TY - JOUR
T1 - Diastolic Dysfunction in Patients With Human Immunodeficiency Virus Receiving Antiretroviral Therapy
T2 - Results From the CHART Study
AU - Butler, Javed
AU - Greene, Stephen J.
AU - Shah, Svati H.
AU - Shah, Sanjiv J.
AU - Anstrom, Kevin J.
AU - Kim, Raymond J.
AU - Kalogeropoulos, Andreas P.
AU - Velazquez, Eric J.
AU - Hernandez, Adrian F.
AU - Desvigne-Nickens, Patrice
AU - Scherzer, Rebecca
AU - Hsue, Priscilla Y.
AU - Braunwald, Eugene
N1 - Funding Information:
The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. J.B. has received research support from the National Institutes of Health, Patient Centered Outcomes Research, and the European Union. He serves on the speaker bureau for Novartis, Janssen, and NovoNordisk. He serves as a consultant and/or serves on steering committee, clinical events committee, or data safety monitoring boards for Abbott, Adrenomed, Amgen, Array, Astra Zeneca, Bayer, BerlinCures, Boehringer Ingelheim, Bristol Myers Squib, Cardiocell, CVRx, G3 Pharmaceutical, Innolife, Janssen, Lantheus, LinaNova, Luitpold, Medscape, Medtronic, Merck, Novartis, NovoNordisk, Relypsa, Roche, Sanofi, StealthPeptide, SC Pharma, V-Wave Limited, Vifor, and ZS Pharma. S.J.G. has received support from a Heart Failure Society of America/ Emergency Medicine Foundation Acute Heart Failure Young Investigator Award funded by Novartis; has received research support from Amgen, Bristol-Myers Squibb, and Novartis; and serves on an advisory board for Amgen. S.H.S. has received support from the National Institutes of Health and the American Heart Association; holds a patent on an unrelated finding. S.J.S. has received research support from the National Institutes of Health (R01 HL127028 and R01 HL107577) and the American Heart Association, Actelion, Astra Zeneca, Bayer, and Novartis; consultant to Actelion, Amgen, Astra Zeneca, Bayer, Boehringer-Ingelheim, Cardiora, Eisai, Gilead, Ironwood, Merck, Myokardia, Novartis, Sanofi, and United Therapeutics. R.J.K. has received research support from Bayer, Stealth Biotherapeutics, and Astellas. A.P.K. has received research support from the American Heart Association; and has been a consultant to Roche Diagnostics. E.J.V. has received research support from National Institutes of Health, Novartis, Amgen, Pfizer, Alnylam, Philips, GE, and Bay Labs; honoraria from Novartis, Amgen, Merck, Pfizer, Expert Exchange, and Abiomed. A.F.H. reports consulting fees from AstraZeneca, Bayer, Boston Scientific, Merck, Novartis, Sanofi, and research support from AstraZeneca, GlaxoSmithKline, Luitpold, Merck, Novartis. P.Y.H. has received research support from the National Institutes of Health and Pfizer; honoraria received from Gilead. E.B. has received grant support from Duke University as Chair of the Heart Failure Network of the National Heart, Lung, and Blood Institute Heart Failure Network and from Merck and Company, Astra Zeneca, Novartis, Daiichi Sankyo, and Glaxo Smith Kline; and consulting fees from The Medicines Company and Theravance; personal fees for lectures from Medscape and Menarini International. He was also uncompensated for consultancies and lectures from Merck and Novartis. All other authors report no conflicts. Research reported in this publication was supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health under award numbers U10 HL084904, U10 HL110297, U10 HL110342, U10 HL110309, U10 HL110262, U10 HL110338, U10 HL110312, U10 HL110302, U10 HL110336, and U10 HL110337.
Funding Information:
Research reported in this publication was supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health under award numbers U10 HL084904, U10 HL110297, U10 HL110342, U10 HL110309, U10 HL110262, U10 HL110338, U10 HL110312, U10 HL110302, U10 HL110336, and U10 HL110337.
Publisher Copyright:
© 2019 Elsevier Inc.
PY - 2020/5
Y1 - 2020/5
N2 - Background: Diastolic dysfunction (DD) is common and occurs at an earlier age among human immunodeficiency virus-infected (HIV+) individuals, but the mechanisms and consequences of DD among HIV+ individuals are unclear. Methods and Results: The Characterization of Heart Function on Antiretroviral Therapy (CHART) study was a multicenter cross-sectional case-control study of treated and virally suppressed HIV+ individuals with (DD+) and without DD (DD−). All patients had normal ejection fraction (>50%), no significant valvular disease, and no history of coronary revascularization or persistent atrial fibrillation. Overall, 94 DD+ and 101 DD− patients were included. DD+ patients were older with higher body mass index (BMI) and more likely to have hypertension, renal dysfunction, and dyslipidemia. Groups were similar with respect to sex, race, CD4 count, and HIV RNA copies. N-terminal pro-B-type natriuretic peptide levels (median 36 [23, 85] vs 26 [12, 49] pg/mL, P < .01) and high-sensitivity troponin I (3.6 [2.6, 5.1] vs 2.5 [1.8, 3.5] pg/mL, P < .01) were higher among DD+ patients. The latter had similar left atrial size, but increased stiffness (conduit strain: 23.5 [17.5, 36.9] vs 30.0 [22.9, 37.0], P < .01) and impaired relaxation (reservoir strain: 39.7 [32.0, 58.0] vs 45.9 [37.0, 60.6], P = .04). On cardiac magnetic resonance, the prevalence of focal fibrosis was higher among DD+ patients (19.0% vs 5.3%, P < .01). DD+ patients demonstrated higher levels of carboxyl-terminal telopeptide of collagen type I (P = .04), and trends toward higher interleukin-6 and oxidized low-density lipoprotein levels (P ≤. 08). Kansas City Cardiomyopathy Questionnaire physical limitation (87.1±21.4 vs 93.1±18.1, P = .01) and symptom frequency scores were lower among DD+ patients (86.0±21.5 vs 92.5±16.8, P = .01). Conclusions: In this contemporary HIV+ population receiving antiretroviral therapy, DD was associated with multiple alterations in cardiac structure and function, including myocardial fibrosis and left atrial abnormalities, and worse quality of life. Further studies are needed to assess longitudinal changes in these parameters and their potential as therapeutic targets to prevent progressive cardiac remodeling and dysfunction in HIV.
AB - Background: Diastolic dysfunction (DD) is common and occurs at an earlier age among human immunodeficiency virus-infected (HIV+) individuals, but the mechanisms and consequences of DD among HIV+ individuals are unclear. Methods and Results: The Characterization of Heart Function on Antiretroviral Therapy (CHART) study was a multicenter cross-sectional case-control study of treated and virally suppressed HIV+ individuals with (DD+) and without DD (DD−). All patients had normal ejection fraction (>50%), no significant valvular disease, and no history of coronary revascularization or persistent atrial fibrillation. Overall, 94 DD+ and 101 DD− patients were included. DD+ patients were older with higher body mass index (BMI) and more likely to have hypertension, renal dysfunction, and dyslipidemia. Groups were similar with respect to sex, race, CD4 count, and HIV RNA copies. N-terminal pro-B-type natriuretic peptide levels (median 36 [23, 85] vs 26 [12, 49] pg/mL, P < .01) and high-sensitivity troponin I (3.6 [2.6, 5.1] vs 2.5 [1.8, 3.5] pg/mL, P < .01) were higher among DD+ patients. The latter had similar left atrial size, but increased stiffness (conduit strain: 23.5 [17.5, 36.9] vs 30.0 [22.9, 37.0], P < .01) and impaired relaxation (reservoir strain: 39.7 [32.0, 58.0] vs 45.9 [37.0, 60.6], P = .04). On cardiac magnetic resonance, the prevalence of focal fibrosis was higher among DD+ patients (19.0% vs 5.3%, P < .01). DD+ patients demonstrated higher levels of carboxyl-terminal telopeptide of collagen type I (P = .04), and trends toward higher interleukin-6 and oxidized low-density lipoprotein levels (P ≤. 08). Kansas City Cardiomyopathy Questionnaire physical limitation (87.1±21.4 vs 93.1±18.1, P = .01) and symptom frequency scores were lower among DD+ patients (86.0±21.5 vs 92.5±16.8, P = .01). Conclusions: In this contemporary HIV+ population receiving antiretroviral therapy, DD was associated with multiple alterations in cardiac structure and function, including myocardial fibrosis and left atrial abnormalities, and worse quality of life. Further studies are needed to assess longitudinal changes in these parameters and their potential as therapeutic targets to prevent progressive cardiac remodeling and dysfunction in HIV.
KW - Antiretroviral therapy
KW - diastolic dysfunction
KW - human immunodeficiency virus
KW - myocardial fibrosis
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U2 - 10.1016/j.cardfail.2019.10.011
DO - 10.1016/j.cardfail.2019.10.011
M3 - Article
C2 - 31682908
AN - SCOPUS:85076578578
SN - 1071-9164
VL - 26
SP - 371
EP - 380
JO - Journal of Cardiac Failure
JF - Journal of Cardiac Failure
IS - 5
ER -