Sulfido-peptide leukotrienes in coronary heart disease - relationship with disease instability and myocardial ischaemia

Eur J Clin Invest 2010; 40 (3): 258–272 Background  Urinary excretion of leukotriene (LT) E4 is an index of LTC4 biosynthesis and platelet–neutrophil interactions, which may occur in coronary heart disease and contribute to myocardial ischaemia. Enhanced LTC4 biosynthesis may be a consequence of myo...

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Veröffentlicht in:European journal of clinical investigation 2010-03, Vol.40 (3), p.258-272
Hauptverfasser: De Caterina, R., Giannessi, D., Lazzerini, G., Bernini, W., Sicari, R., Cupelli, F., Lenzi, S., Rugolotto, M. M., Madonna, R., Maclouf, J.
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container_issue 3
container_start_page 258
container_title European journal of clinical investigation
container_volume 40
creator De Caterina, R.
Giannessi, D.
Lazzerini, G.
Bernini, W.
Sicari, R.
Cupelli, F.
Lenzi, S.
Rugolotto, M. M.
Madonna, R.
Maclouf, J.
description Eur J Clin Invest 2010; 40 (3): 258–272 Background  Urinary excretion of leukotriene (LT) E4 is an index of LTC4 biosynthesis and platelet–neutrophil interactions, which may occur in coronary heart disease and contribute to myocardial ischaemia. Enhanced LTC4 biosynthesis may be a consequence of myocardial ischaemia or be linked to its pathogenetic substrate. Methods and results  Overnight urine collections were obtained from 17 patients with chronic stable angina, three patients with Prinzmetal’s angina, 16 patients with non ST‐elevation acute coronary syndromes (NSTE‐ACS) and six patients with acute ST‐elevation myocardial infarction (STEMI). LTE4 excretion was measured by enzyme immunoassay after HPLC separation. Compared with healthy controls (51·1 ± 21·3 pg mg−1 creatinine, mean ± SD, n = 11) and with non‐coronary cardiac controls (36·6 ± 9·8 pg mg−1 creatinine, n = 9), LTE4 excretion was unchanged in stable angina (40·5 ± 25·8 pg mg−1 creatinine), but significantly (P 
doi_str_mv 10.1111/j.1365-2362.2010.02261.x
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M. ; Madonna, R. ; Maclouf, J.</creator><creatorcontrib>De Caterina, R. ; Giannessi, D. ; Lazzerini, G. ; Bernini, W. ; Sicari, R. ; Cupelli, F. ; Lenzi, S. ; Rugolotto, M. M. ; Madonna, R. ; Maclouf, J.</creatorcontrib><description>Eur J Clin Invest 2010; 40 (3): 258–272 Background  Urinary excretion of leukotriene (LT) E4 is an index of LTC4 biosynthesis and platelet–neutrophil interactions, which may occur in coronary heart disease and contribute to myocardial ischaemia. Enhanced LTC4 biosynthesis may be a consequence of myocardial ischaemia or be linked to its pathogenetic substrate. Methods and results  Overnight urine collections were obtained from 17 patients with chronic stable angina, three patients with Prinzmetal’s angina, 16 patients with non ST‐elevation acute coronary syndromes (NSTE‐ACS) and six patients with acute ST‐elevation myocardial infarction (STEMI). LTE4 excretion was measured by enzyme immunoassay after HPLC separation. Compared with healthy controls (51·1 ± 21·3 pg mg−1 creatinine, mean ± SD, n = 11) and with non‐coronary cardiac controls (36·6 ± 9·8 pg mg−1 creatinine, n = 9), LTE4 excretion was unchanged in stable angina (40·5 ± 25·8 pg mg−1 creatinine), but significantly (P &lt; 0·01) increased in NSTE‐ACS (122·7 ± 137·2 pg mg−1 creatinine) and STEMI (213·4 ± 172·4 pg mg−1 creatinine). In these patients, LTE4 excretion rapidly dropped after day 1, consistent with effective coronary reperfusion. In patients with NSTE‐ACS, the increase in LTE4 excretion was entirely restricted to patients with recent (&lt; 48 h) spontaneous anginal episodes. Myocardial ischaemia elicited by a positive exercise stress test was not accompanied by any detectable increase in LTE4 excretion, while a significant (P &lt; 0·01) increase was detected after a single‐vessel percutaneous coronary interventions (PCI) procedure (n = 10), as compared with diagnostic angiography (n = 9). Conclusions  In coronary heart disease, increased LTC4 biosynthesis is restricted to ACS and not linked to myocardial ischaemia per se, but likely to the occurrence of plaque disruption.</description><identifier>ISSN: 0014-2972</identifier><identifier>EISSN: 1365-2362</identifier><identifier>DOI: 10.1111/j.1365-2362.2010.02261.x</identifier><identifier>PMID: 20415701</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Acute Coronary Syndrome - urine ; Adult ; Aged ; Angina Pectoris - urine ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Biomarkers - urine ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Chromatography, High Pressure Liquid ; Coronary artery plaque ; Coronary heart disease ; Cross-Sectional Studies ; Female ; General aspects ; Heart ; Humans ; Immunoenzyme Techniques ; leukocytes ; Leukotriene E4 - urine ; leukotrienes ; Male ; Medical sciences ; Middle Aged ; Myocardial Infarction - urine ; myocardial ischaemia ; thrombosis</subject><ispartof>European journal of clinical investigation, 2010-03, Vol.40 (3), p.258-272</ispartof><rights>2010 The Authors. 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M.</creatorcontrib><creatorcontrib>Madonna, R.</creatorcontrib><creatorcontrib>Maclouf, J.</creatorcontrib><title>Sulfido-peptide leukotrienes in coronary heart disease - relationship with disease instability and myocardial ischaemia</title><title>European journal of clinical investigation</title><addtitle>Eur J Clin Invest</addtitle><description>Eur J Clin Invest 2010; 40 (3): 258–272 Background  Urinary excretion of leukotriene (LT) E4 is an index of LTC4 biosynthesis and platelet–neutrophil interactions, which may occur in coronary heart disease and contribute to myocardial ischaemia. Enhanced LTC4 biosynthesis may be a consequence of myocardial ischaemia or be linked to its pathogenetic substrate. Methods and results  Overnight urine collections were obtained from 17 patients with chronic stable angina, three patients with Prinzmetal’s angina, 16 patients with non ST‐elevation acute coronary syndromes (NSTE‐ACS) and six patients with acute ST‐elevation myocardial infarction (STEMI). LTE4 excretion was measured by enzyme immunoassay after HPLC separation. Compared with healthy controls (51·1 ± 21·3 pg mg−1 creatinine, mean ± SD, n = 11) and with non‐coronary cardiac controls (36·6 ± 9·8 pg mg−1 creatinine, n = 9), LTE4 excretion was unchanged in stable angina (40·5 ± 25·8 pg mg−1 creatinine), but significantly (P &lt; 0·01) increased in NSTE‐ACS (122·7 ± 137·2 pg mg−1 creatinine) and STEMI (213·4 ± 172·4 pg mg−1 creatinine). In these patients, LTE4 excretion rapidly dropped after day 1, consistent with effective coronary reperfusion. In patients with NSTE‐ACS, the increase in LTE4 excretion was entirely restricted to patients with recent (&lt; 48 h) spontaneous anginal episodes. Myocardial ischaemia elicited by a positive exercise stress test was not accompanied by any detectable increase in LTE4 excretion, while a significant (P &lt; 0·01) increase was detected after a single‐vessel percutaneous coronary interventions (PCI) procedure (n = 10), as compared with diagnostic angiography (n = 9). Conclusions  In coronary heart disease, increased LTC4 biosynthesis is restricted to ACS and not linked to myocardial ischaemia per se, but likely to the occurrence of plaque disruption.</description><subject>Acute Coronary Syndrome - urine</subject><subject>Adult</subject><subject>Aged</subject><subject>Angina Pectoris - urine</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - urine</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Chromatography, High Pressure Liquid</subject><subject>Coronary artery plaque</subject><subject>Coronary heart disease</subject><subject>Cross-Sectional Studies</subject><subject>Female</subject><subject>General aspects</subject><subject>Heart</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>leukocytes</subject><subject>Leukotriene E4 - urine</subject><subject>leukotrienes</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - urine</subject><subject>myocardial ischaemia</subject><subject>thrombosis</subject><issn>0014-2972</issn><issn>1365-2362</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE2P0zAQhi0EYsvCX0C-IE7p-it2cuCAusuyaAXSsnyIizV1Jqq7bhLsRG3__Sa0lCu-2PI873j8EEI5m_NxXaznXOo8E1KLuWDjLRNC8_nuCZmdCk_JjDGuMlEacUZepLRmjBVciufkTDDFc8P4jGy_DqH2VZt12PW-QhpweGj76LHBRH1DXRvbBuKerhBiTyufEBLSjEYM0Pu2SSvf0a3vV6eab1IPSx98v6fQVHSzbx3EykOgPrkV4MbDS_KshpDw1XE_J98-XN0vPma3X65vFu9vM6ek5hnPCyMYK8EoJ6VShtc6Lzgo54AXClheMCxr7pjQWvEqd2WxNLxA7RiUlZTn5O2hbxfb3wOm3m7GGTAEaLAdkjVjVyNVno9kcSBdbFOKWNsu-s34c8uZnazbtZ3k2kmunazbP9btboy-Pj4yLDdYnYJ_NY_AmyMAyUGoIzTOp3-cULrQ5TTtuwO39QH3_z2AvVrcTKcxnx3yPvW4O-UhPlhtpMntj8_Xll3--vTz7vu9vZOPR6mthw</recordid><startdate>201003</startdate><enddate>201003</enddate><creator>De Caterina, R.</creator><creator>Giannessi, D.</creator><creator>Lazzerini, G.</creator><creator>Bernini, W.</creator><creator>Sicari, R.</creator><creator>Cupelli, F.</creator><creator>Lenzi, S.</creator><creator>Rugolotto, M. 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M.</creatorcontrib><creatorcontrib>Madonna, R.</creatorcontrib><creatorcontrib>Maclouf, J.</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>MEDLINE - Academic</collection><jtitle>European journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>De Caterina, R.</au><au>Giannessi, D.</au><au>Lazzerini, G.</au><au>Bernini, W.</au><au>Sicari, R.</au><au>Cupelli, F.</au><au>Lenzi, S.</au><au>Rugolotto, M. M.</au><au>Madonna, R.</au><au>Maclouf, J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sulfido-peptide leukotrienes in coronary heart disease - relationship with disease instability and myocardial ischaemia</atitle><jtitle>European journal of clinical investigation</jtitle><addtitle>Eur J Clin Invest</addtitle><date>2010-03</date><risdate>2010</risdate><volume>40</volume><issue>3</issue><spage>258</spage><epage>272</epage><pages>258-272</pages><issn>0014-2972</issn><eissn>1365-2362</eissn><abstract>Eur J Clin Invest 2010; 40 (3): 258–272 Background  Urinary excretion of leukotriene (LT) E4 is an index of LTC4 biosynthesis and platelet–neutrophil interactions, which may occur in coronary heart disease and contribute to myocardial ischaemia. Enhanced LTC4 biosynthesis may be a consequence of myocardial ischaemia or be linked to its pathogenetic substrate. Methods and results  Overnight urine collections were obtained from 17 patients with chronic stable angina, three patients with Prinzmetal’s angina, 16 patients with non ST‐elevation acute coronary syndromes (NSTE‐ACS) and six patients with acute ST‐elevation myocardial infarction (STEMI). LTE4 excretion was measured by enzyme immunoassay after HPLC separation. Compared with healthy controls (51·1 ± 21·3 pg mg−1 creatinine, mean ± SD, n = 11) and with non‐coronary cardiac controls (36·6 ± 9·8 pg mg−1 creatinine, n = 9), LTE4 excretion was unchanged in stable angina (40·5 ± 25·8 pg mg−1 creatinine), but significantly (P &lt; 0·01) increased in NSTE‐ACS (122·7 ± 137·2 pg mg−1 creatinine) and STEMI (213·4 ± 172·4 pg mg−1 creatinine). In these patients, LTE4 excretion rapidly dropped after day 1, consistent with effective coronary reperfusion. In patients with NSTE‐ACS, the increase in LTE4 excretion was entirely restricted to patients with recent (&lt; 48 h) spontaneous anginal episodes. Myocardial ischaemia elicited by a positive exercise stress test was not accompanied by any detectable increase in LTE4 excretion, while a significant (P &lt; 0·01) increase was detected after a single‐vessel percutaneous coronary interventions (PCI) procedure (n = 10), as compared with diagnostic angiography (n = 9). Conclusions  In coronary heart disease, increased LTC4 biosynthesis is restricted to ACS and not linked to myocardial ischaemia per se, but likely to the occurrence of plaque disruption.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>20415701</pmid><doi>10.1111/j.1365-2362.2010.02261.x</doi><tpages>15</tpages></addata></record>
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subjects Acute Coronary Syndrome - urine
Adult
Aged
Angina Pectoris - urine
Atherosclerosis (general aspects, experimental research)
Biological and medical sciences
Biomarkers - urine
Blood and lymphatic vessels
Cardiology. Vascular system
Chromatography, High Pressure Liquid
Coronary artery plaque
Coronary heart disease
Cross-Sectional Studies
Female
General aspects
Heart
Humans
Immunoenzyme Techniques
leukocytes
Leukotriene E4 - urine
leukotrienes
Male
Medical sciences
Middle Aged
Myocardial Infarction - urine
myocardial ischaemia
thrombosis
title Sulfido-peptide leukotrienes in coronary heart disease - relationship with disease instability and myocardial ischaemia
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