© 1997 American Heart Association, Inc.
Articles |
Circulating Vascular Cell Adhesion Molecule-1 Correlates With the Extent of Human Atherosclerosis in Contrast to Circulating Intercellular Adhesion Molecule-1, E-Selectin, P-Selectin, and Thrombomodulin
From the Departments of Cardiology (K.P., T.N., T.W., W.K., C.B.), Endocrinology (P.N.), Gastroenterology (M.B.), Vascular Surgery (A.W., J.A.), and Medical Biometry (C.C.), University of Heidelberg, Germany.
Correspondence to Dr Karlheinz Peter, Internal Medicine III, University of Heidelberg, Bergheimer Straße 58, 69115 Heidelberg, Germany. E-mail kpeter{at}krzmail.krz.uni-heidelberg.de
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Abstract |
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Abstract Secondary prevention of atherosclerosis, especially before the onset of symptoms, appears desirable and could be possible with a serum marker detecting atherosclerosis. Circulating, shedded forms of adhesion molecules may serve as such because their expression is upregulated in atherosclerotic plaques. In 52 patients with peripheral arterial vascular disease (Fontaine class IIa, 7 patients; class IIb, 29 patients; and class III, 16 patients), the extent of atherosclerosis was evaluated on the basis of angiograms of a large portion of the arterial system. The area diseased by atherosclerosis was determined by the percentage of vessel wall irregularities of the following calculated segments: aorta (distal from the kidney arteries), common iliac artery, external iliac artery, common femoral artery, lateral circumflex femoral artery, and popliteal artery. The maximal surface area that could exhibit atherosclerotic changes was 250 cm2. The serum concentration of circulating vascular cell adhesion molecule-1 (VCAM-1) correlated with the extent of atherosclerosis (r=.8, P<.001). In contrast, circulating intercellular adhesion molecule-1, E-selectin, P-selectin, and thrombomodulin (as markers for endothelial cell damage) did not correlate with the extent of atherosclerosis. Furthermore, circulating VCAM-1 could be used to indicate stages of atherosclerosis with a high degree of statistical significance. The potential bias of factors such as age, diabetes mellitus, hypercholesterolemia, arterial hypertension, renal failure, and history of myocardial infarction on the correlation of circulating VCAM-1 with the extent of atherosclerosis could be excluded by multivariate analysis. These findings suggest an important role of VCAM-1 in atherosclerosis and may serve as the basis for further evaluation of circulating VCAM-1 as a potential serum marker for atherosclerosis.
Key Words: VCAM-1 • atherosclerosis • adhesion molecules • serum marker
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Introduction |
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In the early stages of atherogenesis, aggregations of lipid-rich macrophages and T lymphocytes can be demonstrated within the intima.1 The adhesion of leukocytes on endothelial cells and their transendothelial migration are mediated by adhesion molecules on the endothelial cell membrane that mainly belong to two protein families: the selectins and adhesion molecules of the immunoglobulin superfamily.2 For two members of the first group (E-selectin and P-selectin) and two members of the latter group (ICAM-1 and VCAM-1), expression has been demonstrated in various cell types forming the atherosclerotic plaque, for example, endothelial cells, vascular smooth muscle cells, and macrophages.3 4 5 6 7 8 Especially in intimal neovasculature, the expression of VCAM-1, ICAM-1, and E-selectin is upregulated.8 Circulating, shedded forms of adhesion molecules have been described that are probably generated by cleavage at a site close to the membrane insertion.9 The amount of soluble ICAM-1 and E-selectin released has been demonstrated to be directly correlated with the surface expression of ICAM-1 and E-selectin in endothelial cells in culture.10 Furthermore, a correlation of circulating VCAM-1 with VCAM-1 mRNA expression in human atherosclerotic aorta has been reported.11 On the basis of these findings, we hypothesized that serum levels of circulating adhesion molecules can provide information on human atherosclerosis.
In two previous reports,12 13 patients with ischemic heart disease and pAVD have been compared with asymptomatic control subjects with respect to their serum levels of circulating adhesion molecules. In those studies, circulating P-selectin and ICAM-1 were elevated in the patient groups compared with the control subjects. Elevated circulating VCAM-1 levels have been reported in patients with an atherosclerotic aorta compared with asymptomatic control subjects.11 Furthermore, patients with dyslipidemia, in whom advanced atherosclerosis can be expected, demonstrated elevated levels of circulating adhesion molecules.14 Thus, there are reports supporting the hypothesis that serum levels of circulating adhesion molecules may provide information on atherosclerosis. The present study focuses on the question of whether there is a correlation between the extent of human atherosclerosis and serum levels of circulating adhesion molecules.
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Methods |
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Patients
Patients (n=52) were recruited from the Department of Internal Medicine and Vascular Surgery at the University of Heidelberg. All patients demonstrated symptoms of pAVD. The following classification of pAVD according to Fontaine was used: class I, asymptomatic pAVD; class IIa, mild claudication with a walking distance >200 m; class IIb, severe claudication with a walking distance <200 m; class III, rest pain; and class IV, gangrene. The patients were distributed as follows: class IIa, 7; class IIb, 29; and class III, 16. Patients with Fontaine class IV were not included in the study because their inflammatory status might have interfered with the serum concentrations of circulating adhesion molecules. Because malignancies can influence levels of circulating adhesion molecule,15 patients with malignancies were excluded. Patient characteristics are described in Table 1
. The study was performed as a cross-sectional
study, and all angiographies were done for routine diagnostic purposes
within 7 days after blood drawing. Hospitalized patients and employees
from the Department of Internal Medicine who were without symptoms of
pAVD as well as without abnormalities on physical examination were
recruited as asymptomatic control subjects. Informed written consent
was obtained from every individual for the drawing of 10 mL venous
blood.
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Quantification of Human Atherosclerosis
Because clinical staging of pAVD does not necessarily correlate
with the extent of human atherosclerosis, the quantification of
atherosclerosis was based on angiograms of the abdominal aorta and
pelvic and leg arteries. Thus, a large portion of the human arterial
system could be evaluated directly by use of defined criteria. To allow
for the comparison of patients of different sizes and weights, a mean
area of the evaluated arteries was determined as follows: the mean
length (l) and radius (r) of arterial segments of
all 52 evaluated patients with pAVD were determined on the angiograms,
and the mean internal vessel surface area of each segment was
calculated according to 2
rxl (total of all
segments=250 cm2; see Fig 1). The percentage
of irregular surface on both sides of the vessel in the angiogram (one
view) was determined by two independent observers, and the
atherosclerotic area was calculated as the percentage of the average
surface area of the segments depicted in Fig 1. These values do not
establish an absolute measurement of atherosclerosis, but they can be
used for the comparison of different extents of atherosclerosis.
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Determination of Serum Levels of Circulating Adhesion Molecules,
Thrombomodulin, and Fibrinogen
Fasting venous blood was obtained after nontraumatic
venipuncture and was allowed to clot at room temperature for 30
minutes. Serum was withdrawn after centrifugation in a bench-top
centrifuge for 15 minutes at 3000 rpm and was stored at -20°C. In a
blinded manner, ELISAs were used to determine serum concentrations of
VCAM-1 (capture MAB, BBA22; detection MAB, BBIG-V3/1I10), ICAM-1
(capture MAB, BBIG-12/14C11; detection MAB, BBIG-I1/11C81), E-selectin
(capture MAB, BBA2; detection MAB, BBIG-I5/10C10), P-selectin
(capture MAB, BBA30; detection with polyclonal sheep antibody; British
Biotechnology), and thrombomodulin (Diagnostica Stago).16
According to the commercial suppliers, no cross-reactivity between the
above ELISAs was observed. The mean value of two determinations in each
patient was used for the statistical analysis. Standard curves based on
six reference concentrations were created according to the
manufacturer's recommendations. Intra-assay and interassay precision
were controlled in each assay for patients and control subjects. In
both, the variation was <7.5%. In three patients, sera drawn on 7
consecutive days were tested for reproducibility. The variation of
circulating VCAM-1 was within the range of 17%. Fibrinogen was
determined according to the method of Clauss (Baxter Diagnostics
AG).
Statistical Analysis
The relationship between circulating adhesion molecules and the
determined atherosclerotic area was estimated by correlation and
multiple linear regression analysis. To assess for statistical
significance, Student's t test was applied (null
hypothesis: no correlation). For the comparison of patient
characteristics, the Mann-Whitney test was performed for continuous
data and Fisher's exact test for categorical data. For age-matched
comparisons, the Mann-Whitney test for matched pairs was applied. The
95% confidence interval for predicting the atherosclerotic area from
the serum level of circulating VCAM-1 was calculated with the use of
Statistical Analysis System software (SAS Institute Inc).
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Results |
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Serum concentrations of circulating VCAM-1 correlated with the determined atherosclerotic area of angiographically examined patients (Fig 2
; r=.8, P<.001,
y=7.3x+294). In contrast, for circulating ICAM-1,
E-selectin, and P-selectin, no correlation with the determined
atherosclerotic area could be demonstrated (Fig 3). The
circulating part of the endothelial cell surface receptor
thrombomodulin, as a marker of endothelial cell damage, also did not
demonstrate a correlation with the determined atherosclerotic area.
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To further evaluate the possibility of grading the extent of
atherosclerosis by circulating VCAM-1 levels, the median serum
concentration (800 ng/mL) of circulating VCAM-1 was used as an
arbitrary cutoff point, and two subgroups were thus established
comprising 26 patients each (Table 2). The
atherosclerotic area in these two groups was significantly different
(Fig 4 and Table 2; 46±25 versus 110±39
cm2; P<.001). The two patient groups did not
differ significantly in levels of circulating ICAM-1, E-selectin,
P-selectin, or thrombomodulin. To evaluate a potential bias on
circulating VCAM-1 levels by the unequal distribution of factors such
as diabetes mellitus, arterial hypertension, hypercholesterolemia,
history of myocardial infarction, and elevation of serum creatinine, a
multivariate regression analysis was performed. After adjustment for
these potential covariates, the correlation between circulating VCAM-1
and the atherosclerotic area was still highly significant
(P<.001). None of the potential covariates reached a
significance level of .05. Thus, the correlation between circulating
VCAM-1 and the atherosclerotic area was not due to a bias of the
unbalanced distribution of the above factors.
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The subgroups in Table 2
differed in age. This difference was not
significant, but a clear trend could be seen. An increase of the
overall atherosclerotic burden is expected with increasing age.
Nevertheless, there may be a bias of increasing VCAM-1 levels with
increasing age. However, patients with angiographically similar
atherosclerosis did not demonstrate an increase of circulating VCAM-1
with increasing age. To further exclude a potential bias of age, 15
age-matched pairs selected from the two patient groups in Table 2 were
compared, with a mean atherosclerotic area of 48.5±25.8
cm2 for circulating VCAM-1 <800 ng/mL and 106.7±30.5
cm2 for circulating VCAM-1 >800 ng/mL
(P<.001). This result is not significantly different from
the overall comparison of the patient groups in Table 2. Furthermore,
age as a potential covariate in a multivariate regression analysis did
not reach statistical significance (P=.3). Thus, the
differences in age between the two groups in Table 2 were probably a
result of age-related atherosclerosis, and age per se does not seem to
determine the circulating VCAM-1 level.
When values of the atherosclerotic area and circulating VCAM-1 were
used to divide the 52 pAVD patients into two subgroups with 26 patients
each, a serum concentration of circulating VCAM-1 >800 ng/mL indicated
an atherosclerotic area >75 cm2, with a sensitivity and a
specificity of 88.5% each. Additionally, the individual prediction of
the atherosclerotic area based on the circulating VCAM-1 level
demonstrated a high statistical confidence (95% confidence interval
for individual prediction; Fig 2).
For the present study, the ideal control group would be a group of
individuals demonstrating no atherosclerotic changes in angiograms. But
for ethical reasons, angiography on asymptomatic individuals cannot be
performed at our institution. Individuals who do not demonstrate
symptoms of pAVD or pathological findings on physical examination can
be used with limitations as a control group and were therefore compared
with patients with proven advanced atherosclerosis (>75
cm2 atherosclerotic area). Two groups of individuals were
evaluated: an age-matched group (matched to 26 patients with an
atherosclerotic area >75 cm2) and a group of younger
individuals (age, 32±7 years; n=67) with an expected low
atherosclerotic burden. Circulating VCAM-1 in the first asymptomatic
control group was significantly different from the group with
angiographically proven advanced atherosclerosis (845±248 versus
1157±552 ng/mL; P<.01, 26 age-matched pairs; see Fig 5). The second group of younger individuals demonstrated
low circulating VCAM-1 serum concentrations (581±127 ng/mL) that were
significantly different from the serum concentrations of the group with
proven advanced atherosclerosis (>75 cm2 atherosclerotic
area; 1157±552 ng/mL, n=26, P<.001) as well as from the
older asymptomatic control group (845±248 ng/mL, n=26,
P<.01; see Fig 5). Thus, individuals who were not
angiographically defined in their extent of atherosclerosis but were
expected to have a low extent of atherosclerosis demonstrated
significantly lower circulating VCAM-1 levels than a group of patients
with angiographically proven advanced atherosclerosis. Furthermore, in
the control group with young individuals, in whom a low atherosclerotic
burden was expected, the circulating VCAM-1 level was lower than in the
older asymptomatic control group.
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There was no correlation between Fontaine class and the overall atherosclerotic area in the evaluated angiograms (class IIa, 101±36.5 cm2; class IIb, 120.5±71.5 cm2; and class III, 71±45.5 cm2). This finding reflects the fact that it is not the overall atherosclerotic burden but the existence of arterial stenoses or occlusions that determines the Fontaine class. The circulating VCAM-1 levels demonstrate a distribution similar to the angiographically determined atherosclerotic area (class IIa, 731±101 ng/mL; class IIb, 984±563 ng/mL; and class III, 684±260 ng/mL). Thus, circulating VCAM-1 did not reflect clinical stages of pAVD, but at the same time, the Fontaine classification was not reflected in the extent of atherosclerosis in the evaluated angiograms.
Because inflammatory disease in patients can increase serum
concentrations of circulating adhesion molecules,17 the
serum concentration of C-reactive protein, the blood sedimentation
rate, and the leukocyte counts were determined. Neither a correlation
of these parameters with circulating VCAM-1 nor differences in the
distribution between the two established groups (Table 2) were found.
Because severe renal dysfunction may cause a retention of circulating
adhesion molecules, patients with serum creatinine concentrations >2.0
mg/dL were not included in the present study. The nine patients (Table 2) with mild elevation of serum creatinine who were included did not
demonstrate a high level of the evaluated circulating molecules in
general, arguing against a retention of the evaluated circulating serum
molecules.
Fibrinogen levels were assessed in 40 of the evaluated patients. A
slight trend, which was not statistically significant, toward a higher
fibrinogen level in patients with a higher extent of atherosclerosis
could be demonstrated (Fig 3D).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Serum levels of circulating adhesion molecules were evaluated for a correlation with the extent of human atherosclerosis. On the basis of angiograms of the abdominal aorta and pelvic and leg arteries, the extent of atherosclerosis of a large part of the human arterial system could be quantified. The serum concentrations of the adhesion molecules VCAM-1, ICAM-1, E-selectin, and P-selectin were determined. Of these, circulating VCAM-1 demonstrates a high correlation with the extent of human atherosclerosis. This finding is important in two respects: first, it suggests an important role of VCAM-1 in atherosclerosis, and second, it may be the basis for further evaluation of circulating VCAM-1 as a potential serum marker for atherosclerosis.
Several reports suggest an important role of VCAM-1 in atherogenesis.
The focal expression of VCAM-1 on endothelial cells has been
demonstrated in diet-induced atherogenesis in rabbits, even before the
accumulation of macrophages.3 4 For atherosclerotic
plaques in humans, several studies demonstrate VCAM-1
expression.5 6 8 11 Whereas VCAM-1 expression in
endothelial cells covering atherosclerotic lesions is not always
found,18 the neovasculature and nonendothelial cells in
atherosclerotic plaques particularly seem to upregulate VCAM-1
expression.5 8 Furthermore, there is a striking
association between the degree of macrophage accumulation and
expression of VCAM-1 on neovasculature and nonendothelial cells in
human atherosclerotic plaques.8 Risk and protective
factors of atherosclerosis influence VCAM-1 expression in a way that
complements its potential role in atherogenesis.
Lysophosphatidylcholine, a component of atherogenic lipoproteins,
induces VCAM-1 expression and increases adhesion of monocytes on
endothelium in cell culture.19 Modified LDL and its
constituents augment cytokine-activated VCAM-1 expression in human
vascular endothelial cells.20 In contrast, HDL inhibits
cytokine-induced expression of endothelial cell adhesion
molecules.21 The finding that two therapeutic agents for
which a beneficial effect on atherosclerosis has been proposed
influence VCAM-1 expression on endothelial cells further suggests the
importance of VCAM-1 in atherogenesis. 
3 Fatty acids have been found
to decrease mRNA levels and surface expression of VCAM-1 in endothelial
cells.22 Aspirin inhibits induction of mRNA and cell
surface expression of VCAM-1 by tumor necrosis factor-
and thereby
inhibits monocyte adhesion on stimulated endothelial
cells.23 Furthermore, in contrast to ICAM-1, E-selectin,
and P-selectin, endothelial VCAM-1 can mediate leukocyte adhesion via
its sole interaction with the integrins
4ß1 or
4ß7,24 whereas E-selectin,
P-selectin, and ICAM-1 only mediate parts of the multistep adhesion
process.2 Thus, several observations suggest a dominant
role of VCAM-1 in atherogenesis compared with other adhesion
molecules.
P-selectin in resting platelets is stored in -granules and in
endothelial cells in Weibel-Palade bodies, which allows translocation
to the surface of both cell types within seconds after cell
stimulation.25 This mechanism may be the reason for an
increase in circulating P-selectin in acute syndromes such as coronary
spasm26 and unstable angina.27 Although
P-selectin, among other adhesion molecules, has been demonstrated on
endothelium covering atherosclerotic plaques,7 no
correlation with the extent of atherosclerosis could be observed in the
present study.
The circulating form of the endothelial cell surface receptor
thrombomodulin has been proposed as a marker of endothelial cell
damage.28 29 Nevertheless, no correlation between
circulating thrombomodulin and the atherosclerotic area was found. In
addition, the two established patient groups (Table 2) did not differ
significantly in circulating serum thrombomodulin. Thus,
atherosclerosis seems not to be associated with endothelial cell damage
detectable by measuring circulating thrombomodulin.
Cell surface expression of VCAM-1 has been demonstrated for several cell types, such as endothelial cells, smooth muscle cells, macrophages, nonendothelial cells in atherosclerotic plaques, and several others.8 30 As is the case with endothelial cells, it has been demonstrated for smooth muscle cells that cytokines can induce surface expression.31 The finding of O'Brien et al8 that the neovasculature and nonendothelial cells in atherosclerotic plaques rather than arterial luminal endothelial cells express VCAM-1 suggests that several cell types may contribute to circulating VCAM-1. Recently, it has been found that soluble forms of E-selectin and VCAM-1 can directly mediate angiogenesis,32 a mechanism that may be important in the context of our results and the formation of collateral vessels in atherosclerosis.
A recently published comparison between symptomatic pAVD patients and asymptomatic patients did not reveal significant differences in circulating VCAM-1 levels.12 However, asymptomatic patients may have hitherto asymptomatic atherosclerosis, which actually has been elegantly demonstrated for a high percentage of asymptomatic individuals by the use of ultrafast computed tomography.33 On the other hand, symptomatic patients may have a low atherosclerotic burden but nevertheless have a significant stenosis or an occlusion. The finding that the Fontaine classification does not correlate with the atherosclerotic area in the evaluated angiograms argues that clinical classification does not correlate with the overall atherosclerotic burden. Nevertheless, in comparisons between patients with proven advanced atherosclerosis and patients demonstrating no symptoms of pAVD or abnormalities on physical examination, a significant difference in the circulating VCAM-1 level can be demonstrated. Moreover, two asymptomatic control groups differing in age and thus probably differing in their atherosclerotic burden revealed significant differences in circulating VCAM-1 levels. Thus, the circulating VCAM-1 level may indicate hitherto asymptomatic atherosclerosis.
Our data are supported by a recently published study by Nakai et al11 demonstrating a higher serum concentration of circulating VCAM-1 in 13 patients with atherosclerotic aortic disease (circulating VCAM-1, 850±298 ng/mL; mean age, 64 years) compared with 40 healthy volunteers (494±94 ng/mL and 32 years, respectively). Additionally, the authors found a correlation between VCAM-1 mRNA expression and the concentration of circulating VCAM-1.11 The latter finding is important because this result suggests that the circulating VCAM-1 level can be used as an indicator of VCAM-1 expression in atherosclerotic plaques.
Elevated fibrinogen levels have been demonstrated to be related to the existence and extent of atherosclerosis.34 35 Consistent with these results, the present study describes a trend for higher fibrinogen levels with increasing extent of atherosclerosis. To obtain a statistically significant difference of fibrinogen levels between various extents of atherosclerosis, a large number of patients have been evaluated in the studies published by Levenson et al34 and Heinrich et al,35 which is probably needed to prove a significant correlation between fibrinogen and the angiographically determined atherosclerotic area.
In conclusion, the serum concentration of circulating VCAM-1 strongly correlates with the extent of human atherosclerosis and can be used to grade atherosclerosis. These findings suggest an important role of VCAM-1 in atherosclerosis and may be the basis for further evaluation of circulating VCAM-1 as a potential serum marker for atherosclerosis. Additional prospective studies, particularly large-scale studies, will be required to prove that circulating VCAM-1 can detect asymptomatic atherosclerosis and thus eventually serve as a diagnostic basis for early secondary prevention.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported by the German Research Foundation with a grant to Drs Peter and Bode (SFB 320: C/3). The expert technical assistance of Simone Bauer and Wolfram Schief is gratefully acknowledged.
Received March 21, 1996; accepted August 13, 1996.
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