vessels</subject><subject>Cross-Sectional Studies</subject><subject>Cyclooxygenase-1</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diagnosis</subject><subject>Dosage and administration</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Female</subject><subject>Health sciences</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>Heart surgery</subject><subject>Hematology</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Interleukin</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - blood</subject><subject>Laboratories</subject><subject>Leukocyte L1 Antigen Complex - blood</subject><subject>Leukocytes</subject><subject>Male</subject><subject>Medication Adherence</subject><subject>Middle Aged</subject><subject>P-selectin</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Platelet Aggregation</subject><subject>Platelet Aggregation Inhibitors - therapeutic use</subject><subject>Proteins</subject><subject>Quality</subject><subject>Risk</subject><subject>Risk factors</subject><subject>Smoking</subject><subject>Studies</subject><subject>Therapy</subject><subject>Thromboxane B2 - blood</subject><subject>Type 2 diabetes</subject><subject>Unsaturated fatty acids</subject><subject>Weight control</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7rr6D0QLgujFjGmSJs2NsAx-DCwsqOttSNPTTpZMU5PUj39vutNdprIXUkjCyXPec3L6ZtnzAq0Lwot31270vbLrwfWwRgUuhcAPstNCELxiGJGHR-eT7EkI1wiVpGLscXaSYI4IJafZ1UbZwbsIOpo-V32TD1ZFsBBz1XUeOhWN6_N0N6QT9DHkv0zc5SGq2kKunXe98n9y5SOkrTEBVICn2aNW2QDP5v0su_r44dvm8-ri8tN2c36x0kzguOJAoS5rwnhTCYaqVjQFF61CNWiutBYYtG6bFpcNIQ2uKp0CQmNdlZQjTslZ9vKgO1gX5DyRIAtWEc6IKFEitgeicepaDt7sU7fSKSNvAs53MrVutAXJGMGMi1oQjmjJkKC8SEVbTgROC0ta7-dqY72HRqdpeGUXosub3uxk535KSgkq8dTum1nAux8jhCj3JmiwVvXgxpu-C8xoRadar_5B73_dTHUqPcD0rUt19SQqzynBqKCkIIla30Olr4G90ck-rUnxRcLbRUJiIvyOnRpDkNuvX_6fvfy-ZF8fsTtQNu6Cs-NksbAE6QHU3oXgob0bcoHk5P7bacjJ_XJ2f0p7cfyD7pJu7U7-AoyW_rc</recordid><startdate>20150513</startdate><enddate>20150513</enddate><creator>Larsen, Sanne Bøjet</creator><creator>Grove, Erik Lerkevang</creator><creator>Pareek, Manan</creator><creator>Kristensen, Steen Dalby</creator><creator>Hvas, Anne-Mette</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150513</creationdate><title>Calprotectin and platelet aggregation in patients with stable coronary artery disease</title><author>Larsen, Sanne Bøjet ; Grove, Erik Lerkevang ; Pareek, Manan ; Kristensen, Steen Dalby ; Hvas, Anne-Mette</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-7e4eb5b367d89608f9d179fa0bec7acc92eccfdf25d33d288c2ec9c2c85470743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Activation</topic><topic>Aged</topic><topic>Agglomeration</topic><topic>Arachidonic acid</topic><topic>Aspirin</topic><topic>Aspirin - therapeutic use</topic><topic>Atherosclerosis</topic><topic>Blood platelets</topic><topic>Body mass</topic><topic>Body mass index</topic><topic>Body size</topic><topic>C-Reactive Protein - metabolism</topic><topic>Cardiology</topic><topic>Cardiovascular disease</topic><topic>Care and treatment</topic><topic>Collagen</topic><topic>Coronary artery</topic><topic>Coronary artery disease</topic><topic>Coronary Artery Disease - blood</topic><topic>Coronary Artery Disease - drug therapy</topic><topic>Coronary Artery Disease - physiopathology</topic><topic>Coronary heart disease</topic><topic>Coronary vessels</topic><topic>Cross-Sectional Studies</topic><topic>Cyclooxygenase-1</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diagnosis</topic><topic>Dosage and administration</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Female</topic><topic>Health sciences</topic><topic>Heart attacks</topic><topic>Heart diseases</topic><topic>Heart surgery</topic><topic>Hematology</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Interleukin</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Larsen, Sanne Bøjet</au><au>Grove, Erik Lerkevang</au><au>Pareek, Manan</au><au>Kristensen, Steen Dalby</au><au>Hvas, Anne-Mette</au><au>Freson, Kathleen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Calprotectin and platelet aggregation in patients with stable coronary artery disease</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-05-13</date><risdate>2015</risdate><volume>10</volume><issue>5</issue><spage>e0125992</spage><epage>e0125992</epage><pages>e0125992-e0125992</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Recent studies suggest that the inflammation-associated protein calprotectin may be implicated in the pathogenesis of coronary artery disease (CAD). However, the impact of calprotectin levels on platelet aggregation in CAD patients has never been investigated.
We investigated the association between calprotectin levels and platelet aggregation in stable, high-risk CAD patients receiving aspirin as mono antiplatelet therapy. Furthermore, we aimed to investigate independent clinical and laboratory determinants of calprotectin levels.
We performed a cross-sectional study including 581 stable, high-risk CAD patients. All patients received 75 mg aspirin daily as mono antiplatelet therapy. Platelet aggregation was assessed by 1) impedance aggregometry (Multiplate Analyzer) using arachidonic acid (AA) and collagen as agonists and by 2) the VerifyNow Aspirin Assay. Low-grade inflammation was evaluated by calprotectin, high-sensitive C-reactive-protein (hs-CRP) and interleukin-6. Platelet activation was assessed by soluble P-selectin, and cyclooxygenase-1 inhibition was evaluated by serum thromboxane B2, both measured by ELISA.
Calprotectin levels correlated positively with platelet aggregation according to Multiplate Analyzer (r=0.12, p=0.01). Additionally, calprotectin was positively associated with leukocytes (r=0.33, p<0.0001), hs-CRP (r=0.31, p<0.0001), interleukin-6 (r=0.28, p<0.0001), soluble P-selectin (r=0.10, p=0.02) and serum thromboxane B2 (r=0.10, p=0.02). Type 2 diabetes mellitus was an independent predictor of increased calprotectin levels (p=0.004), and trends were seen for body mass index (p=0.06) and smoking (p=0.07). Compliance with aspirin was confirmed by low serum thromboxane B2 levels in all patients (median [25%;75%]: 1.07 [0.52;1.87] ng/mL).
Calprotectin levels correlated positively, though weakly, with platelet aggregation and activation as well as serum thromboxane B2 in high-risk, stable CAD patients treated with aspirin.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25970343</pmid><doi>10.1371/journal.pone.0125992</doi><oa>free_for_read</oa></addata></record> |
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recordid | cdi_plos_journals_1683763950 |
source | PubMed Central Free; Publicly Available Content Database |
subjects | Activation Aged Agglomeration Arachidonic acid Aspirin Aspirin - therapeutic use Atherosclerosis Blood platelets Body mass Body mass index Body size C-Reactive Protein - metabolism Cardiology Cardiovascular disease Care and treatment Collagen Coronary artery Coronary artery disease Coronary Artery Disease - blood Coronary Artery Disease - drug therapy Coronary Artery Disease - physiopathology Coronary heart disease Coronary vessels Cross-Sectional Studies Cyclooxygenase-1 Diabetes Diabetes mellitus Diagnosis Dosage and administration Enzyme-linked immunosorbent assay Female Health sciences Heart attacks Heart diseases Heart surgery Hematology Hospitals Humans Inflammation Interleukin Interleukin 6 Interleukin-6 - blood Laboratories Leukocyte L1 Antigen Complex - blood Leukocytes Male Medication Adherence Middle Aged P-selectin Pathogenesis Patients Platelet Aggregation Platelet Aggregation Inhibitors - therapeutic use Proteins Quality Risk Risk factors Smoking Studies Therapy Thromboxane B2 - blood Type 2 diabetes Unsaturated fatty acids Weight control |
title | Calprotectin and platelet aggregation in patients with stable coronary artery disease |
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