TY - JOUR
T1 - Association of Hepatic Steatosis With Major Adverse Cardiovascular Events, Independent of Coronary Artery Disease
AU - Meyersohn, Nandini M.
AU - Mayrhofer, Thomas
AU - Corey, Kathleen E.
AU - Bittner, Daniel O.
AU - Staziaki, Pedro V.
AU - Szilveszter, Balint
AU - Hallett, Travis
AU - Lu, Michael T.
AU - Puchner, Stefan B.
AU - Simon, Tracey G.
AU - Foldyna, Borek
AU - Voora, Deepak
AU - Ginsburg, Geoffrey S.
AU - Douglas, Pamela S.
AU - Hoffmann, Udo
AU - Ferencik, Maros
N1 - Funding Information:
Conflicts of interest These authors disclose the following: Nandini M. Meyersohn was supported by NIH/NHLBI T32 HL076136. Daniel O. Bittner was supported by grant from NIH/NHLBI 5K24HL113128. Michael T. Lu received grant support from the American Roentgen Ray Society Scholarship; and personal fees from PQBypass outside the submitted work. Pamela S. Douglas reports receiving grant support from HeartFlow; and serves on a data and safety monitoring board for GE HealthCare outside the submitted work. Udo Hoffmann reports receiving grants from the ACR Imaging Network and HeartFlow during the conduct of the study, and from Siemens Healthcare outside the submitted work. Maros Ferencik was supported by a grant from the American Heart Association (13FTF16450001). The other authors disclose no conflicts.
Funding Information:
Funding The PROMISE trial was funded by grants R01HL098237, R01HL098236, R01HL98305, and R01HL098235 from the National Heart, Lung, and Blood Institute. Conflicts of interest These authors disclose the following: Nandini M. Meyersohn was supported by NIH/NHLBI T32 HL076136. Daniel O. Bittner was supported by grant from NIH/NHLBI 5K24HL113128. Michael T. Lu received grant support from the American Roentgen Ray Society Scholarship; and personal fees from PQBypass outside the submitted work. Pamela S. Douglas reports receiving grant support from HeartFlow; and serves on a data and safety monitoring board for GE HealthCare outside the submitted work. Udo Hoffmann reports receiving grants from the ACR Imaging Network and HeartFlow during the conduct of the study, and from Siemens Healthcare outside the submitted work. Maros Ferencik was supported by a grant from the American Heart Association (13FTF16450001). The other authors disclose no conflicts.
Funding Information:
Funding The PROMISE trial was funded by grants R01HL098237, R01HL098236, R01HL98305, and R01HL098235 from the National Heart, Lung, and Blood Institute .
Publisher Copyright:
© 2021 AGA Institute
PY - 2021/7
Y1 - 2021/7
N2 - Background & Aims: Hepatic steatosis has been associated with increased risk of major adverse cardiovascular events (MACE) but it is not clear whether steatosis is independently associated with risk of MACE. We investigated whether steatosis is associated with risk of MACE independently of the presence and extent of baseline coronary artery disease, assessed by comprehensive contrast-enhanced computed tomography angiography (CTA). Methods: We conducted a nested cohort study of 3756 subjects (mean age, 60.6 years; 48.4% men) who underwent coronary CTA at 193 sites in North America, from July 2010 through September 2013, as part of the PROMISE study, which included noninvasive cardiovascular analyses of symptomatic outpatients without coronary artery disease. Independent core laboratory readers measured hepatic and splenic attenuation, using non-contrast computed tomography images to identify steatosis, and evaluated coronary plaques and stenosis in coronary CTA images. We collected data on participants’ cardiovascular risk factors, presence of metabolic syndrome, and body mass index. The primary endpoint was an adjudicated composite of MACE (death, myocardial infarction, or unstable angina) during a median follow-up time of 25 months. Results: Among the 959 subjects who had steatosis (25.5% of the cohort), 42 had MACE (4.4%), whereas among the 2797 subjects without steatosis, 73 had MACE (2.6%) (hazard ratio [HR] for MACE in subjects with steatosis, 1.69; 95% CI, 1.16–2.48; P = .006 for MACE in subjects with vs without steatosis). This association remained after adjustment for atherosclerotic cardiovascular disease risk scores, significant stenosis, and metabolic syndrome (adjusted HR, 1.72; 95% CI, 1.16–2.54; P = .007) or obesity (adjusted HR, 1.75; 95% CI, 1.19–2.59; P = .005). Steatosis remained independently associated with MACE after adjustment for all CTA measures of plaques and stenosis. Conclusions: Hepatic steatosis is associated with MACE independently of other cardiovascular risk factors or extent of coronary artery disease. Strategies to reduce steatosis might reduce risk of MACE. ClinicalTrials.gov
AB - Background & Aims: Hepatic steatosis has been associated with increased risk of major adverse cardiovascular events (MACE) but it is not clear whether steatosis is independently associated with risk of MACE. We investigated whether steatosis is associated with risk of MACE independently of the presence and extent of baseline coronary artery disease, assessed by comprehensive contrast-enhanced computed tomography angiography (CTA). Methods: We conducted a nested cohort study of 3756 subjects (mean age, 60.6 years; 48.4% men) who underwent coronary CTA at 193 sites in North America, from July 2010 through September 2013, as part of the PROMISE study, which included noninvasive cardiovascular analyses of symptomatic outpatients without coronary artery disease. Independent core laboratory readers measured hepatic and splenic attenuation, using non-contrast computed tomography images to identify steatosis, and evaluated coronary plaques and stenosis in coronary CTA images. We collected data on participants’ cardiovascular risk factors, presence of metabolic syndrome, and body mass index. The primary endpoint was an adjudicated composite of MACE (death, myocardial infarction, or unstable angina) during a median follow-up time of 25 months. Results: Among the 959 subjects who had steatosis (25.5% of the cohort), 42 had MACE (4.4%), whereas among the 2797 subjects without steatosis, 73 had MACE (2.6%) (hazard ratio [HR] for MACE in subjects with steatosis, 1.69; 95% CI, 1.16–2.48; P = .006 for MACE in subjects with vs without steatosis). This association remained after adjustment for atherosclerotic cardiovascular disease risk scores, significant stenosis, and metabolic syndrome (adjusted HR, 1.72; 95% CI, 1.16–2.54; P = .007) or obesity (adjusted HR, 1.75; 95% CI, 1.19–2.59; P = .005). Steatosis remained independently associated with MACE after adjustment for all CTA measures of plaques and stenosis. Conclusions: Hepatic steatosis is associated with MACE independently of other cardiovascular risk factors or extent of coronary artery disease. Strategies to reduce steatosis might reduce risk of MACE. ClinicalTrials.gov
KW - CT
KW - Heart Disease
KW - MAFLD
KW - NAFLD
UR - http://www.scopus.com/inward/record.url?scp=85108065894&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85108065894&partnerID=8YFLogxK
U2 - 10.1016/j.cgh.2020.07.030
DO - 10.1016/j.cgh.2020.07.030
M3 - Article
C2 - 32707340
AN - SCOPUS:85108065894
SN - 1542-3565
VL - 19
SP - 1480-1488.e14
JO - Clinical Gastroenterology and Hepatology
JF - Clinical Gastroenterology and Hepatology
IS - 7
ER -