{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T06:43:56Z","timestamp":1780469036800,"version":"3.54.1"},"reference-count":41,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2017,2,2]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Volumes of paracardial adipose tissue (\n              <jats:styled-content style=\"fixed-case\">PAT<\/jats:styled-content>\n              ) and epicardial adipose tissue (\n              <jats:styled-content style=\"fixed-case\">EAT<\/jats:styled-content>\n              ) are greater after menopause. Interestingly,\n              <jats:styled-content style=\"fixed-case\">PAT<\/jats:styled-content>\n              but not\n              <jats:styled-content style=\"fixed-case\">EAT<\/jats:styled-content>\n              is associated with estradiol decline, suggesting a potential role of menopause in\n              <jats:styled-content style=\"fixed-case\">PAT<\/jats:styled-content>\n              accumulation. We assessed whether volumes of heart fat depot (\n              <jats:styled-content style=\"fixed-case\">EAT<\/jats:styled-content>\n              and\n              <jats:styled-content style=\"fixed-case\">PAT<\/jats:styled-content>\n              ) were associated with coronary artery calcification (\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              ) in women at midlife and whether these associations were modified by menopausal status and estradiol levels.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              <jats:styled-content style=\"fixed-case\">EAT<\/jats:styled-content>\n              and\n              <jats:styled-content style=\"fixed-case\">PAT<\/jats:styled-content>\n              volumes and\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              were measured using electron beam computed tomography scans.\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              was evaluated as (1) the presence of\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              (\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              Agatston score \u226510) and (2) the extent of any\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              (log\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              Agatston score &gt;0). The study included 478 women aged 50.9\u00a0years (58% pre\u2010 or early perimenopausal, 10% late perimenopausal, and 32% postmenopausal).\n              <jats:styled-content style=\"fixed-case\">EAT<\/jats:styled-content>\n              was significantly associated with\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              measures, and these associations were not modified by menopausal status or estradiol. In contrast, associations between\n              <jats:styled-content style=\"fixed-case\">PAT<\/jats:styled-content>\n              and\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              measures were modified by menopausal status (interaction\u2010\n              <jats:italic>P<\/jats:italic>\n              \u22640.01). Independent of study covariates including other adiposity measures, each 1\u2010SD unit increase in log\n              <jats:styled-content style=\"fixed-case\">PAT<\/jats:styled-content>\n              was associated with 102% higher risk of\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              presence (\n              <jats:italic>P<\/jats:italic>\n              =0.04) and an 80% increase in\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              extent (\n              <jats:italic>P<\/jats:italic>\n              =0.008) in postmenopausal women compared with pre\u2010 or early perimenopausal women. Additional adjustment for estradiol and hormone therapy attenuated these differences. Moreover, the association between\n              <jats:styled-content style=\"fixed-case\">PAT<\/jats:styled-content>\n              and\n              <jats:styled-content style=\"fixed-case\">CAC<\/jats:styled-content>\n              extent was stronger in women with lower estradiol levels (interaction\n              <jats:italic>P<\/jats:italic>\n              =0.004).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              The findings suggest that\n              <jats:styled-content style=\"fixed-case\">PAT<\/jats:styled-content>\n              is a potential menopause\u2010specific coronary artery disease risk marker, supporting the need to monitor and target this fat depot for intervention in women at midlife.\n            <\/jats:p>\n          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