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• W2954927487 abstract "Improvement in survival in patients living with human immunodeficiency virus (PLHIV) has led to increased prevalence of cardiovascular disease. Whether HIV-associated immune dysfunction is associated with preclinical left ventricular (LV) dysfunction despite normal LV ejection fraction (LVEF) is unclear. Accordingly, we investigated the relation of immune status and LV function in PLHIV. Global longitudinal strain (GLS) analyses were performed retrospectively on all echocardiograms for PLHIV who had available HIV-1 RNA viral load, nadir, and proximal CD4 cell count data at Duke University Medical Center between 2001 and 2012. The relation between HIV-1 RNA viral load, nadir, and proximal CD4 count and GLS as a continuous dependent variable was assessed with unadjusted and adjusted linear regression. GLS was calculated for 253 PLHIV. Median GLS in our cohort was – 15.1% with interquartile range from (−16.7 to −13.6). All participants had an LVEF ≥50%. In adjusted analyses, proximal CD4 <500 cells/mm3 and nadir CD4 <250 cells/mm3 were significantly inversely correlated with GLS (p = 0.01 and p = 0.004, respectively). In PLHIV, patient with plasma HIV RNA <400 copies/ml at baseline had a trend toward significantly more negative values of GLS compared with those patients without viral suppression at baseline (p = 0.08). In conclusion, this study is the first to demonstrate such a high prevalence of abnormal GLS in PLHIV, and the first to identify that proximal and nadir CD4 cell count are independently associated with GLS despite normal LVEF. Improvement in survival in patients living with human immunodeficiency virus (PLHIV) has led to increased prevalence of cardiovascular disease. Whether HIV-associated immune dysfunction is associated with preclinical left ventricular (LV) dysfunction despite normal LV ejection fraction (LVEF) is unclear. Accordingly, we investigated the relation of immune status and LV function in PLHIV. Global longitudinal strain (GLS) analyses were performed retrospectively on all echocardiograms for PLHIV who had available HIV-1 RNA viral load, nadir, and proximal CD4 cell count data at Duke University Medical Center between 2001 and 2012. The relation between HIV-1 RNA viral load, nadir, and proximal CD4 count and GLS as a continuous dependent variable was assessed with unadjusted and adjusted linear regression. GLS was calculated for 253 PLHIV. Median GLS in our cohort was – 15.1% with interquartile range from (−16.7 to −13.6). All participants had an LVEF ≥50%. In adjusted analyses, proximal CD4 <500 cells/mm3 and nadir CD4 <250 cells/mm3 were significantly inversely correlated with GLS (p = 0.01 and p = 0.004, respectively). In PLHIV, patient with plasma HIV RNA <400 copies/ml at baseline had a trend toward significantly more negative values of GLS compared with those patients without viral suppression at baseline (p = 0.08). In conclusion, this study is the first to demonstrate such a high prevalence of abnormal GLS in PLHIV, and the first to identify that proximal and nadir CD4 cell count are independently associated with GLS despite normal LVEF." @default.
• W2954927487 created "2019-07-12" @default.
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• W2954927487 date "2019-09-01" @default.
• W2954927487 modified "2023-09-24" @default.
• W2954927487 title "Global Longitudinal Strain and Immune Status in Patients Living With Human Immunodeficiency Virus" @default.
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• W2954927487 doi "https://doi.org/10.1016/j.amjcard.2019.06.013" @default.
• W2954927487 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6887515" @default.
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