HIV replication alters the composition of extrinsic pathway coagulation factors and increases thrombin generation

Jason V Baker, Kathleen Brummel-Ziedins, Jacqueline Neuhaus, Daniel Duprez, Nathan Cummins, David Dalmau, Jack DeHovitz, Clara Lehmann, Ann Sullivan, Ian John Woolley, Lewis H Kuller, James D Neaton, Russell Tracy

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Background HIV infection leads to activation of coagulation, which may increase the risk for atherosclerosis and venous thromboembolic disease. We hypothesized that HIV replication increases coagulation potentially through alterations in extrinsic pathway factors. Methods and Results Extrinsic pathway factors were measured among a subset of HIV participants from the Strategies for Management of Anti-Retroviral Therapy (SMART) trial. Thrombin generation was estimated using validated computational modeling based on factor composition. We characterized the effect of antiretroviral therapy (ART) treatment versus the untreated state (HIV replication) via 3 separate analyses: (1) a cross-sectional comparison of those on and off ART (n=717); (2) a randomized comparison of deferring versus starting ART (n=217); and (3) a randomized comparison of stopping versus continuing ART (n=500). Compared with viral suppression, HIV replication consistently showed short-term increases in some procoagulants (eg, 15 to 23 higher FVIII; P
Original languageEnglish
Pages (from-to)1 - 13
Number of pages13
JournalJournal of the American Heart Association
Issue number4 (Art. No.: e000264)
Publication statusPublished - 2013

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