Joo Myung Lee1, Ki Hong Choi1, Bon-Kwon Koo2, Jonghanne Park3, Jihoon Kim1, Doyeon Hwang3, Tae-Min Rhee3, Hyung Yoon Kim4, Hae Won Jung5, Kyung-Jin Kim6, Kawase Yoshiaki7, Eun-Seok Shin8, Joon-Hyung Doh9, Hyuk-Jae Chang10, Yun-Kyeong Cho11, Hyuck-Jun Yoon11, Chang-Wook Nam11, Seung-Ho Hur11, Jianan Wang12, Shaoliang Chen13, Shoichi Kuramitsu14, Nobuhiro Tanaka15, Hitoshi Matsuo7, Takashi Akasaka16. 1. Division of Cardiology, Department of Internal Medicine, Heart Vascular Stroke Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. 2. Department of Internal Medicine and Cardiovascular Center, Seoul National University Hospital, Seoul, Korea; Institute on Aging, Seoul National University, Seoul, Korea. Electronic address: bkkoo@snu.ac.kr. 3. Department of Internal Medicine and Cardiovascular Center, Seoul National University Hospital, Seoul, Korea. 4. Department of Cardiovascular Medicine, Chonnam National University Hospital, Gwangju, Korea. 5. Department of Cardiology, Daegu Catholic University Medical Center, Daegu, Korea. 6. Department of Internal Medicine, Ewha Womans University Medical Center, Ewha Womans University School of Medicine, Seoul, Korea. 7. Department of Cardiology, Gifu Heart Center, Gifu, Japan. 8. Department of Cardiology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea; Division of Cardiology, Ulsan Hospital, Ulsan, Korea. 9. Department of Medicine, Inje University Ilsan Paik Hospital, Goyang, Korea. 10. Division of Cardiology, Severance Cardiovascular Hospital, Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Seoul, Korea. 11. Department of Medicine, Keimyung University Dongsan Medical Center, Daegu, Korea. 12. Department of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China. 13. Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China. 14. Department of Cardiology, Kokura Memorial Hospital, Kitakyushu, Japan. 15. Department of Cardiology, Tokyo Medical University, Tokyo, Japan. 16. Wakayama Medical University, Wakayama, Japan.
Abstract
BACKGROUND: Although the presence of ischemia is a key prognostic factor in patients with coronary artery disease, the presence of high-risk plaque characteristics (HRPC) is also associated with increased risk of cardiovascular events. Limited data exist regarding the prognostic implications of combined information on physiological stenosis severity assessed by fractional flow reserve (FFR) and plaque vulnerability by coronary computed tomography angiography (CTA)-defined HRPC. OBJECTIVES: The current study aimed to evaluate the: 1) association between physiological stenosis severity and coronary CTA-defined HRPC; and 2) prognostic implications of coronary CTA-defined HRPC according to physiological stenosis severity in patients with coronary artery disease. METHODS: A total of 772 vessels (299 patients) evaluated by both coronary CTA and FFR were analyzed. The presence and number of HRPC (minimum lumen area <4 mm2, plaque burden ≥70%, low attenuating plaque, positive remodeling, napkin-ring sign, or spotty calcification) were assessed using coronary CTA images. The risk of vessel-oriented composite outcome (VOCO) (a composite of vessel-related ischemia-driven revascularization, vessel-related myocardial infarction, or cardiac death) at 5 years was compared according to the number of HRPC and FFR categories. RESULTS: The proportion of lesions with ≥3 HRPC was significantly decreased according to the increase in FFR values (58.6%, 46.5%, 36.8%, 15.7%, and 3.5% for FFR ≤0.60, 0.61 to ≤0.70, 0.71 to ≤0.80, 0.81 to ≤0.90, and >0.90, respectively; overall p value <0.001). Both FFR and number of HRPC showed significant association with the estimated risk of VOCO (p = 0.008 and p = 0.023, respectively). In the FFR >0.80 group, lesions with ≥3 HRPC showed significantly higher risk of VOCO than those with <3 HRPC (15.0% vs. 4.3%; hazard ratio: 3.964; 95% confidence interval: 1.451 to 10.828; p = 0.007). However, there was no significant difference in the risk of VOCO according to HRPC in the FFR ≤0.80 group. By multivariable analysis, the presence of ≥3 HRPC was independently associated with the risk of VOCO in the FFR >0.80 group. CONCLUSIONS: Physiological stenosis severity and the number of HRPC were closely related, and both components had significant association with the risk of clinical events. However, the prognostic implication of HRPC was different according to FFR. Integration of both physiological stenosis severity and plaque vulnerability would provide better prognostic stratification of patients than either individual component alone, especially in patients with FFR >0.80. (Clinical Implication of 3-vessel Fractional Flow Reserve [3V FFR-FRIENDS study]; NCT01621438).
BACKGROUND: Although the presence of ischemia is a key prognostic factor in patients with coronary artery disease, the presence of high-risk plaque characteristics (HRPC) is also associated with increased risk of cardiovascular events. Limited data exist regarding the prognostic implications of combined information on physiological stenosis severity assessed by fractional flow reserve (FFR) and plaque vulnerability by coronary computed tomography angiography (CTA)-defined HRPC. OBJECTIVES: The current study aimed to evaluate the: 1) association between physiological stenosis severity and coronary CTA-defined HRPC; and 2) prognostic implications of coronary CTA-defined HRPC according to physiological stenosis severity in patients with coronary artery disease. METHODS: A total of 772 vessels (299 patients) evaluated by both coronary CTA and FFR were analyzed. The presence and number of HRPC (minimum lumen area <4 mm2, plaque burden ≥70%, low attenuating plaque, positive remodeling, napkin-ring sign, or spotty calcification) were assessed using coronary CTA images. The risk of vessel-oriented composite outcome (VOCO) (a composite of vessel-related ischemia-driven revascularization, vessel-related myocardial infarction, or cardiac death) at 5 years was compared according to the number of HRPC and FFR categories. RESULTS: The proportion of lesions with ≥3 HRPC was significantly decreased according to the increase in FFR values (58.6%, 46.5%, 36.8%, 15.7%, and 3.5% for FFR ≤0.60, 0.61 to ≤0.70, 0.71 to ≤0.80, 0.81 to ≤0.90, and >0.90, respectively; overall p value <0.001). Both FFR and number of HRPC showed significant association with the estimated risk of VOCO (p = 0.008 and p = 0.023, respectively). In the FFR >0.80 group, lesions with ≥3 HRPC showed significantly higher risk of VOCO than those with <3 HRPC (15.0% vs. 4.3%; hazard ratio: 3.964; 95% confidence interval: 1.451 to 10.828; p = 0.007). However, there was no significant difference in the risk of VOCO according to HRPC in the FFR ≤0.80 group. By multivariable analysis, the presence of ≥3 HRPC was independently associated with the risk of VOCO in the FFR >0.80 group. CONCLUSIONS: Physiological stenosis severity and the number of HRPC were closely related, and both components had significant association with the risk of clinical events. However, the prognostic implication of HRPC was different according to FFR. Integration of both physiological stenosis severity and plaque vulnerability would provide better prognostic stratification of patients than either individual component alone, especially in patients with FFR >0.80. (Clinical Implication of 3-vessel Fractional Flow Reserve [3V FFR-FRIENDS study]; NCT01621438).
Authors: Khaled M Abdelrahman; Marcus Y Chen; Amit K Dey; Renu Virmani; Aloke V Finn; Ramzi Y Khamis; Andrew D Choi; James K Min; Michelle C Williams; Andrew J Buckler; Charles A Taylor; Campbell Rogers; Habib Samady; Charalambos Antoniades; Leslee J Shaw; Matthew J Budoff; Udo Hoffmann; Ron Blankstein; Jagat Narula; Nehal N Mehta Journal: J Am Coll Cardiol Date: 2020-09-08 Impact factor: 24.094