Supplementary Components1. and stenosis 50% for both HIV+ [PR 1.25 per SD (95% CI 1.07C1.43)] and HIV? males [PR 1.46 per SD (95% CI 1.08C1.85)]. Summary: The organizations between lipids and coronary atherosclerosis c-JUN peptide tended to become weaker for HIV+ in comparison to HIV? males, although TC/HDL had the most powerful association for both HIV and HIV+? males. A weaker association between lipid amounts and coronary atherosclerosis for HIV+ males may donate to the reduced discrimination of CVD risk seen in HIV+ individuals. strong class=”kwd-title” Keywords: Lipids, HIV, coronary artery disease, atherosclerosis Introduction Human immunodeficiency virus (HIV) infected individuals have an estimated 40C75% increased risk for atherosclerotic cardiovascular disease (ASCVD), a leading cause of death for HIV+ individuals receiving highly active antiretroviral therapies (HAART) in the United States.[1C3] The pathophysiology for this increased rate of ASCVD is multifactorial and includes heightened inflammation and immune dysregulation, an increased prevalence of ASCVD risk factors, coagulation disorders, and impaired endothelial function.[4C9] There may also be differences in the pathophysiology of atherosclerosis for HIV-infected (HIV+) individuals and we, and others, have previously demonstrated that HIV+ men have a higher prevalence of non-calcified plaque compared to HIV? men.[10, 11] Treatment with older HAART regimens is associated with an increase in total cholesterol (TC) and low-density lipoprotein (LDL) cholesterol, which is also known as the return to health phenomenon.[12, 13] Use of some protease inhibitors in particular are also associated with a rise in triglycerides and initial era protease inhibitors are also suggested to improve the chance for CVD.[14] This upsurge in lipid amounts c-JUN peptide with HAART may be because of decreased swelling, connected improved virologic control and potentially represent somebody’s pre-HIV infection lipid baseline. Accordingly, these lipid changes make accurate ASCVD risk assessment more difficult and the 2013 American College of Cardiology (ACC)/American Heart Association (AHA) Pooled Cohort Equation (PCE) underestimates the ASCVD risk among individuals with HIV contamination and acquired immunodeficiency syndrome (AIDS).[15C18] Coronary CT angiography provides a detailed assessment of the coronary anatomy for both coronary stenosis and plaque composition. Therefore, a detailed description of the relationship between traditional lipid values and coronary atherosclerosis is usually imperative to better understand potential differences in the pathophysiology of coronary atherosclerosis for HIV+ individuals and to improve ASCVD risk prediction. We used data from the Multicenter AIDS Cohort Study (MACS), which included a detailed assessment of the coronary anatomy for both coronary Notch1 stenosis and plaque composition using coronary computed tomography (CT) angiography in order 1) to determine associations between lipid levels and various components of coronary atherosclerotic plaque composition and 2) to examine whether the relationship between traditional lipid values and subclinical coronary atherosclerosis differs by HIV serostatus and. Methods MACS is usually a cohort study comprised of HIV+ and HIV? bi-sexual and homosexual men who are at risk for HIV contamination. Participants were initially enrolled from 1984C1985 in Baltimore, Maryland/Washington, DC; Chicago, Illinois; Pittsburgh, Pennsylvania; and Los Angeles, California with subsequent enrollment occurring between 1987 to 1991 and 2001 to 2003.[19] Semi-annual visits include standardized interviews, physical examination, and collection of blood. Participants in the MACS cardiovascular ancillary study were between 40 to 70 years of age, weighed less than 300 pounds, had no prior history of cardiac surgery or percutaneous coronary intervention, or current atrial fibrillation, and were oversampled for HIV+ men. Participants were excluded from coronary CT angiography if they had chronic kidney disease (estimated glomerular filtration rate 60 mL/min/1.73 m2) or a known history of intravenous contrast c-JUN peptide allergy. The current analysis included 732 men who underwent coronary CT angiography after excluding men with missing fasting lipid data (n=27). The study was approved by the institutional review boards of all participating sites and participants provided informed consent. The computed tomography (CT) non-contrast and contrast scan protocols used in this study have been previously described in detail and the CT angiogram scans were performed between January 2010 and June 2013.[20] Three centers used 64-slice multi-detector CT and one center used 320-row multi-detector CT. The coronary artery calcium (CAC) score was calculated using the Agatston method and in this analysis was classified as either absent (CAC 10) or present (CAC 10).[21]. A c-JUN peptide prospective EKG triggered protocol was useful for CT angiography (CTA) research to minimize rays exposure, except where the heartrate was.