Association of autoantibodies targeting endothelin type-A receptors with no-reflow in ST-elevation myocardial infarction
No-reflow (NR), where the coronary artery is patent after treatment of ST-elevation myocardial infarction (STEMI) but tissue perfusion is not restored, is associated with worse outcomes. We aimed to investigate the relationship between autoantibodies activating endothelin-1 receptor type A (ETAR-AAs...
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creator | Tona, Francesco Vadori, Marta Civieri, Giovanni Masiero, Giulia Iop, Laura Antonelli, Giorgia Perazzolo Marra, Martina Bianco, Federica Cecere, Annagrazia Lorenzoni, Giulia Naumova, Natalia Bernava, Giacomo Basso, Daniela Plebani, Mario Cozzi, Emanuele Iliceto, Sabino |
description | No-reflow (NR), where the coronary artery is patent after treatment of ST-elevation myocardial infarction (STEMI) but tissue perfusion is not restored, is associated with worse outcomes. We aimed to investigate the relationship between autoantibodies activating endothelin-1 receptor type A (ETAR-AAs) and NR after primary percutaneous coronary intervention (PPCI) in STEMI.
We studied 50 patients (age 59 ± 11 years, 40 males) with STEMI who underwent PPCI within 6 h after the onset of symptoms. Blood samples were obtained from all patients within 12 h following PPCI for ETAR-AA level measurement. The seropositive threshold was provided by the manufacturer (>10 U/ml). NR was assessed by cardiac magnetic resonance imaging (MVO, microvascular obstruction). As a control group, 40 healthy subjects matched for age and sex were recruited from the general population.
MVO was observed in 24 patients (48%). The prevalence of MVO was higher in patients with ETAR-AAs seropositivity (72% vs. 38%, p = 0.03). ETAR-AAs were higher in patients with MVO (8.9 U/mL (interquartile range [IQR] 6.8–16.2 U/mL) vs. 5.7 U/mL [IQR 4.3–7.7 U/mL], p = 0.003). ETAR-AAs seropositivity was independently associated with MVO (OR 3.2, 95% CI 1.3–7.1; p = 0.03). We identified ≥6.74 U/mL as the best cut-off for prediction of MVO (sensitivity 79%; specificity 65%; NPV 71%; PPV 74%; accuracy 72%).
The ETAR-AAs seropositivity is associated with NR in STEMI patients. These findings may open up new options in the management of myocardial infarction even if confirmation in a larger trial is needed.
[Display omitted]
•No-reflow, where the coronary artery is patent after treatment of STEMI but tissue perfusion is not restored, is associated with worse outcomes.•Autoantibodies targeting endothelin type A receptor (ETAR-AAs) can bind to these receptors and regulate their function.•ETAR-AAs may contribute to no-reflow in STEMI after successful primary percutaneous coronary intervention.•This finding, for the first time, shows an autoimmune predisposition to a worse outcome after myocardial infarction. |
doi_str_mv | 10.1016/j.atherosclerosis.2023.06.970 |
format | Article |
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We studied 50 patients (age 59 ± 11 years, 40 males) with STEMI who underwent PPCI within 6 h after the onset of symptoms. Blood samples were obtained from all patients within 12 h following PPCI for ETAR-AA level measurement. The seropositive threshold was provided by the manufacturer (>10 U/ml). NR was assessed by cardiac magnetic resonance imaging (MVO, microvascular obstruction). As a control group, 40 healthy subjects matched for age and sex were recruited from the general population.
MVO was observed in 24 patients (48%). The prevalence of MVO was higher in patients with ETAR-AAs seropositivity (72% vs. 38%, p = 0.03). ETAR-AAs were higher in patients with MVO (8.9 U/mL (interquartile range [IQR] 6.8–16.2 U/mL) vs. 5.7 U/mL [IQR 4.3–7.7 U/mL], p = 0.003). ETAR-AAs seropositivity was independently associated with MVO (OR 3.2, 95% CI 1.3–7.1; p = 0.03). We identified ≥6.74 U/mL as the best cut-off for prediction of MVO (sensitivity 79%; specificity 65%; NPV 71%; PPV 74%; accuracy 72%).
The ETAR-AAs seropositivity is associated with NR in STEMI patients. These findings may open up new options in the management of myocardial infarction even if confirmation in a larger trial is needed.
[Display omitted]
•No-reflow, where the coronary artery is patent after treatment of STEMI but tissue perfusion is not restored, is associated with worse outcomes.•Autoantibodies targeting endothelin type A receptor (ETAR-AAs) can bind to these receptors and regulate their function.•ETAR-AAs may contribute to no-reflow in STEMI after successful primary percutaneous coronary intervention.•This finding, for the first time, shows an autoimmune predisposition to a worse outcome after myocardial infarction.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/j.atherosclerosis.2023.06.970</identifier><identifier>PMID: 37422357</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><ispartof>Atherosclerosis, 2023-08, Vol.378, p.117179-117179, Article 117179</ispartof><rights>2023 The Authors</rights><rights>Copyright © 2023 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c444t-b717a60491672dcf3e18fb033d9d2c312bcb9c2b7cee8b84eb50cc143c5af2303</citedby><cites>FETCH-LOGICAL-c444t-b717a60491672dcf3e18fb033d9d2c312bcb9c2b7cee8b84eb50cc143c5af2303</cites><orcidid>0000-0003-4828-7875</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.atherosclerosis.2023.06.970$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37422357$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tona, Francesco</creatorcontrib><creatorcontrib>Vadori, Marta</creatorcontrib><creatorcontrib>Civieri, Giovanni</creatorcontrib><creatorcontrib>Masiero, Giulia</creatorcontrib><creatorcontrib>Iop, Laura</creatorcontrib><creatorcontrib>Antonelli, Giorgia</creatorcontrib><creatorcontrib>Perazzolo Marra, Martina</creatorcontrib><creatorcontrib>Bianco, Federica</creatorcontrib><creatorcontrib>Cecere, Annagrazia</creatorcontrib><creatorcontrib>Lorenzoni, Giulia</creatorcontrib><creatorcontrib>Naumova, Natalia</creatorcontrib><creatorcontrib>Bernava, Giacomo</creatorcontrib><creatorcontrib>Basso, Daniela</creatorcontrib><creatorcontrib>Plebani, Mario</creatorcontrib><creatorcontrib>Cozzi, Emanuele</creatorcontrib><creatorcontrib>Iliceto, Sabino</creatorcontrib><title>Association of autoantibodies targeting endothelin type-A receptors with no-reflow in ST-elevation myocardial infarction</title><title>Atherosclerosis</title><addtitle>Atherosclerosis</addtitle><description>No-reflow (NR), where the coronary artery is patent after treatment of ST-elevation myocardial infarction (STEMI) but tissue perfusion is not restored, is associated with worse outcomes. We aimed to investigate the relationship between autoantibodies activating endothelin-1 receptor type A (ETAR-AAs) and NR after primary percutaneous coronary intervention (PPCI) in STEMI.
We studied 50 patients (age 59 ± 11 years, 40 males) with STEMI who underwent PPCI within 6 h after the onset of symptoms. Blood samples were obtained from all patients within 12 h following PPCI for ETAR-AA level measurement. The seropositive threshold was provided by the manufacturer (>10 U/ml). NR was assessed by cardiac magnetic resonance imaging (MVO, microvascular obstruction). As a control group, 40 healthy subjects matched for age and sex were recruited from the general population.
MVO was observed in 24 patients (48%). The prevalence of MVO was higher in patients with ETAR-AAs seropositivity (72% vs. 38%, p = 0.03). ETAR-AAs were higher in patients with MVO (8.9 U/mL (interquartile range [IQR] 6.8–16.2 U/mL) vs. 5.7 U/mL [IQR 4.3–7.7 U/mL], p = 0.003). ETAR-AAs seropositivity was independently associated with MVO (OR 3.2, 95% CI 1.3–7.1; p = 0.03). We identified ≥6.74 U/mL as the best cut-off for prediction of MVO (sensitivity 79%; specificity 65%; NPV 71%; PPV 74%; accuracy 72%).
The ETAR-AAs seropositivity is associated with NR in STEMI patients. These findings may open up new options in the management of myocardial infarction even if confirmation in a larger trial is needed.
[Display omitted]
•No-reflow, where the coronary artery is patent after treatment of STEMI but tissue perfusion is not restored, is associated with worse outcomes.•Autoantibodies targeting endothelin type A receptor (ETAR-AAs) can bind to these receptors and regulate their function.•ETAR-AAs may contribute to no-reflow in STEMI after successful primary percutaneous coronary intervention.•This finding, for the first time, shows an autoimmune predisposition to a worse outcome after myocardial infarction.</description><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNqNkD1vFDEQhi1ERI7AX0BukGh28deudwuKU0QCUiSKhNqyx7OJT3vrw_Yl3L-PTxcoqGjG0viZeTUPIR85aznj_edNa8sDpphhPtaQW8GEbFnfjpq9Iis-6LHhalCvyYoxwZuRd-ycvM15wxhTmg9vyLnUSgjZ6RX5vc45QrAlxIXGidp9iXYpwUUfMNNi0z2WsNxTXHyswXNYaDnssFnThIC7ElOmT6E80CU2Cac5PtGK3N41OOPjae32EMEmH-xcvyab4Nh9R84mO2d8__JekJ9XX-8uvzU3P66_X65vGlBKlcZprm3P1Mh7LTxMEvkwOSalH70AyYUDN4JwGhAHNyh0HQPgSkJnJyGZvCCfTnt3Kf7aYy5mGzLgPNsF4z4bMchODExoWdEvJxSq2FyPMbsUtjYdDGfmKN9szD_yzVG-Yb2p8uv8h5eovdui_zv9x3YFrk8A1oMfAyaTIeAC6EOVWYyP4T-jngFQ-KNW</recordid><startdate>202308</startdate><enddate>202308</enddate><creator>Tona, Francesco</creator><creator>Vadori, Marta</creator><creator>Civieri, Giovanni</creator><creator>Masiero, Giulia</creator><creator>Iop, Laura</creator><creator>Antonelli, Giorgia</creator><creator>Perazzolo Marra, Martina</creator><creator>Bianco, Federica</creator><creator>Cecere, Annagrazia</creator><creator>Lorenzoni, Giulia</creator><creator>Naumova, Natalia</creator><creator>Bernava, Giacomo</creator><creator>Basso, Daniela</creator><creator>Plebani, Mario</creator><creator>Cozzi, Emanuele</creator><creator>Iliceto, Sabino</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-4828-7875</orcidid></search><sort><creationdate>202308</creationdate><title>Association of autoantibodies targeting endothelin type-A receptors with no-reflow in ST-elevation myocardial infarction</title><author>Tona, Francesco ; Vadori, Marta ; Civieri, Giovanni ; Masiero, Giulia ; Iop, Laura ; Antonelli, Giorgia ; Perazzolo Marra, Martina ; Bianco, Federica ; Cecere, Annagrazia ; Lorenzoni, Giulia ; Naumova, Natalia ; Bernava, Giacomo ; Basso, Daniela ; Plebani, Mario ; Cozzi, Emanuele ; Iliceto, Sabino</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-b717a60491672dcf3e18fb033d9d2c312bcb9c2b7cee8b84eb50cc143c5af2303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tona, Francesco</creatorcontrib><creatorcontrib>Vadori, Marta</creatorcontrib><creatorcontrib>Civieri, Giovanni</creatorcontrib><creatorcontrib>Masiero, Giulia</creatorcontrib><creatorcontrib>Iop, Laura</creatorcontrib><creatorcontrib>Antonelli, Giorgia</creatorcontrib><creatorcontrib>Perazzolo Marra, Martina</creatorcontrib><creatorcontrib>Bianco, Federica</creatorcontrib><creatorcontrib>Cecere, Annagrazia</creatorcontrib><creatorcontrib>Lorenzoni, Giulia</creatorcontrib><creatorcontrib>Naumova, Natalia</creatorcontrib><creatorcontrib>Bernava, Giacomo</creatorcontrib><creatorcontrib>Basso, Daniela</creatorcontrib><creatorcontrib>Plebani, Mario</creatorcontrib><creatorcontrib>Cozzi, Emanuele</creatorcontrib><creatorcontrib>Iliceto, Sabino</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tona, Francesco</au><au>Vadori, Marta</au><au>Civieri, Giovanni</au><au>Masiero, Giulia</au><au>Iop, Laura</au><au>Antonelli, Giorgia</au><au>Perazzolo Marra, Martina</au><au>Bianco, Federica</au><au>Cecere, Annagrazia</au><au>Lorenzoni, Giulia</au><au>Naumova, Natalia</au><au>Bernava, Giacomo</au><au>Basso, Daniela</au><au>Plebani, Mario</au><au>Cozzi, Emanuele</au><au>Iliceto, Sabino</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of autoantibodies targeting endothelin type-A receptors with no-reflow in ST-elevation myocardial infarction</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2023-08</date><risdate>2023</risdate><volume>378</volume><spage>117179</spage><epage>117179</epage><pages>117179-117179</pages><artnum>117179</artnum><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>No-reflow (NR), where the coronary artery is patent after treatment of ST-elevation myocardial infarction (STEMI) but tissue perfusion is not restored, is associated with worse outcomes. We aimed to investigate the relationship between autoantibodies activating endothelin-1 receptor type A (ETAR-AAs) and NR after primary percutaneous coronary intervention (PPCI) in STEMI.
We studied 50 patients (age 59 ± 11 years, 40 males) with STEMI who underwent PPCI within 6 h after the onset of symptoms. Blood samples were obtained from all patients within 12 h following PPCI for ETAR-AA level measurement. The seropositive threshold was provided by the manufacturer (>10 U/ml). NR was assessed by cardiac magnetic resonance imaging (MVO, microvascular obstruction). As a control group, 40 healthy subjects matched for age and sex were recruited from the general population.
MVO was observed in 24 patients (48%). The prevalence of MVO was higher in patients with ETAR-AAs seropositivity (72% vs. 38%, p = 0.03). ETAR-AAs were higher in patients with MVO (8.9 U/mL (interquartile range [IQR] 6.8–16.2 U/mL) vs. 5.7 U/mL [IQR 4.3–7.7 U/mL], p = 0.003). ETAR-AAs seropositivity was independently associated with MVO (OR 3.2, 95% CI 1.3–7.1; p = 0.03). We identified ≥6.74 U/mL as the best cut-off for prediction of MVO (sensitivity 79%; specificity 65%; NPV 71%; PPV 74%; accuracy 72%).
The ETAR-AAs seropositivity is associated with NR in STEMI patients. These findings may open up new options in the management of myocardial infarction even if confirmation in a larger trial is needed.
[Display omitted]
•No-reflow, where the coronary artery is patent after treatment of STEMI but tissue perfusion is not restored, is associated with worse outcomes.•Autoantibodies targeting endothelin type A receptor (ETAR-AAs) can bind to these receptors and regulate their function.•ETAR-AAs may contribute to no-reflow in STEMI after successful primary percutaneous coronary intervention.•This finding, for the first time, shows an autoimmune predisposition to a worse outcome after myocardial infarction.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>37422357</pmid><doi>10.1016/j.atherosclerosis.2023.06.970</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0003-4828-7875</orcidid><oa>free_for_read</oa></addata></record> |
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title | Association of autoantibodies targeting endothelin type-A receptors with no-reflow in ST-elevation myocardial infarction |
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