CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 7, August 2013
272
AFRICA
Our results suggest that elevated levels of hs-CRP are
manifestations of atherosclerotic plaque instability and a sign
of increased risk of acute coronary events. In the study by
Ghazala and Mansoor, they confirmed that inflammation can
be implicated in the transformation of stable coronary plaque
to unstable plaques, rupture and thrombus.
29
Kadi
et al
. found
in patients with stable coronary artery disease and insufficient
coronary circulation, serum hs-CRP levels were higher than in
patients with adequate coronary collateral circulation.
30
Zhumin
et al
. found that the values of hs-CRP were higher in patients
with unstable carotid atherosclerotic plaques than in patients
with stable plaques or without plaques.
31
According to Ridker
et al
., hs-CRP has been established as an
independent risk factor for future cardiovascular events. It adds
prognostic information to the Framingham risk score and at all
levels of the metabolic syndrome.
32
The findings of our study
support this opinion.
We believe that the presumed pathophysiological mechanism
of atherosclerotic plaque destabilisation in patients with stable
coronary artery disease could be via activation of themacrophages
in plaques, which leads to secretion of metalloproteinases,
cathepsins and collagenases. These enzymes digest the fibrous
cap, particularly at the edges, causing the cap to thin and
ultimately rupture and initiate plaque thrombosis.
Pre-interventional intravascular ultrasound studies of patients
with acute myocardial infarction have shown significantly more
plaque rupture in patients with elevated hs-CRP levels, suggesting
that this may reflect the inflammatory activity of a ruptured
plaque and/or the plausible intensification of focal inflammatory
processes that destabilise vulnerable plaques.
33
Results from this
study have shown that measurement of CIMT should be used
as a tool to identify individuals with coronary atherosclerosis,
but when these changes are associated with increased levels of
hs-CRP (in the absence of other causes for the increase in hs-CRP
levels) then destabilisation of stable CAD should be considered.
The small sample size was a major limitation of this
study. Larger epidemiological studies are needed to clarify the
diagnostic value of CIMT to identify CAD, and the usefulness of
hS-CRP for the prediction of acute coronary syndromes in cases
with increased CIMT.
Conclusion
Measurement of CIMT is a non-invasive predictor of CAD but
it has little prognostic value in predicting CAD events. While
hs-CRP is a good predictor of acute coronary events, normal
values of hs-CRP do not exclude the presence of stable CAD.
The determination of hs-CRP and CIMT together could help in
the diagnosis of CAD, and for predicting coronary events. We
support the consensual statements for the assessment of CIMT
and hs-CRP in individuals who are traditionally considered to be
at moderate cardiovascular risk.
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