(Circulation. 2001;103:1064.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Chronic Infections and the Risk of Carotid Atherosclerosis
Prospective Results From a Large Population Study
From the Departments of Neurology (S.K., W.P., J.W.) and Internal Medicine (C.J.W.), University Clinic Innsbruck, the Institute for Biomedical Aging Research, Austrian Academy of Science (M. Mayr, Q.X., G.W.), and the Institute of General and Experimental Pathology, University of Innsbruck (G.W.), Innsbruck, Austria; the Department of Internal Medicine, Bruneck Hospital, Bruneck (G.E., F.O.), and the Department of Endocrinology and Metabolism, University of Verona, Verona (E.B., M. Muggeo), Italy; and the Department of Cardiological Sciences, St George’s Hospital Medical School, London, UK (Q.X.).
Correspondence to Dr S. Kiechl, Department of Neurology, Innsbruck University Clinic, Anichstraße 35, A-6020 Innsbruck, Austria.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background—Chronic infections have been implicated in the pathogenesis of atherosclerosis, yet from an epidemiological perspective, this concept remains controversial.
Methods and Results—The Bruneck Study is a prospective population-based survey on the pathogenesis of atherosclerosis. In 826 men and women 40 to 79 years old (1990 baseline), 5-year changes in carotid atherosclerosis were thoroughly assessed by high-resolution duplex scanning. The presence of chronic respiratory, urinary tract, dental, and other infections was ascertained by standard diagnostic criteria. Chronic infections amplified the risk of atherosclerosis development in the carotid arteries. The association was most pronounced in subjects free of carotid atherosclerosis at baseline (age-/sex-adjusted odds ratio [95% CI] for any chronic infection versus none, 4.08 [2.42 to 6.85]; P<0.0001) and applied to all types of chronic (bacterial) infections. It remained independently significant after adjustment for classic vascular risk attributes and extended to low-risk individuals free of conventional risk factors. Among subjects with chronic infections, atherosclerosis risk was highest in those with a prominent inflammatory response. Markers of systemic inflammation, such as soluble adhesion molecules and circulating bacterial endotoxin, and levels of soluble human heat-shock protein 60 and antibodies to mycobacterial heat-shock protein 65 were elevated in subjects with chronic infections and predictive of an increased risk of atherosclerosis.
Conclusions—The present study provides solid evidence for a role of common chronic infections in human atherogenesis. Induction of systemic inflammation and autoimmunity may be potential pathophysiological links.
Key Words: atherosclerosis • inflammation • infection • carotid arteries • cardiovascular disease
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Among the recent advances in understanding atherogenesis, the "infection hypothesis" is one of the most compelling, given the high prevalence of this putative risk factor in the general community and the potential availability of preventive interventions. Actually, this hypothesis is astonishingly old, with roots going back to the 19th century,1 2 3 although the bulk of supportive evidence has accumulated in the past few decades.4 5 6 7 8 9 10 11 12 13 14 15 Reasons for the remaining uncertainty and skepticism lie in the difficulties surrounding the ascertainment of atherogenesis and chronic infections in large clinically healthy populations. Previous prospective studies have focused on clinical end points rather than on the extent of and changes in underlying vessel pathological lesions, and most applied serological testing to define infection status. Accordingly, epidemiological evidence of an infectious risk factor in atherogenesis at this time is mainly indirect and restricted to certain pathogens.
The Bruneck Study16 17 18 is appropriate for directly addressing the key hypothesis, given the thorough clinical characterization and diagnostic workup of study subjects, its focus on atherosclerosis, and the availability of extensive laboratory evaluations involving measurements of antibody titers of common bacterial and viral pathogens.13
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Study Subjects
The Bruneck Study is a prospective population-based survey of the epidemiology and pathogenesis of atherosclerosis.16 17 18 At the 1990 baseline evaluation (July to November), the study population was recruited as a sex- and age-stratified random sample of all inhabitants of Bruneck (Bolzano Province, Italy) 40 to 79 years old (125 women and 125 men in the fifth to eighth decades each). A total of 93.6% participated, with data assessment completed in 919 subjects. During 1990 and the reevaluation in 1995 (July to October), a subgroup of 63 individuals died or moved away. In the remaining population, follow-up was 96.5% complete (n=826).16 17 18
Clinical History and Examination
The average number of cigarettes smoked per day and
the pack-years were noted for each smoker and ex-smoker. Regular
alcohol consumption was quantified in terms of grams per day.
Hypertension was defined as blood pressure (mean of 3 measurements)
160/95 mm Hg or the use of antihypertensive drugs. Diabetes mellitus
was coded as present for subjects with fasting glucose levels 140
mg/dL and/or a 2-hour value (oral glucose tolerance test) 200 mg/dL.
High, moderate, and low socioeconomic status were assumed if the
subject had 12, 11 to 9, or 
8 years of education and/or the average
monthly income of the person with the highest income in the household
was $2000, $2000 to $1000, or $1000, respectively.
In an effort to identify subjects with chronic infections or
conditions known to be associated with recurrent episodes of infectious
exacerbation, such as chronic obstructive pulmonary disease, we began
an extensive screening consisting of 2 consecutive
phases.19 20 The
first step involved a detailed self-reported medical and medication
history, thorough clinical examination, spirometry, extensive
laboratory evaluations including urinary analysis, and a review of the
Bruneck Hospital databases and other medical records. If the data were
inconclusive, in a second step individuals were referred for further
optional examinations. The diagnosis of common chronic infections was
established according to standard diagnostic criteria by an expert
committee including specialists from various medical fields. The
diagnosis of chronic obstructive pulmonary disease required
documentation of airway obstruction by spirometry
(FEV1/FVC ratio <0.70) and the presence of
typical symptoms, such as dyspnea, cough, expectoration, or wheeze.
Bronchitis was defined as chronic when cough with expectoration lasted
3 months in >2 consecutive years. Urinary tract infections were
regarded as recurrent in the case of 3 documented episodes.
Periodontitis was defined by self-report. Chronic infections were
considered in the present analysis when manifest at study entry
(baseline 1990).
Laboratory Methods
Blood samples were drawn after an overnight fast and
12 hours’ abstinence from smoking. In subjects with acute infection,
blood drawing was delayed for 6 weeks, ie, until 4 to 5 weeks after
recovery from infectious illness. Markers of infection/inflammation
were assayed as follows: C-reactive protein,
1-antitrypsin, and ceruloplasmin
(nephelometry, Behring); soluble vascular-cell and intracellular
adhesion molecules 1 and E-selectin (ELISA, R&D Systems and Bender);
and endotoxin (limulus amoebocyte lysate test,
Chromogenix19 ). ELISAs were
used to determine antibody titers to mycobacterial heat-shock protein
(HSP) 65,21
anti–C pneumoniae IgA
(seroCP-IgA, Savyon Diagnostics Ltd),
anti–H pylori IgG (Medac), and
anti-cytomegalovirus IgG antibodies
(Medac13 ) and levels of
soluble human HSP60. For the latter, monoclonal antibodies directed
against the II-13 epitope (coated at microtiter plates) and the ML-30
epitope (labeled with biotin) were used. Standard curves were obtained
by use of recombinant human HSP60 (StressGen
Biotechnologies).22 Other
parameters were assayed by standard
methods.18 20
Scanning Protocol and Definition of Ultrasound
End Points
The ultrasound protocol involves the scanning of the
internal (bulbous and distal segments) and common carotid arteries
(proximal and distal segments) of either side with a 10-MHz imaging
probe and a 5-MHz Doppler
probe.16 17
Atherosclerotic lesions were defined according to 2 ultrasound
criteria: (1) wall surface (protrusion or roughness of the arterial
boundary) and (2) wall texture (echogenicity). The maximum axial
diameter of plaques was assessed in each of the 8 vessel segments, and
an atherosclerosis score was calculated by addition of all diameters.
The intima-media thickness was measured at the far wall of the common
carotid arteries (intraobserver coefficient of variation, 7.9%
[n=100]).16 17
Scanning was performed twice in 1990 and 1995 by the same experienced
sonographer, who was unaware of the subjects’ clinical and laboratory
characteristics. The development of new carotid plaques (early
atherogenesis) and occurrence/progression of vessel stenosis >40%
(advanced atherogenesis) was assessed in all
subjects.16 17 18
Reproducibility of the ultrasound categories was "nearly perfect"
(
coefficients >0.8 as derived from 2 independent measurements
performed by the same sonographer in a reproducibility sample,
n=10016 17 ).
Statistical Analysis
Differences in the means of vascular risk attributes
and markers of inflammation in subjects with and without chronic
infections were analyzed with Student’s
t test
(
2 test for proportions). The association
of chronic infection status with the development of carotid plaques and
carotid stenosis was examined by logistic regression
analysis.23 Multivariate
equations were adjusted for a fixed set of
covariates18 or fitted by a
forward stepwise selection procedure. Analyses performed in the entire
population sample
(Figures 1 through 4
) included the baseline atherosclerosis
score as a covariate, because there is evidence that preexisting vessel
disease promotes atherogenesis beyond the injurious action of the
vascular risk profile. This procedure had virtually no effect on the
risk estimates. Population attributive fractions were adjusted for
other risk variables.24
Logistic regression models were supplemented and confirmed by linear
regression analysis by use of 5-year changes in the atherosclerosis
score or the intima-media thickness as continuous outcome
variables.
|
) + LDL and HDL cholesterol, lipoprotein (a), hypertension, smoking (pack-years), alcohol consumption, ferritin, hypothyroidism, and microalbuminuria (
).
|
|
|
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Of the 826 study subjects, 268 met the diagnostic criteria of chronic infections (Table 1
). Susceptibility to infectious illness
increased with advancing age, low social status, and risk behaviors
such as cigarette smoking and heavy drinking. Serum levels of various
markers of inflammation and infection were substantially enhanced in
the chronic infection condition
(Table 2). Furthermore, subjects with chronic infections
showed multiple unfavorable changes in vascular risk factors, most of
which were quantitatively low
(Table 2).
|
|
During a mean of 5 years’ follow-up, new carotid plaques
emerged in 332 of 826 subjects (41%, population-adjusted rate 33%),
with the risk of atherosclerosis development being markedly elevated
among individuals with chronic infection (adjusted OR for any chronic
infection versus none, 2.78,
P<0.001;
Figure 1
). In the subgroup of subjects free of carotid
atherosclerosis at baseline (n=500), a total of 125 (25%,
population-adjusted rate 20%) showed a manifestation of first carotid
plaques. Again, those with chronic infections faced a several-fold risk
of atherosclerosis regardless of whether the analysis was adjusted for
age and sex only (OR [95% CI], 4.08 [2.42 to 6.85];
P<0.0001) or fitted with a
forward-stepwise logistic regression procedure (adjusted OR, 4.10;
Table 3). Exclusion of subjects with manifest
cardiovascular diseases had little effect on the risk estimates
obtained (adjusted OR, 4.05). In the subgroup of subjects with
preexisting carotid atherosclerosis, chronic infection status was of
predictive significance for the development of further lesions (disease
extension) as well (adjusted OR, 2.31;
P<0.001).
|
To account for the potentially confounding effect of
cigarette smoking, which increases susceptibility to infections and per
se represents a vascular risk factor, the analyses were repeated in
lifetime nonsmokers. This and the following analyses were performed in
the entire population sample to ensure adequate sample sizes. Results
were not substantially attenuated
(Figure 1). In line with this, separate analyses limited to
abstainers or various age and other subgroups yielded results similar
to those derived from the original computation
(Figure 1), as did analyses performed after exclusion of
subjects receiving aspirin and/or those with manifest cardiovascular
disease and/or the few subjects reporting repeated or long-term therapy
with antibiotics (n=21).
The strong association with the development of new
atherosclerotic lesions applied to respiratory, urinary, and other
types of chronic infectious illness, including infections with
C pneumoniae
(Figure 2). In contrast, seropositivity to the
cytomegalovirus, manifest infections with the herpes zoster virus, and
chronic active hepatitis B/C appeared to be unrelated to this early
stage in atherogenesis.
Chronic infection status conferred a markedly increased risk
of atherosclerosis development, even in the absence of other vascular
risk factors
(Figure 1). Among subjects with chronic infections, there was
a clear tendency for atherosclerosis risk to increase when C-reactive
protein levels exceeded 1 mg/L (60th percentile)
(Figure 3).
In subjects with preexisting carotid atherosclerosis (n=326), chronic infections conferred an increased risk for the manifestation/progression of carotid stenosis >40% (OR [95% CI] 1.63 [1.03 to 2.58]; P<0.05), which disappeared after adjustment for other risk variables, some of which were increased in the chronic infection condition (eg, fibrinogen). Finally, analyses that applied continuous measures of atherosclerosis extension replicated the results derived from our categorical progression model. In linear regression analyses adjusted for age, sex, and other vascular risk factors, chronic infection status ranked among the variables most strongly associated with atherosclerosis progression (regression coefficients [95% CI] for change in atherosclerosis score, 0.85 [0.47 to 1.23] and intima-media thickness, 0.05 [0.02 to 0.08]; P<0.01 each).
Figure 4 depicts various markers of infection, inflammation,
and immunity. Baseline levels of these variables were significantly
enhanced in subjects who developed atherosclerotic lesions during
follow-up.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Experimental work in the late 1970s and 1980s has prompted a revival of interest in the old hypothesis of an infectious risk factor for atherosclerosis.1 4 5 6 7 Epidemiological confirmation of this concept has not yet been furnished, although (mainly) indirect supportive evidence recently became available.7 8 10 11 12 13 14 15 19 21 22 25 26 High concentrations of C-reactive protein were observed to predict the risk of future cardiovascular disease and may arise in part from the chronic inflammatory state evident in persistent infections.25 26 In most but not all seroepidemiological evaluations, subjects with a prominent immune response to C pneumoniae or (virulent strains of) H pylori, as indicative of chronic infection status, faced an excess risk of coronary heart disease, stroke, and vascular death.7 13 14 15 27 28 29 Finally, chronic bronchitis, as defined by self-reported clinical symptoms, and periodontal disease have been suggested to constitute risk factors for cardiovascular disease.10 11 12
In the Bruneck Study, common chronic infections, as defined
by standard diagnostic procedures, predicted a markedly increased risk
of atherogenesis in the carotid arteries. All major results were
consistently obtained from 2 ultrasound progression models of
atherosclerosis. The one commonly used in the literature uses
continuous outcome variables, such as atherosclerosis scores or
intima-media thickness, and analyzes changes in these variables over
time. The second, person-based approach, developed and validated in the
Bruneck Study, permits differentiation of 2 distinct stages of
atherogenesis, namely the development of new (early) plaques and the
occurrence/progression of vessel stenosis, which was shown to rely
primarily on atherothrombotic
pathomechanisms.16 17 18
As expected, chronic infections were preferentially related to the
former stage. In subjects without atherosclerosis at baseline, 
40%
of newly developed atherosclerosis was attributable to chronic
infection (population attributable risk), making it a leading risk
predictor for this initiating stage of vessel pathology
(Table 3). Chronic infections conferred an increased risk of
atherosclerosis development even in low-risk subjects free of
conventional vascular risk factors.
Subjects with respiratory, urinary, and other types of
infections all faced an increased risk of atherosclerosis
(Figure 2), with the spectrum of underlying pathogens being
highly heterogeneous. C
pneumoniae, which attracted preferential attention in past
research, ranked among these
pathogens.13 In accordance
with our results, atherosclerosis can be induced in animal models by a
variety of microorganisms, such as chlamydia, streptococci, and
salmonella.1 3 9 30
As to infection with the cytomegalovirus (assessed by serological
criteria)13 and other viral
agents, our study did not furnish evidence of a role in atherogenesis,
which, however, may be a peculiarity of our study population and does
not rule out pathogenetic relevance in special subgroups, such as
subjects receiving immune-suppressive therapy or undergoing coronary
angioplasty.4 5 6 7 8 31
Among subjects with chronic infections, risk of
atherosclerosis tended to be higher in those with a prominent
inflammatory response
(Figure 3), which may indicate high virulence of the
underlying pathogen or atherogenic host-pathogen
interactions.13 14 27 31
Induction of systemic inflammation has been proposed to be of
pathogenetic relevance in the association of infection and
atherosclerosis and may rely in part on the endothelial toxicity of
bacterial endotoxin and the action of proinflammatory
cytokines.7 19
Recently, we demonstrated that in smokers and subjects with chronic
infections, high concentrations of circulating endotoxin predict a
substantially increased risk of atherosclerosis
(Figure 4).19 The
present evaluation extends this finding to various other markers of
inflammation, all of which predicted the development of atherosclerosis
and were substantially enhanced in subjects with chronic infections
(Table 2,
Figure 4).
Another well-founded proatherogenic property of infectious illness may be the induction of autoimmunity.32 All bacteria expose immunogenic HSP60 on their surface, which shows a high structure homology to its human counterpart. Human HSP60 expression is increased in atherosclerotic lesions, notably in areas subject to hemodynamic stress.32 Serum antibodies to mycobacterial HSP65 correlate with the prevalence and incidence of carotid atherosclerosis,21 cross-react with human HSP60, and mediate cytotoxicity on stressed endothelial cells.33 Chronic infections may contribute to vascular injury by causing a breakdown of self-tolerance and subsequent immune attack against human HSP exposed on endothelium stressed by atherogenic risk factors.
In the interpretation of our results, it must be considered that no consensus exists on the types of illness to be subsumed under the term "chronic infections." In the present analysis, this potential source of bias was at least in part overcome by an a priori definition of the variable. Infection status was defined by standard diagnostic guidelines, which closely resembles diagnostic practice in clinical routine and thus warrants high accuracy. As a further potential limitation, the study population is purely white. Results are not necessarily representative of other ethnic populations, which may differ in the genetic background of immune defense as well as target cell (endothelial cell) antigen expression.
In conclusion, the present study advocates a prominent role of common (bacterial) infections in atherogenesis and suggests 2 important pathophysiological clues: the induction of systemic inflammation and autoimmunity. Our findings may assist in identifying subjects at high risk of atherosclerosis and offer a preliminary basis for future anti-infectious and anti-inflammatory prevention trials.
Received August 10, 2000; revision received October 27, 2000; accepted October 27, 2000.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Nieto FJ. Infections and atherosclerosis: new clues from an old hypothesis. Am J Epidemiol. 1998;148:937–948.
2. Virchow R. Cellular Pathology as Based Upon Physiological and Pathological Histology. (English translation of German edition 1859). Philadelphia, Pa: JB Lippincott; 1971.
3. Gilbert A, Lion G. Artérites infectieuses expérimentales. CR Séances Soc Biol Fil. 1889;41:583–584.
4.
Speir E, Modali R,
Huang ES, et al. Potential role of human cytomegalovirus and p53
interaction in coronary restenosis.
Science. 1994;265:391–394.
5. Minick CR, Fabricant CG, Fabricant J, et al. Atheroarteriosclerosis induced by infection with a herpesvirus. Am J Pathol. 1979;96:673–706.[Abstract]
6.
Fabricant CG,
Fabricant J, Litrenta MM, et al. Virus-induced atherosclerosis.
J Exp Med. 1978;148:335–340.
7.
Libby P, Egan D,
Skarlatos S. Roles of infectious agents in atherosclerosis and
restenosis: an assessment of the evidence and need for future research.
Circulation. 1997;96:4095–4103.
8.
Nicholson AC,
Hajjar DP. Herpesvirus in atherosclerosis and thrombosis: etiologic
agents or ubiquitous bystanders?
Arterioscler Thromb Vasc Biol. 1998;18:339–348.
9.
Muhlestein JB,
Anderson JL, Hammond EH, et al. Infection with
Chlamydia pneumoniae
accelerates the development of atherosclerosis and treatment with
azithromycin prevents it in a rabbit model.
Circulation. 1998;97:633–636.
10. Jousilahti P, Vartiainen E, Tuomilehto J, et al. Symptoms of chronic bronchitis and the risk of coronary disease. Lancet. 1996;348:567–572.[Medline] [Order article via Infotrieve]
11. DeStefano F, Anda RF, Kahn HS, et al. Dental disease and risk of coronary heart disease and mortality. BMJ. 1993;306:688–691.
12. Mattila KJ, Valtonen VV, Nieminen M, et al. Dental infection and the risk of new coronary events: prospective study of patients with documented coronary artery disease. Clin Infect Dis. 1995;20:588–592.[Medline] [Order article via Infotrieve]
13.
Mayr M, Kiechl S,
Willeit J, et al. Infections, immunity, and atherosclerosis:
associations of antibodies to Chlamydia
pneumoniae, Helicobacter
pylori, and cytomegalovirus with immune reactions to
heat-shock protein 60 and carotid and femoral atherosclerosis.
Circulation. 2000;102:833–839.
14.
Pasceri V,
Cammarota G, Patti G, et al. Association of virulent
Helicobacter pylori strains
with ischemic heart disease.
Circulation. 1998;97:1675–1679.
15.
Strachan DP,
Carrington D, Mendall MA, et al. Relation of
Chlamydia pneumoniae serology
to mortality and incidence of ischaemic heart disease over 13 years in
the Caerphilly prospective heart disease study.
BMJ. 1999;318:1035–1039.
16.
Kiechl S, Willeit
J. The natural course of atherosclerosis, I: incidence and progression.
Arterioscler Thromb Vasc Biol. 1999;19:1484–1490.
17.
Kiechl S, Willeit
J. The natural course of atherosclerosis, II: vascular remodeling.
Arterioscler Thromb Vasc Biol. 1999;19:1491–1498.
18.
Willeit J, Kiechl
S, Oberhollenzer F, et al. Distinct risk profiles of early and advanced
atherosclerosis: prospective results from the Bruneck Study.
Arterioscler Thromb Vasc Biol. 2000;20:529–537.
19.
Wiedermann
CI, Kiechl S, Dunzendorfer S, et al. Association of endotoxemia with
carotid atherosclerosis and cardiovascular disease: prospective results
from the Bruneck Study. J Am Coll
Cardiol. 1999;34:1975–1981.
20.
Kiechl S, Willeit
J, Egger G, et al. Body iron stores and the risk of carotid
atherosclerosis: prospective results from the Bruneck Study.
Circulation. 1997;96:3300–3307.
21.
Xu Q, Kiechl S,
Mayr M, et al. Association of serum antibodies to heat-shock protein 65
with carotid atherosclerosis: clinical significance determined in a
follow-up study. Circulation. 1999;100:1169–1174.
22.
Xu Q, Schett G,
Perschinka H, et al. Serum soluble heat shock protein 60 is elevated in
subjects with atherosclerosis in a general population.
Circulation. 2000;102:14–20.
23. Hosmer DW, Lemeshow S. Applied Logistic Regression. New York, NY: John Wiley & Sons Inc; 1988.
24.
Whittemore AS.
Estimating attributable risk from case-control studies.
Am J Epidemiol. 1983;117:76–85.
25.
Ridker PM,
Cushman M, Stampfer MJ, et al. Inflammation, aspirin, and the risk of
cardiovascular disease in apparently healthy men.
N Engl J Med. 1997;336:973–979.
26.
Kuller LH, Tracy
RP, Shaten J, et al. Relation of C-reactive protein and coronary heart
disease in the MRFIT nested case-control study.
Am J Epidemiol. 1996;144:537–547.
27.
Epstein SE, Zhu
J. Lack of association of infectious agents with risk of future
myocardial infarction and stroke: definite evidence disproving the
infection/coronary artery disease hypothesis?
Circulation. 1999;100:1366–1368.
28.
Markus HS, Sitzer
M, Carrington D, et al. Chlamydia
pneumoniae infection and early asymptomatic carotid
atherosclerosis. Circulation. 1999;100:832–837.
29.
Folsom AR, Nieto
FJ, Sorlie P, et al, Atherosclerosis Risk In Communities (ARIC) Study
Investigators. Helicobacter
pylori seropositivity and coronary heart disease incidence.
Circulation. 1998;98:845–850.
30. Benson RL, Smith KG, Semenov H. Experimental arteritis and arteriosclerosis associated with streptococcal inoculations. Arch Pathol. 1931;12:924–940.
31.
Zhu J, Quyyumi
AA, Norman JE, et al. Cytomegalovirus in the pathogenesis of
atherosclerosis: the role of inflammation as reflected by elevated
C-reactive protein levels. J Am Coll
Cardiol. 1999;34:1738–1743.
32. Wick G, Romen M, Amberger A, et al. Atherosclerosis, autoimmunity and vascular-associated lymphoid tissue (VALT). FASEB J. 1997;11:1199–1207.[Medline] [Order article via Infotrieve]
33.
Mayr M, Metzler
B, Kiechl S, et al. Endothelial cytotoxicity mediated by serum
antibodies to heat shock proteins of
Escherichia coli and
Chlamydia pneumoniae: immune
reactions to heat shock proteins as a possible link between infection
and atherosclerosis.
Circulation. 1999;99:1560–1566.
This article has been cited by other articles:
 |
|
 |
|
  A. S. Reece Improved parameters of metabolic glycaemic and immune function and arterial stiffness with naltrexone implant therapy BMJ Case Reports, April 14, 2009; 2009(apr07_2): bcr0820080799 - bcr0820080799. [Abstract] [Full Text]
|
|
|
|
 |
|
 E. Pesonen, E. Andsberg, A. Grubb, H. Rautelin, S. Meri, K. Persson, M. Puolakkainen, S. Sarna, and H. Ohlin Elevated infection parameters and infection symptoms predict an acute coronary event Therapeutic Advances in Cardiovascular Disease, December 1, 2008; 2(6): 419 - 424. [Abstract] [PDF]
|
|
|
|
 |
|
 S. Kato, M. Chmielewski, H. Honda, R. Pecoits-Filho, S. Matsuo, Y. Yuzawa, A. Tranaeus, P. Stenvinkel, and B. Lindholm Aspects of Immune Dysfunction in End-stage Renal Disease Clin. J. Am. Soc. Nephrol., September 1, 2008; 3(5): 1526 - 1533. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K.A. E. Kallio, K. Buhlin, M. Jauhiainen, R. Keva, A. M. Tuomainen, B. Klinge, A. Gustafsson, and P. J. Pussinen Lipopolysaccharide associates with pro-atherogenic lipoproteins in periodontitis patients Innate Immunity, August 1, 2008; 14(4): 247 - 253. [Abstract] [PDF]
|
|
|
|
 |
|
 A. R. Afzal, S. Kiechl, Y. P. Daryani, A. Weerasinghe, Y. Zhang, M. Reindl, A. Mayr, S. Weger, Q. Xu, and J. Willeit Common CCR5-del32 Frameshift Mutation Associated With Serum Levels of Inflammatory Markers and Cardiovascular Disease Risk in the Bruneck Population Stroke, July 1, 2008; 39(7): 1972 - 1978. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Loppnow, K. Werdan, and M. Buerke Invited review: Vascular cells contribute to atherosclerosis by cytokine- and innate-immunity-related inflammatory mechanisms Innate Immunity, April 1, 2008; 14(2): 63 - 87. [Abstract] [PDF]
|
|
|
|
 |
|
 A. M. Guiltinan, Z. Kaidarova, B. Custer, J. Orland, A. Strollo, S. Cyrus, M. P. Busch, and E. L. Murphy Increased All-Cause, Liver, and Cardiac Mortality among Hepatitis C Virus-seropositive Blood Donors Am. J. Epidemiol., March 15, 2008; 167(6): 743 - 750. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C.-C. Szeto, B. C.-H. Kwan, K.-M. Chow, K.-B. Lai, K.-Y. Chung, C.-B. Leung, and P. K.-T. Li Endotoxemia is Related to Systemic Inflammation and Atherosclerosis in Peritoneal Dialysis Patients Clin. J. Am. Soc. Nephrol., March 1, 2008; 3(2): 431 - 436. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A Steptoe, A Shamaei-Tousi, A Gylfe, B Henderson, S Bergstrom, and M Marmot Socioeconomic status, pathogen burden and cardiovascular disease risk Heart, December 1, 2007; 93(12): 1567 - 1570. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Kiechl, G. Schett, J. Schwaiger, K. Seppi, P. Eder, G. Egger, P. Santer, A. Mayr, Q. Xu, and J. Willeit Soluble Receptor Activator of Nuclear Factor-{kappa}B Ligand and Risk for Cardiovascular Disease Circulation, July 24, 2007; 116(4): 385 - 391. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D.-F. Dai, J.-W. Lin, J.-H. Kao, C.-N. Hsu, F.-T. Chiang, J.-L. Lin, Y.-H. Chou, K.-L. Hsu, C.-D. Tseng, Y.-Z. Tseng, et al. The Effects of Metabolic Syndrome Versus Infectious Burden on Inflammation, Severity of Coronary Atherosclerosis, and Major Adverse Cardiovascular Events J. Clin. Endocrinol. Metab., July 1, 2007; 92(7): 2532 - 2537. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. J. Pussinen, K. Tuomisto, P. Jousilahti, A. S. Havulinna, J. Sundvall, and V. Salomaa Endotoxemia, Immune Response to Periodontal Pathogens, and Systemic Inflammation Associate With Incident Cardiovascular Disease Events Arterioscler. Thromb. Vasc. Biol., June 1, 2007; 27(6): 1433 - 1439. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Sung, Y.-M. Song, Y.-H. Choi, S. Ebrahim, and G. Davey Smith Hepatitis B Virus Seropositivity and the Risk of Stroke and Myocardial Infarction Stroke, May 1, 2007; 38(5): 1436 - 1441. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Erridge, C. M. Spickett, and D. J. Webb Non-enterobacterial endotoxins stimulate human coronary artery but not venous endothelial cell activation via Toll-like receptor 2 Cardiovasc Res, January 1, 2007; 73(1): 181 - 189. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F.-Y. Lin, Y.-H. Chen, J.-S. Tasi, J.-W. Chen, T.-L. Yang, H.-J. Wang, C.-Y. Li, Y.-L. Chen, and S.-J. Lin Endotoxin Induces Toll-Like Receptor 4 Expression in Vascular Smooth Muscle Cells via NADPH Oxidase Activation and Mitogen-Activated Protein Kinase Signaling Pathways Arterioscler. Thromb. Vasc. Biol., December 1, 2006; 26(12): 2630 - 2637. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Tarasiuk, S. Greenberg-Dotan, T. Simon, A. Tal, A. Oksenberg, and H. Reuveni Low socioeconomic status is a risk factor for cardiovascular disease among adult obstructive sleep apnea syndrome patients requiring treatment. Chest, September 1, 2006; 130(3): 766 - 773. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. S. Markus, R. Labrum, S. Bevan, M. Reindl, G. Egger, C. J. Wiedermann, Q. Xu, S. Kiechl, and J. Willeit Genetic and Acquired Inflammatory Conditions Are Synergistically Associated With Early Carotid Atherosclerosis Stroke, September 1, 2006; 37(9): 2253 - 2259. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Schillinger, W. Kluger, M. Exner, W. Mlekusch, S. Sabeti, J. Amighi, O. Wagner, E. Minar, and M. Schillinger Dental and Periodontal Status and Risk for Progression of Carotid Atherosclerosis: The Inflammation and Carotid Artery Risk for Atherosclerosis Study Dental Substudy Stroke, September 1, 2006; 37(9): 2271 - 2276. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Erdogan, C. A. Schaefer, A. K. Most, M. B. Schaefer, K. Mayer, H. Tillmanns, and C. R. W. Kuhlmann Lipopolysaccharide-induced proliferation and adhesion of U937 cells to endothelial cells involves barium chloride sensitive hyperpolarization Innate Immunity, August 1, 2006; 12(4): 224 - 230. [Abstract] [PDF]
|
|
|
|
 |
|
 M. Mayr, S. Kiechl, S. Tsimikas, E. Miller, J. Sheldon, J. Willeit, J. L. Witztum, and Q. Xu Oxidized Low-Density Lipoprotein Autoantibodies, Chronic Infections, and Carotid Atherosclerosis in a Population-Based Study J. Am. Coll. Cardiol., June 20, 2006; 47(12): 2436 - 2443. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Volanen, M. J. Jarvisalo, R. Vainionpaa, M. Arffman, K. Kallio, S. Angle, T. Ronnemaa, J. Viikari, J. Marniemi, O. T. Raitakari, et al. Increased Aortic Intima-Media Thickness in 11-Year-Old Healthy Children With Persistent Chlamydia pneumoniae Seropositivity Arterioscler. Thromb. Vasc. Biol., March 1, 2006; 26(3): 649 - 655. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. Chen, G. Yang, M. Zhou, M. Smith, A. Offer, J. Ma, L. Wang, H. Pan, G. Whitlock, R. Collins, et al. Body mass index and mortality from ischaemic heart disease in a lean population: 10 year prospective study of 220 000 adult men Int. J. Epidemiol., February 1, 2006; 35(1): 141 - 150. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Q. Xiao, K. Mandal, G. Schett, M. Mayr, G. Wick, F. Oberhollenzer, J. Willeit, S. Kiechl, and Q. Xu Association of Serum-Soluble Heat Shock Protein 60 With Carotid Atherosclerosis: Clinical Significance Determined in a Follow-Up Study Stroke, December 1, 2005; 36(12): 2571 - 2576. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Knoflach, S. Kiechl, A. Mayr, J. Willeit, W. Poewe, and G. Wick Allergic Rhinitis, Asthma, and Atherosclerosis in the Bruneck and ARMY Studies Arch Intern Med, November 28, 2005; 165(21): 2521 - 2526. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Bruunsgaard Physical activity and modulation of systemic low-level inflammation J. Leukoc. Biol., October 1, 2005; 78(4): 819 - 835. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Kivimaki, D. A. Lawlor, M. Juonala, G. Davey Smith, M. Elovainio, L. Keltikangas-Jarvinen, J. Vahtera, J. S.A. Viikari, and O. T. Raitakari Lifecourse Socioeconomic Position, C-Reactive Protein, and Carotid Intima-Media Thickness in Young Adults: The Cardiovascular Risk in Young Finns Study Arterioscler. Thromb. Vasc. Biol., October 1, 2005; 25(10): 2197 - 2202. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R-S Koskela, P Mutanen, J-A Sorsa, and M Klockars Respiratory disease and cardiovascular morbidity Occup. Environ. Med., September 1, 2005; 62(9): 650 - 655. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D H Birnie, L E Vickers, W S Hillis, J Norrie, and S M Cobbe Increased titres of anti-human heat shock protein 60 predict an adverse one year prognosis in patients with acute cardiac chest pain Heart, September 1, 2005; 91(9): 1148 - 1153. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Pfister, C. M. Stroh, H. Perschinka, M. Kind, M. Knoflach, P. Hinterdorfer, and G. Wick Detection of HSP60 on the membrane surface of stressed human endothelial cells by atomic force and confocal microscopy J. Cell Sci., April 15, 2005; 118(8): 1587 - 1594. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Desvarieux, R. T. Demmer, T. Rundek, B. Boden-Albala, D. R. Jacobs Jr, R. L. Sacco, and P. N. Papapanou Periodontal Microbiota and Carotid Intima-Media Thickness: The Oral Infections and Vascular Disease Epidemiology Study (INVEST) Circulation, February 8, 2005; 111(5): 576 - 582. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. L. Stoll, G. M. Denning, and N. L. Weintraub Potential Role of Endotoxin as a Proinflammatory Mediator of Atherosclerosis Arterioscler. Thromb. Vasc. Biol., December 1, 2004; 24(12): 2227 - 2236. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. S. Michelsen, T. M. Doherty, P. K. Shah, and M. Arditi TLR Signaling: An Emerging Bridge from Innate Immunity to Atherogenesis J. Immunol., November 15, 2004; 173(10): 5901 - 5907. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. H. Meurman, M. Sanz, and S.-J. Janket ORAL HEALTH, ATHEROSCLEROSIS, AND CARDIOVASCULAR DISEASE Critical Reviews in Oral Biology & Medicine, November 1, 2004; 15(6): 403 - 413. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Lu, M. Raptis, E. Black, M. Stan, S. Amar, and D. T. Graves Influence of Diabetes on the Exacerbation of an Inflammatory Response in Cardiovascular Tissue Endocrinology, November 1, 2004; 145(11): 4934 - 4939. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. J. Chilton Pathophysiology of Coronary Heart Disease: A Brief Review J Am Osteopath Assoc, September 1, 2004; 104(9_suppl): 5S - 8S. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. M. Miller, G. Rodgers, J. A. Charlesworth, B. Kirkland, S. R. Severson, T. E. Rasmussen, M. Yagubyan, J. C. Rodgers, F. R. Cockerill III, R. L. Folk, et al. Evidence of nanobacterial-like structures in calcified human arteries and cardiac valves Am J Physiol Heart Circ Physiol, September 1, 2004; 287(3): H1115 - H1124. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. L. Stoll, G. M. Denning, W.-G. Li, J. B. Rice, A. L. Harrelson, S. A. Romig, S. T. Gunnlaugsson, F. J. Miller Jr, and N. L. Weintraub Regulation of Endotoxin-Induced Proinflammatory Activation in Human Coronary Artery Cells: Expression of Functional Membrane-Bound CD14 by Human Coronary Artery Smooth Muscle Cells J. Immunol., July 15, 2004; 173(2): 1336 - 1343. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Khovidhunkit, M.-S. Kim, R. A. Memon, J. K. Shigenaga, A. H. Moser, K. R. Feingold, and C. Grunfeld Thematic review series: The Pathogenesis of Atherosclerosis. Effects of infection and inflammation on lipid and lipoprotein metabolism mechanisms and consequences to the host J. Lipid Res., July 1, 2004; 45(7): 1169 - 1196. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Kiechl, G. Schett, G. Wenning, K. Redlich, M. Oberhollenzer, A. Mayr, P. Santer, J. Smolen, W. Poewe, and J. Willeit Osteoprotegerin Is a Risk Factor for Progressive Atherosclerosis and Cardiovascular Disease Circulation, May 11, 2004; 109(18): 2175 - 2180. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C Vassalle, S Masini, F Bianchi, and G C Zucchelli Evidence for association between hepatitis C virus seropositivity and coronary artery disease Heart, May 1, 2004; 90(5): 565 - 566. [Full Text] [PDF]
|
|
|
|
|
|
M. Naghavi, P. Libby, E. Falk, S. W. Casscells, S. Litovsky, J. Rumberger, J. J. Badimon, C. Stefanadis, P. Moreno, G. Pasterkamp, et al. From Vulnerable Plaque to Vulnerable Patient: A Call for New Definitions and Risk Assessment Strategies: Part II Circulation, October 14, 2003; 108(15): 1772 - 1778. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Girndt and H. Kohler Interleukin-10 (IL-10): an update on its relevance for cardiovascular risk Nephrol. Dial. Transplant., October 1, 2003; 18(10): 1976 - 1979. [Full Text] [PDF]
|
|
|
|
|
|
M. P. Reilly, M. L. Wolfe, A. R. Localio, and D. J. Rader C-Reactive Protein and Coronary Artery Calcification: The Study of Inherited Risk of Coronary Atherosclerosis (SIRCA) Arterioscler. Thromb. Vasc. Biol., October 1, 2003; 23(10): 1851 - 1856. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. J. Lindsberg and A. J. Grau Inflammation and Infections as Risk Factors for Ischemic Stroke Stroke, October 1, 2003; 34(10): 2518 - 2532. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. B. Rice, L. L. Stoll, W.-G. Li, G. M. Denning, J. Weydert, E. Charipar, W. E. Richenbacher, F. J. Miller Jr, and N. L. Weintraub Low-Level Endotoxin Induces Potent Inflammatory Activation of Human Blood Vessels: Inhibition by Statins Arterioscler. Thromb. Vasc. Biol., September 1, 2003; 23(9): 1576 - 1582. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Desvarieux, R. T. Demmer, T. Rundek, B. Boden-Albala, D. R. Jacobs Jr, P. N. Papapanou, and R. L. Sacco Relationship Between Periodontal Disease, Tooth Loss, and Carotid Artery Plaque: The Oral Infections and Vascular Disease Epidemiology Study (INVEST) Stroke, September 1, 2003; 34(9): 2120 - 2125. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. A. Holly and P. M. Bracci Population-based Study of Non-Hodgkin Lymphoma, Histology, and Medical History among Human Immunodeficiency Virus-negative Participants in San Francisco Am. J. Epidemiol., August 15, 2003; 158(4): 316 - 327. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. K. Kiecolt-Glaser, K. J. Preacher, R. C. MacCallum, C. Atkinson, W. B. Malarkey, and R. Glaser Chronic stress and age-related increases in the proinflammatory cytokine IL-6 PNAS, July 22, 2003; 100(15): 9090 - 9095. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Perschinka, M. Mayr, G. Millonig, C. Mayerl, R. van der Zee, S. G. Morrison, R. P. Morrison, Q. Xu, and G. Wick Cross-Reactive B-Cell Epitopes of Microbial and Human Heat Shock Protein 60/65 in Atherosclerosis Arterioscler. Thromb. Vasc. Biol., June 1, 2003; 23(6): 1060 - 1065. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Huittinen, M. Leinonen, L. Tenkanen, H. Virkkunen, M. Manttari, T. Palosuo, V. Manninen, and P. Saikku Synergistic Effect of Persistent Chlamydia pneumoniae Infection, Autoimmunity, and Inflammation on Coronary Risk Circulation, May 27, 2003; 107(20): 2566 - 2570. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Bonora, S. Kiechl, J. Willeit, F. Oberhollenzer, G. Egger, R. C. Bonadonna, and M. Muggeo Carotid Atherosclerosis and Coronary Heart Disease in the Metabolic Syndrome: Prospective data from the Bruneck Study Diabetes Care, April 1, 2003; 26(4): 1251 - 1257. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Mayr, S. Kiechl, M. A. Mendall, J. Willeit, G. Wick, and Q. Xu Increased Risk of Atherosclerosis Is Confined to CagA-Positive Helicobacter pylori Strains: Prospective Results From the Bruneck Study Stroke, March 1, 2003; 34(3): 610 - 615. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. B. Muhlestein and J. L. Anderson Infectious Serology and Atherosclerosis: How Burdensome Is the Risk? Circulation, January 21, 2003; 107(2): 220 - 222. [Full Text] [PDF]
|
|
|
|
 |
|
 G. S. Cooke, S. Segal, A. V.S. Hill, the Tuberculosis, Genetics, and Environment (TBGEN, B. Beutler, E. Beutler, S. Kiechl, J. Willeit, and D. A. Schwartz Toll-like Receptor 4 Polymorphisms and Atherogenesis N. Engl. J. Med., December 12, 2002; 347(24): 1978 - 1980. [Full Text] [PDF]
|
|
|
|
|
|
M. Prager, Z. Turel, W. S. Speidl, G. Zorn, C. Kaun, A. Niessner, G. Heinze, I. Huk, G. Maurer, K. Huber, et al. Chlamydia pneumoniae in Carotid Artery Atherosclerosis: A Comparison of Its Presence in Atherosclerotic Plaque, Healthy Vessels, and Circulating Leukocytes From the Same Individuals Stroke, December 1, 2002; 33(12): 2756 - 2761. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Espinola-Klein, H.-J. Rupprecht, S. Blankenberg, C. Bickel, H. Kopp, A. Victor, G. Hafner, W. Prellwitz, W. Schlumberger, and J. Meyer Impact of Infectious Burden on Progression of Carotid Atherosclerosis Stroke, November 1, 2002; 33(11): 2581 - 2586. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Temelkova-Kurktschiev, C. Koehler, E. Henkel, and M. Hanefeld Leukocyte count and fibrinogen are associated with carotid and femoral intima-media thickness in a risk population for diabetes Cardiovasc Res, November 1, 2002; 56(2): 277 - 283. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.A. Erkens, O.H. Klungel, R.M.C. Herings, R.P. Stolk, J.A. Spoelstra, D.E. Grobbee, and H.G.M. Leufkens Use of fluorquinolones is associated with a reduced risk of coronary heart disease in diabetes mellitus type 2 patients Eur. Heart J., October 2, 2002; 23(20): 1575 - 1579. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Q. Xu Role of Heat Shock Proteins in Atherosclerosis Arterioscler. Thromb. Vasc. Biol., October 1, 2002; 22(10): 1547 - 1559. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Kiechl, P. Werner, G. Egger, F. Oberhollenzer, M. Mayr, Q. Xu, W. Poewe, and J. Willeit Active and Passive Smoking, Chronic Infections, and the Risk of Carotid Atherosclerosis: Prospective Results From the Bruneck Study Stroke, September 1, 2002; 33(9): 2170 - 2176. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
E. Lutgens, M. Gijbels, M. Smook, P. Heeringa, P. Gotwals, V. E. Koteliansky, and M. J.A.P. Daemen Transforming Growth Factor-{beta} Mediates Balance Between Inflammation and Fibrosis During Plaque Progression Arterioscler. Thromb. Vasc. Biol., June 1, 2002; 22(6): 975 - 982. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Ishizaka, Y. Ishizaka, E. Takahashi, E.-i. Toda, H. Hashimoto, M. Ohno, R. Nagai, and M. Yamakado Increased Prevalence of Carotid Atherosclerosis in Hepatitis B Virus Carriers Circulation, March 5, 2002; 105(9): 1028 - 1030. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Huittinen, M. Leinonen, L. Tenkanen, M. Manttari, H. Virkkunen, T. Pitkanen, E. Wahlstrom, T. Palosuo, V. Manninen, and P. Saikku Autoimmunity to Human Heat Shock Protein 60, Chlamydia pneumoniae Infection, and Inflammation in Predicting Coronary Risk Arterioscler. Thromb. Vasc. Biol., March 1, 2002; 22(3): 431 - 437. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Saikku Seroepidemiology in Chlamydia pneumoniae -- atherosclerosis association Eur. Heart J., February 2, 2002; 23(4): 263 - 264. [Full Text] [PDF]
|
|
|
|
 |
|
 H. Nassar, H.-H. Chou, M. Khlgatian, F. C. Gibson III, T. E. V. Dyke, and C. A. Genco Role for Fimbriae and Lysine-Specific Cysteine Proteinase Gingipain K in Expression of Interleukin-8 and Monocyte Chemoattractant Protein in Porphyromonas gingivalis-Infected Endothelial Cells Infect. Immun., January 1, 2002; 70(1): 268 - 276. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. K. Kiecolt-Glaser, L. McGuire, T. F. Robles, and R. Glaser Psychoneuroimmunology and Psychosomatic Medicine: Back to the Future Psychosom Med, January 1, 2002; 64(1): 15 - 28. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Lutgens and M. J.A.P. Daemen Transforming Growth Factor-{beta}: A Local or Systemic Mediator of Plaque Stability? Circ. Res., November 9, 2001; 89(10): 853 - 855. [Full Text] [PDF]
|
|
|
|
|
|
C. J. Wiedermann, S. Kiechl, P. Schratzberger, S. Dunzendorfer, G. Weiss, and J. Willeit The role of immune activation in endotoxin-induced atherogenesis Innate Immunity, August 1, 2001; 7(4): 322 - 326. [Abstract] [PDF]
|
|
|
|
|
|
L. Li, E. Messas, E. L. Batista Jr, R. A. Levine, and S. Amar Porphyromonas gingivalis Infection Accelerates the Progression of Atherosclerosis in a Heterozygous Apolipoprotein E-Deficient Murine Model Circulation, February 19, 2002; 105(7): 861 - 867. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||