(Circulation. 2000;101:2149.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Elevation of Tumor Necrosis Factor-
and Increased Risk of Recurrent Coronary Events After Myocardial Infarction
From the Leducq Center for Molecular and Genetic Epidemiology of Cardiovascular Disorders (P.M.R.), the Center for Cardiovascular Prevention (P.M.R.), Division of Cardiovascular Diseases (P.M.R., M.P., F.S., E.B.) and the Division of Preventive Medicine (P.M.R.), Brigham and Women’s Hospital; the Department of Pathology, Children’s Hospital Medical Center (N.R.), Harvard Medical School, Boston, Mass; and the Centre Universitaire de Sante de l’Estrie (S.L.), Sherbrooke, Quebec, Canada.
Correspondence to Dr Paul M. Ridker, Cardiovascular Diseases, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115.
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionReferences |
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Background—Levels of tumor necrosis factor-
(TNF-) increase with acute ischemia.
However, whether elevations of TNF- in the stable phase after
myocardial ischemia (MI) are associated with increased risk of
recurrent coronary events is unknown.
Methods and Results—A nested case-control design was used to
compare TNF- levels obtained an average of 8.9 months after initial
MI among 272 participants in the Cholesterol And Recurrent
Events (CARE) trial who subsequently developed recurrent nonfatal MI or
a fatal cardiovascular event (cases) and from an equal
number of age- and sex-matched participants who remained free of these
events during follow-up (controls). Overall, TNF- levels were
significantly higher among cases than controls (2.84 versus 2.57 pg/mL,
P=0.02). The excess risk of recurrent coronary
events after MI was predominantly seen among those with the highest
levels of TNF-, such that those with levels in excess of 4.17 pg/mL
(the 95th percentile of the control distribution) had an 
3-fold
increase in risk (RR=2.7, 95% CI 1.4 to 5.2, P=0.004).
Risk estimates were independent of other risk factors and were similar
in subgroup analyses limited to cardiovascular
death (RR=2.1) or to recurrent nonfatal MI (RR=3.2).
Conclusions—Plasma concentrations of TNF- are persistently
elevated among post-MI patients at increased risk for recurrent
coronary events. These data support the hypothesis that a
persistent inflammatory instability is present among stable
patients at increased vascular risk. Novel therapies designed to
attenuate inflammation may thus represent a new direction in
the treatment of MI.
Key Words: inflammation • myocardial infarction • tumor necrosis factor • atherosclerosis
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Tumor necrosis factor-
(TNF-) is a multifunctional
circulating cytokine derived from endothelial
and smooth muscle cells as well as macrophages associated with
coronary atheroma.1 2 3 Initially
identified as a factor that promoted hemorrhagic necrosis in
transplanted tumors,4 TNF- is involved in several
cardiovascular processes. For example, TNF- levels
are markedly elevated in advanced heart failure,5 6 and in
experimental settings, TNF- can produce left ventricular
dysfunction,7 pulmonary edema,8 9 and
cardiomyopathy.10 Furthermore, TNF-
is upregulated in the myocardium in response to both
transient myocardial ischemia and
reperfusion,11 12 13 14 and it has been hypothesized that
persistent overexpression of TNF- after ischemia might lead
to adverse coronary outcomes.15 However, although
some studies suggest that TNF- levels increase acutely with
coronary ischemia,16 17 it is unknown
whether elevations of TNF- measured several months after myocardial
infarction (MI) are associated with increased risk of recurrent
coronary events.
To address this hypothesis, we measured circulating TNF- levels
among post-MI patients enrolled in the Cholesterol And
Recurrent Events (CARE)18 trial who were prospectively
monitored for incident events of recurrent MI and coronary
death. Specifically, we evaluated post-MI TNF- levels in a nested
case-control analysis involving 272 CARE study participants who
subsequently suffered recurrent coronary events (cases) and
among 272 age- and sex-matched study participants who remained free of
recurrent coronary disease during a 5-year follow-up period
(controls).
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Study participants were patients enrolled in the CARE trial, a randomized, double-blind, placebo-controlled evaluation of 40 mg of pravastatin daily in the secondary prevention of cardiovascular disease conducted among 4159 individuals with a prior history of MI.17 Post-MI patients aged 21 to 75 years were eligible for CARE if the qualifying index event occurred 3 to 20 months before randomization and if they had left ventricular ejection fraction >25% and no clinical evidence of congestive heart failure. The primary end point of CARE was death due to coronary heart disease or nonfatal MI confirmed by creatine kinase enzyme measurements. Blood samples were collected in CARE during prerandomization visits designed primarily to determine baseline lipid levels; to be eligible for randomization, levels of total cholesterol were required to be <240 mg/dL and levels of LDL cholesterol were required to be between 115 and 175 mg/dL. On average, prerandomization blood samples were obtained 8.9 months after the qualifying acute MI. Samples were collected in EDTA and stored at -80°C until the time of analysis.
To evaluate the potential role of TNF- as a marker of
coronary risk in the CARE study population, prerandomization
blood samples were assayed for this cytokine among 272 study
participants who subsequently developed recurrent MI or death due to
coronary heart disease during study follow-up (cases) and from
272 age- and sex-matched study participants who remained free of
recurrent coronary events over a 5-year follow-up period
(controls). Stored plasma obtained from each case and control subject
was thawed and assayed for TNF- with a commercially available
quantitative enzyme immunoassay (Quantikine High Sensitivity human
TNF-, R&D Systems). This assay has a lower limit of detection for
TNF- of 0.1 pg/mL and a coefficient of variation between 5% and
8%. Blood specimens were analyzed in pairs, with the position
of the case specimen varied at random within pairs to reduce systematic
bias and limit interassay variability. Laboratory personnel were
unaware of case or control status.
The significance of any differences in baseline levels of TNF-,
total cholesterol, HDL cholesterol, LDL
cholesterol, triglycerides, and blood pressure
between case and control subjects was evaluated with the Student’s
t test; differences in proportions for other baseline
characteristics were evaluated with the 
2
statistic. Because preliminary data suggested that relationships
between TNF- and subsequent risk might be limited to those with high
levels in a nonlinear fashion, we conducted evaluations for evidence of
association between TNF- and recurrent coronary events among
study subjects with levels at baseline above or below the 50th, 75th,
90th, and 95th percentile cut points, as defined by the control values.
All analyses of risk took into consideration the matching
variables of age and sex. Adjusted estimates of risk were obtained
in conditional logistic regression models that further accounted
for HDL and LDL cholesterol and triglycerides
(lipid-adjusted analysis), as well as for smoking status
(current/past/never), body mass index, history of diabetes,
diastolic blood pressure, and randomized treatment
assignment (fully adjusted analysis). Additional
analyses were performed to compute risks across increasing
levels of TNF- in which the referent group was those with TNF-
levels at or below the 50th percentile of the control distribution. All
probability values are 2-tailed, and all confidence intervals were
computed at the 95% level.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Baseline characteristics of the study participants are shown in Table 1
. Due to matching, age
(60±9.3 years) and sex distributions (84% male) were similar between
case and control subjects. Other baseline characteristics of the study
participants are similar to those reported for the CARE trial as a
whole; as previously described,18 those individuals who
suffered recurrent coronary events were more likely to smoke,
suffer from diabetes, or to have a greater mean body mass index than
those who remained free of recurrent coronary events. At study
entry, 83% of patients in the CARE trial were taking oral aspirin.
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Overall, TNF- levels among study participants were normally
distributed (Figure 1). In these data,
which derive from frozen plasma samples, the range (95% of values
between 0.4 and 4.8 pg/mL), mean (2.7 pg/mL), and median (2.5 pg/mL)
TNF- levels were similar to those reported in prior population-based
studies based on fresh blood samples (range 0.5 to 4.1 pg/mL; data on
file, R&D Systems).
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Table 2 presents mean TNF- levels
among case and control subjects measured at entry into the CARE trial,
an average of 8.9 months after the qualifying initial MI. Overall,
TNF- levels were significantly higher among those in whom
coronary events subsequently developed than among those who
remained free of recurrent disease (2.84 versus 2.57 pg/mL,
P=0.02). As also shown in Table 2, these differences
were present in all low-risk subgroups evaluated, including
nonsmokers (2.91 versus 2.56 pg/mL, P=0.008), those without
diabetes (2.84 versus 2.54 pg/mL, P=0.02), those without
hypertension (2.87 versus 2.61 pg/mL, P=0.05), and those
without obesity (3.06 versus 2.62 pg/mL, P=0.02).
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Although mean TNF- levels were significantly higher among cases, the
excess risk of recurrent coronary events after MI was
predominantly seen among those with the highest levels of TNF-.
Specifically, the relative risks associated with TNF- levels
exceeding the 50th, 75th, 90th, and 95th percentiles of the control
distribution were 1.1 (P=0.7), 1.3 (P=0.2), 1.8
(P=0.02), and 2.7 (P=0.004) (Table 3). Thus, as illustrated in Figure 2, nearly all of the excess risk of
recurrent coronary events associated with post-MI TNF-
levels was among those with levels >4.17 pg/mL (the 95th percentile
cutoff point of the control distribution). Risk estimates were similar
in subgroup analyses limited to cardiovascular
death (RR=2.1, 95% CI 0.9 to 5.2) or to recurrent nonfatal MI (RR=3.2,
95% CI 1.5 to 6.7).
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We found no evidence of association in these data between TNF-
levels and total cholesterol or LDL
cholesterol, although small correlations were observed
between TNF- and HDL cholesterol (r=-0.10,
P=0.03) and triglycerides (r=0.12,
P=0.01). There were no significant correlations between
TNF- and systolic (r=0.02, P=0.7) or
diastolic (r=-0.03, P=0.5) blood
pressure, nor were there significant differences in mean TNF- levels
for those with and without diabetes (2.8 versus 2.7 pg/mL,
P=0.3) or for those who did and did not smoke (2.7 versus
2.6 pg/mL, P=0.4). As shown in Table 3
, adjustment
for lipid fractions had no impact on the relative risk of recurrent
coronary events associated with elevated levels of TNF-,
such that those with levels above the 95th percentile of the control
distribution had a lipid-adjusted relative risk 2.5 times higher than
those with lower levels of TNF- (95% CI 1.3 to 5.0,
P=0.007). Similarly, after further adjustment for body mass
index, diabetes, and blood pressure (in addition to the matching
variables of age and sex), an 2.5-fold increase in risk was
observed for those with high levels of TNF- (fully adjusted RR=2.5,
95% CI 1.3 to 5.1, P=0.008). Additional control for
randomized treatment assignment and for aspirin use had no effect on
these findings; however, because the observed excess risk associated
with TNF- was limited to those with the highest levels, the power
in this study to detect evidence of an interaction between
pravastatin use, levels of TNF- above the 95th
percentile, and the risk of recurrent clinical events is low.
In a previous report from this cohort,19 plasma levels of
C-reactive protein (CRP) and serum amyloid A (SAA), 2 nonspecific
markers of inflammation, were found to be elevated among those at risk
for recurrent coronary events. In these data, modest but
statistically significant correlations were observed between TNF-
levels and both log-normalized concentration of CRP (r=0.21,
P=0.001) and log-normalized concentration of SAA
(r=0.18, P=0.001). However, in
multivariate analyses that adjusted for both
CRP and SAA, the relative risk of recurrent coronary events
associated with elevated levels of TNF- remained statistically
significant (RR=2.3, 95% CI 1.1 to 4.5, P=0.02); by
contrast, the relationship between CRP or SAA and risk of recurrent
coronary events was no longer significant after adjustment for
TNF- (P=0.6 and 0.5 for CRP and SAA, respectively).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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These data indicate that plasma concentration of TNF-
, a
multifunctional cytokine with diverse systemic effects, is
elevated many months after MI among individuals at increased risk for
recurrent coronary events. Specifically, in these data for
which blood samples were obtained a minimum of 3 months after initial
infarction (mean 8.9 months), those individuals with the highest levels
of TNF- were found to have a 3-fold increase in the risk of
recurrent MI or coronary death (RR=2.7, 95% CI 1.4 to 5.2,
P=0.004). This increased risk was present in all
subgroups evaluated, including nonsmokers and those without obesity, 2
factors known to increase TNF- levels. In this regard, the elevated
risk associated with elevations of TNF- was independent of other
traditional markers of risk evaluated and was present in subgroup
analyses limited to the end point of
cardiovascular death (RR=2.1) or nonfatal recurrent MI
(RR=3.2). The strongest correlates of TNF in these data were CRP and
SAA, 2 nonspecific markers of systemic inflammation; however, the
increased risk of recurrent coronary events associated with
persistent elevations of TNF- was also independent of these latter 2
parameters.
The fact that blood samples were obtained in this study an average of 9
months after MI suggests that the increased risk of recurrent
coronary events associated with TNF- is not simply the
result of a transient increase in TNF- after coronary
occlusion.20 However, the source of persistently elevated
levels of TNF- among those at risk in our study is uncertain. Prior
studies of acute MI suggest that cytokines are preferentially
produced by inflammatory cells in the peri-infarct zone and thus that
persistent cytokine elevations result from an increased
infiltration of inflammatory cells.21 By contrast, in a
recent experimental study of MI induced by ligation of the left
anterior descending coronary artery in rats, TNF- expression
in myocardium was found to persist after infarction even in
otherwise normal myocardial segments.15 In that study,
TNF- gene and protein expression persisted in myocytes over time,
which suggests a possible long-term role of this cytokine in
vascular remodeling. Additional experimental studies will be required
to determine the source of the TNF- elevations observed in these
data.
Our data demonstrating evidence of persistent inflammation several
months after MI among individuals at high risk for recurrent events is
consistent with prior work from other investigators indicating
persistent elevations of CRP among high-risk individuals recovering
from unstable angina22 and extend data demonstrating that
both CRP19 23 24 25 and interleukin-626 have
predictive value in the setting of acute coronary
ischemia. Thus, taken together, these data suggest that
subclinical persistent instability, or a susceptibility to recurrent
instability, can be detected by the presence of inflammatory markers
such as TNF- or CRP, even among apparently stable patients well into
clinical recovery.
Potential limitations of our study should be considered. First, plasma
concentrations of TNF- increase with both smoking and obesity, and
thus it is possible that the current results reflect confounding by
these factors. We believe this is unlikely, however, because
statistically significant differences in baseline TNF- levels were
observed between case and control subjects in subgroup analyses
that specifically excluded such individuals. Furthermore, in
multivariate analysis, adjustment for these
factors had no discernable impact on our results. Second, because our
study relied on frozen plasma samples, we cannot exclude the
possibility that protein degradation may have affected our study.
However, as shown in Figure 1, the TNF- levels observed in
our data are similar to those reported in prior studies that used fresh
blood samples. Furthermore, even if protein degradation was a problem
in our study, this effect could not have lead to any systematic bias
because samples from case and control subjects were obtained at
baseline and were handled identically throughout the collection,
storage, and analytic phases of this analysis. Third, prior
data have demonstrated that those individuals with evidence of severely
reduced ejection fraction and clinical heart failure have markedly
elevated levels of TNF-.5 6 Thus, differential levels
of ventricular dysfunction after MI among case and control
subjects must be considered as an alternative explanation for our
results. However, because the CARE trial specifically excluded
individuals with any evidence of clinical congestive heart failure, the
possibility that systematic differences in ventricular
function had a major influence on these data also seems unlikely.
Finally, we recognize that the plasma half-life of TNF- is brief and
that basal levels are low in most patients. However, these effects
would not result in a false-positive finding. Moreover, our data for
TNF- are in concordance with recent work in unstable angina that
indicates that levels of interleukin-1 receptor antagonist
and interleukin-6 are in turn associated with increased risk of
in-hospital coronary events.27
Previous investigators have suggested that persistence of TNF- into
the late stages of MI may contribute to cardiac myocyte loss and
cardiac decompensation.15 In our data, those individuals
with elevated levels of TNF- were at increased risk for
coronary death and recurrent MI. Thus, these data are
consistent with the hypothesis that inflammation plays a major
role in the acute coronary syndromes,28 29 as well
as having long-term prognostic value among apparently stable
patients.30 31 Finally, because individuals with elevated
levels of TNF- were at increased risk independent of other risk
factors, these data also support the possibility that novel therapies
designed to attenuate the inflammatory response after acute
coronary occlusion may represent a new direction in the
treatment of MI.28 29
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Acknowledgments |
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This study was supported by grants from the National Heart, Lung, and Blood Institute, Bethesda, Md, and by an Established Investigator Award from the American Heart Association, Dallas, Tex (P.M.R.).
Received September 21, 1999; revision received December 1, 1999; accepted December 10, 1999.
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References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Warner SJC, Libby P. Human vascular smooth muscles: target for and source of tumor necrosis factor. J Immunol. 1989;142:100–109.[Abstract]
2. Tipping PG, Hancock WW. Production of tumor necrosis factor and interleukin-1 by macrophages from human atheromatous plaques. Am J Pathol. 1994;142:1721–1782.[Abstract]
3. Barath P, Fishbein MC, Cao J, Berenson J, Helfant RH, Forrester JS. Detection and localization of tumor necrosis factor in human atheroma. Am J Cardiol. 1990;65:297–302.[Medline] [Order article via Infotrieve]
4.
Old LJ. Tumor necrosis factor (TNF).
Science. 1985;230:630–632.
5. Levine B, Kalman J, Mayer L, Fillit HM, Packer M. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N Engl J Med. 1990;323:236–241.[Abstract]
6.
McMurray J, Abdullah I, Dargie H, Shapiro D. Increased
concentrations of tumour necrosis factor in "cachectic" patients
with severe heart failure. Br Heart J. 1991;66:356–358.
7. Yokoyama T, Vaca L, Rossen RD, Durante W, Hazarika P, Mann DL. Cellular basis for the negative inotropic effects of tumor necrosis factor-alpha in the adult mammalian heart. J Clin Invest. 1993;92:2303–2312.
8. Lo SK, Everitt J, Gu J, Malik AB. Tumor necrosis factor mediates experimental pulmonary edema by ICAM-1 and CD18-dependent mechanisms. J Clin Invest. 1992;89:981–988.
9.
Horgan MJ, Palace GP, Everitt JE, Malik AB.
TNF- release in endotoxemia contributes to neutrophil-dependent
pulmonary edema. Am J Physiol. 1993;264:H1161–H1165.
10. Hegewisch S, Weh HJ, Hossfeld DK. TNF-induced cardiomyopathy. Lancet. 1990;2:294–295.
11.
Vaddi K, Nicolini FA, Mehta P, Mehta JL. Increased
secretion of tumour necrosis factor-alpha and interferon-gamma by
mononuclear leukocytes in patients with ischemic heart disease:
relevance in superoxide anion generation. Circulation. 1994;90:694–699.
12.
Kulkeilka GL, Smith CW, Maning AM, Yonker KA, Micheal
KH, Entman ML. Induction of interleukin synthesis in the
myocardium. Circulation. 1995;92:1866–1875.
13. Herskowitz A, Choi S, Ansari AA, Wesselingh S. Cytokine mRNA expression in postischemic/reperfused myocardium. Am J Pathol. 1995;146:419–428.[Abstract]
14.
Chandrasekar B, Freeman GL. Induction of nuclear
factor 
B and activation of protein 1 in
postischemic myocardium. FEBS Lett. 1997;401:30–34.[Medline]
[Order article via Infotrieve]
15.
Irwin MW, Mak S, Mann DL, Qu R, Penninger JM, Yan A,
Dawood F, Wen W-H, Shou Z, Liu P. Tissue expression and
immunolocalization of tumor necrosis factor- in postinfarction
dysfunctional myocardium. Circulation. 1999;99:1492–1498.
16.
Maury CPJ, Teppo AM. Circulating tumor necrosis
factor- (cachectin) in myocardial infarction. J
Intern Med. 1989;225:333–336.[Medline]
[Order article via Infotrieve]
17. Basaran Y, Basaran MM, Babacan KF, Ener B, Okay T, Gok H, Ozdemir M. Serum tumor necrosis factor levels in acute myocardial infarction and unstable angina pectoris. Angiology. 1993;44:332–337.
18.
Sacks FM, Pfeffer MA, Moye LA, Rouleau JL, Rutherford
JD, Cole TG, Brown L, Warnica JW, Arnold JMO, Wun C, Davis BR,
Braunwald E, for the Cholesterol And Recurrent Events Trial
Investigators. The effect of pravastatin on
coronary events after myocardial infarction in patients with
average cholesterol levels. N Engl J
Med. 1996;335:1001–1009.
19.
Ridker PM, Rifai N, Pfeffer MA, Sacks FM, Moye LA,
Goldman S, Flaker GC, Braunwald E, for the Cholesterol And
Recurrent Events (CARE) Investigators. Inflammation,
pravastatin, and the risk of coronary events after
myocardial infarction in patients with average cholesterol
levels. Circulation. 1998;98:839–844.
20.
Gabay C, Kushner I. Acute-phase proteins and other
systemic responses to inflammation. N Engl J Med. 1999;340:448–454.
21. Marx N, Neumann F-J, Ott I, Gawaz M, Koch W, Pinkau T, Schomig A. Induction of cytokine expression in leukocytes in acute myocardial infarction. J Am Coll Cardiol. 1997;30:165–170.[Abstract]
22.
Biasucci LM, Liuzzo G, Grillo RL, Caligiuri G, Rebuzzi
AG, Buffon A, Summaria F, Ginnetti F, Fadda G, Maseri A. Elevated
levels of C-reactive protein at discharge in patients with unstable
angina predict recurrent instability. Circulation. 1999;99:855–860.
23. Haverkate F, Thompson SG, Pyke SDM, Gallimore JR, Pepys MB, for the European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. Production of C-reactive protein and risk of coronary events in stable and unstable angina. Lancet. 1997;349:462–466.[Medline] [Order article via Infotrieve]
24.
Liuzzo G, Biasucci LM, Gallimore JR, Grillo RL, Rebuzzi
AG, Pepys MB, Maseri A. The prognostic value of C-reactive protein and
serum amyloid A protein in severe unstable angina. N Engl
J Med. 1994;331:417–424.
25.
Morrow DA, Rifai N, Antman EM, Weiner DL, McCabe C,
Cannon CP, Braunwald E. C-reactive protein is a potent predictor of
mortality independently of and in combination with troponin T in acute
coronary syndromes: a TIMI 11A substudy. J Am Coll
Cardiol. 1998;31:1460–1465.
26.
Biasucci LM, Bitelli A, Liuzzo G, Altamura S, Caligiuri
G, Monaco C, Rebuzzi AG, Ciliberto G, Maseri A. Elevated levels of
interleukin-6 in unstable angina. Circulation. 1996;94:874–877.
27.
Biasucci LM, Liuzzo G, Fantuzzi G, Caligiuri G, Rebuzzi
AG, Ginnetti F, Dinarello CA, Maseri A. Increasing levels of
interleukin (IL)-1Ra and IL-6 during the first 2 days of
hospitalization in unstable angina are associated with increased risk
of in-hospital coronary events. Circulation. 1999;99:2079–2084.
28.
Libby P. Molecular bases of the acute coronary
syndromes. Circulation. 1995;91:2844–2850.
29.
Ross R. Mechanisms of disease:
atherosclerosis: an inflammatory disease. N
Engl J Med. 1999;340:115–126.
30.
Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens
CH. Inflammation, aspirin, and the risk of
cardiovascular disease in apparently healthy men.
N Engl J Med. 1997;336:973–979.
31.
Ridker PM, Glynn RJ, Hennekens CH. C-reactive protein
adds to the predictive value of total and HDL cholesterol
in determining risk of first myocardial infarction.
Circulation. 1998;97:2007–2011.
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 S. S. Martin, A. Qasim, and M. P. Reilly Leptin Resistance: A Possible Interface of Inflammation and Metabolism in Obesity-Related Cardiovascular Disease J. Am. Coll. Cardiol., October 7, 2008; 52(15): 1201 - 1210. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Welsh, G. D.O. Lowe, J. Chalmers, D. J. Campbell, A. Rumley, B. C. Neal, S. W. MacMahon, and M. Woodward Associations of Proinflammatory Cytokines With the Risk of Recurrent Stroke Stroke, August 1, 2008; 39(8): 2226 - 2230. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. S Lund, L. Tarnow, C. D A Stehouwer, C. G Schalkwijk, T. Teerlink, J. Gram, K. Winther, M. Frandsen, U. M Smidt, O. Pedersen, et al. Impact of metformin versus repaglinide on non-glycaemic cardiovascular risk markers related to inflammation and endothelial dysfunction in non-obese patients with type 2 diabetes Eur. J. Endocrinol., May 1, 2008; 158(5): 631 - 641. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Radaelli, C. Loardi, M. Cazzaniga, G. Balestri, C. DeCarlini, M. G. Cerrito, E. N. Cusa, L. Guerra, S. Garducci, D. Santo, et al. Inflammatory Activation During Coronary Artery Surgery and Its Dose-Dependent Modulation by Statin/ACE-Inhibitor Combination Arterioscler Thromb Vasc Biol, December 1, 2007; 27(12): 2750 - 2755. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. G. Schneider, Y. Zhu, T. Coleman, and C. F. Semenkovich Macrophage 3 Integrin Suppresses Hyperlipidemia-Induced Inflammation by Modulating TNF{alpha} Expression Arterioscler Thromb Vasc Biol, December 1, 2007; 27(12): 2699 - 2706. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. A. Yialamas, A. A. Dwyer, E. Hanley, H. Lee, N. Pitteloud, and F. J. Hayes Acute Sex Steroid Withdrawal Reduces Insulin Sensitivity in Healthy Men with Idiopathic Hypogonadotropic Hypogonadism J. Clin. Endocrinol. Metab., November 1, 2007; 92(11): 4254 - 4259. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Zhang, K. Peppel, P. Sivashanmugam, E. S. Orman, L. Brian, S. T. Exum, and N. J. Freedman Expression of Tumor Necrosis Factor Receptor-1 in Arterial Wall Cells Promotes Atherosclerosis Arterioscler Thromb Vasc Biol, May 1, 2007; 27(5): 1087 - 1094. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. H.Y. Wu, N. C. Ward, A. P. Indrawan, C.-A. Almeida, J. M. Hodgson, J. M. Proudfoot, I. B. Puddey, and K. D. Croft Effects of {alpha}-Tocopherol and Mixed Tocopherol Supplementation on Markers of Oxidative Stress and Inflammation in Type 2 Diabetes Clin. Chem., March 1, 2007; 53(3): 511 - 519. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. De Lorenzo, V. Del Gobbo, M. G. Premrov, M. Bigioni, F. Galvano, and L. Di Renzo Normal-weight obese syndrome: early inflammation? Am. J. Clinical Nutrition, January 1, 2007; 85(1): 40 - 45. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R.-E. W. Kavey, V. Allada, S. R. Daniels, L. L. Hayman, B. W. McCrindle, J. W. Newburger, R. S. Parekh, and J. Steinberger Cardiovascular Risk Reduction in High-Risk Pediatric Patients: A Scientific Statement From the American Heart Association Expert Panel on Population and Prevention Science; the Councils on Cardiovascular Disease in the Young, Epidemiology and Prevention, Nutrition, Physical Activity and Metabolism, High Blood Pressure Research, Cardiovascular Nursing, and the Kidney in Heart Disease; and the Interdisciplinary Working Group on Quality of Care and Outcomes Research: Endorsed by the American Academy of Pediatrics Circulation, December 12, 2006; 114(24): 2710 - 2738. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. M. Howard-Alpe, J. W. Sear, and P. Foex Methods of detecting atherosclerosis in non-cardiac surgical patients; the role of biochemical markers Br. J. Anaesth., December 1, 2006; 97(6): 758 - 769. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Vlachopoulos, K. Aznaouridis, N. Ioakeimidis, K. Rokkas, C. Vasiliadou, N. Alexopoulos, E. Stefanadi, A. Askitis, and C. Stefanadis Unfavourable endothelial and inflammatory state in erectile dysfunction patients with or without coronary artery disease Eur. Heart J., November 2, 2006; 27(22): 2640 - 2648. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. S. V. Elkind, W. Tai, K. Coates, M. C. Paik, and R. L. Sacco High-sensitivity C-reactive protein, lipoprotein-associated phospholipase A2, and outcome after ischemic stroke. Arch Intern Med, October 23, 2006; 166(19): 2073 - 2080. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Ryan, C. T. Taylor, and W. T. McNicholas Predictors of Elevated Nuclear Factor-{kappa}B-dependent Genes in Obstructive Sleep Apnea Syndrome Am. J. Respir. Crit. Care Med., October 1, 2006; 174(7): 824 - 830. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Takaoka, S. Uemura, H. Kawata, K.-i. Imagawa, Y. Takeda, K. Nakatani, N. Naya, M. Horii, S. Yamano, Y. Miyamoto, et al. Inflammatory Response to Acute Myocardial Infarction Augments Neointimal Hyperplasia After Vascular Injury in a Remote Artery Arterioscler Thromb Vasc Biol, September 1, 2006; 26(9): 2083 - 2089. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Giugliano, A. Ceriello, and K. Esposito The Effects of Diet on Inflammation: Emphasis on the Metabolic Syndrome J. Am. Coll. Cardiol., August 15, 2006; 48(4): 677 - 685. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. M.A.C. Martens, T. J. Rabelink, J. op 't Roodt, E. J.P. de Koning, and F. L.J. Visseren TNF-{alpha} induces endothelial dysfunction in diabetic adults, an effect reversible by the PPAR-{gamma} agonist pioglitazone Eur. Heart J., July 1, 2006; 27(13): 1605 - 1609. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. E. Bernstein, J. Berry, S. Kim, B. Canavan, and S. K. Grinspoon Effects of Etanercept in Patients With the Metabolic Syndrome. Arch Intern Med, April 24, 2006; 166(8): 902 - 908. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Matsushita, H. Yatsuya, K. Tamakoshi, K. Wada, R. Otsuka, S. Takefuji, K. Sugiura, T. Kondo, T. Murohara, and H. Toyoshima Comparison of Circulating Adiponectin and Proinflammatory Markers Regarding Their Association With Metabolic Syndrome in Japanese Men Arterioscler Thromb Vasc Biol, April 1, 2006; 26(4): 871 - 876. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. E. Marketou, E. A. Zacharis, D. Nikitovic, E. S. Ganotakis, F. I. Parthenakis, N. Maliaraki, and P. E. Vardas Early Effects of Simvastatin versus Atorvastatin on Oxidative Stress and Proinflammatory Cytokines in Hyperlipidemic Subjects Angiology, March 1, 2006; 57(2): 211 - 218. [Abstract] [PDF]
|
|
|
|
 |
|
 J. M. McCaffery, N. Frasure-Smith, M.-P. Dube, P. Theroux, G. A. Rouleau, Q. Duan, and F. Lesperance Common genetic vulnerability to depressive symptoms and coronary artery disease: a review and development of candidate genes related to inflammation and serotonin. Psychosom Med, March 1, 2006; 68(2): 187 - 200. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Rutschow, J. Li, H.-P. Schultheiss, and M. Pauschinger Myocardial proteases and matrix remodeling in inflammatory heart disease Cardiovasc Res, February 15, 2006; 69(3): 646 - 656. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. J. Armstrong, D. A. Morrow, and M. S. Sabatine Inflammatory Biomarkers in Acute Coronary Syndromes: Part I: Introduction and Cytokines Circulation, February 14, 2006; 113(6): e72 - e75. [Full Text] [PDF]
|
|
|
|
|
|
P. Libby Inflammation and cardiovascular disease mechanisms Am. J. Clinical Nutrition, February 1, 2006; 83(2): 456S - 460S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. K. Koh, S. H. Han, and M. J. Quon Inflammatory Markers and the Metabolic Syndrome: Insights From Therapeutic Interventions J. Am. Coll. Cardiol., December 6, 2005; 46(11): 1978 - 1985. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U. Singh, J. Tabibian, S. K. Venugopal, S. Devaraj, and I. Jialal Development of an In Vitro Screening Assay to Test the Antiinflammatory Properties of Dietary Supplements and Pharmacologic Agents Clin. Chem., December 1, 2005; 51(12): 2252 - 2256. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. C. Hall and N. Dalbeth Disease modification and cardiovascular risk reduction: two sides of the same coin? Rheumatology, December 1, 2005; 44(12): 1473 - 1482. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. S. Speidl, M. Exner, J. Amighi, S. P. Kastl, G. Zorn, G. Maurer, O. Wagner, K. Huber, E. Minar, J. Wojta, et al. Complement component C5a predicts future cardiovascular events in patients with advanced atherosclerosis Eur. Heart J., November 1, 2005; 26(21): 2294 - 2299. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Ryan, C. T. Taylor, and W. T. McNicholas Selective Activation of Inflammatory Pathways by Intermittent Hypoxia in Obstructive Sleep Apnea Syndrome Circulation, October 25, 2005; 112(17): 2660 - 2667. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Minoguchi, T. Yokoe, T. Tazaki, H. Minoguchi, A. Tanaka, N. Oda, S. Okada, S. Ohta, H. Naito, and M. Adachi Increased Carotid Intima-Media Thickness and Serum Inflammatory Markers in Obstructive Sleep Apnea Am. J. Respir. Crit. Care Med., September 1, 2005; 172(5): 625 - 630. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Hetzel, B. Balletshofer, K. Rittig, D. Walcher, W. Kratzer, V. Hombach, H.-U. Haring, W. Koenig, and N. Marx Rapid Effects of Rosiglitazone Treatment on Endothelial Function and Inflammatory Biomarkers Arterioscler Thromb Vasc Biol, September 1, 2005; 25(9): 1804 - 1809. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Shai, M. B. Schulze, J. E. Manson, K. M. Rexrode, M. J. Stampfer, C. Mantzoros, and F. B. Hu A Prospective Study of Soluble Tumor Necrosis Factor-{alpha} Receptor II (sTNF-RII) and Risk of Coronary Heart Disease Among Women With Type 2 Diabetes Diabetes Care, June 1, 2005; 28(6): 1376 - 1382. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. Seddon, S. George, B. Rosner, and N. Rifai Progression of Age-Related Macular Degeneration: Prospective Assessment of C-Reactive Protein, Interleukin 6, and Other Cardiovascular Biomarkers Arch Ophthalmol, June 1, 2005; 123(6): 774 - 782. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. M. Stuveling, S. J. L. Bakker, H. L. Hillege, P. E. de Jong, R. O. B. Gans, and D. de Zeeuw Biochemical risk markers: a novel area for better prediction of renal risk? Nephrol. Dial. Transplant., March 1, 2005; 20(3): 497 - 508. [Full Text] [PDF]
|
|
|
|
|
|
M. Valgimigli, C. Ceconi, P. Malagutti, E. Merli, O. Soukhomovskaia, G. Francolini, G. Cicchitelli, A. Olivares, G. Parrinello, G. Percoco, et al. Tumor Necrosis Factor-{alpha} Receptor 1 Is a Major Predictor of Mortality and New-Onset Heart Failure in Patients With Acute Myocardial Infarction: The Cytokine-Activation and Long-Term Prognosis in Myocardial Infarction (C-ALPHA) Study Circulation, February 22, 2005; 111(7): 863 - 870. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. K. Kharbanda, S. Wallace, B. Walton, A. Donald, J. M. Cross, and J. Deanfield Systemic Acyl-CoA:Cholesterol Acyltransferase Inhibition Reduces Inflammation and Improves Vascular Function in Hypercholesterolemia Circulation, February 15, 2005; 111(6): 804 - 807. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Tedgui The role of inflammation in atherothrombosis: implications for clinical practice Vascular Medicine, February 1, 2005; 10(1): 45 - 53. [Abstract] [PDF]
|
|
|
|
|
|
W. S. Speidl, A. Zeiner, M. Nikfardjam, A. Geppert, N. Jordanova, A. Niessner, G. Zorn, G. Maurer, W. Schreiber, J. Wojta, et al. An increase of C-reactive protein is associated with enhanced activation of endogenous fibrinolysis at baseline but an impaired endothelial fibrinolytic response after venous occlusion J. Am. Coll. Cardiol., January 4, 2005; 45(1): 30 - 34. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. M. Biasucci CDC/AHA Workshop on Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: Clinical Use of Inflammatory Markers in Patients With Cardiovascular Diseases: A Background Paper Circulation, December 21, 2004; 110(25): e560 - e567. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. K. Pai, T. Pischon, J. Ma, J. E. Manson, S. E. Hankinson, K. Joshipura, G. C. Curhan, N. Rifai, C. C. Cannuscio, M. J. Stampfer, et al. Inflammatory Markers and the Risk of Coronary Heart Disease in Men and Women N. Engl. J. Med., December 16, 2004; 351(25): 2599 - 2610. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Minoguchi, T. Tazaki, T. Yokoe, H. Minoguchi, Y. Watanabe, M. Yamamoto, and M. Adachi Elevated Production of Tumor Necrosis Factor-{alpha} by Monocytes in Patients With Obstructive Sleep Apnea Syndrome Chest, November 1, 2004; 126(5): 1473 - 1479. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Kaushal, A. H. Heald, K. W. Siddals, M. S. Sandhu, D. B. Dunger, J. M. Gibson, and N. J. Wareham The Impact of Abnormalities in IGF and Inflammatory Systems on the Metabolic Syndrome Diabetes Care, November 1, 2004; 27(11): 2682 - 2688. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. J. DeGraba Immunogenetic Susceptibility of Atherosclerotic Stroke: Implications on Current and Future Treatment of Vascular Inflammation Stroke, November 1, 2004; 35(11_suppl_1): 2712 - 2719. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Walcher and N. Marx Insulin resistance and cardiovascular disease: the role of PPAR{gamma} activators beyond their anti-diabetic action Diabetes and Vascular Disease Research, October 1, 2004; 1(2): 76 - 81. [Abstract] [PDF]
|
|
|
|
 |
|
 P H Wirtz, R von Kanel, N Rohleder, and J E Fischer Monocyte proinflammatory cytokine release is higher and glucocorticoid sensitivity is lower in middle aged men than in women independent of cardiovascular risk factors Heart, August 1, 2004; 90(8): 853 - 858. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C J Malkin, P J Pugh, P D Morris, K E Kerry, R D Jones, T H Jones, and K S Channer Testosterone replacement in hypogonadal men with angina improves ischaemic threshold and quality of life Heart, August 1, 2004; 90(8): 871 - 876. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. J. Malkin, P. J. Pugh, R. D. Jones, D. Kapoor, K. S. Channer, and T. H. Jones The Effect of Testosterone Replacement on Endogenous Inflammatory Cytokines and Lipid Profiles in Hypogonadal Men J. Clin. Endocrinol. Metab., July 1, 2004; 89(7): 3313 - 3318. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Jeanmonod, R. von Kanel, F. E. Maly, and J. E. Fischer Elevated Plasma C-Reactive Protein in Chronically Distressed Subjects Who Carry the A Allele of the TNF-{alpha} -308 G/A Polymorphism Psychosom Med, July 1, 2004; 66(4): 501 - 506. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Lekander, S. Elofsson, I.-M. Neve, L.-O. Hansson, and A.-L. Unden Self-rated Health Is Related to Levels of Circulating Cytokines Psychosom Med, July 1, 2004; 66(4): 559 - 563. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Iwashima, T. Katsuya, K. Ishikawa, N. Ouchi, M. Ohishi, K. Sugimoto, Y. Fu, M. Motone, K. Yamamoto, A. Matsuo, et al. Hypoadiponectinemia Is an Independent Risk Factor for Hypertension Hypertension, June 1, 2004; 43(6): 1318 - 1323. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. T. Willerson and P. M. Ridker Inflammation as a Cardiovascular Risk Factor Circulation, June 1, 2004; 109(21_suppl_1): II-2 - II-10. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Monakier, M. Mates, M. W. Klutstein, J. A. Balkin, B. Rudensky, D. Meerkin, and D. Tzivoni Rofecoxib, a COX-2 Inhibitor, Lowers C-Reactive Protein and Interleukin-6 Levels in Patients With Acute Coronary Syndromes Chest, May 1, 2004; 125(5): 1610 - 1615. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A.D. Booth, D.R.W. Jayne, R.K. Kharbanda, C.M. McEniery, I.S. Mackenzie, J. Brown, and I.B. Wilkinson Infliximab Improves Endothelial Dysfunction in Systemic Vasculitis: A Model of Vascular Inflammation Circulation, April 13, 2004; 109(14): 1718 - 1723. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Ohashi, N. Ouchi, S. Kihara, T. Funahashi, T. Nakamura, S. Sumitsuji, T. Kawamoto, S. Matsumoto, H. Nagaretani, M. Kumada, et al. Adiponectin I164T mutation is associated with the metabolic syndrome and coronary artery disease J. Am. Coll. Cardiol., April 7, 2004; 43(7): 1195 - 1200. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Lind, G. Engstrom, L. Stavenow, L. Janzon, F. Lindgarde, and B. Hedblad Risk of Myocardial Infarction and Stroke in Smokers Is Related to Plasma Levels of Inflammation-Sensitive Proteins Arterioscler Thromb Vasc Biol, March 1, 2004; 24(3): 577 - 582. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L S Rallidis, M G Zolindaki, P C Pentzeridis, K P Poulopoulos, A H Velissaridou, and T S Apostolou Raised concentrations of macrophage colony stimulating factor in severe unstable angina beyond the acute phase are strongly predictive of long term outcome Heart, January 1, 2004; 90(1): 25 - 29. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Lutgens, R.-J. van Suylen, B. C. Faber, M. J. Gijbels, P. M. Eurlings, A.-P. Bijnens, K. B. Cleutjens, S. Heeneman, and M. J.A.P. Daemen Atherosclerotic Plaque Rupture: Local or Systemic Process? Arterioscler Thromb Vasc Biol, December 1, 2003; 23(12): 2123 - 2130. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Mazurek, L. Zhang, A. Zalewski, J. D. Mannion, J. T. Diehl, H. Arafat, L. Sarov-Blat, S. O'Brien, E. A. Keiper, A. G. Johnson, et al. Human Epicardial Adipose Tissue Is a Source of Inflammatory Mediators Circulation, November 18, 2003; 108(20): 2460 - 2466. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Schoenhagen, G. W. Stone, S. E. Nissen, C. L. Grines, J. Griffin, B. S. Clemson, D. G. Vince, K. Ziada, T. Crowe, C. Apperson-Hanson, et al. Coronary Plaque Morphology and Frequency of Ulceration Distant From Culprit Lesions in Patients With Unstable and Stable Presentation Arterioscler Thromb Vasc Biol, October 1, 2003; 23(10): 1895 - 1900. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. P. Miller, Y.-F. Chen, D. Xing, W. Feng, and S. Oparil Hormone Replacement Therapy and Inflammation: Interactions in Cardiovascular Disease Hypertension, October 1, 2003; 42(4): 657 - 663. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. J. Dacey, J. DeSimone, J. H. Braxton, B. J. Leavitt, S. J. Lahey, J. D. Klemperer, B. M. Westbrook, E. M. Olmstead, and G. T. O'Connor Preoperative white blood cell count and mortality and morbidity after coronary artery bypass grafting Ann. Thorac. Surg., September 1, 2003; 76(3): 760 - 764. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Pischon, S. E. Hankinson, G. S. Hotamisligil, N. Rifai, W. C. Willett, and E. B. Rimm Habitual Dietary Intake of n-3 and n-6 Fatty Acids in Relation to Inflammatory Markers Among US Men and Women Circulation, July 15, 2003; 108(2): 155 - 160. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. F. Berg, B. Maraha, G.-J. Scheffer, M. F. Peeters, and J. A. J. W. Kluytmans Effect of Clarithromycin on Inflammatory Markers in Patients with Atherosclerosis Clin. Vaccine Immunol., July 1, 2003; 10(4): 525 - 528. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E Svenungsson, G-Z Fei, K Jensen-Urstad, U de Faire, A Hamsten, and J Frostegard TNF-{alpha}: a link between hypertriglyceridaemia and inflammation in SLE patients with cardiovascular disease Lupus, June 1, 2003; 12(6): 454 - 461. [Abstract] [PDF]
|
|
|
|
|
|
E. C. Suarez, R. R. Krishnan, and J. G. Lewis The Relation of Severity of Depressive Symptoms to Monocyte-Associated Proinflammatory Cytokines and Chemokines in Apparently Healthy Men Psychosom Med, May 1, 2003; 65(3): 362 - 368. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-P. Despres, I. Lemieux, A. Pascot, N. Almeras, M. Dumont, A. Nadeau, J. Bergeron, and D. Prud'homme Gemfibrozil Reduces Plasma C-Reactive Protein Levels in Abdominally Obese Men With the Atherogenic Dyslipidemia of the Metabolic Syndrome Arterioscler Thromb Vasc Biol, April 1, 2003; 23(4): 702 - 703. [Full Text] [PDF]
|
|
|
|
|
|
S. Chia, M. Qadan, R. Newton, C. A. Ludlam, K. A.A. Fox, and D. E. Newby Intra-Arterial Tumor Necrosis Factor-{alpha} Impairs Endothelium-Dependent Vasodilatation and Stimulates Local Tissue Plasminogen Activator Release in Humans Arterioscler Thromb Vasc Biol, April 1, 2003; 23(4): 695 - 701. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Blankenberg, H. J. Rupprecht, O. Poirier, C. Bickel, M. Smieja, G. Hafner, J. Meyer, F. Cambien, L. Tiret, and for the AtheroGene Investigators Plasma Concentrations and Genetic Variation of Matrix Metalloproteinase 9 and Prognosis of Patients With Cardiovascular Disease Circulation, April 1, 2003; 107(12): 1579 - 1585. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. R. Murray and G. L. Freeman Proinflammatory Cytokines: Predictors of a Failing Heart? Circulation, March 25, 2003; 107(11): 1460 - 1462. [Full Text] [PDF]
|
|
|
|
|
|
R. S. Vasan, L. M. Sullivan, R. Roubenoff, C. A. Dinarello, T. Harris, E. J. Benjamin, D. B. Sawyer, D. Levy, P. W.F. Wilson, and R. B. D'Agostino Inflammatory Markers and Risk of Heart Failure in Elderly Subjects Without Prior Myocardial Infarction: The Framingham Heart Study Circulation, March 25, 2003; 107(11): 1486 - 1491. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. H. Von der Thusen, J. Kuiper, T. J. C. Van Berkel, and E. A. L. Biessen Interleukins in Atherosclerosis: Molecular Pathways and Therapeutic Potential Pharmacol. Rev., March 1, 2003; 55(1): 133 - 166. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Chia, C. A. Ludlam, K. A. A. Fox, and D. E. Newby Acute systemic inflammation enhances endothelium-dependent tissue plasminogen activator release in men J. Am. Coll. Cardiol., January 15, 2003; 41(2): 333 - 339. [Abstract] [Full Text] [PDF]
|
|
|
|
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K. Esposito, F. Nappo, R. Marfella, G. Giugliano, F. Giugliano, M. Ciotola, L. Quagliaro, A. Ceriello, and D. Giugliano Inflammatory Cytokine Concentrations Are Acutely Increased by Hyperglycemia in Humans: Role of Oxidative Stress Circulation, October 15, 2002; 106(16): 2067 - 2072. [Abstract] [Full Text] [PDF]
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D. Tanne, M. Haim, V. Boyko, U. Goldbourt, T. Reshef, S. Matetzky, Y. Adler, Y. A. Mekori, and S. Behar Soluble Intercellular Adhesion Molecule-1 and Risk of Future Ischemic Stroke: A Nested Case-Control Study From the Bezafibrate Infarction Prevention (BIP) Study Cohort Stroke, September 1, 2002; 33(9): 2182 - 2186. [Abstract] [Full Text] [PDF]
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K. K. Koh, J. Y. Ahn, D. K. Jin, B.-K. Yoon, H. S. Kim, D. S. Kim, M.-S. Shin, J. W. Son, I. S. Choi, and E. K. Shin Effects of Continuous Combined Hormone Replacement Therapy on Inflammation in Hypertensive and/or Overweight Postmenopausal Women Arterioscler Thromb Vasc Biol, September 1, 2002; 22(9): 1459 - 1464. [Abstract] [Full Text] [PDF]
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K. K. Koh Effects of estrogen on the vascular wall: vasomotor function and inflammation Cardiovasc Res, September 1, 2002; 55(4): 714 - 726. [Full Text] [PDF]
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P. Schoenhagen, E. M. Tuzcu, and S. G. Ellis Plaque Vulnerability, Plaque Rupture, and Acute Coronary Syndromes: (Multi)-Focal Manifestation of a Systemic Disease Process Circulation, August 13, 2002; 106(7): 760 - 762. [Full Text] [PDF]
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K. Esposito, A. Pontillo, M. Ciotola, C. Di Palo, E. Grella, G. Nicoletti, and D. Giugliano Weight Loss Reduces Interleukin-18 Levels in Obese Women J. Clin. Endocrinol. Metab., August 1, 2002; 87(8): 3864 - 3866. [Abstract] [Full Text] [PDF]
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S. Kiechl, E. Lorenz, M. Reindl, C. J. Wiedermann, F. Oberhollenzer, E. Bonora, J. Willeit, and D. A. Schwartz Toll-like Receptor 4 Polymorphisms and Atherogenesis N. Engl. J. Med., July 18, 2002; 347(3): 185 - 192. [Abstract] [Full Text] [PDF]
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P. Libby, P. M. Ridker, and A. Maseri Inflammation and Atherosclerosis Circulation, March 5, 2002; 105(9): 1135 - 1143. [Abstract] [Full Text] [PDF]
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G.J. Blake and P.M. Ridker Tumour necrosis factor-{alpha}, inflammatory biomarkers, and atherogenesis Eur. Heart J., March 1, 2002; 23(5): 345 - 347. [Full Text] [PDF]
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T. Skoog, W. Dichtl, S. Boquist, C. Skoglund-Andersson, F. Karpe, R. Tang, M.G. Bond, U. de Faire, J. Nilsson, P. Eriksson, et al. Plasma tumour necrosis factor-{alpha} and early carotid atherosclerosis in healthy middle-aged men Eur. Heart J., March 1, 2002; 23(5): 376 - 383. [Abstract] [Full Text] [PDF]
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M. S. Elkind, J. Cheng, B. Boden-Albala, T. Rundek, J. Thomas, H. Chen, L. E. Rabbani, R. L. Sacco, and A. G. Thrift Tumor Necrosis Factor Receptor Levels Are Associated With Carotid Atherosclerosis * Editorial Comment Stroke, January 1, 2002; 33(1): 31 - 38. [Abstract] [Full Text] [PDF]
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