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Effective long-term inhibition of thromboxane production but not of serotonin release in patients with coronary heart disease by 30 mg/d acetylsalicylic acid dosage
Efficacy of aspirin (Acetylsalicylic acid, ASA) antiaggregatory prevention was demonstrated in a series of clinical trials. The recommended ASA doses decreased gradually and doses 50-30 mg ASA/d are intensively studied at the present time. A group of 42 patients with coronary heart disease was evalu...
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Published in: | Prostaglandins, leukotrienes and essential fatty acids leukotrienes and essential fatty acids, 1998-07, Vol.59 (1), p.17-21 |
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container_title | Prostaglandins, leukotrienes and essential fatty acids |
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creator | GAJDOS, M SPUSTOVA, V SEBEKOVA, K KRIVOSIKOVA, Z DZURIK, R |
description | Efficacy of aspirin (Acetylsalicylic acid, ASA) antiaggregatory prevention was demonstrated in a series of clinical trials. The recommended ASA doses decreased gradually and doses 50-30 mg ASA/d are intensively studied at the present time.
A group of 42 patients with coronary heart disease was evaluated: (1) Basal TXB
2 production during spontaneous blood clotting was 360 ± 37.6 ng/ml; (2) Two initial doses were tested: while 200 mg ASA inhibited, during spontaneous blood clotting, median TXB
2 production by 99.9% (serum TXB
2 concentration 1.35 ng/ml), 30 mg ASA median inhibition was just 42.0% (serum TXB
2 151 ng/ml); (3) 30 mg ASA/d maintenance dose was evaluated for 3 months. The median TXB
2 production inhibition was 98.5% (serum TXB
2 3.75 ng/ml, first month) and 94.0% (serum TXB
2 14.2 ng/ml, third month); (4) Four patients did not respond sufficiently, because of noncompliance verified by the determination of salicyluric acid urinary excretion, the lower limit of excretion being |
doi_str_mv | 10.1016/S0952-3278(98)90047-3 |
format | article |
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A group of 42 patients with coronary heart disease was evaluated: (1) Basal TXB
2 production during spontaneous blood clotting was 360 ± 37.6 ng/ml; (2) Two initial doses were tested: while 200 mg ASA inhibited, during spontaneous blood clotting, median TXB
2 production by 99.9% (serum TXB
2 concentration 1.35 ng/ml), 30 mg ASA median inhibition was just 42.0% (serum TXB
2 151 ng/ml); (3) 30 mg ASA/d maintenance dose was evaluated for 3 months. The median TXB
2 production inhibition was 98.5% (serum TXB
2 3.75 ng/ml, first month) and 94.0% (serum TXB
2 14.2 ng/ml, third month); (4) Four patients did not respond sufficiently, because of noncompliance verified by the determination of salicyluric acid urinary excretion, the lower limit of excretion being <3 μmol/2 h; (5) Both initial and maintenance ASA dose decreased metabolic TXA
2 endproducts in urine; (6) 5HT platelet release did not decrease; (7) Potential changes of 5HT metabolic elimination were excluded by the simultaneous determination of 5-hydroxyindoleacetic acid (5HIAA).
In conclusion, 200 mg initial dose and 30 mg ASA/d maintenance dose are suggested to be maximally inhibitory for TXB
2 production without influence on 5HT release.</description><identifier>ISSN: 0952-3278</identifier><identifier>EISSN: 1532-2823</identifier><identifier>DOI: 10.1016/S0952-3278(98)90047-3</identifier><identifier>PMID: 9758203</identifier><language>eng</language><publisher>Kidlington: Elsevier Ltd</publisher><subject>Aspirin - therapeutic use ; Biological and medical sciences ; Blood Coagulation - drug effects ; Blood. Blood coagulation. Reticuloendothelial system ; Coronary Disease - physiopathology ; Dose-Response Relationship, Drug ; Humans ; Medical sciences ; Myocardial Ischemia - prevention & control ; Pharmacology. Drug treatments ; Serotonin - secretion ; Thromboxane A2 - antagonists & inhibitors ; Thromboxane A2 - urine ; Thromboxane B2 - metabolism</subject><ispartof>Prostaglandins, leukotrienes and essential fatty acids, 1998-07, Vol.59 (1), p.17-21</ispartof><rights>1998</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-edd079be8e5a5be5285751e722422155b5a8f05625cae7d4f9a2d1a019a48d923</citedby><cites>FETCH-LOGICAL-c389t-edd079be8e5a5be5285751e722422155b5a8f05625cae7d4f9a2d1a019a48d923</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2407937$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9758203$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GAJDOS, M</creatorcontrib><creatorcontrib>SPUSTOVA, V</creatorcontrib><creatorcontrib>SEBEKOVA, K</creatorcontrib><creatorcontrib>KRIVOSIKOVA, Z</creatorcontrib><creatorcontrib>DZURIK, R</creatorcontrib><title>Effective long-term inhibition of thromboxane production but not of serotonin release in patients with coronary heart disease by 30 mg/d acetylsalicylic acid dosage</title><title>Prostaglandins, leukotrienes and essential fatty acids</title><addtitle>Prostaglandins Leukot Essent Fatty Acids</addtitle><description>Efficacy of aspirin (Acetylsalicylic acid, ASA) antiaggregatory prevention was demonstrated in a series of clinical trials. The recommended ASA doses decreased gradually and doses 50-30 mg ASA/d are intensively studied at the present time.
A group of 42 patients with coronary heart disease was evaluated: (1) Basal TXB
2 production during spontaneous blood clotting was 360 ± 37.6 ng/ml; (2) Two initial doses were tested: while 200 mg ASA inhibited, during spontaneous blood clotting, median TXB
2 production by 99.9% (serum TXB
2 concentration 1.35 ng/ml), 30 mg ASA median inhibition was just 42.0% (serum TXB
2 151 ng/ml); (3) 30 mg ASA/d maintenance dose was evaluated for 3 months. The median TXB
2 production inhibition was 98.5% (serum TXB
2 3.75 ng/ml, first month) and 94.0% (serum TXB
2 14.2 ng/ml, third month); (4) Four patients did not respond sufficiently, because of noncompliance verified by the determination of salicyluric acid urinary excretion, the lower limit of excretion being <3 μmol/2 h; (5) Both initial and maintenance ASA dose decreased metabolic TXA
2 endproducts in urine; (6) 5HT platelet release did not decrease; (7) Potential changes of 5HT metabolic elimination were excluded by the simultaneous determination of 5-hydroxyindoleacetic acid (5HIAA).
In conclusion, 200 mg initial dose and 30 mg ASA/d maintenance dose are suggested to be maximally inhibitory for TXB
2 production without influence on 5HT release.</description><subject>Aspirin - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Blood Coagulation - drug effects</subject><subject>Blood. Blood coagulation. Reticuloendothelial system</subject><subject>Coronary Disease - physiopathology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Myocardial Ischemia - prevention & control</subject><subject>Pharmacology. Drug treatments</subject><subject>Serotonin - secretion</subject><subject>Thromboxane A2 - antagonists & inhibitors</subject><subject>Thromboxane A2 - urine</subject><subject>Thromboxane B2 - metabolism</subject><issn>0952-3278</issn><issn>1532-2823</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><recordid>eNqFkV1rHCEUhqU0pNu0PyHgRSntxTR-jBm9KiGkHxDIRdprcfTMrmVGt-qk3f_THxpnd9nbgiLyPufoe16ELin5RAm9vnokSrCGs05-UPKjIqTtGv4CrajgrGGS8ZdodUJeodc5_yKEMErbc3SuOiEZ4Sv0724YwBb_BHiMYd0USBP2YeN7X3wMOA64bFKc-vjXBMDbFN1s90o_FxxiWYgMKZYYfMAJRjAZage8NcVDKBn_8WWDbUwxmLTDGzCpYOfznut3mBM8ra8cNhbKbsxm9HZXd717h13MZg1v0Nlgxgxvj-cF-vnl7sftt-b-4ev325v7xnKpSgPOkU71IEEY0YNgUnSCQsdYyxgVohdGDkRcM2ENdK4dlGGOGkKVaaVTjF-g94e-1ebvGXLRk88WxrFaj3PWHVctk5xXUBxAm2LOCQa9TX6q9jQleklH79PRy-i1qmtJRy91l8cH5n4Cd6o6xlH1d0fdZGvGIZlgfT5hrK3-eFexzwcM6jCePCSdbZ21BedTDVO76P_zkWe2ea8v</recordid><startdate>19980701</startdate><enddate>19980701</enddate><creator>GAJDOS, M</creator><creator>SPUSTOVA, V</creator><creator>SEBEKOVA, K</creator><creator>KRIVOSIKOVA, Z</creator><creator>DZURIK, R</creator><general>Elsevier Ltd</general><general>Elsevier</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>19980701</creationdate><title>Effective long-term inhibition of thromboxane production but not of serotonin release in patients with coronary heart disease by 30 mg/d acetylsalicylic acid dosage</title><author>GAJDOS, M ; SPUSTOVA, V ; SEBEKOVA, K ; KRIVOSIKOVA, Z ; DZURIK, R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-edd079be8e5a5be5285751e722422155b5a8f05625cae7d4f9a2d1a019a48d923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Aspirin - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Blood Coagulation - drug effects</topic><topic>Blood. Blood coagulation. Reticuloendothelial system</topic><topic>Coronary Disease - physiopathology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Myocardial Ischemia - prevention & control</topic><topic>Pharmacology. Drug treatments</topic><topic>Serotonin - secretion</topic><topic>Thromboxane A2 - antagonists & inhibitors</topic><topic>Thromboxane A2 - urine</topic><topic>Thromboxane B2 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GAJDOS, M</creatorcontrib><creatorcontrib>SPUSTOVA, V</creatorcontrib><creatorcontrib>SEBEKOVA, K</creatorcontrib><creatorcontrib>KRIVOSIKOVA, Z</creatorcontrib><creatorcontrib>DZURIK, R</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>Prostaglandins, leukotrienes and essential fatty acids</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GAJDOS, M</au><au>SPUSTOVA, V</au><au>SEBEKOVA, K</au><au>KRIVOSIKOVA, Z</au><au>DZURIK, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effective long-term inhibition of thromboxane production but not of serotonin release in patients with coronary heart disease by 30 mg/d acetylsalicylic acid dosage</atitle><jtitle>Prostaglandins, leukotrienes and essential fatty acids</jtitle><addtitle>Prostaglandins Leukot Essent Fatty Acids</addtitle><date>1998-07-01</date><risdate>1998</risdate><volume>59</volume><issue>1</issue><spage>17</spage><epage>21</epage><pages>17-21</pages><issn>0952-3278</issn><eissn>1532-2823</eissn><abstract>Efficacy of aspirin (Acetylsalicylic acid, ASA) antiaggregatory prevention was demonstrated in a series of clinical trials. The recommended ASA doses decreased gradually and doses 50-30 mg ASA/d are intensively studied at the present time.
A group of 42 patients with coronary heart disease was evaluated: (1) Basal TXB
2 production during spontaneous blood clotting was 360 ± 37.6 ng/ml; (2) Two initial doses were tested: while 200 mg ASA inhibited, during spontaneous blood clotting, median TXB
2 production by 99.9% (serum TXB
2 concentration 1.35 ng/ml), 30 mg ASA median inhibition was just 42.0% (serum TXB
2 151 ng/ml); (3) 30 mg ASA/d maintenance dose was evaluated for 3 months. The median TXB
2 production inhibition was 98.5% (serum TXB
2 3.75 ng/ml, first month) and 94.0% (serum TXB
2 14.2 ng/ml, third month); (4) Four patients did not respond sufficiently, because of noncompliance verified by the determination of salicyluric acid urinary excretion, the lower limit of excretion being <3 μmol/2 h; (5) Both initial and maintenance ASA dose decreased metabolic TXA
2 endproducts in urine; (6) 5HT platelet release did not decrease; (7) Potential changes of 5HT metabolic elimination were excluded by the simultaneous determination of 5-hydroxyindoleacetic acid (5HIAA).
In conclusion, 200 mg initial dose and 30 mg ASA/d maintenance dose are suggested to be maximally inhibitory for TXB
2 production without influence on 5HT release.</abstract><cop>Kidlington</cop><pub>Elsevier Ltd</pub><pmid>9758203</pmid><doi>10.1016/S0952-3278(98)90047-3</doi><tpages>5</tpages></addata></record> |
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subjects | Aspirin - therapeutic use Biological and medical sciences Blood Coagulation - drug effects Blood. Blood coagulation. Reticuloendothelial system Coronary Disease - physiopathology Dose-Response Relationship, Drug Humans Medical sciences Myocardial Ischemia - prevention & control Pharmacology. Drug treatments Serotonin - secretion Thromboxane A2 - antagonists & inhibitors Thromboxane A2 - urine Thromboxane B2 - metabolism |
title | Effective long-term inhibition of thromboxane production but not of serotonin release in patients with coronary heart disease by 30 mg/d acetylsalicylic acid dosage |
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