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Burden of premature ventricular contractions beyond nonsustained ventricular tachycardia is related to the myocardial extracellular space expansion in patients with hypertrophic-cardiomyopathy

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dc.contributor.author권혁문-
dc.contributor.author김윤정-
dc.contributor.author김종윤-
dc.contributor.author김태훈-
dc.contributor.author민필기-
dc.contributor.author박철환-
dc.contributor.author윤영원-
dc.contributor.author이경아-
dc.contributor.author이병권-
dc.contributor.author임세중-
dc.contributor.author최의영-
dc.contributor.author홍범기-
dc.date.accessioned2020-12-11T07:57:44Z-
dc.date.available2020-12-11T07:57:44Z-
dc.date.issued2020-11-
dc.identifier.issn0160-9289-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/180727-
dc.description.abstractBackground: Although nonsustained ventricular tachycardia (NSVT) is a risk factor for sudden cardiac death in hypertrophic-cardiomyopathy (HCM), the impact of premature ventricular contraction (PVC) burden, in the absence of NSVT, is not well-known. Hypothesis: PVC burden may be associated with myocardial fibrosis and genetic mutations in patients with HCM. Methods: Of the 212 patients prospectively enrolled to the HCM registry of genetics, 84 were evaluated with both cardiac magnetic resonance, 24-hour Holter monitoring and genetic analysis. Among them, 71 patients have not been diagnosed with NSVT. Results: Patients with NSVT (n = 13) had a higher late gadolinium enhancement (LGE) amount, extracellular volume fraction (ECV), and prevalence of sarcomere mutations compared with patients without NSVT. Among patients without NSVT, those with LGE (n = 46) had a higher total PVC (109 ± 332 vs 7 ± 13, P = .003) and PVC burden (0.114 ± 0.225 vs 0.008 ± 0.014%, P = .003) during 24-hour Holter monitoring compared with others. The %LGE and global ECV were correlated with PVC burden (r = 0.377, P = .001; r = 0.401, P = .001). The optimal cutoff value for PVC number for LGE was 45 (37.0% and 100% sensitivity and specificity, respectively) with 0.733 of the area under the receiver operating characteristic-curve (P < .001). Thick filament gene mutation was more prevalent in the higher PVC burden group (41.2% vs 16.7%, P = .048). Conclusion: Total PVC burden is significantly related to increase in myocardial fibrosis in HCM patients without NSVT.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherJohn Wiley & Sons, Inc.-
dc.relation.isPartOfCLINICAL CARDIOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleBurden of premature ventricular contractions beyond nonsustained ventricular tachycardia is related to the myocardial extracellular space expansion in patients with hypertrophic-cardiomyopathy-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학교실)-
dc.contributor.googleauthorHyemoon Chung-
dc.contributor.googleauthorChul-Hwan Park-
dc.contributor.googleauthorYoonjung Kim-
dc.contributor.googleauthorJong-Youn Kim-
dc.contributor.googleauthorPil-Ki Min-
dc.contributor.googleauthorYoung Won Yoon-
dc.contributor.googleauthorKyung-A Lee-
dc.contributor.googleauthorByoung Kwon Lee-
dc.contributor.googleauthorBum-Kee Hong-
dc.contributor.googleauthorTae Hoon Kim-
dc.contributor.googleauthorSe-Joong Rim-
dc.contributor.googleauthorHyuck Moon Kwon-
dc.contributor.googleauthorEui-Young Choi-
dc.identifier.doi10.1002/clc.23445-
dc.contributor.localIdA00260-
dc.contributor.localIdA00793-
dc.contributor.localIdA00926-
dc.contributor.localIdA01086-
dc.contributor.localIdA01412-
dc.contributor.localIdA01722-
dc.contributor.localIdA02580-
dc.contributor.localIdA02647-
dc.contributor.localIdA02793-
dc.contributor.localIdA03372-
dc.contributor.localIdA04165-
dc.contributor.localIdA04394-
dc.relation.journalcodeJ00565-
dc.identifier.eissn1932-8737-
dc.identifier.pmid32815161-
dc.subject.keywordhypertrophic-cardiomyopathy-
dc.subject.keywordlate gadolinium enhancement-
dc.subject.keywordmyocardial fibrosis-
dc.subject.keywordpremature ventricular contraction-
dc.contributor.alternativeNameKwon, Hyuck Moon-
dc.contributor.affiliatedAuthor권혁문-
dc.contributor.affiliatedAuthor김윤정-
dc.contributor.affiliatedAuthor김종윤-
dc.contributor.affiliatedAuthor김태훈-
dc.contributor.affiliatedAuthor민필기-
dc.contributor.affiliatedAuthor박철환-
dc.contributor.affiliatedAuthor윤영원-
dc.contributor.affiliatedAuthor이경아-
dc.contributor.affiliatedAuthor이병권-
dc.contributor.affiliatedAuthor임세중-
dc.contributor.affiliatedAuthor최의영-
dc.contributor.affiliatedAuthor홍범기-
dc.citation.volume43-
dc.citation.number11-
dc.citation.startPage1317-
dc.citation.endPage1325-
dc.identifier.bibliographicCitationCLINICAL CARDIOLOGY, Vol.43(11) : 1317-1325, 2020-11-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Laboratory Medicine (진단검사의학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Radiology (영상의학교실) > 1. Journal Papers

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