We assessed the relation of inflammatory and coagulation biomarkers with electrocardiographic
(ECG) evidence of myocardial ischemia. High-sensitivity C-reactive protein (hsCRP),
interleukin-6 (IL-6), and D-dimer levels were measured at study entry for 3,085 human
immunodeficiency virus-infected participants (mean age 44 years; 26.4% women; 24.6%
black) in the Strategies for Management of Antiretroviral Therapy trial. Logistic
regression models were used to examine the associations of these biomarkers with prevalent
and incident myocardial ischemia. The latter analyses were performed for 1,411 participants
who were randomly assigned to receive continuous antiretroviral therapy during follow-up
to suppress the human immunodeficiency virus viral load and had ≥1 ECG reading during
the follow-up period. The median hsCRP, IL-6, and D-dimer level was 1.65 μg/ml (interquartile
range 0.69 to 4.11), 1.60 pg/ml (interquartile range 1.00 to 2.75), and 0.18 μg/ml
(interquartile range 0.11 to 0.32), respectively. At baseline, the prevalence of major
or minor Q-QS or ST-T ECG abnormalities was 18.6%. The biomarker levels were associated
with prevalent major or minor ischemic abnormalities on the univariate analyses; however,
adjustment for traditional risk factors attenuated these associations. The adjusted
odds ratio for major or minor ischemic abnormalities and 95% confidence intervals
for the greatest versus lowest quartiles was 1.3 (95% confidence interval 0.9 to 1.7)
for hsCRP, 1.0 (95% confidence interval 0.7 to 1.3) for IL-6, and 1.1 (95% confidence
interval 0.9 to 1.5) for D-dimer. During a median follow-up of 2.3 years, new definite
or probable ischemic ECG abnormalities developed in 11.7% of participants receiving
continuous antiretroviral therapy. Biomarker levels were not associated with incident
abnormalities on unadjusted or adjusted analyses. In conclusion, higher levels of
hsCRP, IL-6, and D-dimer were not associated with ischemic ECG abnormalities. Elevated
biomarker levels and ECG abnormalities indicating myocardial ischemia might reflect
different risk pathways for cardiovascular disease.
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Article info
Publication history
Published online: January 07, 2013
Accepted:
November 14,
2012
Received in revised form:
November 14,
2012
Received:
August 27,
2012
Footnotes
This study was supported by grants U01AI068641, U01AI042170, and U01AI046362 from the National Institute of Allergy and Infectious Disease, National Institutes of Health (Bethesda, Maryland); Mr. Miller was supported by grant AI007432-15 from the National Institute of Allergy and Infectious Disease, National Institutes of Health (Bethesda, Maryland).
See page 763 for disclosure information.
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© 2013 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
