循环 PCSK9 与急性 STEV 心肌梗死缺血再灌注损伤的关系

IF 6.5 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Circulation: Cardiovascular Imaging Pub Date : 2024-08-01 Epub Date: 2024-08-20 DOI:10.1161/CIRCIMAGING.123.016482
Christina Tiller, Magdalena Holzknecht, Ivan Lechner, Fritz Oberhollenzer, Sebastian von der Emde, Thomas Kremser, Can Gollmann-Tepeköylü, Agnes Mayr, Axel Bauer, Bernhard Metzler, Sebastian J Reinstadler, Martin Reindl
{"title":"循环 PCSK9 与急性 STEV 心肌梗死缺血再灌注损伤的关系","authors":"Christina Tiller, Magdalena Holzknecht, Ivan Lechner, Fritz Oberhollenzer, Sebastian von der Emde, Thomas Kremser, Can Gollmann-Tepeköylü, Agnes Mayr, Axel Bauer, Bernhard Metzler, Sebastian J Reinstadler, Martin Reindl","doi":"10.1161/CIRCIMAGING.123.016482","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Beyond therapeutic implications, PCSK9 (proprotein convertase subtilisin/kexin 9) has emerged as a promising cardiovascular biomarker. The exact role of PCSK9 in the setting of acute ST-elevation myocardial infarction (STEMI) is incompletely understood. We aimed to investigate the association of PCSK9 with ischemia-reperfusion injury, visualized by cardiac magnetic resonance imaging, in patients with STEMI revascularized by primary percutaneous coronary intervention (PCI).</p><p><strong>Methods: </strong>In this prespecified substudy from the prospective MARINA-STEMI (NCT04113356) registry, we included 205 patients with STEMI. PCSK9 concentrations were measured from venous blood samples by an immunoassay 24 and 48 hours after PCI. The primary end point was defined as presence of intramyocardial hemorrhage according to cardiac magnetic resonance T2* mapping. Secondary imaging end points were the presence of microvascular obstruction (MVO) and infarct size. The clinical end point was the occurrence of major adverse cardiac events.</p><p><strong>Results: </strong>We observed a significant increase in PCSK9 levels from 24 to 48 hours (268-304 ng/mL; <i>P</i><0.001) after PCI. PCSK9 24 hours after PCI did not show any relation to intramyocardial hemorrhage, MVO, and infarct size (all <i>P</i>>0.05). PCSK9 concentrations 48 hours post-STEMI were higher in patients with intramyocardial hemorrhage (333 versus 287 ng/mL; <i>P</i>=0.004), MVO (320 versus 292 ng/mL; <i>P</i>=0.020), and large infarct size (323 versus 296 ng/mL; <i>P</i>=0.013). Furthermore, patients with increased PCSK9 levels >361 ng/mL at 48 hours were more likely to experience major adverse cardiac events (15% versus 8%; <i>P</i>=0.002) during a median follow-up of 12 months.</p><p><strong>Conclusions: </strong>In patients with STEMI, a significant increase in PCSK9 was observed from 24 to 48 hours after PCI. While PCSK9 levels after 24 hours were not related to myocardial or microvascular injury, PCSK9 after 48 hours was significantly associated with intramyocardial hemorrhage, MVO, and infarct size as well as worse subsequent clinical outcomes.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier; NCT04113356.</p>","PeriodicalId":10202,"journal":{"name":"Circulation: Cardiovascular Imaging","volume":"17 8","pages":"e016482"},"PeriodicalIF":6.5000,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Association of Circulating PCSK9 With Ischemia-Reperfusion Injury in Acute ST-Elevation Myocardial Infarction.\",\"authors\":\"Christina Tiller, Magdalena Holzknecht, Ivan Lechner, Fritz Oberhollenzer, Sebastian von der Emde, Thomas Kremser, Can Gollmann-Tepeköylü, Agnes Mayr, Axel Bauer, Bernhard Metzler, Sebastian J Reinstadler, Martin Reindl\",\"doi\":\"10.1161/CIRCIMAGING.123.016482\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Beyond therapeutic implications, PCSK9 (proprotein convertase subtilisin/kexin 9) has emerged as a promising cardiovascular biomarker. The exact role of PCSK9 in the setting of acute ST-elevation myocardial infarction (STEMI) is incompletely understood. We aimed to investigate the association of PCSK9 with ischemia-reperfusion injury, visualized by cardiac magnetic resonance imaging, in patients with STEMI revascularized by primary percutaneous coronary intervention (PCI).</p><p><strong>Methods: </strong>In this prespecified substudy from the prospective MARINA-STEMI (NCT04113356) registry, we included 205 patients with STEMI. PCSK9 concentrations were measured from venous blood samples by an immunoassay 24 and 48 hours after PCI. The primary end point was defined as presence of intramyocardial hemorrhage according to cardiac magnetic resonance T2* mapping. Secondary imaging end points were the presence of microvascular obstruction (MVO) and infarct size. The clinical end point was the occurrence of major adverse cardiac events.</p><p><strong>Results: </strong>We observed a significant increase in PCSK9 levels from 24 to 48 hours (268-304 ng/mL; <i>P</i><0.001) after PCI. PCSK9 24 hours after PCI did not show any relation to intramyocardial hemorrhage, MVO, and infarct size (all <i>P</i>>0.05). PCSK9 concentrations 48 hours post-STEMI were higher in patients with intramyocardial hemorrhage (333 versus 287 ng/mL; <i>P</i>=0.004), MVO (320 versus 292 ng/mL; <i>P</i>=0.020), and large infarct size (323 versus 296 ng/mL; <i>P</i>=0.013). Furthermore, patients with increased PCSK9 levels >361 ng/mL at 48 hours were more likely to experience major adverse cardiac events (15% versus 8%; <i>P</i>=0.002) during a median follow-up of 12 months.</p><p><strong>Conclusions: </strong>In patients with STEMI, a significant increase in PCSK9 was observed from 24 to 48 hours after PCI. While PCSK9 levels after 24 hours were not related to myocardial or microvascular injury, PCSK9 after 48 hours was significantly associated with intramyocardial hemorrhage, MVO, and infarct size as well as worse subsequent clinical outcomes.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier; NCT04113356.</p>\",\"PeriodicalId\":10202,\"journal\":{\"name\":\"Circulation: Cardiovascular Imaging\",\"volume\":\"17 8\",\"pages\":\"e016482\"},\"PeriodicalIF\":6.5000,\"publicationDate\":\"2024-08-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Circulation: Cardiovascular Imaging\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1161/CIRCIMAGING.123.016482\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/8/20 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Circulation: Cardiovascular Imaging","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1161/CIRCIMAGING.123.016482","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/8/20 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0

摘要

背景:除了治疗意义外,PCSK9(proprotein convertase subtilisin/kexin 9)已成为一种有前途的心血管生物标志物。目前还不完全清楚 PCSK9 在急性 ST 段抬高型心肌梗死(STEMI)中的确切作用。我们的目的是研究通过初级经皮冠状动脉介入治疗(PCI)进行血运重建的 STEMI 患者中,PCSK9 与心脏磁共振成像显示的缺血再灌注损伤的关系:在这项来自前瞻性 MARINA-STEMI (NCT04113356)登记的预设子研究中,我们纳入了 205 名 STEMI 患者。PCI术后24小时和48小时用免疫测定法测定静脉血样本中的PCSK9浓度。根据心脏磁共振 T2* 图谱,主要终点定义为是否存在心肌内出血。次要成像终点为是否存在微血管阻塞(MVO)和梗塞大小。临床终点是重大心脏不良事件的发生率:我们观察到,从 24 小时到 48 小时,PCSK9 的水平明显升高(268-304 ng/mL;PP>0.05)。心肌内出血(333 对 287 ng/mL;P=0.004)、MVO(320 对 292 ng/mL;P=0.020)和大面积梗死(323 对 296 ng/mL;P=0.013)患者在经胸膜后 48 小时的 PCSK9 浓度较高。此外,在中位随访12个月期间,48小时时PCSK9水平升高>361纳克/毫升的患者更有可能发生重大心脏不良事件(15%对8%;P=0.002):在 STEMI 患者中,PCI 后 24 至 48 小时内 PCSK9 水平显著升高。虽然24小时后的PCSK9水平与心肌或微血管损伤无关,但48小时后的PCSK9与心肌内出血、MVO和梗死面积以及更差的后续临床预后显著相关:URL:https://www.clinicaltrials.gov;唯一标识符;NCT04113356。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Association of Circulating PCSK9 With Ischemia-Reperfusion Injury in Acute ST-Elevation Myocardial Infarction.

Background: Beyond therapeutic implications, PCSK9 (proprotein convertase subtilisin/kexin 9) has emerged as a promising cardiovascular biomarker. The exact role of PCSK9 in the setting of acute ST-elevation myocardial infarction (STEMI) is incompletely understood. We aimed to investigate the association of PCSK9 with ischemia-reperfusion injury, visualized by cardiac magnetic resonance imaging, in patients with STEMI revascularized by primary percutaneous coronary intervention (PCI).

Methods: In this prespecified substudy from the prospective MARINA-STEMI (NCT04113356) registry, we included 205 patients with STEMI. PCSK9 concentrations were measured from venous blood samples by an immunoassay 24 and 48 hours after PCI. The primary end point was defined as presence of intramyocardial hemorrhage according to cardiac magnetic resonance T2* mapping. Secondary imaging end points were the presence of microvascular obstruction (MVO) and infarct size. The clinical end point was the occurrence of major adverse cardiac events.

Results: We observed a significant increase in PCSK9 levels from 24 to 48 hours (268-304 ng/mL; P<0.001) after PCI. PCSK9 24 hours after PCI did not show any relation to intramyocardial hemorrhage, MVO, and infarct size (all P>0.05). PCSK9 concentrations 48 hours post-STEMI were higher in patients with intramyocardial hemorrhage (333 versus 287 ng/mL; P=0.004), MVO (320 versus 292 ng/mL; P=0.020), and large infarct size (323 versus 296 ng/mL; P=0.013). Furthermore, patients with increased PCSK9 levels >361 ng/mL at 48 hours were more likely to experience major adverse cardiac events (15% versus 8%; P=0.002) during a median follow-up of 12 months.

Conclusions: In patients with STEMI, a significant increase in PCSK9 was observed from 24 to 48 hours after PCI. While PCSK9 levels after 24 hours were not related to myocardial or microvascular injury, PCSK9 after 48 hours was significantly associated with intramyocardial hemorrhage, MVO, and infarct size as well as worse subsequent clinical outcomes.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier; NCT04113356.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
6.30
自引率
2.70%
发文量
225
审稿时长
6-12 weeks
期刊介绍: Circulation: Cardiovascular Imaging, an American Heart Association journal, publishes high-quality, patient-centric articles focusing on observational studies, clinical trials, and advances in applied (translational) research. The journal features innovative, multimodality approaches to the diagnosis and risk stratification of cardiovascular disease. Modalities covered include echocardiography, cardiac computed tomography, cardiac magnetic resonance imaging and spectroscopy, magnetic resonance angiography, cardiac positron emission tomography, noninvasive assessment of vascular and endothelial function, radionuclide imaging, molecular imaging, and others. Article types considered by Circulation: Cardiovascular Imaging include Original Research, Research Letters, Advances in Cardiovascular Imaging, Clinical Implications of Molecular Imaging Research, How to Use Imaging, Translating Novel Imaging Technologies into Clinical Applications, and Cardiovascular Images.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信