Clinical outcomes of low-intensity area without attenuation and cholesterol crystals in non-culprit lesions assessed by optical coherence tomography.

Cholesterol crystal Intraplaque hemorrhage Low-intensity area without attenuation Major adverse cardiac event Optical coherence tomography

Journal

Atherosclerosis
ISSN: 1879-1484
Titre abrégé: Atherosclerosis
Pays: Ireland
ID NLM: 0242543

Informations de publication

Date de publication:
09 2021
Historique:
received: 06 02 2021
revised: 07 07 2021
accepted: 03 08 2021
pubmed: 14 8 2021
medline: 27 10 2021
entrez: 13 8 2021
Statut: ppublish

Résumé

Pathologists have shown that intraplaque hemorrhage contributes to plaque destabilization and is frequently co-located with cholesterol crystals (CC). Optical coherence tomography (OCT)-detected low-intensity area without attenuation (LIA) may represent intraplaque hemorrhage. We aimed to examine the prevalence and impact of OCT-detected LIA + CC in untreated non-culprit lesions (NCLs) on subsequent major adverse cardiac events (MACE). OCT imaged NCLs in the culprit vessel in the patients who underwent OCT-guided percutaneous coronary intervention were included. An NCL was a lesion with >90° of diseased arc (≥0.5 mm intimal thickness), length ≥2 mm, and >5 mm away from stent edge. CC was defined as a thin linear region of high intensity. NCL-related MACE includes cardiac death, myocardial infarction, or ischemia-driven revascularization attributed to NCLs. We included 735 NCLs in 566 patients with 2.5 ± 0.7 years follow-up. The prevalence of concomitant LIA with CC (LIA + CC) was 15.5% (114/735). Three-year NCL-related MACE rate was 2.9% (20 events) at a lesion level and 15.6% (78 events) at a patient level. Untreated NCLs with LIA + CC had an increased risk for NCL-MACE (adjusted hazard ratio [HR] 3.09, 95% confidence interval [CI] 1.27-7.50, p = 0.01) along with thin-cap fibroatheroma (adjusted HR 4.38, 95% CI 1.44-13.30, p < 0.01) and minimum lumen area <3.5 mm An OCT-detected LIA + CC in an NCL was associated with subsequent NCL-MACE.

Sections du résumé

BACKGROUND AND AIMS
Pathologists have shown that intraplaque hemorrhage contributes to plaque destabilization and is frequently co-located with cholesterol crystals (CC). Optical coherence tomography (OCT)-detected low-intensity area without attenuation (LIA) may represent intraplaque hemorrhage. We aimed to examine the prevalence and impact of OCT-detected LIA + CC in untreated non-culprit lesions (NCLs) on subsequent major adverse cardiac events (MACE).
METHODS
OCT imaged NCLs in the culprit vessel in the patients who underwent OCT-guided percutaneous coronary intervention were included. An NCL was a lesion with >90° of diseased arc (≥0.5 mm intimal thickness), length ≥2 mm, and >5 mm away from stent edge. CC was defined as a thin linear region of high intensity. NCL-related MACE includes cardiac death, myocardial infarction, or ischemia-driven revascularization attributed to NCLs.
RESULTS
We included 735 NCLs in 566 patients with 2.5 ± 0.7 years follow-up. The prevalence of concomitant LIA with CC (LIA + CC) was 15.5% (114/735). Three-year NCL-related MACE rate was 2.9% (20 events) at a lesion level and 15.6% (78 events) at a patient level. Untreated NCLs with LIA + CC had an increased risk for NCL-MACE (adjusted hazard ratio [HR] 3.09, 95% confidence interval [CI] 1.27-7.50, p = 0.01) along with thin-cap fibroatheroma (adjusted HR 4.38, 95% CI 1.44-13.30, p < 0.01) and minimum lumen area <3.5 mm
CONCLUSIONS
An OCT-detected LIA + CC in an NCL was associated with subsequent NCL-MACE.

Identifiants

pubmed: 34384955
pii: S0021-9150(21)01264-8
doi: 10.1016/j.atherosclerosis.2021.08.003
pii:
doi:

Substances chimiques

Cholesterol 97C5T2UQ7J

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

41-47

Informations de copyright

Copyright © 2021 Elsevier B.V. All rights reserved.

Auteurs

Eisuke Usui (E)

Clinical Trials Center, Cardiovascular Research Foundation, New York, USA; NewYork-Presbyterian Hospital/Columbia University Irving Medical Center, New York, USA.

Mitsuaki Matsumura (M)

Clinical Trials Center, Cardiovascular Research Foundation, New York, USA.

Gary S Mintz (GS)

Clinical Trials Center, Cardiovascular Research Foundation, New York, USA.

Zhipeng Zhou (Z)

Clinical Trials Center, Cardiovascular Research Foundation, New York, USA.

Masahiro Hada (M)

Cardiovascular Medicine, Tsuchiura Kyodo General Hospital, Ibaraki, Japan.

Masao Yamaguchi (M)

Cardiovascular Medicine, Tsuchiura Kyodo General Hospital, Ibaraki, Japan.

Masahiro Hoshino (M)

Cardiovascular Medicine, Tsuchiura Kyodo General Hospital, Ibaraki, Japan.

Yoshihisa Kanaji (Y)

Cardiovascular Medicine, Tsuchiura Kyodo General Hospital, Ibaraki, Japan.

Tomoyo Sugiyama (T)

Cardiovascular Medicine, Tsuchiura Kyodo General Hospital, Ibaraki, Japan.

Tadashi Murai (T)

Cardiovascular Medicine, Tsuchiura Kyodo General Hospital, Ibaraki, Japan.

Tetsumin Lee (T)

Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.

Taishi Yonetsu (T)

Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.

Tsunekazu Kakuta (T)

Cardiovascular Medicine, Tsuchiura Kyodo General Hospital, Ibaraki, Japan.

Mie Kunio (M)

Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Canon U.S.A., Inc., Cambridge, MA, USA.

Guillermo J Tearney (GJ)

Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

Akiko Maehara (A)

Clinical Trials Center, Cardiovascular Research Foundation, New York, USA; NewYork-Presbyterian Hospital/Columbia University Irving Medical Center, New York, USA. Electronic address: amaehara@crf.org.

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