{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T04:21:42Z","timestamp":1791346902402,"version":"4.3.1"},"reference-count":58,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"12","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2016,12]]},"abstract":"<jats:sec id=\"jah31935-sec-0001\" xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Compared to uninfected adults,\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">HIV<\/jats:styled-content>\n              \u2010infected adults on antiretroviral therapy are at increased risk of cardiovascular disease. Given the increase in T\u2010cell dysfunction, inflammation, and coagulation in\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">HIV<\/jats:styled-content>\n              infection, microvascular dysfunction is thought to contribute to this excess cardiovascular risk. However, the relationships between these variables remain undefined.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec id=\"jah31935-sec-0002\" xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              This was a cross\u2010sectional study of 358\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">HIV<\/jats:styled-content>\n              \u2010infected adults from the\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">SCOPE<\/jats:styled-content>\n              cohort. Macrovascular endothelial function was assessed using flow\u2010mediated dilation of the brachial artery and microvascular function by reactive hyperemia. T\u2010cell phenotype was determined by flow cytometry. Plasma markers of inflammation (tumor necrosis factor\u2010\u03b1, interleukin\u20106, high\u2010sensitivity C\u2010reactive protein,\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">sCD<\/jats:styled-content>\n              14) and coagulation (fibrinogen, D\u2010dimer) were also measured. In all\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">HIV<\/jats:styled-content>\n              + subjects, markers of inflammation (tumor necrosis factor\u2010\u03b1, high\u2010sensitivity C\u2010reactive protein), coagulation (D\u2010dimer) and T\u2010cell activation (\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">CD<\/jats:styled-content>\n              8+\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">PD<\/jats:styled-content>\n              1+,\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">CD<\/jats:styled-content>\n              4+interferon+cytomegalovirus\u2010specific) were associated with worse reactive hyperemia after adjusting for traditional cardiovascular risk factors and co\u2010infections. In treated and suppressed subjects, tumor necrosis factor\u2010\u03b1 and\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">CD<\/jats:styled-content>\n              8+\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">PD<\/jats:styled-content>\n              1+ cells remained associated with worse reactive hyperemia after adjustment. Compared to the untreated subjects,\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">CD<\/jats:styled-content>\n              8+\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">PD<\/jats:styled-content>\n              1+ cells were increased in the virally suppressed group. Reactive hyperemia was predictive of flow\u2010mediated dilation.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec id=\"jah31935-sec-0003\" xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">CD<\/jats:styled-content>\n              8+\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">PD<\/jats:styled-content>\n              1+ cells and tumor necrosis factor\u2010\u03b1 were associated with microvascular dysfunction in all\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">HIV<\/jats:styled-content>\n              + subjects and the treated and suppressed group. Additionally, D\u2010dimer, high\u2010sensitivity C\u2010reactive protein,\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">sCD<\/jats:styled-content>\n              \u201014, and interleukin\u20106 were associated with microvascular dysfunction in all\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">HIV<\/jats:styled-content>\n              + subjects. Although T\u2010cell dysfunction, inflammation, and microvascular dysfunction are thought to play a role in cardiovascular disease in\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">HIV<\/jats:styled-content>\n              , this study is the first to look at which T\u2010cell and inflammatory markers are associated with microvascular dysfunction in\n              <jats:styled-content style=\"fixed-case\" toggle=\"no\">HIV<\/jats:styled-content>\n              \u2010infected individuals.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.116.004243","type":"journal-article","created":{"date-parts":[[2016,12,21]],"date-time":"2016-12-21T01:40:28Z","timestamp":1482284428000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":59,"title":["Role of T\u2010Cell Dysfunction, Inflammation, and Coagulation in Microvascular Disease in HIV"],"prefix":"10.1161","volume":"5","author":[{"given":"Arjun","family":"Sinha","sequence":"first","affiliation":[{"name":"University of California","place":["San Francisco"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yifei","family":"Ma","sequence":"additional","affiliation":[{"name":"University of California","place":["San Francisco"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebecca","family":"Scherzer","sequence":"additional","affiliation":[{"name":"University of California","place":["San Francisco"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sophia","family":"Hur","sequence":"additional","affiliation":[{"name":"University of California","place":["San Francisco"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Danny","family":"Li","sequence":"additional","affiliation":[{"name":"University of California","place":["San Francisco"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Ganz","sequence":"additional","affiliation":[{"name":"University of California","place":["San Francisco"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven G.","family":"Deeks","sequence":"additional","affiliation":[{"name":"San Francisco General Hospital","place":["San Francisco"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Priscilla Y.","family":"Hsue","sequence":"additional","affiliation":[{"name":"University of California","place":["San Francisco"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"crossref","first-page":"1228","DOI":"10.1097\/QAD.0b013e328339192f","article-title":"Increased risk of myocardial infarction in HIV\u2010infected patients in France, relative to the general population","volume":"24","author":"Lang S","year":"2010","unstructured":"Lang S, Mary\u2010Krause M, Cotte L, Gilquin J, Partisani M, Simon A, Boccara F, Bingham A, Costagliola D; French Hospital Database on HIV\u2010ANRS CO4 . 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