Heesun Lee1, Jung Hye Kim2, Minkwan Kim3, Hyo Eun Park1, Su-Yeon Choi1, Hye Kyung Kim4, Byoung Kwon Lee5, Jin-Young Min6, Kyoung-Bok Min7, Shinae Kang8, Seung-Pyo Lee9. 1. Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea; Healthcare System Gangnam Center, Seoul National University Hospital, Seoul, South Korea. 2. Department of Internal Medicine, Yonsei Health Promotion Internal Clinic, Seoul, South Korea. 3. Department of Internal Medicine, Yongin Severance Hospital, Yonsei University College of Medicine and Cardiovascular Center, Yongin, Gyeonggi-do, South Korea. 4. Department of Family Medicine, Health Promotion Center, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. 5. Department of Cardiology and Cardiovascular Center, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. 6. Institute of Health and Environment, Seoul National University, Seoul, South Korea. 7. Department of Preventive Medicine, College of Medicine, Seoul National University, Seoul, South Korea. 8. Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. Electronic address: shinae95@yuhs.ac. 9. Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea; Cardiovascular Center, Seoul National University Hospital, Seoul, South Korea. Electronic address: sproll1@snu.ac.kr.
Abstract
BACKGROUND: We investigated the change of coronary atherosclerosis with long-term exposure to fine particulate matter of aerodynamic diameter <2.5 μm (PM2.5) using coronary computed tomography angiography (CCTA). METHODS: Subjects undergoing serial CCTAs between January 2007 and December 2017 (n = 3,127) were analyzed. Each individual's cumulative amount of PM2.5 exposure between the two CCTAs was evaluated by Kriging interpolation and zonal analysis, considering the time interval between the two CCTAs. The main outcome was progression of coronary artery calcium (CAC) with additional semiquantitative analysis on the changes in the severity and composition of atherosclerotic plaques. RESULTS: The CAC scores increased by 30.8 Agatston units per-year under a median PM2.5 concentration 24.9 μg/m3 and tended to increase with the cumulative amount of PM2.5 exposure (r = 0.321, p <0.001). The CAC progressed in 1,361 (43.5%) subjects during a median 53 months follow-up. The cumulative amount of PM2.5 exposure was independently associated with CAC progression (adjusted OR 1.09, p <0.001). By random forest analysis, the relative impact of cumulative amount of PM2.5 exposure on CAC progression was higher than that of traditional cardiovascular risk factors and the average concentration of PM2.5. The extent of coronary atherosclerosis and newly developed calcified plaque on follow-up were also significantly associated with the cumulative amount of PM2.5 exposure. CONCLUSIONS: Cumulative exposure to air pollution is associated with the progression of diffuse coronary calcification, the importance of which may be more significant than other traditional cardiovascular risk factors. Further investigations into the causality between PM2.5 and coronary atherosclerosis are warranted to improve global cardiovascular health.
BACKGROUND: We investigated the change of coronary atherosclerosis with long-term exposure to fine particulate matter of aerodynamic diameter <2.5 μm (PM2.5) using coronary computed tomography angiography (CCTA). METHODS: Subjects undergoing serial CCTAs between January 2007 and December 2017 (n = 3,127) were analyzed. Each individual's cumulative amount of PM2.5 exposure between the two CCTAs was evaluated by Kriging interpolation and zonal analysis, considering the time interval between the two CCTAs. The main outcome was progression of coronary artery calcium (CAC) with additional semiquantitative analysis on the changes in the severity and composition of atherosclerotic plaques. RESULTS: The CAC scores increased by 30.8 Agatston units per-year under a median PM2.5 concentration 24.9 μg/m3 and tended to increase with the cumulative amount of PM2.5 exposure (r = 0.321, p <0.001). The CAC progressed in 1,361 (43.5%) subjects during a median 53 months follow-up. The cumulative amount of PM2.5 exposure was independently associated with CAC progression (adjusted OR 1.09, p <0.001). By random forest analysis, the relative impact of cumulative amount of PM2.5 exposure on CAC progression was higher than that of traditional cardiovascular risk factors and the average concentration of PM2.5. The extent of coronary atherosclerosis and newly developed calcified plaque on follow-up were also significantly associated with the cumulative amount of PM2.5 exposure. CONCLUSIONS: Cumulative exposure to air pollution is associated with the progression of diffuse coronary calcification, the importance of which may be more significant than other traditional cardiovascular risk factors. Further investigations into the causality between PM2.5 and coronary atherosclerosis are warranted to improve global cardiovascular health.