β-Amyloid and mitochondrial-derived peptide-c are additive predictors of adverse outcome to high-on-treatment platelet reactivity in type 2 diabetics with revascularized coronary artery disease
Background and aims Increased β-amyloid and decreased mitochondrial-derived peptide (MOTS-c), are reported in diabetes. We investigated their additive value to high on-clopidogrel platelet reactivity (HPR) for adverse outcome in type 2 diabetics after recent revascularization. Patients and methods I...
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| Veröffentlicht in: | Journal of thrombosis and thrombolysis 2020-04, Vol.49 (3), p.365-376 |
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| creator | Ikonomidis, Ignatios Katogiannis, Konstantinos Kyriakou, Elias Taichert, Maria Katsimaglis, Georgios Tsoumani, Maria Andreadou, Ioanna Maratou, Eirini Lambadiari, Vaia Kousathana, Foteini Papadopoulou, Anna Varlamos, Charalampos Plotas, Panagiotis Parissis, John Stamatelopoulos, Kimon Alexopoulos, Dimitrios Dimitriadis, George Tsantes, Argirios E. |
| description | Background and aims
Increased β-amyloid and decreased mitochondrial-derived peptide (MOTS-c), are reported in diabetes. We investigated their additive value to high on-clopidogrel platelet reactivity (HPR) for adverse outcome in type 2 diabetics after recent revascularization.
Patients and methods
In 121 type II diabetics, treated with clopidogrel and aspirin, (93 males, mean age 67.2 years) we measured: (a) maximum platelet aggregation to adenosine diphosphate (ADP) by light transmission aggregometry (LTAmax), (b) malondialdehyde (MDA), as oxidative stress marker, (c) MOTS-c, (d) β-amyloid blood levels. Cardiac death and acute coronary syndromes (MACE) were recorded during 2 years of follow-up.
Results
Out of 121 patients, 32 showed HPR (LTAmax > 48%,). At baseline, HPR was associated with β-amyloid > 51 pg/ml (
p
= 0.006) after adjusting clinical variables, HbA1c, MOTS-c, MDA and medication. During follow-up, 22 patients suffered a MACE. HPR, β-amyloid > 51 pg/ml and MOTS-c |
| doi_str_mv | 10.1007/s11239-020-02060-4 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2354741580</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2387925776</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-7116939da628729fd177449aecaa9f67344472fb3089d62b6033b19b677dd4813</originalsourceid><addsrcrecordid>eNp9kc9qFTEYxYNY7LX6Ai4k4Kab2PybyWRZilqh4EbBXcgk3_SmzEzGJHPL9bF8hD6Az9TUWxVcuAgfnPy-kxMOQq8YfcsoVWeZMS40oZw-nJYS-QRtWKMEUZJ_fYo2VHNNGkGbY_Q85xtKqdaUP0PHgtOGC9Zs0N3PH-R82o8xeGxnj6dQotvG2adgR-IhhR14vMBSggfisE2ArfehVB0vCXxwJaaM41DlHaQMOK7FxQlwiXgbrrckzqQksGWCueBltAVGKLgqrpqEssdhxmW_AObYB9tDCS7j21C2ldnZ7NbRpvC9pnAxxdmmfQ1RoA4fMtgML9DRYMcMLx_nCfry_t3ni0ty9enDx4vzK-KEagpRjLVaaG9b3imuB8-UklJbcNbqoVVCSqn40Avaad_yvqVC9Ez3rVLey46JE3R68F1S_LZCLmYK2cE42hnimg0XjVSSNR2t6Jt_0Ju4prmmq1SnNG-UaivFD5RLMecEg1lSmOoHDaPmoWFzaNjUds2vho2sS68frdd-Av9n5XelFRAHINer-RrS37f_Y3sPnxm1kQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2387925776</pqid></control><display><type>article</type><title>β-Amyloid and mitochondrial-derived peptide-c are additive predictors of adverse outcome to high-on-treatment platelet reactivity in type 2 diabetics with revascularized coronary artery disease</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Ikonomidis, Ignatios ; Katogiannis, Konstantinos ; Kyriakou, Elias ; Taichert, Maria ; Katsimaglis, Georgios ; Tsoumani, Maria ; Andreadou, Ioanna ; Maratou, Eirini ; Lambadiari, Vaia ; Kousathana, Foteini ; Papadopoulou, Anna ; Varlamos, Charalampos ; Plotas, Panagiotis ; Parissis, John ; Stamatelopoulos, Kimon ; Alexopoulos, Dimitrios ; Dimitriadis, George ; Tsantes, Argirios E.</creator><creatorcontrib>Ikonomidis, Ignatios ; Katogiannis, Konstantinos ; Kyriakou, Elias ; Taichert, Maria ; Katsimaglis, Georgios ; Tsoumani, Maria ; Andreadou, Ioanna ; Maratou, Eirini ; Lambadiari, Vaia ; Kousathana, Foteini ; Papadopoulou, Anna ; Varlamos, Charalampos ; Plotas, Panagiotis ; Parissis, John ; Stamatelopoulos, Kimon ; Alexopoulos, Dimitrios ; Dimitriadis, George ; Tsantes, Argirios E.</creatorcontrib><description>Background and aims
Increased β-amyloid and decreased mitochondrial-derived peptide (MOTS-c), are reported in diabetes. We investigated their additive value to high on-clopidogrel platelet reactivity (HPR) for adverse outcome in type 2 diabetics after recent revascularization.
Patients and methods
In 121 type II diabetics, treated with clopidogrel and aspirin, (93 males, mean age 67.2 years) we measured: (a) maximum platelet aggregation to adenosine diphosphate (ADP) by light transmission aggregometry (LTAmax), (b) malondialdehyde (MDA), as oxidative stress marker, (c) MOTS-c, (d) β-amyloid blood levels. Cardiac death and acute coronary syndromes (MACE) were recorded during 2 years of follow-up.
Results
Out of 121 patients, 32 showed HPR (LTAmax > 48%,). At baseline, HPR was associated with β-amyloid > 51 pg/ml (
p
= 0.006) after adjusting clinical variables, HbA1c, MOTS-c, MDA and medication. During follow-up, 22 patients suffered a MACE. HPR, β-amyloid > 51 pg/ml and MOTS-c < 167 ng/ml were predictors of MACE (relative risk 3.1, 3.5 and 3.8 respectively,
p
< 0.05) after adjusting for confounders and medication. There was significant interaction between HPR and β-amyloid or MOTS-c for the prediction of MACE (
p
< 0.05). Patients with HPR and β-amyloid > 51 mg/dl or HPR and MOTS-c concentration < 167 ng/ml had a fourfold higher risk for MACE than patients without these predictors (relative risk 4.694 and 4.447 respectively
p
< 0.01). The above results were confirmed in an external validation cohort of 90 patients with diabetes and CAD.
Conclusions
Increased β-amyloid or low MOTS-c are additive predictors to high on-clopidogrel platelet reactivity for adverse outcome in diabetics with CAD during 2-years follow-up. Clinical Trial Registration-URL:
https://www.clinicaltrials.gov
. Unique identifier: NCT04027712.</description><identifier>ISSN: 0929-5305</identifier><identifier>EISSN: 1573-742X</identifier><identifier>DOI: 10.1007/s11239-020-02060-4</identifier><identifier>PMID: 32052315</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adenosine ; Aged ; Alzheimer's disease ; Amyloid beta-Peptides - blood ; Aspirin ; Blood levels ; Blood Platelets ; Cardiology ; Cardiovascular disease ; Clopidogrel ; Clopidogrel - administration & dosage ; Coronary artery ; Coronary Artery Disease - blood ; Coronary Artery Disease - therapy ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - therapy ; Female ; Follow-Up Studies ; Hematology ; Humans ; Male ; Malondialdehyde ; Malondialdehyde - blood ; Medicine ; Medicine & Public Health ; Middle Aged ; Mitochondria ; Mitochondrial Proteins - blood ; Myocardial Revascularization ; Oxidative stress ; Patients ; Peptides ; Platelet Activation - drug effects ; Platelet aggregation ; Risk Factors ; β-Amyloid</subject><ispartof>Journal of thrombosis and thrombolysis, 2020-04, Vol.49 (3), p.365-376</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-7116939da628729fd177449aecaa9f67344472fb3089d62b6033b19b677dd4813</citedby><cites>FETCH-LOGICAL-c375t-7116939da628729fd177449aecaa9f67344472fb3089d62b6033b19b677dd4813</cites><orcidid>0000-0001-8241-7886</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11239-020-02060-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11239-020-02060-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32052315$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ikonomidis, Ignatios</creatorcontrib><creatorcontrib>Katogiannis, Konstantinos</creatorcontrib><creatorcontrib>Kyriakou, Elias</creatorcontrib><creatorcontrib>Taichert, Maria</creatorcontrib><creatorcontrib>Katsimaglis, Georgios</creatorcontrib><creatorcontrib>Tsoumani, Maria</creatorcontrib><creatorcontrib>Andreadou, Ioanna</creatorcontrib><creatorcontrib>Maratou, Eirini</creatorcontrib><creatorcontrib>Lambadiari, Vaia</creatorcontrib><creatorcontrib>Kousathana, Foteini</creatorcontrib><creatorcontrib>Papadopoulou, Anna</creatorcontrib><creatorcontrib>Varlamos, Charalampos</creatorcontrib><creatorcontrib>Plotas, Panagiotis</creatorcontrib><creatorcontrib>Parissis, John</creatorcontrib><creatorcontrib>Stamatelopoulos, Kimon</creatorcontrib><creatorcontrib>Alexopoulos, Dimitrios</creatorcontrib><creatorcontrib>Dimitriadis, George</creatorcontrib><creatorcontrib>Tsantes, Argirios E.</creatorcontrib><title>β-Amyloid and mitochondrial-derived peptide-c are additive predictors of adverse outcome to high-on-treatment platelet reactivity in type 2 diabetics with revascularized coronary artery disease</title><title>Journal of thrombosis and thrombolysis</title><addtitle>J Thromb Thrombolysis</addtitle><addtitle>J Thromb Thrombolysis</addtitle><description>Background and aims
Increased β-amyloid and decreased mitochondrial-derived peptide (MOTS-c), are reported in diabetes. We investigated their additive value to high on-clopidogrel platelet reactivity (HPR) for adverse outcome in type 2 diabetics after recent revascularization.
Patients and methods
In 121 type II diabetics, treated with clopidogrel and aspirin, (93 males, mean age 67.2 years) we measured: (a) maximum platelet aggregation to adenosine diphosphate (ADP) by light transmission aggregometry (LTAmax), (b) malondialdehyde (MDA), as oxidative stress marker, (c) MOTS-c, (d) β-amyloid blood levels. Cardiac death and acute coronary syndromes (MACE) were recorded during 2 years of follow-up.
Results
Out of 121 patients, 32 showed HPR (LTAmax > 48%,). At baseline, HPR was associated with β-amyloid > 51 pg/ml (
p
= 0.006) after adjusting clinical variables, HbA1c, MOTS-c, MDA and medication. During follow-up, 22 patients suffered a MACE. HPR, β-amyloid > 51 pg/ml and MOTS-c < 167 ng/ml were predictors of MACE (relative risk 3.1, 3.5 and 3.8 respectively,
p
< 0.05) after adjusting for confounders and medication. There was significant interaction between HPR and β-amyloid or MOTS-c for the prediction of MACE (
p
< 0.05). Patients with HPR and β-amyloid > 51 mg/dl or HPR and MOTS-c concentration < 167 ng/ml had a fourfold higher risk for MACE than patients without these predictors (relative risk 4.694 and 4.447 respectively
p
< 0.01). The above results were confirmed in an external validation cohort of 90 patients with diabetes and CAD.
Conclusions
Increased β-amyloid or low MOTS-c are additive predictors to high on-clopidogrel platelet reactivity for adverse outcome in diabetics with CAD during 2-years follow-up. Clinical Trial Registration-URL:
https://www.clinicaltrials.gov
. Unique identifier: NCT04027712.</description><subject>Adenosine</subject><subject>Aged</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - blood</subject><subject>Aspirin</subject><subject>Blood levels</subject><subject>Blood Platelets</subject><subject>Cardiology</subject><subject>Cardiovascular disease</subject><subject>Clopidogrel</subject><subject>Clopidogrel - administration & dosage</subject><subject>Coronary artery</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - therapy</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - therapy</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Hematology</subject><subject>Humans</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Malondialdehyde - blood</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Mitochondria</subject><subject>Mitochondrial Proteins - blood</subject><subject>Myocardial Revascularization</subject><subject>Oxidative stress</subject><subject>Patients</subject><subject>Peptides</subject><subject>Platelet Activation - drug effects</subject><subject>Platelet aggregation</subject><subject>Risk Factors</subject><subject>β-Amyloid</subject><issn>0929-5305</issn><issn>1573-742X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc9qFTEYxYNY7LX6Ai4k4Kab2PybyWRZilqh4EbBXcgk3_SmzEzGJHPL9bF8hD6Az9TUWxVcuAgfnPy-kxMOQq8YfcsoVWeZMS40oZw-nJYS-QRtWKMEUZJ_fYo2VHNNGkGbY_Q85xtKqdaUP0PHgtOGC9Zs0N3PH-R82o8xeGxnj6dQotvG2adgR-IhhR14vMBSggfisE2ArfehVB0vCXxwJaaM41DlHaQMOK7FxQlwiXgbrrckzqQksGWCueBltAVGKLgqrpqEssdhxmW_AObYB9tDCS7j21C2ldnZ7NbRpvC9pnAxxdmmfQ1RoA4fMtgML9DRYMcMLx_nCfry_t3ni0ty9enDx4vzK-KEagpRjLVaaG9b3imuB8-UklJbcNbqoVVCSqn40Avaad_yvqVC9Ez3rVLey46JE3R68F1S_LZCLmYK2cE42hnimg0XjVSSNR2t6Jt_0Ju4prmmq1SnNG-UaivFD5RLMecEg1lSmOoHDaPmoWFzaNjUds2vho2sS68frdd-Av9n5XelFRAHINer-RrS37f_Y3sPnxm1kQ</recordid><startdate>20200401</startdate><enddate>20200401</enddate><creator>Ikonomidis, Ignatios</creator><creator>Katogiannis, Konstantinos</creator><creator>Kyriakou, Elias</creator><creator>Taichert, Maria</creator><creator>Katsimaglis, Georgios</creator><creator>Tsoumani, Maria</creator><creator>Andreadou, Ioanna</creator><creator>Maratou, Eirini</creator><creator>Lambadiari, Vaia</creator><creator>Kousathana, Foteini</creator><creator>Papadopoulou, Anna</creator><creator>Varlamos, Charalampos</creator><creator>Plotas, Panagiotis</creator><creator>Parissis, John</creator><creator>Stamatelopoulos, Kimon</creator><creator>Alexopoulos, Dimitrios</creator><creator>Dimitriadis, George</creator><creator>Tsantes, Argirios E.</creator><general>Springer US</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</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>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8241-7886</orcidid></search><sort><creationdate>20200401</creationdate><title>β-Amyloid and mitochondrial-derived peptide-c are additive predictors of adverse outcome to high-on-treatment platelet reactivity in type 2 diabetics with revascularized coronary artery disease</title><author>Ikonomidis, Ignatios ; Katogiannis, Konstantinos ; Kyriakou, Elias ; Taichert, Maria ; Katsimaglis, Georgios ; Tsoumani, Maria ; Andreadou, Ioanna ; Maratou, Eirini ; Lambadiari, Vaia ; Kousathana, Foteini ; Papadopoulou, Anna ; Varlamos, Charalampos ; Plotas, Panagiotis ; Parissis, John ; Stamatelopoulos, Kimon ; Alexopoulos, Dimitrios ; Dimitriadis, George ; Tsantes, Argirios E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-7116939da628729fd177449aecaa9f67344472fb3089d62b6033b19b677dd4813</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adenosine</topic><topic>Aged</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides - blood</topic><topic>Aspirin</topic><topic>Blood levels</topic><topic>Blood Platelets</topic><topic>Cardiology</topic><topic>Cardiovascular disease</topic><topic>Clopidogrel</topic><topic>Clopidogrel - administration & dosage</topic><topic>Coronary artery</topic><topic>Coronary Artery Disease - blood</topic><topic>Coronary Artery Disease - therapy</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes Mellitus, Type 2 - therapy</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Hematology</topic><topic>Humans</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Malondialdehyde - blood</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Mitochondria</topic><topic>Mitochondrial Proteins - blood</topic><topic>Myocardial Revascularization</topic><topic>Oxidative stress</topic><topic>Patients</topic><topic>Peptides</topic><topic>Platelet Activation - drug effects</topic><topic>Platelet aggregation</topic><topic>Risk Factors</topic><topic>β-Amyloid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ikonomidis, Ignatios</creatorcontrib><creatorcontrib>Katogiannis, Konstantinos</creatorcontrib><creatorcontrib>Kyriakou, Elias</creatorcontrib><creatorcontrib>Taichert, Maria</creatorcontrib><creatorcontrib>Katsimaglis, Georgios</creatorcontrib><creatorcontrib>Tsoumani, Maria</creatorcontrib><creatorcontrib>Andreadou, Ioanna</creatorcontrib><creatorcontrib>Maratou, Eirini</creatorcontrib><creatorcontrib>Lambadiari, Vaia</creatorcontrib><creatorcontrib>Kousathana, Foteini</creatorcontrib><creatorcontrib>Papadopoulou, Anna</creatorcontrib><creatorcontrib>Varlamos, Charalampos</creatorcontrib><creatorcontrib>Plotas, Panagiotis</creatorcontrib><creatorcontrib>Parissis, John</creatorcontrib><creatorcontrib>Stamatelopoulos, Kimon</creatorcontrib><creatorcontrib>Alexopoulos, Dimitrios</creatorcontrib><creatorcontrib>Dimitriadis, George</creatorcontrib><creatorcontrib>Tsantes, Argirios E.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</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>Journal of thrombosis and thrombolysis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ikonomidis, Ignatios</au><au>Katogiannis, Konstantinos</au><au>Kyriakou, Elias</au><au>Taichert, Maria</au><au>Katsimaglis, Georgios</au><au>Tsoumani, Maria</au><au>Andreadou, Ioanna</au><au>Maratou, Eirini</au><au>Lambadiari, Vaia</au><au>Kousathana, Foteini</au><au>Papadopoulou, Anna</au><au>Varlamos, Charalampos</au><au>Plotas, Panagiotis</au><au>Parissis, John</au><au>Stamatelopoulos, Kimon</au><au>Alexopoulos, Dimitrios</au><au>Dimitriadis, George</au><au>Tsantes, Argirios E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>β-Amyloid and mitochondrial-derived peptide-c are additive predictors of adverse outcome to high-on-treatment platelet reactivity in type 2 diabetics with revascularized coronary artery disease</atitle><jtitle>Journal of thrombosis and thrombolysis</jtitle><stitle>J Thromb Thrombolysis</stitle><addtitle>J Thromb Thrombolysis</addtitle><date>2020-04-01</date><risdate>2020</risdate><volume>49</volume><issue>3</issue><spage>365</spage><epage>376</epage><pages>365-376</pages><issn>0929-5305</issn><eissn>1573-742X</eissn><abstract>Background and aims
Increased β-amyloid and decreased mitochondrial-derived peptide (MOTS-c), are reported in diabetes. We investigated their additive value to high on-clopidogrel platelet reactivity (HPR) for adverse outcome in type 2 diabetics after recent revascularization.
Patients and methods
In 121 type II diabetics, treated with clopidogrel and aspirin, (93 males, mean age 67.2 years) we measured: (a) maximum platelet aggregation to adenosine diphosphate (ADP) by light transmission aggregometry (LTAmax), (b) malondialdehyde (MDA), as oxidative stress marker, (c) MOTS-c, (d) β-amyloid blood levels. Cardiac death and acute coronary syndromes (MACE) were recorded during 2 years of follow-up.
Results
Out of 121 patients, 32 showed HPR (LTAmax > 48%,). At baseline, HPR was associated with β-amyloid > 51 pg/ml (
p
= 0.006) after adjusting clinical variables, HbA1c, MOTS-c, MDA and medication. During follow-up, 22 patients suffered a MACE. HPR, β-amyloid > 51 pg/ml and MOTS-c < 167 ng/ml were predictors of MACE (relative risk 3.1, 3.5 and 3.8 respectively,
p
< 0.05) after adjusting for confounders and medication. There was significant interaction between HPR and β-amyloid or MOTS-c for the prediction of MACE (
p
< 0.05). Patients with HPR and β-amyloid > 51 mg/dl or HPR and MOTS-c concentration < 167 ng/ml had a fourfold higher risk for MACE than patients without these predictors (relative risk 4.694 and 4.447 respectively
p
< 0.01). The above results were confirmed in an external validation cohort of 90 patients with diabetes and CAD.
Conclusions
Increased β-amyloid or low MOTS-c are additive predictors to high on-clopidogrel platelet reactivity for adverse outcome in diabetics with CAD during 2-years follow-up. Clinical Trial Registration-URL:
https://www.clinicaltrials.gov
. Unique identifier: NCT04027712.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>32052315</pmid><doi>10.1007/s11239-020-02060-4</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-8241-7886</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0929-5305 |
| ispartof | Journal of thrombosis and thrombolysis, 2020-04, Vol.49 (3), p.365-376 |
| issn | 0929-5305 1573-742X |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2354741580 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Adenosine Aged Alzheimer's disease Amyloid beta-Peptides - blood Aspirin Blood levels Blood Platelets Cardiology Cardiovascular disease Clopidogrel Clopidogrel - administration & dosage Coronary artery Coronary Artery Disease - blood Coronary Artery Disease - therapy Diabetes Diabetes mellitus Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - therapy Female Follow-Up Studies Hematology Humans Male Malondialdehyde Malondialdehyde - blood Medicine Medicine & Public Health Middle Aged Mitochondria Mitochondrial Proteins - blood Myocardial Revascularization Oxidative stress Patients Peptides Platelet Activation - drug effects Platelet aggregation Risk Factors β-Amyloid |
| title | β-Amyloid and mitochondrial-derived peptide-c are additive predictors of adverse outcome to high-on-treatment platelet reactivity in type 2 diabetics with revascularized coronary artery disease |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-29T17%3A52%3A45IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=%CE%B2-Amyloid%20and%20mitochondrial-derived%20peptide-c%20are%20additive%20predictors%20of%20adverse%20outcome%20to%20high-on-treatment%20platelet%20reactivity%20in%20type%202%20diabetics%20with%20revascularized%20coronary%20artery%20disease&rft.jtitle=Journal%20of%20thrombosis%20and%20thrombolysis&rft.au=Ikonomidis,%20Ignatios&rft.date=2020-04-01&rft.volume=49&rft.issue=3&rft.spage=365&rft.epage=376&rft.pages=365-376&rft.issn=0929-5305&rft.eissn=1573-742X&rft_id=info:doi/10.1007/s11239-020-02060-4&rft_dat=%3Cproquest_cross%3E2387925776%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2387925776&rft_id=info:pmid/32052315&rfr_iscdi=true |