Platelet function in patients with obstructive sleep apnoea syndrome
Patients with obstructive sleep apnoea syndrome (OSAS) are subject to an increased cardiovascular morbidity including myocardial infarction and stroke. Platelets play an important role in the pathogenesis and triggering of acute cardiovascular syndromes. So far, the influence of OSAS on platelet fun...
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Veröffentlicht in: | The European respiratory journal 2000-10, Vol.16 (4), p.648-652 |
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description | Patients with obstructive sleep apnoea syndrome (OSAS) are subject to an increased cardiovascular morbidity including myocardial infarction and stroke. Platelets play an important role in the pathogenesis and triggering of acute cardiovascular syndromes. So far, the influence of OSAS on platelet function is not fully understood.
Platelet aggregability to epinephrine, collagen, arachidonic acid, and adenosine diphosphate in vitro was measured in 17 consecutive male patients (53.0±2.1 yrs) with polysomnographically verified OSAS and compared with that of 15 male controls (50.1±3.6 yrs) at 20:00 h, 24:00 h, and 06:00 h. In addition, the long‐term effects of continuous positive airway pressure (CPAP) therapy on platelet aggregability was assessed after 6 months.
Platelet aggregation in vitro induced by epinephrine showed a slight increase overnight in the untreated OSAS patients (
ns) whereas it decreased slightly (
ns) in the controls and in the treated OSAS patients. Pretherapeutic platelet aggregability was significantly lowered by CPAP therapy both at 24:00 h (64.0±6.5 versus 55.3±6.7%, p |
doi_str_mv | 10.1034/j.1399-3003.2000.16d14.x |
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Platelet aggregability to epinephrine, collagen, arachidonic acid, and adenosine diphosphate in vitro was measured in 17 consecutive male patients (53.0±2.1 yrs) with polysomnographically verified OSAS and compared with that of 15 male controls (50.1±3.6 yrs) at 20:00 h, 24:00 h, and 06:00 h. In addition, the long‐term effects of continuous positive airway pressure (CPAP) therapy on platelet aggregability was assessed after 6 months.
Platelet aggregation in vitro induced by epinephrine showed a slight increase overnight in the untreated OSAS patients (
ns) whereas it decreased slightly (
ns) in the controls and in the treated OSAS patients. Pretherapeutic platelet aggregability was significantly lowered by CPAP therapy both at 24:00 h (64.0±6.5 versus 55.3±6.7%, p<0.05) and at 06:00 h (64.1±6.5 versus 45.8±7.6%; p=0.01). Platelet aggregability during sleep in the controls resembled that found in patients with OSAS during CPAP therapy.
The results suggest that obstructive sleep apnoea syndrome contributes, at least in part, to platelet dysfunction and that long‐term continuous positive airway pressure treatment may reduce platelet aggregability.</description><identifier>ISSN: 0903-1936</identifier><identifier>EISSN: 1399-3003</identifier><identifier>DOI: 10.1034/j.1399-3003.2000.16d14.x</identifier><identifier>PMID: 11106207</identifier><language>eng</language><publisher>Sheffield: Eur Respiratory Soc</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Catecholamines ; Chronic obstructive pulmonary disease, asthma ; Humans ; Male ; Medical sciences ; Middle Aged ; obstructive sleep apnoea syndrome ; Platelet Aggregation - physiology ; platelet function ; Pneumology ; Polysomnography ; Positive-Pressure Respiration ; Regression Analysis ; sleep ; Sleep Apnea Syndromes - blood ; Sleep Apnea Syndromes - diagnosis ; Sleep Apnea Syndromes - therapy ; stroke</subject><ispartof>The European respiratory journal, 2000-10, Vol.16 (4), p.648-652</ispartof><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1034%2Fj.1399-3003.2000.16d14.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1034%2Fj.1399-3003.2000.16d14.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1531520$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11106207$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sanner, BM</creatorcontrib><creatorcontrib>Konermann, M</creatorcontrib><creatorcontrib>Tepel, M</creatorcontrib><creatorcontrib>Groetz, J</creatorcontrib><creatorcontrib>Mummenhoff, C</creatorcontrib><creatorcontrib>Zidek, W</creatorcontrib><title>Platelet function in patients with obstructive sleep apnoea syndrome</title><title>The European respiratory journal</title><addtitle>Eur Respir J</addtitle><description>Patients with obstructive sleep apnoea syndrome (OSAS) are subject to an increased cardiovascular morbidity including myocardial infarction and stroke. Platelets play an important role in the pathogenesis and triggering of acute cardiovascular syndromes. So far, the influence of OSAS on platelet function is not fully understood.
Platelet aggregability to epinephrine, collagen, arachidonic acid, and adenosine diphosphate in vitro was measured in 17 consecutive male patients (53.0±2.1 yrs) with polysomnographically verified OSAS and compared with that of 15 male controls (50.1±3.6 yrs) at 20:00 h, 24:00 h, and 06:00 h. In addition, the long‐term effects of continuous positive airway pressure (CPAP) therapy on platelet aggregability was assessed after 6 months.
Platelet aggregation in vitro induced by epinephrine showed a slight increase overnight in the untreated OSAS patients (
ns) whereas it decreased slightly (
ns) in the controls and in the treated OSAS patients. Pretherapeutic platelet aggregability was significantly lowered by CPAP therapy both at 24:00 h (64.0±6.5 versus 55.3±6.7%, p<0.05) and at 06:00 h (64.1±6.5 versus 45.8±7.6%; p=0.01). Platelet aggregability during sleep in the controls resembled that found in patients with OSAS during CPAP therapy.
The results suggest that obstructive sleep apnoea syndrome contributes, at least in part, to platelet dysfunction and that long‐term continuous positive airway pressure treatment may reduce platelet aggregability.</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Catecholamines</subject><subject>Chronic obstructive pulmonary disease, asthma</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>obstructive sleep apnoea syndrome</subject><subject>Platelet Aggregation - physiology</subject><subject>platelet function</subject><subject>Pneumology</subject><subject>Polysomnography</subject><subject>Positive-Pressure Respiration</subject><subject>Regression Analysis</subject><subject>sleep</subject><subject>Sleep Apnea Syndromes - blood</subject><subject>Sleep Apnea Syndromes - diagnosis</subject><subject>Sleep Apnea Syndromes - therapy</subject><subject>stroke</subject><issn>0903-1936</issn><issn>1399-3003</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkU9P3DAQxa2KCrbAV6h8gN6yncl4Q3xBQkBpK6RWqD1bTjxhvXL-ECcs--2bZZdyGmneT08z7wkhEeYIpL6u5khaJwRA8xRg2mYO1fzlg5j9Fw7EDDRQgpqyI_EpxhUAZorwUBwhImQpXMzEze9gBw48yGpsysG3jfSN7OzguRmiXPthKdsiDv04ic8sY2DupO2alq2Mm8b1bc0n4mNlQ-TT_TwWf7_d_rn-ntz_uvtxfXWfLClFlaAjchWpomIiKkpELljbonRphQQaCXNXoFWO3YJ0VQIWaZpr7VxeqgXRsfiy8-369mnkOJjax5JDsA23YzQX6UQB5BP4eQ-ORc3OdL2vbb8xb39PwNkesLG0oeptU_r4zi0IFylM2OUOW_vAm3cZzLYGszLbtM02bbOtwbzWYF7M7cNPzG5QTQbnO4Olf1yufc8m1jaE6Sw03K8wM8pkKqd_HqCIpw</recordid><startdate>200010</startdate><enddate>200010</enddate><creator>Sanner, BM</creator><creator>Konermann, M</creator><creator>Tepel, M</creator><creator>Groetz, J</creator><creator>Mummenhoff, C</creator><creator>Zidek, W</creator><general>Eur Respiratory Soc</general><general>Munksgaard International Publishers</general><general>Maney</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200010</creationdate><title>Platelet function in patients with obstructive sleep apnoea syndrome</title><author>Sanner, BM ; Konermann, M ; Tepel, M ; Groetz, J ; Mummenhoff, C ; Zidek, W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h3214-1d33df34bfe333bc11ebe9abcd2f13091318db1a4ded539fc01b22899dd8c4533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Catecholamines</topic><topic>Chronic obstructive pulmonary disease, asthma</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>obstructive sleep apnoea syndrome</topic><topic>Platelet Aggregation - physiology</topic><topic>platelet function</topic><topic>Pneumology</topic><topic>Polysomnography</topic><topic>Positive-Pressure Respiration</topic><topic>Regression Analysis</topic><topic>sleep</topic><topic>Sleep Apnea Syndromes - blood</topic><topic>Sleep Apnea Syndromes - diagnosis</topic><topic>Sleep Apnea Syndromes - therapy</topic><topic>stroke</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sanner, BM</creatorcontrib><creatorcontrib>Konermann, M</creatorcontrib><creatorcontrib>Tepel, M</creatorcontrib><creatorcontrib>Groetz, J</creatorcontrib><creatorcontrib>Mummenhoff, C</creatorcontrib><creatorcontrib>Zidek, W</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>MEDLINE - Academic</collection><jtitle>The European respiratory journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sanner, BM</au><au>Konermann, M</au><au>Tepel, M</au><au>Groetz, J</au><au>Mummenhoff, C</au><au>Zidek, W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet function in patients with obstructive sleep apnoea syndrome</atitle><jtitle>The European respiratory journal</jtitle><addtitle>Eur Respir J</addtitle><date>2000-10</date><risdate>2000</risdate><volume>16</volume><issue>4</issue><spage>648</spage><epage>652</epage><pages>648-652</pages><issn>0903-1936</issn><eissn>1399-3003</eissn><abstract>Patients with obstructive sleep apnoea syndrome (OSAS) are subject to an increased cardiovascular morbidity including myocardial infarction and stroke. Platelets play an important role in the pathogenesis and triggering of acute cardiovascular syndromes. So far, the influence of OSAS on platelet function is not fully understood.
Platelet aggregability to epinephrine, collagen, arachidonic acid, and adenosine diphosphate in vitro was measured in 17 consecutive male patients (53.0±2.1 yrs) with polysomnographically verified OSAS and compared with that of 15 male controls (50.1±3.6 yrs) at 20:00 h, 24:00 h, and 06:00 h. In addition, the long‐term effects of continuous positive airway pressure (CPAP) therapy on platelet aggregability was assessed after 6 months.
Platelet aggregation in vitro induced by epinephrine showed a slight increase overnight in the untreated OSAS patients (
ns) whereas it decreased slightly (
ns) in the controls and in the treated OSAS patients. Pretherapeutic platelet aggregability was significantly lowered by CPAP therapy both at 24:00 h (64.0±6.5 versus 55.3±6.7%, p<0.05) and at 06:00 h (64.1±6.5 versus 45.8±7.6%; p=0.01). Platelet aggregability during sleep in the controls resembled that found in patients with OSAS during CPAP therapy.
The results suggest that obstructive sleep apnoea syndrome contributes, at least in part, to platelet dysfunction and that long‐term continuous positive airway pressure treatment may reduce platelet aggregability.</abstract><cop>Sheffield</cop><pub>Eur Respiratory Soc</pub><pmid>11106207</pmid><doi>10.1034/j.1399-3003.2000.16d14.x</doi><tpages>5</tpages></addata></record> |
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subjects | Adult Aged Biological and medical sciences Catecholamines Chronic obstructive pulmonary disease, asthma Humans Male Medical sciences Middle Aged obstructive sleep apnoea syndrome Platelet Aggregation - physiology platelet function Pneumology Polysomnography Positive-Pressure Respiration Regression Analysis sleep Sleep Apnea Syndromes - blood Sleep Apnea Syndromes - diagnosis Sleep Apnea Syndromes - therapy stroke |
title | Platelet function in patients with obstructive sleep apnoea syndrome |
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