Magnitude of Soluble ST2 as a Novel Biomarker for Acute Aortic Dissection

BACKGROUND—Misdiagnosis of acute aortic dissection (AAD) can lead to significant morbidity and death. Soluble ST2 (sST2) is a cardiovascular injury-related biomarker. The extent to which sST2 is elevated in AAD and whether sST2 can discriminate AAD from other causes of sudden-onset severe chest pain...

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Published in:Circulation (New York, N.Y.) N.Y.), 2018-01, Vol.137 (3), p.259-269
Main Authors: Wang, Yuan, Tan, Xin, Gao, Hai, Yuan, Hui, Hu, Rong, Jia, Lixin, Zhu, Junming, Sun, Lizhong, Zhang, Hongjia, Huang, Lianjun, Zhao, Dong, Gao, Pei, Du, Jie
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container_issue 3
container_start_page 259
container_title Circulation (New York, N.Y.)
container_volume 137
creator Wang, Yuan
Tan, Xin
Gao, Hai
Yuan, Hui
Hu, Rong
Jia, Lixin
Zhu, Junming
Sun, Lizhong
Zhang, Hongjia
Huang, Lianjun
Zhao, Dong
Gao, Pei
Du, Jie
description BACKGROUND—Misdiagnosis of acute aortic dissection (AAD) can lead to significant morbidity and death. Soluble ST2 (sST2) is a cardiovascular injury-related biomarker. The extent to which sST2 is elevated in AAD and whether sST2 can discriminate AAD from other causes of sudden-onset severe chest pain is unknown. METHODS—We measured plasma concentrations of sST2 (R&D systems assay) in 1360 patients, including 1027 participants in the retrospective discovery set and 333 patients with initial suspicion of AAD enrolled in the prospective validation cohort. Measures of discrimination for differentiating AAD from other causes of chest pain were calculated. RESULTS—In the acute phase, sST2 levels were higher in patients with AAD than those with either acute myocardial infarction (AMI) in the first case-control discovery set within 24h symptom onset or pulmonary embolism (PE) patients in the second discovery set (medians of 129.2 ng/mL vs. 14.7 with p
doi_str_mv 10.1161/CIRCULATIONAHA.117.030469
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Soluble ST2 (sST2) is a cardiovascular injury-related biomarker. The extent to which sST2 is elevated in AAD and whether sST2 can discriminate AAD from other causes of sudden-onset severe chest pain is unknown. METHODS—We measured plasma concentrations of sST2 (R&amp;D systems assay) in 1360 patients, including 1027 participants in the retrospective discovery set and 333 patients with initial suspicion of AAD enrolled in the prospective validation cohort. Measures of discrimination for differentiating AAD from other causes of chest pain were calculated. RESULTS—In the acute phase, sST2 levels were higher in patients with AAD than those with either acute myocardial infarction (AMI) in the first case-control discovery set within 24h symptom onset or pulmonary embolism (PE) patients in the second discovery set (medians of 129.2 ng/mL vs. 14.7 with p&lt;0.001 for AAD vs. AMI and 88.6 vs. 9.3 with p&lt;0.001 for AAD vs. PE). In the prospective validation set, sST2 was most elevated in AAD patients (median [25, 75 percentile]76.4 [49.6, 130.3]) and modestly elevated in AMI (25.0 [15.5, 37.2]), PE (14.9 [10.2, 30.1]) and angina patients (21.5 [13.1, 27.6], all p&lt;0.001 vs. AAD). The area under ROC curve for AAD patients versus all control patients within 24h presenting in emergency department were 0.97 (0.95, 0.98) for sST2, 0.91 (0.88, 0.94) for D-dimer, 0.50 (0.44, 0.56) for cTnI respectively. At a cutoff level of 34.6 ng/mL, sST2 had the sensitivity of 99.1%, specificity of 84.9%, positive predictive value of 68.7%, negative predictive value of 99.7%, positive likelihood ratio of 6.6 and negative likelihood ratio of 0.01. CONCLUSIONS—Among patients with suspected aortic dissection in the emergency department, sST2 showed superior overall diagnostic performance than D-dimer or cTnI. Additional study is needed to determine if sST2 might be a useful “rule-out” marker for AAD in the emergency room.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/CIRCULATIONAHA.117.030469</identifier><identifier>PMID: 29146682</identifier><language>eng</language><publisher>United States: by the American College of Cardiology Foundation and the American Heart Association, Inc</publisher><ispartof>Circulation (New York, N.Y.), 2018-01, Vol.137 (3), p.259-269</ispartof><rights>2017 by the American College of Cardiology Foundation and the American Heart Association, Inc.</rights><rights>2017 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4789-b68d1420795f3d238d39ebf22ea5a488780981633365408c2bb680267f319bf23</citedby><cites>FETCH-LOGICAL-c4789-b68d1420795f3d238d39ebf22ea5a488780981633365408c2bb680267f319bf23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29146682$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Yuan</creatorcontrib><creatorcontrib>Tan, Xin</creatorcontrib><creatorcontrib>Gao, Hai</creatorcontrib><creatorcontrib>Yuan, Hui</creatorcontrib><creatorcontrib>Hu, Rong</creatorcontrib><creatorcontrib>Jia, Lixin</creatorcontrib><creatorcontrib>Zhu, Junming</creatorcontrib><creatorcontrib>Sun, Lizhong</creatorcontrib><creatorcontrib>Zhang, Hongjia</creatorcontrib><creatorcontrib>Huang, Lianjun</creatorcontrib><creatorcontrib>Zhao, Dong</creatorcontrib><creatorcontrib>Gao, Pei</creatorcontrib><creatorcontrib>Du, Jie</creatorcontrib><title>Magnitude of Soluble ST2 as a Novel Biomarker for Acute Aortic Dissection</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>BACKGROUND—Misdiagnosis of acute aortic dissection (AAD) can lead to significant morbidity and death. Soluble ST2 (sST2) is a cardiovascular injury-related biomarker. The extent to which sST2 is elevated in AAD and whether sST2 can discriminate AAD from other causes of sudden-onset severe chest pain is unknown. METHODS—We measured plasma concentrations of sST2 (R&amp;D systems assay) in 1360 patients, including 1027 participants in the retrospective discovery set and 333 patients with initial suspicion of AAD enrolled in the prospective validation cohort. Measures of discrimination for differentiating AAD from other causes of chest pain were calculated. RESULTS—In the acute phase, sST2 levels were higher in patients with AAD than those with either acute myocardial infarction (AMI) in the first case-control discovery set within 24h symptom onset or pulmonary embolism (PE) patients in the second discovery set (medians of 129.2 ng/mL vs. 14.7 with p&lt;0.001 for AAD vs. AMI and 88.6 vs. 9.3 with p&lt;0.001 for AAD vs. PE). In the prospective validation set, sST2 was most elevated in AAD patients (median [25, 75 percentile]76.4 [49.6, 130.3]) and modestly elevated in AMI (25.0 [15.5, 37.2]), PE (14.9 [10.2, 30.1]) and angina patients (21.5 [13.1, 27.6], all p&lt;0.001 vs. AAD). The area under ROC curve for AAD patients versus all control patients within 24h presenting in emergency department were 0.97 (0.95, 0.98) for sST2, 0.91 (0.88, 0.94) for D-dimer, 0.50 (0.44, 0.56) for cTnI respectively. At a cutoff level of 34.6 ng/mL, sST2 had the sensitivity of 99.1%, specificity of 84.9%, positive predictive value of 68.7%, negative predictive value of 99.7%, positive likelihood ratio of 6.6 and negative likelihood ratio of 0.01. CONCLUSIONS—Among patients with suspected aortic dissection in the emergency department, sST2 showed superior overall diagnostic performance than D-dimer or cTnI. 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Soluble ST2 (sST2) is a cardiovascular injury-related biomarker. The extent to which sST2 is elevated in AAD and whether sST2 can discriminate AAD from other causes of sudden-onset severe chest pain is unknown. METHODS—We measured plasma concentrations of sST2 (R&amp;D systems assay) in 1360 patients, including 1027 participants in the retrospective discovery set and 333 patients with initial suspicion of AAD enrolled in the prospective validation cohort. Measures of discrimination for differentiating AAD from other causes of chest pain were calculated. RESULTS—In the acute phase, sST2 levels were higher in patients with AAD than those with either acute myocardial infarction (AMI) in the first case-control discovery set within 24h symptom onset or pulmonary embolism (PE) patients in the second discovery set (medians of 129.2 ng/mL vs. 14.7 with p&lt;0.001 for AAD vs. AMI and 88.6 vs. 9.3 with p&lt;0.001 for AAD vs. PE). In the prospective validation set, sST2 was most elevated in AAD patients (median [25, 75 percentile]76.4 [49.6, 130.3]) and modestly elevated in AMI (25.0 [15.5, 37.2]), PE (14.9 [10.2, 30.1]) and angina patients (21.5 [13.1, 27.6], all p&lt;0.001 vs. AAD). The area under ROC curve for AAD patients versus all control patients within 24h presenting in emergency department were 0.97 (0.95, 0.98) for sST2, 0.91 (0.88, 0.94) for D-dimer, 0.50 (0.44, 0.56) for cTnI respectively. At a cutoff level of 34.6 ng/mL, sST2 had the sensitivity of 99.1%, specificity of 84.9%, positive predictive value of 68.7%, negative predictive value of 99.7%, positive likelihood ratio of 6.6 and negative likelihood ratio of 0.01. CONCLUSIONS—Among patients with suspected aortic dissection in the emergency department, sST2 showed superior overall diagnostic performance than D-dimer or cTnI. Additional study is needed to determine if sST2 might be a useful “rule-out” marker for AAD in the emergency room.</abstract><cop>United States</cop><pub>by the American College of Cardiology Foundation and the American Heart Association, Inc</pub><pmid>29146682</pmid><doi>10.1161/CIRCULATIONAHA.117.030469</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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title Magnitude of Soluble ST2 as a Novel Biomarker for Acute Aortic Dissection
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