한빛사논문
Daichi Fujimoto MD, PhD a, Daisuke Kinoshita MD, PhD a, Keishi Suzuki MD, PhD a, Takayuki Niida MD, PhD a, Haruhito Yuki MD a, Iris McNulty RN a, Hang Lee PhD b, Hiromasa Otake MD, PhD c, Junya Shite MD, PhD d, Maros Ferencik MD, PhD, MCR e, Damini Dey PhD f, Tsunekazu Kakuta MD, PhD g, Ik-Kyung Jang MD, PhD a
aCardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
bBiostatistics Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
cDivision of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan
dDivision of Cardiovascular Medicine, Osaka Saiseikai Nakatsu Hospital, Osaka, Japan
eKnight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon, USA
fBiomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA
gDepartment of Cardiovascular Medicine, Tsuchiura Kyodo General Hospital, Tsuchiura, Ibaraki, Japan
Addresses for correspondence: Dr Ik-Kyung Jang, Tsunekazu Kakuta MD, PhD
Abstract
Background: Coronary artery calcification is an integral part of atherosclerosis. It has been suggested that early coronary artery calcification is associated with active inflammation, and advanced calcification forms as inflammation subsides. Inflammation is also an important factor in plaque vulnerability. However, the relationship between coronary artery calcium burden, vascular inflammation, and plaque vulnerability has not been fully investigated.
Objectives: This study aimed to correlate calcified plaque burden (CPB) at the culprit lesion with vascular inflammation and plaque vulnerability.
Methods: Patients with coronary artery disease who had both computed tomography angiography and optical coherence tomography were included. The authors divided the patients into 4 groups: 1 group without calcification at the culprit lesion; and 3 groups based on the CPB tertiles. CPB was calculated as calcified plaque volume divided by vessel volume in the culprit lesion. The authors compared pericoronary adipose tissue (PCAT) attenuation for vascular inflammation and optical coherence tomography-derived vulnerable features among the 4 groups.
Results: Among 578 patients, the highest CPB tertile showed significantly lower PCAT attenuation of culprit vessel compared with the other groups. The prevalence of features of plaque vulnerability (including lipid-rich plaque, macrophage, and microvessel) was also lowest in the highest CPB tertile. In the patients with calcification, higher age, statin use, and lower PCAT attenuation were independently associated with CPB.
Conclusions: Greater calcium burden is associated with a lower level of vascular inflammation and plaque vulnerability. A greater calcium burden may represent advanced stable plaque without significant inflammatory activity. (Massachusetts General Hospital and Tsuchiura Kyodo General Hospital Coronary Imaging Collaboration; NCT04523194).
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