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We calculated Agatston-scores, number of coronary plaques and segment stenosis score (SSS). Linear mixed models were used to assess the effects of HIV-infection, atherosclerotic cardiovascular disease (ASCVD) risk, years of cocaine use on CAD. There was no significant difference in annual progression rates between HIV-infected and\u2014uninfected regarding Agatston-scores (10.8\u2009\u00b1\u200925.1\/year vs. 7.2\u2009\u00b1\u200917.8\/year, <jats:italic>p<\/jats:italic>\u2009=\u20090.17), the number of plaques (0.2\u2009\u00b1\u20090.3\/year vs. 0.3\u2009\u00b1\u20090.5\/year, <jats:italic>p<\/jats:italic>\u2009=\u20090.11) or SSS (0.5\u2009\u00b1\u20090.8\/year vs. 0.5\u2009\u00b1\u20091.3\/year, <jats:italic>p<\/jats:italic>\u2009=\u20090.96). Multivariately, HIV-infection was not associated with Agatston-scores (8.3, CI: [\u2212\u200937.2\u201353.7], <jats:italic>p<\/jats:italic>\u2009=\u20090.72), the number of coronary plaques (\u2212\u20090.1, CI: [\u2212\u20090.5\u20130.4], <jats:italic>p<\/jats:italic>\u2009=\u20090.73) or SSS (\u2212\u20090.1, CI: [\u2212\u20091.0\u20130.8], <jats:italic>p<\/jats:italic>\u2009=\u20090.84). ASCVD risk scores and years of cocaine-use significantly increased all CAD outcomes among HIV-infected individuals, but not among HIV-uninfected. Importantly, none of the HIV-medications were associated with any of the CAD outcomes. HIV-infection is not directly associated with CAD and therefore HIV-infected are not destined to have worse CAD profiles. However, HIV-infection may indirectly promote CAD progression as risk factors may have a more prominent role in the acceleration of CAD in these patients.<\/jats:p>","DOI":"10.1038\/s41598-021-02556-w","type":"journal-article","created":{"date-parts":[[2021,11,30]],"date-time":"2021-11-30T17:53:32Z","timestamp":1638294812000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["HIV indirectly accelerates coronary artery disease by promoting the effects of risk factors: longitudinal observational study"],"prefix":"10.1038","volume":"11","author":[{"given":"M\u00e1rton","family":"Kolossv\u00e1ry","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Celentano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gary","family":"Gerstenblith","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David A.","family":"Bluemke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raul N.","family":"Mandler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elliot K.","family":"Fishman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandeepan","family":"Bhatia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shaoguang","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shenghan","family":"Lai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Lai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,11,30]]},"reference":[{"key":"2556_CR1","doi-asserted-by":"publisher","first-page":"39","DOI":"10.1097\/QAI.0000000000001014","volume":"73","author":"JL Marcus","year":"2016","unstructured":"Marcus, J. 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