Platelet microparticles and calcium homeostasis in acute coronary ischemias
Elevation of free cytoplasmic calcium is the common pathway of platelet activation, leading to shape change, shedding of platelet microparticles (PMP), aggregation, and secretion of internal granules, including expression of CD62p on the surface. Platelet activation is well documented in unstable an...
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Veröffentlicht in: | American journal of hematology 1997-02, Vol.54 (2), p.95-101 |
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creator | Katopodis, John N. Kolodny, Luciano Jy, Wenche Horstman, Lawrence L. De Marchena, E.J. Tao, Jian G. Haynes, Duncan H. Ahn, Yeon S. |
description | Elevation of free cytoplasmic calcium is the common pathway of platelet activation, leading to shape change, shedding of platelet microparticles (PMP), aggregation, and secretion of internal granules, including expression of CD62p on the surface. Platelet activation is well documented in unstable angina (UA) and acute myocardial infarction (MI). We investigated the following markers of platelet activation in 55 patients undergoing coronary angiography for suspected CAD: free cytoplasmic calcium, [Ca2+]cyt, PMP, CD62p expression, and platelet/leukocyte (P/L) interaction. [CA2+]cyt was measured by Fluo‐3 and the other measurements were by flow cytometry. Patients were classified into three groups: unstable angina (UA, n = 11), recent myocardial infarction (MI, n = 11), and patient controls (CTL, n = 33). Blood was drawn before infusion of heparin through femoral lines at the time of catheterization for assays. Results: (1) PMP values were significantly higher in both UA and MI than in CTL, P < 0.05. There was no difference between UA and MI. (2) P/L interaction was significantly elevated only in UA, P < 0.05. (3) CD62p expression on free platelets did not differ significantly between any of the three groups. (4) The resting [Ca2+]cyt, thrombin‐induced CA2+ influx, and release of CA2+ from internal stores were all significantly higher in platelets from the combined patient group (UA + MI) than in the patient group, P < 0.001 Conclusions: Results on calcium hemostasis and PMP were significantly different in patients with acute coronary syndromes than those with stable angina or no coronay ischemia; this may reflect underlying pathophysiology of acute coronary ischemia. P/L interaction was higher only in the UA group, suggesting a role of leukocytes in the UA. Am. J. Hematol. 54:95–101, 1997 © 1997 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/(SICI)1096-8652(199702)54:2<95::AID-AJH1>3.0.CO;2-Z |
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Platelet activation is well documented in unstable angina (UA) and acute myocardial infarction (MI). We investigated the following markers of platelet activation in 55 patients undergoing coronary angiography for suspected CAD: free cytoplasmic calcium, [Ca2+]cyt, PMP, CD62p expression, and platelet/leukocyte (P/L) interaction. [CA2+]cyt was measured by Fluo‐3 and the other measurements were by flow cytometry. Patients were classified into three groups: unstable angina (UA, n = 11), recent myocardial infarction (MI, n = 11), and patient controls (CTL, n = 33). Blood was drawn before infusion of heparin through femoral lines at the time of catheterization for assays. Results: (1) PMP values were significantly higher in both UA and MI than in CTL, P < 0.05. There was no difference between UA and MI. (2) P/L interaction was significantly elevated only in UA, P < 0.05. (3) CD62p expression on free platelets did not differ significantly between any of the three groups. (4) The resting [Ca2+]cyt, thrombin‐induced CA2+ influx, and release of CA2+ from internal stores were all significantly higher in platelets from the combined patient group (UA + MI) than in the patient group, P < 0.001 Conclusions: Results on calcium hemostasis and PMP were significantly different in patients with acute coronary syndromes than those with stable angina or no coronay ischemia; this may reflect underlying pathophysiology of acute coronary ischemia. P/L interaction was higher only in the UA group, suggesting a role of leukocytes in the UA. Am. J. Hematol. 54:95–101, 1997 © 1997 Wiley‐Liss, Inc.</description><identifier>ISSN: 0361-8609</identifier><identifier>EISSN: 1096-8652</identifier><identifier>DOI: 10.1002/(SICI)1096-8652(199702)54:2<95::AID-AJH1>3.0.CO;2-Z</identifier><identifier>PMID: 9034282</identifier><identifier>CODEN: AJHEDD</identifier><language>eng</language><publisher>New York: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Acute Disease ; Adult ; Aged ; Biological and medical sciences ; Biomarkers ; Blood Platelets - metabolism ; Blood Platelets - physiology ; Calcium - metabolism ; calcium homeostasis ; Cardiology. Vascular system ; Cell Communication ; Coronary heart disease ; Female ; Heart ; Homeostasis ; Humans ; immune thrombocytopenic ; Leukocytes - physiology ; Male ; Medical sciences ; Middle Aged ; myocardial infarction ; Myocardial Ischemia - blood ; P-Selectin - metabolism ; Platelet Activation ; platelet microparticles ; purpura (ITP) ; unstable angina</subject><ispartof>American journal of hematology, 1997-02, Vol.54 (2), p.95-101</ispartof><rights>Copyright © 1997 Wiley‐Liss, Inc.</rights><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c5281-778e77705762ec1a9cc4c100fcbe8de69072730b661552eea42f33d9b3e3df803</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2F%28SICI%291096-8652%28199702%2954%3A2%3C95%3A%3AAID-AJH1%3E3.0.CO%3B2-Z$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2F%28SICI%291096-8652%28199702%2954%3A2%3C95%3A%3AAID-AJH1%3E3.0.CO%3B2-Z$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2566339$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9034282$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Katopodis, John N.</creatorcontrib><creatorcontrib>Kolodny, Luciano</creatorcontrib><creatorcontrib>Jy, Wenche</creatorcontrib><creatorcontrib>Horstman, Lawrence L.</creatorcontrib><creatorcontrib>De Marchena, E.J.</creatorcontrib><creatorcontrib>Tao, Jian G.</creatorcontrib><creatorcontrib>Haynes, Duncan H.</creatorcontrib><creatorcontrib>Ahn, Yeon S.</creatorcontrib><title>Platelet microparticles and calcium homeostasis in acute coronary ischemias</title><title>American journal of hematology</title><addtitle>Am J Hematol</addtitle><description>Elevation of free cytoplasmic calcium is the common pathway of platelet activation, leading to shape change, shedding of platelet microparticles (PMP), aggregation, and secretion of internal granules, including expression of CD62p on the surface. Platelet activation is well documented in unstable angina (UA) and acute myocardial infarction (MI). We investigated the following markers of platelet activation in 55 patients undergoing coronary angiography for suspected CAD: free cytoplasmic calcium, [Ca2+]cyt, PMP, CD62p expression, and platelet/leukocyte (P/L) interaction. [CA2+]cyt was measured by Fluo‐3 and the other measurements were by flow cytometry. Patients were classified into three groups: unstable angina (UA, n = 11), recent myocardial infarction (MI, n = 11), and patient controls (CTL, n = 33). Blood was drawn before infusion of heparin through femoral lines at the time of catheterization for assays. Results: (1) PMP values were significantly higher in both UA and MI than in CTL, P < 0.05. There was no difference between UA and MI. (2) P/L interaction was significantly elevated only in UA, P < 0.05. (3) CD62p expression on free platelets did not differ significantly between any of the three groups. (4) The resting [Ca2+]cyt, thrombin‐induced CA2+ influx, and release of CA2+ from internal stores were all significantly higher in platelets from the combined patient group (UA + MI) than in the patient group, P < 0.001 Conclusions: Results on calcium hemostasis and PMP were significantly different in patients with acute coronary syndromes than those with stable angina or no coronay ischemia; this may reflect underlying pathophysiology of acute coronary ischemia. P/L interaction was higher only in the UA group, suggesting a role of leukocytes in the UA. Am. J. Hematol. 54:95–101, 1997 © 1997 Wiley‐Liss, Inc.</description><subject>Acute Disease</subject><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Biomarkers</subject><subject>Blood Platelets - metabolism</subject><subject>Blood Platelets - physiology</subject><subject>Calcium - metabolism</subject><subject>calcium homeostasis</subject><subject>Cardiology. Vascular system</subject><subject>Cell Communication</subject><subject>Coronary heart disease</subject><subject>Female</subject><subject>Heart</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>immune thrombocytopenic</subject><subject>Leukocytes - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>myocardial infarction</subject><subject>Myocardial Ischemia - blood</subject><subject>P-Selectin - metabolism</subject><subject>Platelet Activation</subject><subject>platelet microparticles</subject><subject>purpura (ITP)</subject><subject>unstable angina</subject><issn>0361-8609</issn><issn>1096-8652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1v1DAQhi0EKkvhJyDlgFB7yOKPOLa3CGmVlnah0iIVLr2MvM5ENcrHNk6E-u_rdFfLgYqTP-bVzDMPIWeMzhml_NPJzapYnTJq8lTnkp8wYxTlpzJb8M9GLhbL1Xm6_HbFvog5nRfrM57eviCzQ_4lmVGRs3in5jV5E8JvShnLND0iR4aKjGs-I99_1HbAGoek8a7vtrYfvKsxJLYtE2dr58cmuesa7MJggw-JbxPrxgET1_Vda_uHxAd3h4234S15Vdk64Lv9eUx-fb34WVyl1-vLVbG8Tp3kmqVKaVRKUalyjo5Z41zm4sKV26AuMTdUcSXoJs-ZlBzRZrwSojQbgaKsNBXH5OOu77bv7kcMAzSRAevattiNAZTWXHA1BW92wbhZCD1WsO19E5mBUZgUA0yKYVIGkzLYKQaZAQcjAaJimBSDAArFOv7exq7v9-PHTYPloefeaax_2NdtiAar3rbOh0OMyzwXwvyF--NrfPiH7P9gz3A9vcUjjH-isg</recordid><startdate>199702</startdate><enddate>199702</enddate><creator>Katopodis, John N.</creator><creator>Kolodny, Luciano</creator><creator>Jy, Wenche</creator><creator>Horstman, Lawrence L.</creator><creator>De Marchena, E.J.</creator><creator>Tao, Jian G.</creator><creator>Haynes, Duncan H.</creator><creator>Ahn, Yeon S.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</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>199702</creationdate><title>Platelet microparticles and calcium homeostasis in acute coronary ischemias</title><author>Katopodis, John N. ; Kolodny, Luciano ; Jy, Wenche ; Horstman, Lawrence L. ; De Marchena, E.J. ; Tao, Jian G. ; Haynes, Duncan H. ; Ahn, Yeon S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5281-778e77705762ec1a9cc4c100fcbe8de69072730b661552eea42f33d9b3e3df803</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Acute Disease</topic><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Biomarkers</topic><topic>Blood Platelets - metabolism</topic><topic>Blood Platelets - physiology</topic><topic>Calcium - metabolism</topic><topic>calcium homeostasis</topic><topic>Cardiology. Vascular system</topic><topic>Cell Communication</topic><topic>Coronary heart disease</topic><topic>Female</topic><topic>Heart</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>immune thrombocytopenic</topic><topic>Leukocytes - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>myocardial infarction</topic><topic>Myocardial Ischemia - blood</topic><topic>P-Selectin - metabolism</topic><topic>Platelet Activation</topic><topic>platelet microparticles</topic><topic>purpura (ITP)</topic><topic>unstable angina</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Katopodis, John N.</creatorcontrib><creatorcontrib>Kolodny, Luciano</creatorcontrib><creatorcontrib>Jy, Wenche</creatorcontrib><creatorcontrib>Horstman, Lawrence L.</creatorcontrib><creatorcontrib>De Marchena, E.J.</creatorcontrib><creatorcontrib>Tao, Jian G.</creatorcontrib><creatorcontrib>Haynes, Duncan H.</creatorcontrib><creatorcontrib>Ahn, Yeon S.</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>American journal of hematology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Katopodis, John N.</au><au>Kolodny, Luciano</au><au>Jy, Wenche</au><au>Horstman, Lawrence L.</au><au>De Marchena, E.J.</au><au>Tao, Jian G.</au><au>Haynes, Duncan H.</au><au>Ahn, Yeon S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet microparticles and calcium homeostasis in acute coronary ischemias</atitle><jtitle>American journal of hematology</jtitle><addtitle>Am J Hematol</addtitle><date>1997-02</date><risdate>1997</risdate><volume>54</volume><issue>2</issue><spage>95</spage><epage>101</epage><pages>95-101</pages><issn>0361-8609</issn><eissn>1096-8652</eissn><coden>AJHEDD</coden><abstract>Elevation of free cytoplasmic calcium is the common pathway of platelet activation, leading to shape change, shedding of platelet microparticles (PMP), aggregation, and secretion of internal granules, including expression of CD62p on the surface. Platelet activation is well documented in unstable angina (UA) and acute myocardial infarction (MI). We investigated the following markers of platelet activation in 55 patients undergoing coronary angiography for suspected CAD: free cytoplasmic calcium, [Ca2+]cyt, PMP, CD62p expression, and platelet/leukocyte (P/L) interaction. [CA2+]cyt was measured by Fluo‐3 and the other measurements were by flow cytometry. Patients were classified into three groups: unstable angina (UA, n = 11), recent myocardial infarction (MI, n = 11), and patient controls (CTL, n = 33). Blood was drawn before infusion of heparin through femoral lines at the time of catheterization for assays. Results: (1) PMP values were significantly higher in both UA and MI than in CTL, P < 0.05. There was no difference between UA and MI. (2) P/L interaction was significantly elevated only in UA, P < 0.05. (3) CD62p expression on free platelets did not differ significantly between any of the three groups. (4) The resting [Ca2+]cyt, thrombin‐induced CA2+ influx, and release of CA2+ from internal stores were all significantly higher in platelets from the combined patient group (UA + MI) than in the patient group, P < 0.001 Conclusions: Results on calcium hemostasis and PMP were significantly different in patients with acute coronary syndromes than those with stable angina or no coronay ischemia; this may reflect underlying pathophysiology of acute coronary ischemia. P/L interaction was higher only in the UA group, suggesting a role of leukocytes in the UA. Am. J. Hematol. 54:95–101, 1997 © 1997 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>9034282</pmid><doi>10.1002/(SICI)1096-8652(199702)54:2<95::AID-AJH1>3.0.CO;2-Z</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acute Disease Adult Aged Biological and medical sciences Biomarkers Blood Platelets - metabolism Blood Platelets - physiology Calcium - metabolism calcium homeostasis Cardiology. Vascular system Cell Communication Coronary heart disease Female Heart Homeostasis Humans immune thrombocytopenic Leukocytes - physiology Male Medical sciences Middle Aged myocardial infarction Myocardial Ischemia - blood P-Selectin - metabolism Platelet Activation platelet microparticles purpura (ITP) unstable angina |
title | Platelet microparticles and calcium homeostasis in acute coronary ischemias |
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