The Facts About Inflammatory Markers:
C-Reactive Protein (CRP) and Lipoprotein-associated phospholipase
AS (Lp-PLA2)
Over the past decade, researchers have tried to improve cardiovascular
disease risk prediction (Pearson, et al., 2003; Pepys &
Hirschfield, 2003; Ridker, 2003; Yeh & Willerson, 2003).
Traditional risk factors, such as high cholesterol, high blood
pressure, physical inactivity, and smoking have been used
to determine the relative risk of an individual with respect
to their cardiovascular disease risk. However, this method
does not allow for the ability to identify individuals who
do not exhibit any of the traditional risk factors such as
high blood pressure or high cholesterol. This concern triggered
researchers to examine other potential means for predicting
elevated relative risks for cardiovascular disease and stroke.
According to researchers, conventional risk factors account
for approximately 50% to 75% of cardiovascular conditions,
such as heart attack, angina, and stroke (Mayo Clinic, 2003).
This leaves a significant number who experience cardiovascular
events that occur in the absence of the traditional risk factors.
By uncovering other methods of predicting these unexplained
health problems, healthcare professionals can develop additional
strategies for prevention and treatment.
A number of studies have recently focused on examining inflammatory
markers and their potential predictive and prognostic clinical
importance (Libby, Ridker, & Maseri, 2002). In the past
ten years, researchers have accumulated compelling evidence
that inflammatory markers may be the means of augmenting risk
stratification in patients who are borderline (Pearson, Mensah,
et al., 2003). These inflammatory markers can provide support
for or against primary prevention or secondary prevention
strategies. In addition, they might be useful in monitoring
the effects of those treatment strategies. In fact, researchers
are considering inflammatory markers as emerging risk factors,
which potentially can be used as an optional measurement tool
for improving predictive estimates (Expert Panel on Detection,
Evaluation, and Treatment of High Blood Cholesterol in Adults,
2001; Ridker, 2003; Schwartz, et al, 2003; Yeh & Willerson,
2003). Two the inflammatory markers that have recently moved
to the forefront and gained considerable attention are C-reactive
Protein (CRP) and Lipoprotein-associated phospholipase A2
(Lp-PLA2).
CRP is an acute phase protein produced by the liver as part
of the immune system response, and thought to only be present
during episodes of acute systemic inflammation (Mayo Clinic,
2003: National Institutes of Health [NIH], 2003; Yeh &
Willerson, 2003). It is referred to as an inflammatory marker
because it is produced as a response to any inflammation in
the body. CRP has no specificity in differentiating disease
entities, however has risen as one of the more powerful predictors
for cardiovascular disease (Yeh & Willerson, 2003).
Researchers have found in empirical studies that high levels
of CRP in the blood are positively correlated with increased
incidents of myocardial infarction, stroke, cardiovascular
disease, and even sudden cardiac death (Mayo Clinic, 2003;
Ridker, 2003). In fact, some researchers feel that CRP might
become a better predictor of cardiovascular disease than current
traditional risk factors (Mayo Clinic, 2003; Pepys & Hirschfield,
2003; Yeh & Willerson, 2003). Moreover, elevated levels
of CRP have also been associated with other metabolic diseases,
such as type 2 diabetes and metabolic syndrome (Huerta &
Nadler, 2002; Ridker, Buring, et al., 2003). The results of
these studies suggest that baseline CRP levels can have clinical
significance regarding predicting future vascular risks.
Lp-PLA2, also known as platelet activating factor acetylhydrolas
(PAF-AH) is classified as an independent member of the phospholipase
A2 enzyme family (Dada, et al., 2002; Rackard, et al, 2000).
Lp-PLA2 circulates in the blood and binds primarily to low-density
lipoprotein cholesterol (LDL). Lp-PLA2 is considered a potent
pro-inflammatory mediator involved in the vascular inflammation
process. It has been suggested that Lp-PLA2 is partly responsible
for atherosclerosis and therefore contributes to the development
of cardiovascular disease (Ballantyne, et al, 2003; Packard,
et al, 2000). CRP and Lp-PLA2 are not linked to one another.
It is thought that these are independent predictors of elevated
cardiovascular disease risk. The following will review the
information found in the literature regarding both CRP and
Lp-PLA2.
©2004 Aerobics and Fitness
Association of America
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