Highlights
- •Monocyte-platelet aggregates (MPA) are a robust marker of platelet activity and inflammatory monocytes.
- •MPA are higher in patients with cardiovascular disease.
- •MPA are highest in patients with peripheral artery disease (PAD).
Abstract
Background and aims
Platelets are a major culprit in the pathogenesis of cardiovascular disease (CVD).
Circulating monocyte-platelet aggregates (MPA) represent the crossroads between atherothrombosis
and inflammation. However, there is little understanding of the platelets and monocytes
that comprise MPA and the prevalence of MPA in different CVD phenotypes. We aimed
to establish (1) the reproducibility of MPA over time in circulating blood samples
from healthy controls, (2) the effect of aspirin, (3) the relationship between MPA
and platelet activity and monocyte subtype, and (4) the association between MPA and
CVD phenotype (coronary artery disease, peripheral artery disease [PAD], abdominal
aortic aneurysm, and carotid artery stenosis).
Methods and results
MPA were identified by CD14+ monocytes positive for CD61+ platelets in healthy subjects and in patients with CVD. We found that MPA did not
significantly differ over time in healthy controls, nor altered by aspirin use. Compared
with healthy controls, MPA were significantly higher in CVD (9.4% [8.2, 11.1] vs. 21.8% [11.5, 44.1], p < 0.001) which remained significant after multivariable adjustment (β = 9.1 [SER = 3.9],
p = 0.02). We found PAD to be associated with a higher MPA in circulation (β = 19.3
[SER = 6.0], p = 0.001), and among PAD subjects, MPA was higher in subjects with critical limb ischemia
(34.9% [21.9, 51.15] vs. 21.6% [15.1, 40.6], p = 0.0015), and significance remained following multivariable adjustment (β = 14.77
(SE = 4.35), p = 0.001).
Conclusions
Circulating MPA are a robust marker of platelet activity and monocyte inflammation,
unaffected by low-dose aspirin, and are significantly elevated in subjects with CVD,
particularly those with PAD.
Graphical abstract
Graphical Abstract
Keywords
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Article Info
Publication History
Published online: January 02, 2019
Accepted:
December 20,
2018
Received in revised form:
November 2,
2018
Received:
September 4,
2018
Identification
Copyright
© 2018 Published by Elsevier B.V.
