Author + information
- Received October 15, 2017
- Revision received January 8, 2018
- Accepted January 9, 2018
- Published online April 9, 2018.
- Joo Myung Lee, MD, MPH, PhDa,
- Gilwoo Choi, PhDb,
- Bon-Kwon Koo, MD, PhDc,d,∗ (, )
- Doyeon Hwang, MDc,
- Jonghanne Park, MD, PhDc,
- Jinlong Zhang, MDc,
- Kyung-Jin Kim, MDc,
- Yaliang Tong, MDe,
- Hyun Jin Kim, PhDb,
- Leo Grady, PhDb,
- Joon-Hyung Doh, MD, PhDf,
- Chang-Wook Nam, MD, PhDg,
- Eun-Seok Shin, MD, PhDh,
- Young-Seok Cho, MD, PhDi,
- Su-Yeon Choi, MD, PhDj,
- Eun Ju Chun, MD, PhDk,
- Jin-Ho Choi, MD, PhDa,
- Bjarne L. Nørgaard, MD, PhDl,
- Evald H. Christiansen, MD, PhDl,
- Koen Niemen, MD, PhDm,n,
- Hiromasa Otake, MD, PhDo,
- Martin Penicka, MD, PhDp,
- Bernard de Bruyne, MD, PhDp,
- Takashi Kubo, MD, PhDq,
- Takashi Akasaka, MD, PhDq,
- Jagat Narula, MD, PhDr,
- Pamela S. Douglas, MDs,
- Charles A. Taylor, PhDb,t and
- Hyo-Soo Kim, MD, PhDc
- aDepartment of Internal Medicine and Cardiovascular Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea
- bHeartFlow, Inc., Redwood City, California
- cDepartment of Medicine, Seoul National University Hospital, Seoul, South Korea
- dInstitute on Aging, Seoul National University, Seoul, Korea
- eDepartment of Cardiology, China-Japan Union Hospital of Jilin University, Changchun, China
- fDepartment of Medicine, Inje University Ilsan Paik Hospital, Goyang, South Korea
- gDepartment of Medicine, Keimyung University Dongsan Medical Center, Daegu, South Korea
- hDepartment of Cardiology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, South Korea
- iDepartment of Medicine, Seoul National University Bundang Hospital, Seongnam, South Korea
- jDepartment of Internal Medicine, Seoul National University Healthcare System Gangnam Center, Seoul National University College of Medicine, Seoul, South Korea
- kDepartment of Radiology, Seoul National University Bundang Hospital, Seongnam, South Korea
- lDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark
- mErasmus University Medical Center, Rotterdam, the Netherlands
- nCardiovascular Institute, Stanford University, School of Medicine, Stanford, California
- oDepartment of Internal Medicine, Division of Cardiovascular and Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe, Japan
- pCardiovascular Center Aalst, OLV-Clinic, Aalst, Belgium
- qDepartment of Cardiovascular Medicine, Wakayama Medical University, Wakayama, Japan
- rIcahn School of Medicine at Mount Sinai Hospital, New York, New York
- sDuke Clinical Research Institute, Duke University School of Medicine, Durham, North Carolina
- tDepartment of Bioengineering, Stanford University, Stanford, California
- ↵∗Address for correspondence:
Dr. Bon-Kwon Koo, Department of Internal Medicine and Cardiovascular Center, Seoul National University Hospital, 101 Daehang-ro, Chongno-gu, Seoul, 110-744, South Korea.
Objectives We investigated the utility of noninvasive hemodynamic assessment in the identification of high-risk plaques that caused subsequent acute coronary syndrome (ACS).
Background ACS is a critical event that impacts the prognosis of patients with coronary artery disease. However, the role of hemodynamic factors in the development of ACS is not well-known.
Methods Seventy-two patients with clearly documented ACS and available coronary computed tomographic angiography (CTA) acquired between 1 month and 2 years before the development of ACS were included. In 66 culprit and 150 nonculprit lesions as a case-control design, the presence of adverse plaque characteristics (APC) was assessed and hemodynamic parameters (fractional flow reserve derived by coronary computed tomographic angiography [FFRCT], change in FFRCT across the lesion [△FFRCT], wall shear stress [WSS], and axial plaque stress) were analyzed using computational fluid dynamics. The best cut-off values for FFRCT, △FFRCT, WSS, and axial plaque stress were used to define the presence of adverse hemodynamic characteristics (AHC). The incremental discriminant and reclassification abilities for ACS prediction were compared among 3 models (model 1: percent diameter stenosis [%DS] and lesion length, model 2: model 1 + APC, and model 3: model 2 + AHC).
Results The culprit lesions showed higher %DS (55.5 ± 15.4% vs. 43.1 ± 15.0%; p < 0.001) and higher prevalence of APC (80.3% vs. 42.0%; p < 0.001) than nonculprit lesions. Regarding hemodynamic parameters, culprit lesions showed lower FFRCT and higher △FFRCT, WSS, and axial plaque stress than nonculprit lesions (all p values <0.01). Among the 3 models, model 3, which included hemodynamic parameters, showed the highest c-index, and better discrimination (concordance statistic [c-index] 0.789 vs. 0.747; p = 0.014) and reclassification abilities (category-free net reclassification index 0.287; p = 0.047; relative integrated discrimination improvement 0.368; p < 0.001) than model 2. Lesions with both APC and AHC showed significantly higher risk of the culprit for subsequent ACS than those with no APC/AHC (hazard ratio: 11.75; 95% confidence interval: 2.85 to 48.51; p = 0.001) and with either APC or AHC (hazard ratio: 3.22; 95% confidence interval: 1.86 to 5.55; p < 0.001).
Conclusions Noninvasive hemodynamic assessment enhanced the identification of high-risk plaques that subsequently caused ACS. The integration of noninvasive hemodynamic assessments may improve the identification of culprit lesions for future ACS. (Exploring the Mechanism of Plaque Rupture in Acute Coronary Syndrome Using Coronary CT Angiography and Computational Fluid Dynamic [EMERALD]; NCT02374775)
- acute coronary syndrome
- adverse plaque characteristics
- axial plaque stress
- computational fluid dynamics
- coronary computed tomography angiography
- coronary plaque
- wall shear stress
This study was funded by HeartFlow Inc. The company performed the computational fluid dynamics analysis, but had no role in study design, conduct, or manuscript preparation. Drs. G. Choi, H.J. Kim, Grady, and Taylor are employees and shareholders of HeartFlow, Inc., which provides the FFRCT service. Dr. Douglas has received research grants from HeartFlow, Inc. and GE Healthcare. Dr. Nørgaard has received institutional unrestricted research grants from Siemens and HeartFlow, Inc. Dr. De Bruyne has received institutional unrestricted research grants from Abbott, Boston Scientific, Biotronik, and St. Jude Medical; has received consulting fees from St. Jude Medical, Opsens, and Boston Scientific; and is a shareholder for Siemens, GE, Bayer, Philips, HeartFlow, Inc., Edwards Life Sciences, Sanofi, and Omega Pharma. Dr. Niemen has received support from HeartFlow Inc., Siemens Healthineers, and GE Healthcare. Todd Villines, MD, served as the Guest Editor for this paper. Drs. Joo Myung Lee and Gilwoo Choi contributed equally to this work and are joint first authors.
- Received October 15, 2017.
- Revision received January 8, 2018.
- Accepted January 9, 2018.
- 2018 American College of Cardiology Foundation
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