Key result
HIV infection was associated with reduced LVEF (61.4% vs 64.7%, P=0.001) and increased markers of myocardial inflammation and oedema compared to healthy controls.
Why the study?
Pathophysiological mechanisms of cardiac disease in HIV remain elusive, and previous studies focused on ART-treated patients, confounding full understanding of myocardial changes.
Does HIV infection alter myocardial structure and function as detected by CMR compared to healthy controls?
Cross-Sectional (n=72)
No
Does HIV infection alter myocardial structure and function as detected by CMR compared to healthy controls?
Absolute Event Rate: 61.4% vs 64.7%
p-value: p=0.001
HIV patients exhibit subclinical alterations in myocardial function and structure, including inflammation and oedema, which may be partially reversible with anti-retroviral therapy.
May prompt cardiac evaluation in select HIV patients; hypothesis-generating and should not yet change practice.
Funding Acknowledgements: The study was funded by the UK Foreign & Commonwealth Office and The Peruvian Scientific, Technological Development and Technological Innovation Background: HIV-related heart disease remains a major public health problem, despite anti-retroviral therapy (ART). Patients with HIV have high risk of developing cardiac disease, but pathophysiological mechanisms remain elusive. Previous research focused on anti-retro viral (ART) treated HIV patients confounding full understanding. We explored myocardial changes in both ART-treated and ART-naïve HIV patients by deploying advanced quantitative CMR methods in the developing world, where untreated HIV remains prevalent. Methods: As part of multinational CMR outreach, rapidCMR for clinical, and research capability were set up in the Developing World. A single centre, cross-sectional study performed in Lima, Peru. 51 patients with HIV (26 on ART; 25 ART-naïve) without a history of cardiovascular disease were compared with twenty-one (21) age-matched controls, scanned concurrently. All underwent CMR (Siemens Prisma, 3T) for myocardial structure and function, myocardial strain and tissue characterisation (LGE, T1, T2 mapping and ECV). Results: Compared with healthy controls, HIV-infected patients had reduced LVEF (61.4%±4.1 vs 64.7 ± 2.4%, P = 0.001) and strain (Global Longitudinal Strain- GLS -17.6 ± 3.3% vs -21 ± 3.8%, p = 0.002). Native T1 (1294 ± 20.4ms vs 1229 ± 9.1ms, p < 0.001), T2 (41.5 ± 2.4ms vs 36.4 ± 1.4ms, p < 0.0001) and global ECV (28.5 ± 1.5% vs 24.8 ± 0.9%, p < 0.001) were also higher. See Table 1. Pericardial effusions and the presence of LGE (mid and sub-epicardial pattern) were three times more common, Figure 1. When comparing HIV treated and patients naïve to treatment, treated patients had lower (more normal) ECV (27.7 ± 1.3 vs 29.3 ± 0.7, p < 0.001) and lower (more normal) native T1 (1284.9 ± 15.9 vs 1303.9 ± 20.3, p < 0.001). ECV inversely correlated with CD4 count (r2 = 0.22, p = 0.01). Conclusions: Patients with HIV have alterations in myocardial function and structure with effusions, focal LGE and diffuse markers of inflammation/oedema. These changes may be reversible with therapy. The extracellular volume tracks markers of disease severity and treatment. CMR in HIV patients vs control patients ms = milliseconds Abstract 525 Figure. Common findings in HIV patients
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Medina et al. (2019) conducted a cross-sectional in HIV (n=72). HIV infection vs. Age-matched healthy controls was evaluated on Left ventricular ejection fraction (LVEF) (p=0.001). HIV infection was associated with reduced LVEF (61.4% vs 64.7%, P=0.001) and increased markers of myocardial inflammation and oedema compared to healthy controls.
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