상위피인용논문
연세대학교 세브란스병원
Hyuk-Jae Chang MD, PhDa, Fay Y. Lin MDb, Sang-Eun Lee MD, PhDa, Daniele Andreini MD, PhDc, Jeroen Bax MD, PhDd, Filippo Cademartiri MD, PhDe, Kavitha Chinnaiyan MDf, Benjamin J.W. Chow MDg, Edoardo Conte MDc, Ricardo C. Cury MDh, Gudrun Feuchtner MDi, Martin Hadamitzky MDj, Yong-Jin Kim MDk, Jonathon Leipsic MDl, Erica Maffei MDm, Hugo Marques MDn, Fabian Plank MDi, Gianluca Pontone MD, PhDc, Gilbert L. Raff MDf, Alexander R. van Rosendael MDd, Todd C. Villines MDo, Harald G. Weirich MDi, Subhi J. Al’Aref MDb, Lohendran Baskaran MDb, Iksung Cho MDa,b,p, Ibrahim Danad MDq, Donghee Han MDa,b, Ran Heo MDr, Ji Hyun Lee MDa,b, Asim Rivzi MDb,s, Wijnand J. Stuijfzand MDb, Heidi Gransar MSct, Yao Lu MScb, Ji Min Sung PhDa, Hyung-Bok Park MDa, Daniel S. Berman MDt, Matthew J. Budoff MDu, Habib Samady MDv, Leslee J. Shaw PhDv, Peter H. Stone MDw, Renu Virmani MDx, Jagat Narula MD, PhDy, James K. Min MDb,*
aDivision of Cardiology, Severance Cardiovascular Hospital, Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Seoul, South Korea
bDalio Institute of Cardiovascular Imaging, Department of Radiology, New York-Presbyterian Hospital and Weill Cornell Medicine, New York, New York
cDepartment of Clinical Sciences and Community Health, University of Milan, Centro Cardiologico Monzino, IRCCS, Milan, Italy
dDepartment of Cardiology, Heart Lung Center, Leiden University Medical Center, Leiden, the Netherlands
eCardiovascular Imaging Center, SDN IRCCS, Naples, Italy
fDepartment of Cardiology, William Beaumont Hospital, Royal Oaks, Michigan
gDepartment of Medicine and Radiology, University of Ottawa, Ottawa, Ontario, Canada
hBaptist Cardiac and Vascular Institute, Miami, Florida
iDepartment of Radiology, Medical University of Innsbruck, Innsbruck, Austria
jDepartment of Radiology and Nuclear Medicine, German Heart Center Munich, Munich, Germany
kSeoul National University College of Medicine, Seoul National University Hospital, Seoul, South Korea
lDepartment of Medicine and Radiology, University of British Columbia, Vancouver, British Columbia, Canada
mDepartment of Radiology, Area Vasta 1/ASUR Marche, Urbino, Italy
nUNICA, Unit of Cardiovascular Imaging, Hospital da Luz, Lisboa, Portugal
oCardiology Service, Walter Reed National Military Center, Bethesda, Maryland
pChung-Ang University Hospital, Seoul, South Korea
qVU University Medical Center, Amsterdam, the Netherlands
rAsan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea
sDepartment of Radiology, Mayo Clinic, Rochester, Minnesota
tDepartment of Imaging and Medicine, Cedars Sinai Medical Center, Los Angeles, California
uDepartment of Medicine, Los Angeles Biomedical Research Institute, Torrance, California
vDivision of Cardiology, Emory University School of Medicine, Atlanta, Georgia
wDivision of Cardiovascular Medicine, Brigham and Women’s Hospital, Boston, Massachusetts
xCVPath Institute, Gaithersburg, Maryland
yIcahn School of Medicine at Mount Sinai, Mount Sinai Heart, Zena and Michael A. Wiener Cardiovascular Institute, and Marie-Josée and Henry R. Kravis Center for Cardiovascular Health, New York, New York
*Corresponding author
Abstract
Background
The association of atherosclerotic features with first acute coronary syndromes (ACS) has not accounted for plaque burden.
Objectives
The purpose of this study was to identify atherosclerotic features associated with precursors of ACS.
Methods
We performed a nested case-control study within a cohort of 25,251 patients undergoing coronary computed tomographic angiography (CTA) with follow-up over 3.4 ± 2.1 years. Patients with ACS and nonevent patients with no prior coronary artery disease (CAD) were propensity matched 1:1 for risk factors and coronary CTA–evaluated obstructive (≥50%) CAD. Separate core laboratories performed blinded adjudication of ACS and culprit lesions and quantification of baseline coronary CTA for percent diameter stenosis (%DS), percent cross-sectional plaque burden (PB), plaque volumes (PVs) by composition (calcified, fibrous, fibrofatty, and necrotic core), and presence of high-risk plaques (HRPs).
Results
We identified 234 ACS and control pairs (age 62 years, 63% male). More than 65% of patients with ACS had nonobstructive CAD at baseline, and 52% had HRP. The %DS, cross-sectional PB, fibrofatty and necrotic core volume, and HRP increased the adjusted hazard ratio (HR) of ACS (1.010 per %DS, 95% confidence interval [CI]: 1.005 to 1.015; 1.008 per percent cross-sectional PB, 95% CI: 1.003 to 1.013; 1.002 per mm3 fibrofatty plaque, 95% CI: 1.000 to 1.003; 1.593 per mm3 necrotic core, 95% CI: 1.219 to 2.082; all p < 0.05). Of the 129 culprit lesion precursors identified by coronary CTA, three-fourths exhibited <50% stenosis and 31.0% exhibited HRP.
Conclusions
Although ACS increases with %DS, most precursors of ACS cases and culprit lesions are nonobstructive. Plaque evaluation, including HRP, PB, and plaque composition, identifies high-risk patients above and beyond stenosis severity and aggregate plaque burden.
논문정보