The relation between C-reactive protein (CRP) and coronary atherosclerosis is not
fully understood. This study aims to investigate the associations among high-sensitivity
CRP, coronary plaque burden, and the presence of high-risk coronary lesions as measured
by intravascular ultrasound (IVUS) and 1-year cardiovascular outcome. Between 2008
and 2011, grayscale and virtual histology IVUS imaging of a nonculprit coronary artery
was performed in 581 patients who underwent coronary angiography for acute coronary
syndrome (ACS) or stable angina pectoris. Primary end point consisted of 1-year major
adverse cardiac events (MACEs), defined as all-cause mortality, ACS, or unplanned
coronary revascularization. After adjustment for established cardiac risk factors,
baseline CRP levels were independently associated with higher coronary plaque burden
(p = 0.002) and plaque volume (p = 0.002) in the imaged coronary segment. CRP was
also independently associated with the presence of large lesions (plaque burden ≥70%;
p = 0.030) but not with the presence of stenotic lesions (minimal luminal area ≤4.0 mm2; p = 0.62) or IVUS virtual histology-derived thin-cap fibroatheroma lesions (p =
0.36). Cumulative incidence of 1-year MACE was 9.7%. CRP levels >3 mg/L were independently
associated with a higher incidence of MACE (hazard ratio 2.17, 95% confidence interval
[CI] 1.01 to 4.67, p = 0.046) and of all-cause mortality and ACS only (hazard ratio
3.58, 95% CI 1.04 to 13.0, p = 0.043), compared with CRP levels <1 mg/L. In conclusion,
in patients who underwent coronary angiography, high-sensitivity CRP is a marker of
coronary plaque burden but is not related to the presence of virtual histology-derived
thin-cap fibroatheroma lesions and stenotic lesions. CRP levels >3 mg/L are predictive
for adverse cardiovascular outcome at 1 year.
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Article info
Publication history
Published online: August 26, 2014
Accepted:
August 5,
2014
Received in revised form:
August 5,
2014
Received:
June 1,
2014
Footnotes
Cheng and Oemrawsingh contributed equally to this work.
The ATHEROREMO-IVUS study was funded by the European Commission, Seventh Framework Program, Brussels, Belgium, theme FP7-HEALTH-2007-2.4.2-1. JMC and RMO are supported by grant numbers NHS2009B091 and NHS2007B012, respectively, from The Netherlands Heart Foundation, Den Haag, The Netherlands.
See page 1503 for disclosure information.
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© 2014 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
