Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/53072
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dc.contributor.authorManmathan G.P.R.-
dc.contributor.authorWardill T.-
dc.contributor.authorAbdi Z.-
dc.contributor.authorNgwu N.-
dc.contributor.authorJohnson M.A.-
dc.contributor.authorWong D.-
dc.contributor.authorRakhit R.D.-
dc.date.accessioned2025-01-20T00:24:56Z-
dc.date.available2025-01-20T00:24:56Z-
dc.date.copyright2024-
dc.date.issued2025-01-14en
dc.identifier.citationEuropean Heart Journal. Conference: European Society of Cardiology Congress, ESC 2024. London United Kingdom. 45(Supplement 1) (no pagination), 2024. Date of Publication: 01 Oct 2024.-
dc.identifier.urihttps://repository.monashhealth.org/monashhealthjspui/handle/1/53072-
dc.description.abstractBackground: Controversy exists regarding the contribution of HIV, ART or traditional risk factors to CVD risk in PLWH. The H-ART to Heart study investigates the prevalence of subclinical CVD in asymptomatic PLWH without cardiovascular risk factors compared to negative controls(-). Vascular inflammation inhibits local adipogenesis in pericoronary adipose tissue (PCAT) and thus can be detected on coronary computed tomography angiography (CTCA) as an increase in CT attenuation of PCAT surrounding the proximal right coronary artery (RCA). Method(s): This cross-sectional study compared PLWH aged 35-55yrs (diagnosed >10 yrs, on ART) to matched controls. Included were Caucasian men who have sex with men(MSM) and Black African/Caribbean women (BW) with traditional risk factors excluded (hypertension, hyperlipidaemia, diabetes, kidney disease, smoking, depression, inflammatory conditions, etc.). Detailed vitals, 10 year CVD risk calculation (Q-RISK 3) were recorded. CTCA were performed with novel analysis using PCAT to assess for coronary inflammation (Figure 1.) Results: 98 participants were recruited (49M; 51 PLWH). Mean Q Risk 3 (10yr CVD risk - %) was low across the groups (HIV+MSM 4.65+/-2.1, HIV-MSM 3.88+/-2.7;p=0.29; HIV+BW 2.03+/-1.3, HIV-BW 1.38+/-0.98 p=0.66). 79 participants (42 PLWH; 37 controls) completed a CTCA with only 2 PLWH having clinically significant disease (CAD-RAD 3+ ie. >50% luminal stenosis) and none in the control group. (p=0.49) The CT scans of 69 patients were assessed for peri-coronary adipose tissue (PCAT) density, 2 were ruled out due to a small non-dominant RCA. The PCAT density of PLWH was higher than that of the controls (-71.2+/-27.6 vs -75.5+/-30.3 P=<0.05). Multivariate linear regression demonstrated that HIV status was an independent predictor of coronary inflammation (p=0.037) after adjusting for age, gender and BMI. Conclusion(s): PWLH without traditional CV risk factors did not have significant evidence of more clinically relevant stenosis than controls on CTCA. However PCAT demonstrated a higher signal of coronary inflammation, despite stable disease, compliance with ART and low CVD risk scores. PLWH remain at risk of CV disease, this study supports the rationale for early preventative strategies for CVD prevention in PLWH. (Figure Presented).-
dc.publisherOxford University Press-
dc.relation.ispartofEuropean Heart Journal-
dc.subject.meshadipogenesis-
dc.subject.meshadipose tissue-
dc.subject.meshcomputed tomographic angiography-
dc.subject.meshcomputer assisted tomography-
dc.subject.meshcoronary arteritis-
dc.subject.meshdepression-
dc.subject.meshdiabetic nephropathy-
dc.subject.meshHuman immunodeficiency virus infected patient-
dc.subject.meshhyperlipidemia-
dc.subject.meshhypertension-
dc.titlePericoronary adipose tissue computed tomography attenuation (PCAT) as a marker of premature cvd in asymptomatic people living with HIV (PLWH) without traditional risk factors: H-ART to heart study.-
dc.typeConference Abstract-
dc.identifier.affiliationCardiology (MonashHeart)-
dc.description.conferencenameEuropean Society of Cardiology Congress, ESC 2024-
dc.description.conferencelocationLondon, United Kingdom-
dc.type.studyortrialObservational study (cohort, case-control, cross sectional, or survey)-
dc.identifier.doihttp://monash.idm.oclc.org/login?url=https://dx.doi.org/10.1093/eurheartj/ehae666.3241-
local.date.conferencestart2024-08-30-
dc.identifier.institution(Manmathan) University College London, Cardiovascular Sciences, London, United Kingdom-
dc.identifier.institution(Wardill) Monash Heart, Victorian Heart Hospital, Melbourne, Australia-
dc.identifier.institution(Abdi, Ngwu, Johnson, Rakhit) Royal Free Hospital, London, United Kingdom-
dc.identifier.institution(Wong) Monash University, Melbourne, Australia-
local.date.conferenceend2024-09-02-
dc.identifier.affiliationmh(Wardill) Monash Heart, Victorian Heart Hospital, Melbourne, Australia-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.openairetypeConference Abstract-
crisitem.author.deptCardiology (MonashHeart & Victorian Heart Institute)-
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