Effects of HIV Infection and Anti-retroviral Therapy on Cardiovascular Risk Factors

2014 ◽  
Vol 6 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Robert A. Ngala ◽  
Klutse Fianko
2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Kolossvary ◽  
E.K Fishman ◽  
G Gerstenblith ◽  
D.A Bluemke ◽  
R.N Mandler ◽  
...  

Abstract Background/Introduction Cross-sectional studies are inconsistent on the potential independent adverse effects of human immunodeficiency virus (HIV)-infection on coronary artery disease (CAD). Furthermore, there is no information on the potential effects of HIV-infection on plaque volumes. Also, only the independent effects of HIV-infection on CAD have been investigated. Purpose In a prospective longitudinal observational cohort, we wished to assess whether HIV-infection accelerates CAD independently, or by acting in synergistic fashion with conventional and nonconventional cardiovascular risk factors to accelerate disease progression as assessed by clinical and volumetric parameters of CAD on coronary CT angiography (CCTA). Methods Overall, 300 asymptomatic individuals without cardiovascular symptoms but with CCTA-confirmed coronary plaques (210 males, age: 48.0±7.2 years) with or without HIV (226 HIV-infected) prospectively underwent CCTA at two time points (mean follow-up: 4.0±2.3 years). Agatston-score, number of coronary plaques, segment stenosis score were calculated, and we also segmented the coronary plaques to enumerate total, noncalcified (−100–350HU) and calcified (≥351HU) plaque volumes. Linear mixed models were used to assess the effects of HIV-infection, atherosclerotic cardiovascular disease (ASCVD) risk, years of cocaine use and high-sensitivity C-reactive protein on CCTA markers of CAD. Results In univariate analysis, there was no significant difference in CAD characteristics between HIV-infected and -uninfected, neither at baseline nor at follow-up (p>0.05 for all). Furthermore, there was no significant difference in annual progression rates between the two groups (p>0.05 for all). By multivariate analysis, HIV was not associated with any CAD parameter (p>0.05 for all). However, among HIV-infected individuals, each year of cocaine use significantly increased all CAD parameters (p<0.05 for all), while ASCVD risk score was significantly associated with CAD parameters except for Agatston-score (p<0.05). These associations were only present among HIV-infected individuals. Conclusion(s) Instead of directly worsening CAD, HIV may promote CAD through increased susceptibility to conventional and nonconventional cardiovascular risk factors. Therefore, aggressive management of both conventional and nonconventional cardiovascular risk factors is needed to reduce cardiovascular burden of HIV-infection. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): National Institutes of Health, National Institute on Drug Abuse


2010 ◽  
Vol 53 (1) ◽  
pp. 102-106 ◽  
Author(s):  
Leslie Cockerham ◽  
Rebecca Scherzer ◽  
Andrew Zolopa ◽  
David Rimland ◽  
Cora E Lewis ◽  
...  

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Kolossvary ◽  
D.A Bluemke ◽  
E.K Fishman ◽  
G Gerstenblith ◽  
R.N Mandler ◽  
...  

Abstract Background/Introduction Cardiovascular risk factors are assumed to propagate coronary artery disease (CAD) through the lipid and/or inflammatory pathologic pathways. However, we currently do not have any in-vivo information whether these effects may alter CAD morphology and structure differently. Purpose We wished to assess whether conventional cardiovascular risk factors (which are assumed to affect CAD primarily through the lipid pathway), and unconventional risk factors such as cocaine use and human immunodeficiency virus (HIV)-infection (which are assumed to propagate CAD primarily through the inflammatory pathway) affect different coronary plaque structures as assessed by radiomics. Methods In our prospective longitudinal observational study of 300 individuals without cardiovascular symptoms but with coronary CT angiography (CCTA)-confirmed atherosclerosis (210 male, age: 48±7 years) of whom 161 were cocaine users at baseline with or without HIV-infection (226 HIV-infected), underwent CCTA at two time points (mean follow-up: 4.0±2.3 years). Precision phenotyping of CAD was done by calculating 1276 radiomic features on the 861 plaques. Linear mixed models corrected for plaque volume, high-sensitivity C-reactive protein, statin use and positive family history were used to assess the effects of chronic cocaine use, HIV-infection and elevated atherosclerotic cardiovascular disease risk (ASCVD≥7.5%). Hierarchical clustering was used to assess potential clusters among significant radiomic features. Bonferroni corrected p<0.00004 (0.05/1276) was considered significant. Results Overall, 32.0% (409/1276) of the radiomic features showed any significant association, of which 74.1% (303/409), 4.2% (17/409) and 25.4% (104/409) were affected by cocaine use, HIV-infection and elevated ASCVD risk, respectively. There was no overlap among radiomic features significantly associated with increased ASCVD risk and cocaine use or HIV-infection, while 88,2% (15/17) of HIV-infection associated parameters were also affected by cocaine use. Cluster analysis indicated 13 different structural components among significant features, of which eight were unique to chronic cocaine use, three unique to ASCVD risk, and two contained parameters associated with chronic cocaine use, elevated ASCVD risk and/or HIV-infection. Interpretation Chronic cocaine use and HIV-infection modify different CAD morphological components than conventional cardiovascular risk factors, potentially implying independent pathological pathways of disease progression irrespective of each other. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): National Institutes of Health, National Institute on Drug Abuse


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