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Relationship between lipoprotein(a) and spontaneous recanalization of infarct-related arteries in the early phase of acute myocardial infarction

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dc.contributor.authorKim, Jin Won-
dc.contributor.authorSeo, Hong Seog-
dc.contributor.authorSuh, Soon Yong-
dc.contributor.authorChoi, Cheol Ung-
dc.contributor.authorKim, Eung Ju-
dc.contributor.authorRha, Seung-Woon-
dc.contributor.authorPark, Chang Gyu-
dc.contributor.authorOh, Dong Joo-
dc.date.accessioned2021-09-09T08:38:47Z-
dc.date.available2021-09-09T08:38:47Z-
dc.date.created2021-06-10-
dc.date.issued2008-05-
dc.identifier.issn0160-9289-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/123575-
dc.description.abstractBackground: Lipoprotein(a) (Lp[a]) is known to inhibit the fibrinolysis system and promote thrombus formation. Hypothesis: We retrospectively investigated the influences of Lp(a) on infarct-retated artery patency in the early phase of acute myocardial infarction (AMI). Methods: In 144 patients with ST-segment elevation, myocardial, coronary angiography (CAG) was performed within 12 h of the onset of symptoms. Subjects were divided into 2 groups according to the thrombolysis in myocardial infaction (TIMI) grade, Group I (TIMI 0-1, n = 94) versus Group II (TIMI 2-3, n = 50). The Gensini score and 0- to 3-vessel disease score estimated the severity and extent of coronary artery disease (CAD), respectively. Lp(a), lipid profile and c-reactive protein (CRP) were measured before any medications including thrombolytics were given. Results: The Lp(a) level was higher in Group I than in Group II. There was a weak correlation between Lp(a) level and Gensini score. By multivariate logistic regression analysis, a Lp(a) level was a predictor of infarct-related artery patency in the early phase of AMI. There were no significant differences in the location of the infarct-related arteries, extent of CAD, time from pain to CAG, number of risk factors, and hs-CRP values between the 2 groups. Conclusion: The Lp(a) level was significantly higher in patients with persistent occlusion compared with those with spontaneous recanalization of infarct-related arteries in the early phase of AMI.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherWILEY-
dc.subjectHUMAN APOLIPOPROTEIN(A)-
dc.subjectCORONARY-ARTERY-
dc.subjectFIBRINOLYSIS-
dc.subjectREPERFUSION-
dc.subjectOCCLUSION-
dc.subjectPATENCY-
dc.subjectLEVEL-
dc.subjectWALL-
dc.subjectVEIN-
dc.titleRelationship between lipoprotein(a) and spontaneous recanalization of infarct-related arteries in the early phase of acute myocardial infarction-
dc.typeArticle-
dc.contributor.affiliatedAuthorKim, Jin Won-
dc.contributor.affiliatedAuthorSeo, Hong Seog-
dc.contributor.affiliatedAuthorChoi, Cheol Ung-
dc.contributor.affiliatedAuthorKim, Eung Ju-
dc.contributor.affiliatedAuthorRha, Seung-Woon-
dc.contributor.affiliatedAuthorPark, Chang Gyu-
dc.contributor.affiliatedAuthorOh, Dong Joo-
dc.identifier.doi10.1002/clc.20143-
dc.identifier.scopusid2-s2.0-44449148756-
dc.identifier.wosid000256140000005-
dc.identifier.bibliographicCitationCLINICAL CARDIOLOGY, v.31, no.5, pp.211 - 216-
dc.relation.isPartOfCLINICAL CARDIOLOGY-
dc.citation.titleCLINICAL CARDIOLOGY-
dc.citation.volume31-
dc.citation.number5-
dc.citation.startPage211-
dc.citation.endPage216-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaCardiovascular System & Cardiology-
dc.relation.journalWebOfScienceCategoryCardiac & Cardiovascular Systems-
dc.subject.keywordPlusHUMAN APOLIPOPROTEIN(A)-
dc.subject.keywordPlusCORONARY-ARTERY-
dc.subject.keywordPlusFIBRINOLYSIS-
dc.subject.keywordPlusREPERFUSION-
dc.subject.keywordPlusOCCLUSION-
dc.subject.keywordPlusPATENCY-
dc.subject.keywordPlusLEVEL-
dc.subject.keywordPlusWALL-
dc.subject.keywordPlusVEIN-
dc.subject.keywordAuthorlipoprotein(a)-
dc.subject.keywordAuthoracute myocardial infarction-
dc.subject.keywordAuthorrecanalization-
dc.subject.keywordAuthorthrombolysis in myocardial infarction flow-
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