{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T04:40:27Z","timestamp":1789015227812,"version":"build-2803163510"},"reference-count":92,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>Arterial stiffening may contribute to the pathogenesis of metabolic dysfunction\u2013associated steatotic liver disease. We aimed to assess relations of vascular hemodynamic measures with measures of hepatic steatosis and fibrosis in the community.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>Our sample was drawn from the Framingham Offspring, New Offspring Spouse, Third Generation, Omni-1, and Omni-2 cohorts (N=3875; mean age, 56 years; 54% women). We used vibration-controlled transient elastography to assess controlled attenuation parameter and liver stiffness measurements as measures of liver steatosis and liver fibrosis, respectively. We assessed noninvasive vascular hemodynamics using arterial tonometry. We assessed cross-sectional relations of vascular hemodynamic measures with continuous and dichotomous measures of hepatic steatosis and fibrosis using multivariable linear and logistic regression.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              In multivariable models adjusting for cardiometabolic risk factors, higher carotid-femoral pulse wave velocity (estimated \u03b2 per SD, 0.05 [95% CI, 0.01\u20130.09];\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              =0.003), but not forward pressure wave amplitude and central pulse pressure, was associated with more liver steatosis (higher controlled attenuation parameter). Additionally, higher carotid-femoral pulse wave velocity (\u03b2=0.11 [95% CI, 0.07\u20130.15];\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              &lt;0.001), forward pressure wave amplitude (\u03b2=0.05 [95% CI, 0.01\u20130.09];\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              =0.01), and central pulse pressure (\u03b2=0.05 [95% CI, 0.01\u20130.09];\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              =0.01) were associated with more hepatic fibrosis (higher liver stiffness measurement). Associations were more prominent among men and among participants with obesity, diabetes, and metabolic syndrome (interaction\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              values, &lt;0.001\u20130.04). Higher carotid-femoral pulse wave velocity, but not forward pressure wave amplitude and central pulse pressure, was associated with higher odds of hepatic steatosis (odds ratio, 1.16 [95% CI, 1.02\u20131.31];\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              =0.02) and fibrosis (odds ratio, 1.40 [95% CI, 1.19\u20131.64];\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              &lt;0.001).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>Elevated aortic stiffness and pressure pulsatility may contribute to hepatic steatosis and fibrosis.<\/jats:p>\n          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Institute, MA (V.X., E.J.B., R.S.V.)."},{"name":"Evans Department of Medicine, Boston Medical Center, MA (E.J.B., N.M.H.)."},{"name":"Whitaker Cardiovascular Institute, Boston University Chobanian and Avedisian School of Medicine, MA (E.J.B., N.M.H.)."},{"name":"Cardiology and Preventive Medicine Sections, Department of Medicine, Boston University Chobanian and Avedisian School of Medicine, MA (E.J.B.)."},{"name":"Department of Epidemiology, Boston University School of Public Health, MA (E.J.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7357-5970","authenticated-orcid":true,"given":"Ramachandran S.","family":"Vasan","sequence":"additional","affiliation":[{"name":"Framingham Heart Study, Boston University and National Heart, Lung, and Blood Institute, MA (V.X., E.J.B., R.S.V.)."},{"name":"The University of Texas School of Public Health San Antonio (R.S.V.)."},{"name":"The University of Texas Health Science Center, San Antonio 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