Association of HIV Infection With Cardiovascular Pathology Based on Advanced Cardiovascular Imaging

Hudson, Jonathan A; Majonga, Edith; Ferrand, Rashida A; Perel, Pablo; Alam, Shirjel; Shah, Anoop

doi:10.1001/jama.2022.15078

Cited by 15 publications

(22 citation statements)

References 76 publications

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“…Importantly, 18F-FDG-PET studies to date have been restricted to predominantly male participants in their fifth decade in nonendemic regions usually with known cardiovascular risk factors. 9 In contrast, the majority of PLWH in SSA are women, typically younger, and with a lower cardiovascular risk profile. 28,53,134,135 There exists Evidence From Anatomic Imaging Computed tomography coronary angiography (CTCA) has been used to further describe the extent and severity of coronary artery disease in HIV.…”

Section: Molecular Imagingmentioning

confidence: 99%

HIV-Associated Cardiovascular Disease Pathogenesis: An Emerging Understanding Through Imaging and Immunology

Hudson,

Ferrand,

Gitau

et al. 2024

Circulation Research

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Cardiac abnormalities were identified early in the epidemic of AIDS, predating the isolation and characterization of the etiologic agent, HIV. Several decades later, the causation and pathogenesis of cardiovascular disease (CVD) linked to HIV infection continue to be the focus of intense speculation. Before the widespread use of antiretroviral therapy, HIV-associated CVD was primarily characterized by HIV-associated cardiomyopathy linked to profound immunodeficiency. With increasing antiretroviral therapy use, viral load suppression, and establishment of immune competency, the effects of HIV on the cardiovascular system are more subtle. Yet, people living with HIV still face an increased incidence of cardiovascular pathology. Advances in cardiac imaging modalities and immunology have deepened our understanding of the pathogenesis of HIV-associated CVD. This review provides an overview of the pathogenesis of HIV-associated CVD integrating data from imaging and immunologic studies with particular relevance to the HIV population originating from high-endemic regions, such as sub-Saharan Africa. The review highlights key evidence gaps in the field and suggests future directions for research to better understand the complex HIV-CVD interactions.

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Section: Molecular Imagingmentioning

confidence: 99%

HIV-Associated Cardiovascular Disease Pathogenesis: An Emerging Understanding Through Imaging and Immunology

Hudson,

Ferrand,

Gitau

et al. 2024

Circulation Research

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“…Increased MACE in PWH is thought to be related, in part, to traditional mechanisms as well as to residual inflammation and immune activation . Premature CAD in PWH is characterized by increased noncalcified coronary plaque, which may contribute to increased cardiovascular events . As PWH are increasingly likely to die of non–HIV-related causes, including cardiovascular disease (CVD), it is important to develop a strategy to improve CAD and cardiovascular outcomes in PWH.…”

Section: Introductionmentioning

confidence: 99%

Effects of Pitavastatin on Coronary Artery Disease and Inflammatory Biomarkers in HIV

Lu,

Ribaudo,

Foldyna

et al. 2024

JAMA Cardiol

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ImportanceCardiovascular disease (CVD) is increased in people with HIV (PWH) and is characterized by premature noncalcified coronary plaque. In the Randomized Trial to Prevent Vascular Events in HIV (REPRIEVE), pitavastatin reduced major adverse cardiovascular events (MACE) by 35% over a median of 5.1 years.ObjectiveTo investigate the effects of pitavastatin on noncalcified coronary artery plaque by coronary computed tomography angiography (CTA) and on inflammatory biomarkers as potential mechanisms for MACE prevention.Design, Setting, and ParticipantsThis double-blind, placebo-controlled randomized clinical trial enrolled participants from April 2015 to February 2018 at 31 US clinical research sites.PWH without known CVD who were taking antiretroviral therapy and had low to moderate 10-year CVD risk were included. Data were analyzed from April to November 2023.InterventionOral pitavastatin calcium, 4 mg per day.Main Outcomes and MeasuresCoronary CTA and inflammatory biomarkers at baseline and 24 months. The primary outcomes were change in noncalcified coronary plaque volume and progression of noncalcified plaque.ResultsOf 804 enrolled persons, 774 had at least 1 evaluable CTA. Plaque changes were assessed in 611 who completed both CT scans. Of 611 analyzed participants, 513 (84.0%) were male, the mean (SD) age was 51 (6) years, and the median (IQR) 10-year CVD risk was 4.5% (2.6-7.0). A total of 302 were included in the pitavastatin arm and 309 in the placebo arm. The mean noncalcified plaque volume decreased with pitavastatin compared with placebo (mean [SD] change, −1.7 [25.2] mm3 vs 2.6 [27.1] mm3; baseline adjusted difference, −4.3 mm3; 95% CI, −8.6 to −0.1; P = .04; 7% [95% CI, 1-12] greater reduction relative to placebo). A larger effect size was seen among the subgroup with plaque at baseline (−8.8 mm3 [95% CI, −17.9 to 0.4]). Progression of noncalcified plaque was 33% less likely with pitavastatin compared with placebo (relative risk, 0.67; 95% CI, 0.52-0.88; P = .003). Compared with placebo, the mean low-density lipoprotein cholesterol decreased with pitavastatin (mean change: pitavastatin, −28.5 mg/dL; 95% CI, −31.9 to −25.1; placebo, −0.8; 95% CI, −3.8 to 2.2). The pitavastatin arm had a reduction in both oxidized low-density lipoprotein (−29% [95% CI, −32 to −26] vs −13% [95% CI, −17 to −9]; P &lt; .001) and lipoprotein-associated phospholipase A2 (−7% [95% CI, −11 to −4] vs 14% [95% CI, 10-18]; P &lt; .001) compared with placebo at 24 months.Conclusions and RelevanceIn PWH at low to moderate CVD risk, 24 months of pitavastatin reduced noncalcified plaque volume and progression as well as markers of lipid oxidation and arterial inflammation. These changes may contribute to the observed MACE reduction in REPRIEVE.Trial RegistrationClinicalTrials.gov Identifier: NCT02344290

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“…Child death from HIV-associated cardiomyopathy has decreased; however, recent studies have shown both transient and chronic functional and structural changes by echocardiography (7,8). Cardiovascular magnetic resonance image (CMR) has emerged as a premier modality for assessment of CVD in PLWH, as it can detect abnormal structural, functional, and tissue characterization parameters better than other imaging modalities (4,5,9). CMR has demonstrated brosis in assessment of late gadolinium enhancement (LGE) and mapping techniques in PLWH ( 4).…”

Section: Introductionmentioning

confidence: 99%

Diffuse Myocardial Fibrosis is Uncommon in People with Perinatally Acquired Human Immunodeficiency Virus Infection

Williams,

MS,

Jenista

et al. 2023

Preprint

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Background Cardiovascular disease (CVD) remains a leading cause of death in people living with HIV. Myocardial fibrosis is well-described in HIV infection acquired in adulthood. We evaluate the burden of fibrosis by cardiac magnetic resonance in people with perinatal HIV infection. Methods Individuals with perinatally acquired HIV (pnHIV) diagnosed before 10 years-old and on antiretroviral treatment for ≥ 6 months were matched with uninfected controls. Patients with significant cardiometabolic co-morbidities and pregnancy were excluded. Diffuse fibrosis was assessed by cardiac magnetic resonance (CMR). with native T1 mapping for calculation of extracellular volume fraction (ECV). Viability was assessed with late gadolinium enhancement. The normality of fibrosis was assessed using the Komogrov-Smirnov test. Fibrosis between the groups was analyzed using a Mann-Whitney U test, as the data was not normally distributed. Statistical significance was defined as a p-valve < 0.05. Results Fourteen adults with pnHIV group and 26 controls (71% female and 86% Black race) were assessed. The average (± standard deviation) age in the study group was 29 (± 4.3) years-old. All pnHIV had been on ART for decades. Demographic data, CMR functional/volumetric data, and pre-contrast T1 mapping values were similar between groups. Diastolic function was normal in 50% of pnHIV patients and indeterminate in most of the remainder (42%). There was no statistically significant difference in ECV between groups; p = 0.24. Conclusion Perinatally-acquired HIV was not associated with diffuse myocardial fibrosis. Early exposure to ART may be cardioprotective against development of myocardial fibrosis in patients with perinatal HIV.

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Association of HIV Infection With Cardiovascular Pathology Based on Advanced Cardiovascular Imaging

Cited by 15 publications

References 76 publications

HIV-Associated Cardiovascular Disease Pathogenesis: An Emerging Understanding Through Imaging and Immunology

HIV-Associated Cardiovascular Disease Pathogenesis: An Emerging Understanding Through Imaging and Immunology

Effects of Pitavastatin on Coronary Artery Disease and Inflammatory Biomarkers in HIV

Diffuse Myocardial Fibrosis is Uncommon in People with Perinatally Acquired Human Immunodeficiency Virus Infection

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