Asymmetric and Symmetric Dimethylarginines are Markers of Delayed Cerebral Ischemia and Neurological Outcome in Patients with Subarachnoid Hemorrhage
Background Delayed cerebral ischemia (DCI) is the major cause of lethality and neuronal damage in patients who survived the primary subarachnoid hemorrhage (SAH). Asymmetric and symmetric dimethylarginines (ADMA and SDMA) inhibit nitric oxide production from l -arginine via distinct mechanisms. Elev...
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| Veröffentlicht in: | Neurocritical care 2018-08, Vol.29 (1), p.84-93 |
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| creator | Appel, Daniel Seeberger, Miriam Schwedhelm, Edzard Czorlich, Patrick Goetz, Alwin E. Böger, Rainer H. Hannemann, Juliane |
| description | Background
Delayed cerebral ischemia (DCI) is the major cause of lethality and neuronal damage in patients who survived the primary subarachnoid hemorrhage (SAH). Asymmetric and symmetric dimethylarginines (ADMA and SDMA) inhibit nitric oxide production from
l
-arginine via distinct mechanisms. Elevated ADMA levels are associated with vasospasm after SAH. We aimed to study the time course of ADMA and SDMA in plasma and ventricular cerebrospinal fluid (CSF) and their associations with DCI and outcome.
Methods
We measured ADMA and SDMA in 34 SAH patients with an external ventricular drain at admission and on days 3, 6, 8, 12, and 15 and followed them up for clinical status and neurological outcome until 30 days post-discharge. DCI was defined as the appearance of new infarctions on cerebral computed tomography or magnetic resonance imaging.
Results
ADMA and SDMA plasma concentrations did not differ significantly at baseline between patients who suffered DCI (
N
= 14; 41%) and not; however, plasma ADMA reached a peak on days 8 and 15 after hemorrhage in patients with DCI (0.81–0.91 µmol/l). Baseline plasma
l
-arginine/ADMA ratio was significantly lower in patients with DCI (57.1 [34.3; 70.8] vs. 68.7 [55.7; 96.2];
p
|
| doi_str_mv | 10.1007/s12028-018-0520-1 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2016536524</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2919480476</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-c06282add5f4e219af3bd5aca4320d6d2e9b92c846d6d0a125c4168880b545c13</originalsourceid><addsrcrecordid>eNp1kcFu1DAQhi0EoqXwAFyQJS5cArZjO_Gx2hZaqVCkwtma2JONSxIXOxHaB-F98bKlSEgcLM9oPv8e6SPkJWdvOWPNu8wFE23FeDlKsIo_IsdcKV0xo_njfS15pU1dH5FnOd8yJhrTqKfkSBilmTLtMfl5mnfThEsKjsLs6c1DdxZKMexGSNswhxkzhYT0I6RvmDKNPT3DEXbo6QYTdglGepndgFOA30GfcE1xjNvgyuR6XVyckIaZfoYl4Lxk-iMsA71ZO0jghjkGTy9wiikNsMXn5EkPY8YX9_cJ-fr-_Mvmorq6_nC5Ob2qXN2IpXJMi1aA96qXKLiBvu68AgeyFsxrL9B0RrhW6tIw4EI5yXXbtqxTUjlen5A3h9y7FL-vmBc7hexwHGHGuGYrGNeq1krIgr7-B72Na5rLdlYYbmTLZKMLxQ-USzHnhL29S2GCtLOc2b0ze3BmizO7d2b3S7y6T167Cf3Diz-SCiAOQC6jeYvp79f_T_0F2QCjcA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2919480476</pqid></control><display><type>article</type><title>Asymmetric and Symmetric Dimethylarginines are Markers of Delayed Cerebral Ischemia and Neurological Outcome in Patients with Subarachnoid Hemorrhage</title><source>SpringerLink Journals</source><source>ProQuest Central</source><creator>Appel, Daniel ; Seeberger, Miriam ; Schwedhelm, Edzard ; Czorlich, Patrick ; Goetz, Alwin E. ; Böger, Rainer H. ; Hannemann, Juliane</creator><creatorcontrib>Appel, Daniel ; Seeberger, Miriam ; Schwedhelm, Edzard ; Czorlich, Patrick ; Goetz, Alwin E. ; Böger, Rainer H. ; Hannemann, Juliane</creatorcontrib><description>Background
Delayed cerebral ischemia (DCI) is the major cause of lethality and neuronal damage in patients who survived the primary subarachnoid hemorrhage (SAH). Asymmetric and symmetric dimethylarginines (ADMA and SDMA) inhibit nitric oxide production from
l
-arginine via distinct mechanisms. Elevated ADMA levels are associated with vasospasm after SAH. We aimed to study the time course of ADMA and SDMA in plasma and ventricular cerebrospinal fluid (CSF) and their associations with DCI and outcome.
Methods
We measured ADMA and SDMA in 34 SAH patients with an external ventricular drain at admission and on days 3, 6, 8, 12, and 15 and followed them up for clinical status and neurological outcome until 30 days post-discharge. DCI was defined as the appearance of new infarctions on cerebral computed tomography or magnetic resonance imaging.
Results
ADMA and SDMA plasma concentrations did not differ significantly at baseline between patients who suffered DCI (
N
= 14; 41%) and not; however, plasma ADMA reached a peak on days 8 and 15 after hemorrhage in patients with DCI (0.81–0.91 µmol/l). Baseline plasma
l
-arginine/ADMA ratio was significantly lower in patients with DCI (57.1 [34.3; 70.8] vs. 68.7 [55.7; 96.2];
p
< 0.05). ADMA and SDMA concentrations in CSF were significantly higher in patients with DCI than without. In multivariable-adjusted linear regression models, CSF ADMA was negatively associated with the incidence of DCI (OR 0.03 [0.02–0.70];
p
= 0.04), whereas CSF SDMA on the day of hemorrhage predicted poor neurological outcome until 30 days after discharge (OR 22.4 [1.21–416.02];
p
= 0.04).
Conclusions
Our study shows that ADMA and the
l
-arginine/ADMA ratio are associated with the incidence of DCI after SAH. By contrast, SDMA was associated with initial neuronal damage and poor neurological outcome after SAH. These data support the hypothesis that ADMA and
l
-arginine affect the pathophysiology of cerebral ischemia after SAH, while SDMA is a biomarker of neurological outcome after SAH.</description><identifier>ISSN: 1541-6933</identifier><identifier>EISSN: 1556-0961</identifier><identifier>DOI: 10.1007/s12028-018-0520-1</identifier><identifier>PMID: 29560598</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Aneurysms ; Body mass index ; Catheters ; Critical Care Medicine ; Flow velocity ; Glasgow Coma Scale ; Hemorrhage ; Intensive ; Intensive care ; Internal Medicine ; Intracranial pressure ; Ischemia ; Laboratories ; Magnetic resonance imaging ; Medical imaging ; Medicine ; Medicine & Public Health ; Mortality ; Neurology ; Original Article ; Pathogenesis ; Patients ; Plasma ; Stroke ; Surgeons</subject><ispartof>Neurocritical care, 2018-08, Vol.29 (1), p.84-93</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society 2018</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society 2018.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-c06282add5f4e219af3bd5aca4320d6d2e9b92c846d6d0a125c4168880b545c13</citedby><cites>FETCH-LOGICAL-c372t-c06282add5f4e219af3bd5aca4320d6d2e9b92c846d6d0a125c4168880b545c13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12028-018-0520-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2919480476?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,776,780,21367,27901,27902,33721,33722,41464,42533,43781,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29560598$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Appel, Daniel</creatorcontrib><creatorcontrib>Seeberger, Miriam</creatorcontrib><creatorcontrib>Schwedhelm, Edzard</creatorcontrib><creatorcontrib>Czorlich, Patrick</creatorcontrib><creatorcontrib>Goetz, Alwin E.</creatorcontrib><creatorcontrib>Böger, Rainer H.</creatorcontrib><creatorcontrib>Hannemann, Juliane</creatorcontrib><title>Asymmetric and Symmetric Dimethylarginines are Markers of Delayed Cerebral Ischemia and Neurological Outcome in Patients with Subarachnoid Hemorrhage</title><title>Neurocritical care</title><addtitle>Neurocrit Care</addtitle><addtitle>Neurocrit Care</addtitle><description>Background
Delayed cerebral ischemia (DCI) is the major cause of lethality and neuronal damage in patients who survived the primary subarachnoid hemorrhage (SAH). Asymmetric and symmetric dimethylarginines (ADMA and SDMA) inhibit nitric oxide production from
l
-arginine via distinct mechanisms. Elevated ADMA levels are associated with vasospasm after SAH. We aimed to study the time course of ADMA and SDMA in plasma and ventricular cerebrospinal fluid (CSF) and their associations with DCI and outcome.
Methods
We measured ADMA and SDMA in 34 SAH patients with an external ventricular drain at admission and on days 3, 6, 8, 12, and 15 and followed them up for clinical status and neurological outcome until 30 days post-discharge. DCI was defined as the appearance of new infarctions on cerebral computed tomography or magnetic resonance imaging.
Results
ADMA and SDMA plasma concentrations did not differ significantly at baseline between patients who suffered DCI (
N
= 14; 41%) and not; however, plasma ADMA reached a peak on days 8 and 15 after hemorrhage in patients with DCI (0.81–0.91 µmol/l). Baseline plasma
l
-arginine/ADMA ratio was significantly lower in patients with DCI (57.1 [34.3; 70.8] vs. 68.7 [55.7; 96.2];
p
< 0.05). ADMA and SDMA concentrations in CSF were significantly higher in patients with DCI than without. In multivariable-adjusted linear regression models, CSF ADMA was negatively associated with the incidence of DCI (OR 0.03 [0.02–0.70];
p
= 0.04), whereas CSF SDMA on the day of hemorrhage predicted poor neurological outcome until 30 days after discharge (OR 22.4 [1.21–416.02];
p
= 0.04).
Conclusions
Our study shows that ADMA and the
l
-arginine/ADMA ratio are associated with the incidence of DCI after SAH. By contrast, SDMA was associated with initial neuronal damage and poor neurological outcome after SAH. These data support the hypothesis that ADMA and
l
-arginine affect the pathophysiology of cerebral ischemia after SAH, while SDMA is a biomarker of neurological outcome after SAH.</description><subject>Aneurysms</subject><subject>Body mass index</subject><subject>Catheters</subject><subject>Critical Care Medicine</subject><subject>Flow velocity</subject><subject>Glasgow Coma Scale</subject><subject>Hemorrhage</subject><subject>Intensive</subject><subject>Intensive care</subject><subject>Internal Medicine</subject><subject>Intracranial pressure</subject><subject>Ischemia</subject><subject>Laboratories</subject><subject>Magnetic resonance imaging</subject><subject>Medical imaging</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mortality</subject><subject>Neurology</subject><subject>Original Article</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Plasma</subject><subject>Stroke</subject><subject>Surgeons</subject><issn>1541-6933</issn><issn>1556-0961</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp1kcFu1DAQhi0EoqXwAFyQJS5cArZjO_Gx2hZaqVCkwtma2JONSxIXOxHaB-F98bKlSEgcLM9oPv8e6SPkJWdvOWPNu8wFE23FeDlKsIo_IsdcKV0xo_njfS15pU1dH5FnOd8yJhrTqKfkSBilmTLtMfl5mnfThEsKjsLs6c1DdxZKMexGSNswhxkzhYT0I6RvmDKNPT3DEXbo6QYTdglGepndgFOA30GfcE1xjNvgyuR6XVyckIaZfoYl4Lxk-iMsA71ZO0jghjkGTy9wiikNsMXn5EkPY8YX9_cJ-fr-_Mvmorq6_nC5Ob2qXN2IpXJMi1aA96qXKLiBvu68AgeyFsxrL9B0RrhW6tIw4EI5yXXbtqxTUjlen5A3h9y7FL-vmBc7hexwHGHGuGYrGNeq1krIgr7-B72Na5rLdlYYbmTLZKMLxQ-USzHnhL29S2GCtLOc2b0ze3BmizO7d2b3S7y6T167Cf3Diz-SCiAOQC6jeYvp79f_T_0F2QCjcA</recordid><startdate>20180801</startdate><enddate>20180801</enddate><creator>Appel, Daniel</creator><creator>Seeberger, Miriam</creator><creator>Schwedhelm, Edzard</creator><creator>Czorlich, Patrick</creator><creator>Goetz, Alwin E.</creator><creator>Böger, Rainer H.</creator><creator>Hannemann, Juliane</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20180801</creationdate><title>Asymmetric and Symmetric Dimethylarginines are Markers of Delayed Cerebral Ischemia and Neurological Outcome in Patients with Subarachnoid Hemorrhage</title><author>Appel, Daniel ; Seeberger, Miriam ; Schwedhelm, Edzard ; Czorlich, Patrick ; Goetz, Alwin E. ; Böger, Rainer H. ; Hannemann, Juliane</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-c06282add5f4e219af3bd5aca4320d6d2e9b92c846d6d0a125c4168880b545c13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Aneurysms</topic><topic>Body mass index</topic><topic>Catheters</topic><topic>Critical Care Medicine</topic><topic>Flow velocity</topic><topic>Glasgow Coma Scale</topic><topic>Hemorrhage</topic><topic>Intensive</topic><topic>Intensive care</topic><topic>Internal Medicine</topic><topic>Intracranial pressure</topic><topic>Ischemia</topic><topic>Laboratories</topic><topic>Magnetic resonance imaging</topic><topic>Medical imaging</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mortality</topic><topic>Neurology</topic><topic>Original Article</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>Plasma</topic><topic>Stroke</topic><topic>Surgeons</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Appel, Daniel</creatorcontrib><creatorcontrib>Seeberger, Miriam</creatorcontrib><creatorcontrib>Schwedhelm, Edzard</creatorcontrib><creatorcontrib>Czorlich, Patrick</creatorcontrib><creatorcontrib>Goetz, Alwin E.</creatorcontrib><creatorcontrib>Böger, Rainer H.</creatorcontrib><creatorcontrib>Hannemann, Juliane</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Neurocritical care</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Appel, Daniel</au><au>Seeberger, Miriam</au><au>Schwedhelm, Edzard</au><au>Czorlich, Patrick</au><au>Goetz, Alwin E.</au><au>Böger, Rainer H.</au><au>Hannemann, Juliane</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Asymmetric and Symmetric Dimethylarginines are Markers of Delayed Cerebral Ischemia and Neurological Outcome in Patients with Subarachnoid Hemorrhage</atitle><jtitle>Neurocritical care</jtitle><stitle>Neurocrit Care</stitle><addtitle>Neurocrit Care</addtitle><date>2018-08-01</date><risdate>2018</risdate><volume>29</volume><issue>1</issue><spage>84</spage><epage>93</epage><pages>84-93</pages><issn>1541-6933</issn><eissn>1556-0961</eissn><abstract>Background
Delayed cerebral ischemia (DCI) is the major cause of lethality and neuronal damage in patients who survived the primary subarachnoid hemorrhage (SAH). Asymmetric and symmetric dimethylarginines (ADMA and SDMA) inhibit nitric oxide production from
l
-arginine via distinct mechanisms. Elevated ADMA levels are associated with vasospasm after SAH. We aimed to study the time course of ADMA and SDMA in plasma and ventricular cerebrospinal fluid (CSF) and their associations with DCI and outcome.
Methods
We measured ADMA and SDMA in 34 SAH patients with an external ventricular drain at admission and on days 3, 6, 8, 12, and 15 and followed them up for clinical status and neurological outcome until 30 days post-discharge. DCI was defined as the appearance of new infarctions on cerebral computed tomography or magnetic resonance imaging.
Results
ADMA and SDMA plasma concentrations did not differ significantly at baseline between patients who suffered DCI (
N
= 14; 41%) and not; however, plasma ADMA reached a peak on days 8 and 15 after hemorrhage in patients with DCI (0.81–0.91 µmol/l). Baseline plasma
l
-arginine/ADMA ratio was significantly lower in patients with DCI (57.1 [34.3; 70.8] vs. 68.7 [55.7; 96.2];
p
< 0.05). ADMA and SDMA concentrations in CSF were significantly higher in patients with DCI than without. In multivariable-adjusted linear regression models, CSF ADMA was negatively associated with the incidence of DCI (OR 0.03 [0.02–0.70];
p
= 0.04), whereas CSF SDMA on the day of hemorrhage predicted poor neurological outcome until 30 days after discharge (OR 22.4 [1.21–416.02];
p
= 0.04).
Conclusions
Our study shows that ADMA and the
l
-arginine/ADMA ratio are associated with the incidence of DCI after SAH. By contrast, SDMA was associated with initial neuronal damage and poor neurological outcome after SAH. These data support the hypothesis that ADMA and
l
-arginine affect the pathophysiology of cerebral ischemia after SAH, while SDMA is a biomarker of neurological outcome after SAH.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>29560598</pmid><doi>10.1007/s12028-018-0520-1</doi><tpages>10</tpages></addata></record> |
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| subjects | Aneurysms Body mass index Catheters Critical Care Medicine Flow velocity Glasgow Coma Scale Hemorrhage Intensive Intensive care Internal Medicine Intracranial pressure Ischemia Laboratories Magnetic resonance imaging Medical imaging Medicine Medicine & Public Health Mortality Neurology Original Article Pathogenesis Patients Plasma Stroke Surgeons |
| title | Asymmetric and Symmetric Dimethylarginines are Markers of Delayed Cerebral Ischemia and Neurological Outcome in Patients with Subarachnoid Hemorrhage |
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