Abstract
Funding Acknowledgements
Type of funding sources: Public Institution(s). Main funding source(s): University of Stellenbosch Cardiology Research Fund and United States National Institutes of Health/Fogarty International Center
Background
Cardiovascular disease (CVD) is a leading cause of death and disability in people living with HIV (PLWH). The coronary disease burden in high income countries contrast what is experienced in low- and middle-income countries where cardiomyopathy remains prevalent. Cardiovascular magnetic resonance imaging (CMR) has the unique ability to characterise tissues to obtain "virtual histology". Our data support a high burden of myocardial disease, already present at the time of HIV diagnosis in a young South African cohort.
Purpose
Early, undiagnosed myocardial pathology in some antiretroviral therapy (ART) naïve persons appear to precede the development of poorly prognostic HIV associated cardiomyopathy. The burden and mechanisms underlying the progression to more advanced disease in treatment naïve PLWH remain largely unknown, as does the modifying effect of ART on these abnormalities. Studying early myocardial disease and its progression with serial CMR evaluation will improve our understanding of disease evolution.
Methods
24 newly diagnosed, ART naïve adults without known CVD underwent a contrasted, 1.5T CMR study. Assessments included: Left ventricular (LV) volumes, mass, ejection fraction (EF), native and post-contrast T1 mapping, T2 mapping, extracellular volume (ECV) mapping, and late gadolinium enhancement (LGE) imaging. Quantitative measurements were obtained using a semi-automated software. Qualitative LGE findings were reviewed by an EACVI level III accredited cardiologist.
Results
The median age of the cohort was 33, interquartile range (IQR) 30-43 years. Median CD4 count was 250, IQR 152-520 cells/uL. All patients had non-dilated LV"s according to indexed end diastolic volumes (Mean: 85 ± 15ml/m²). No patient had overt systolic dysfunction (Mean EF: 62 ± 6%). Non-trivial pericardial effusions were present in 71% of cases. Indexed LV mass measured normal (Mean: 65 ± 12g/m²). Mean global native T1 and T2 values were 1043 ± 46 and 49 ± 4ms respectively. Native T1 values were highest in the septum and inferior wall (Mean: 1054 ± 50 and 1047 ± 51ms respectively). Mean global ECV was 28 ± 4%. Non-ischaemic LGE was present in 71% of participants. In those with LGE, midmyocardial enhancement of the inferior septum represented 71% of abnormalities (Figure).
Conclusion
In this young cohort of newly diagnosed HIV-infected persons, the prevalence of myocardial abnormalities were high. The midmyocardial LGE and abnormal mapping parameters (high for our scanner and high normal for published data) suggest myocardial inflammation and fibrosis already present at HIV-diagnosis. This was most appreciable in the septum and inferior walls, and likely represents a diffuse process that may progress to symptomatic cardiomyopathy over time. Serial evaluation on ART and comparison with a matched HIV-negative control group is planned. This will allow quantitative comparison of tissue characterisation and explore the nature and evolution of these abnormalities.
Abstract Figure. Late gadolinium enhancement (Arrows)
The prognostic value of T1 mapping and late gadolinium enhancement cardiovascular magnetic resonance imaging in patients with light chain amyloidosis
