(Circulation. 1997;96:4204-4210.)
© 1997 American Heart Association, Inc.
Articles |
Prognostic Influence of Increased Fibrinogen and C-Reactive Protein Levels in Unstable Coronary Artery Disease
From the Department of Cardiology (H.T., B.L., L.W.) and Laboratory for Coagulation Research (A.S.), Department of Clinical Laboratory Sciences, University Hospital, Uppsala, Sweden.
Correspondence to Dr Henrik Toss, Department of Cardiology, University Hospital, S-751 85 Uppsala, Sweden.
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Abstract |
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Background The prognostic influences of fibrinogen and C-reactive protein levels and their relations to myocardial damage in unstable coronary artery syndromes have not been well described.
Methods and Results Fibrinogen and C-reactive protein were
determined at inclusion and related to outcome after 5 months in 965
patients with unstable angina or non–Q-wave myocardial infarction
randomized to 5 weeks with low-molecular-weight heparin or placebo. The
probabilities of death were 1.6%, 4.6%, and 6.9%
(P=.005) and the probabilities of death and/or
myocardial infarction were 9.3%, 14.2%, and 19.1%
(P=.002), respectively, in patients stratified by
tertiles of fibrinogen (<3.38, 3.38 to 3.99, and 
4.0 g/L). The
probabilities of death were 2.2%, 3.6%, and 7.5%
(P=.003) after stratification of patient data by
tertiles of C-reactive protein level (<2, 2 to 10, and >10 mg/L). In
logistic multiple regression analysis, increased fibrinogen
levels were independently associated with the incidence of death and/or
myocardial infarction (P=.013), and elevated C-reactive
protein level was associated with the incidence of death
(P=.012). The increased relative risk of subsequent
death or myocardial infarction in individuals with an elevated
fibrinogen level was consistent in most subgroups evaluated;
although significantly so only in patients with signs of myocardial
damage.
Conclusions Increased levels of both fibrinogen and C-reactive protein are associated with a worse outcome in patients with unstable coronary artery disease. The increased risk associated with elevated fibrinogen levels is independent of, and additive to, the prognostic influence of myocardial damage.
Key Words: angina • fibrinogen • mycardial infarction • prognosis • risk factors
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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There is an association between increased fibrinogen levels and early signs of atherosclerosis in asymptomatic individuals.1,2 Elevated fibrinogen levels might therefore be an indicator of, and contribute to, the formation and progression of atherosclerotic plaques. Increased fibrinogen levels have also been identified as an important risk factor for future cardiovascular events in several prospective long-term studies of apparently healthy individuals3–7 and patients with stable coronary artery disease.8–10 However, the prognostic influence of increased fibrinogen levels in acute coronary syndromes has been investigated in only a few studies and with conflicting results.11–14 In unstable coronary artery disease (ie, unstable angina or non–Q-wave myocardial infarction), plaque rupture with a superimposed thrombus seems to be the main pathophysiological mechanism.15,16 Fibrinogen participates in platelet aggregation and is the substrate for fibrin formation. Fibrinogen also acts as an acute phase protein and increases after myocardial damage, with a maximal level being reached after 5 days.17 There are other signs of inflammation in unstable coronary artery disease, such as increased levels of interleukin-818 and C-reactive protein.19 In a recent study, increased C-reactive protein levels were associated with a more severe short-term prognosis in patients with unstable angina.20 Furthermore, a strong correlation between fibrinogen and C-reactive protein levels was found in a large prospective study of patients with angina pectoris.21
The aim of this study was to investigate and compare the short-term (5-month) prognostic influences of fibrinogen and C-reactive protein levels on death or myocardial infarction in a large population of patients with unstable coronary artery disease.
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Methods |
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Patients
The current study was a substudy of the FRISC trial, in which the efficacy was evaluated of low-molecular-weight heparin in unstable coronary artery disease. Eligible for inclusion in the study were men and women admitted to coronary care units with chest pain and suspicion of acute myocardial infarction or recent (within 2 months)-onset angina, crescendo angina, or angina at rest and with the latest episode of chest pain occurring within the previous 72 hours. ECG criteria to be fulfilled were newly developed or previously unknown
0.1-mV1 ST-segment depression
and/or2 T-wave inversion in two contiguous leads.
Excluded from the study were men below the age of 40 and premenopausal
women, patients with an increased risk of bleeding (gastrointestinal
bleeding or peptic ulcer during past 2 years, cerebral bleeding within
the previous 3 months, recent surgery, known hemostatic defect,
platelet count of <100x109, treatment with
anticoagulants), anemia (hemoglobin of <110 g/L in women and
<125 g/L in men), renal insufficiency (creatinine
of >200 µmol/L), liver insufficiency (prothrombin time
of <50%), indication for thrombolysis, newly
developed Q wave or Q wave in the ECG leads with ST-T changes, left
bundle-branch block, significant aortic stenosis, primary
myocardial disease, endomyopericarditis, previously planned
coronary intervention, uncontrolled hypertension or
hypotension, fever with a temperature of 39°C, other serious
disease, or hypersensitivity to heparin or those participating in
another study or who were not residents in the catchment area. Patients
were also ineligible if they were unable or unwilling to participate in
the study. After giving informed consent, patients were randomized to
receive placebo-controlled, subcutaneous injections of 120 IU/kg body
wt dalteparin sodium (low-molecular-weight heparin) twice daily for 5
to 8 days, followed by 7500 IU once daily for an additional 35 to 45
days. If not contraindicated, all patients were also treated with 75 mg
aspirin as well as ß-blockers and calcium antagonists
and/or organic nitrates as required. Follow-up visits were scheduled at
40 to 50 days and 5 to 7 months after inclusion. Details of the FRISC
trial were recently published.22
The diagnosis of the event qualifying for inclusion (ie, myocardial
infarction or unstable angina pectoris) was based on maximal elevation
of the following myocardial enzymes determined at the local hospital
laboratories: CK-MB (mass) determined with the IMx system (Abbott
Laboratories; discrimination limit, 15 µg/L; n=616) or
Icon-QSR system (Hybritec; discrimination limit, 10 µg/L;
n=45), CK (catalytic activity; discrimination limit, 2.5 µkat/L for
women and 3.0 µkat/L for men; n=150), CK-MB (catalytic activity;
discrimination limit, 0.4 µkat/L; n=104), and
aspartate-aminotransferase (discrimination limit, 0.6 µkat/L for
women and 0.8 µkat/L for men; n=50). Subsequent myocardial
infarctions were classified according to World Health Organization
criteria23 by an independent end point committee,
and the diagnosis was made when two of the following criteria were
fulfilled: (1) severe ischemic chest pain of 20 minutes'
duration, (2) a diagnostic ECG, or (3) an increase in
cardiac enzymes above the upper reference limit at the local hospital
in at least two consecutive samples. The study protocol was approved by
the local ethics committee.
Blood Sampling and Assays
Blood samples from 965 patients were collected at inclusion in
tubes containing EDTA. The samples were immediately centrifuged
for 20 minutes at 2000g. The plasma was aliquoted and stored
at -70°C until analyzed. Fibrinogen was analyzed by
rate nephelometry with a Beckman Array protein system (Beckman
Instruments). The assay was performed according to recommendations of
the manufacturer except that goat anti-human fibrinogen (Atlantic
Antibodies) was used. The assay was calibrated against a human plasma
standard (Behring). C-reactive protein was analyzed
turbidimetrically (Hitachi 717; Boehringer-Mannheim) with sheep
antibodies against C-reactive protein obtained from Orion
Diagnostica. The total coefficient of variance was 4.5% at
a level of 25 mg/L during >4 months.
Troponin T (tn-T) was measured with an Enzymun-Test system
(Boehringer-Mannheim Biochemicals) with a lower detection level
of 0.04 µg/L. The upper reference level in healthy blood
donors is 0.06 µg/L,24 and according to
previous studies, levels of 0.1 µg/L are significant markers
of myocardial damage.25
Statistical Analysis
The Kaplan-Meier technique (log-rank test) was applied in
survival analysis. To evaluate the relations among fibrinogen,
C-reactive protein, and tn-T levels at inclusion, Pearson's
correlation coefficients were calculated. The distributions of
C-reactive protein and tn-T levels were positively skewed, and
therefore the data were log transformed. To evaluate the independent
contribution of the risk factors to the risk of new events,
univariate and forward stepwise multiple logistic
regression analyses were used. Added to this model were age;
sex; body mass index; smoking habits; history of diabetes mellitus,
hypertension, congestive heart failure, or previous myocardial
infarction; number of antianginal drugs (none, one, or two or more);
modified Braunwald class (no rest angina [class I], rest angina
within the past 2 months but not the past 48 hours [class II], rest
angina within the past 48 hours [class III], or non–Q-wave
myocardial infarction [class IV]); degree of ischemic signs
on inclusion ECG (T-wave inversion only, ST-segment depression only, or
T-wave inversion combined with ST-segment depression); tertiles of
fibrinogen; and tertiles of C-reactive protein and tn-T value of
< or >0.1 µg/L. Differences in proportions were evaluated by
2 analysis. Continuous variables
are described as median values with 25th and 75th percentiles, and
comparisons between groups were evaluated with the Mann-Whitney
U test. Values of P<.05 were considered
statistically significant. Statistical analyses were performed
with a computer with the SPSS system 6.1 (Statistical Package for the
Social Sciences, 1994).
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Baseline characteristics are presented in Table 1
. During the 150-day follow-up period,
42 patients (4.4%) died, 118 (12.3%) had a new myocardial infarction,
and 138 (14.4%) died and/or had a new myocardial infarction (combined
end point).
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The mean fibrinogen level was significantly higher in patients who died
or had a new myocardial infarction during the follow-up period: 3.87
(3.45 to 4.46) g/L versus 3.65 (3.22 to 4.12) g/L
(P<.001). The patients were stratified into tertiles based
on fibrinogen levels with cutoff limits of <3.38, 3.38 to 3.99, and
4.0 g/L. In survival analysis after >5 months,
increased probabilities of death (1.6%, 4.6%, and 6.9%;
P=.005) and death and/or myocardial infarction (9.3%,
14.2%, and 19.1%; P=.002) were found in the upper tertiles
(Fig 1).
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A significantly higher median level of C-reactive protein was found in
patients who died during the follow-up period (15 [6 to 26] versus 5
[0 to 14] mg/L; P<.001). However, only a trend of
increased C-reactive protein was found in the group who died and/or had
a new myocardial infarction compared with patients with no such events
during the follow-up period (7.5 [1 to 17] versus 5 [0 to 14]
mg/L; P=.067). Stratification of the patients into
tertiles based on C-reactive protein levels (<2, 2 to 10, and >10
mg/L) revealed an increased probability of death in patients
with increased C-reactive protein levels: 2.2%, 3.6%, and 7.5%,
respectively (P=.003). However, no significant differences
in the combined end point of death and/or myocardial infarction was
seen: 11.8%, 14.9%, and 16.3% (P=.26) (Fig 2).
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Both mean fibrinogen level and median level of C-reactive protein were
lower in patients with a tn-T level of <0.1 µg/L compared
with patients with a level of 0.1 µg/L (3.54 [3.52 to
4.03] versus 3.74 [3.30 to 4.23] g/L; P=.002; and
3 [0 to 10] versus 6 [1 to 17] mg/L; P<.001).
Fibrinogen concentrations were positively correlated with baseline
levels of C-reactive protein (r=.45; P<.001) and
tn-T (r=.14; P<.001). Levels of C-reactive
protein also correlated with the levels of tn-T (r=.29;
P<.001).
To elucidate whether fibrinogen and C-reactive protein levels were
independently associated with the risk of death and/or myocardial
infarction, logistic multiple regression analyses were
performed, with other risk factors at inclusion also taken into
account. In order of strength of significance, risk of death or
myocardial infarction was significantly associated with increased tn-T
level, number of antianginal drugs, elevated fibrinogen level, and
increasing age (Table 2). An increased
C-reactive protein level was not an independent risk factor for the
combined end point, even after exclusion of fibrinogen from the model.
Increased C-reactive protein levels, as well as increased tn-T levels,
number of antianginal drugs, heart failure, and degree of
ischemic changes on ECG at inclusion (Table 2) were independent
risk factors for mortality. However, after exclusion of C-reactive
protein levels from the model, increased fibrinogen level also proved
to be an independent risk factor for death.
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The relative risk of death or a subsequent myocardial infarction in
patients with an elevated fibrinogen level was increased in most
evaluated subgroups but significantly so only in individuals with
increased tn-T levels or non–Q-wave myocardial infarction (Table 3). In the total subgroup of patients
with unstable angina (n=589), the relative risk of death or subsequent
myocardial infarction was 1.60 (CI, 0.89 to 2.88) in individuals with a
fibrinogen level in the highest tertile compared with those with a
level in the lowest tertile. In comparison of the relative risk in
individuals in the highest versus the lowest tertiles of fibrinogen
value, an increased fibrinogen level was associated with an increased
risk of both death (relative risk, 4.24; CI, 1.62 to 11.04) as well as
myocardial infarction (relative risk, 1.69; CI, 1.10 to 2.60). The
relative risk of the combined end point of death or subsequent
myocardial infarction in individuals with a higher C-reactive protein
value was not significantly increased in the total patient population
(Table 4). However, a C-reactive protein
level in the highest tertile, compared with the lowest, was
significantly associated with an increased risk of death (relative
risk, 3.46; CI, 1.51 to 7.92).
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Discussion |
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Despite improved treatment of unstable coronary artery disease during the past decade, there remains a substantial risk of new ischemic events during the first months after the acute episode.22 The identification of new risk markers could improve (1) risk stratification and selection of individuals who might benefit from intensified therapy and (2) the understanding of pathophysiological mechanisms. Increased concentrations of acute phase proteins, such as fibrinogen and C-reactive protein, have been reported in unstable coronary artery disease,19,26 but the prognostic implications of these findings have not been fully elucidated.
The present study is the first to reveal a relation between elevated fibrinogen levels and short-term risk of death or a new myocardial infarction in unstable coronary artery disease. Furthermore, the prognostic importance of elevated fibrinogen levels is independent of, and additive to, the influence of myocardial damage on short-term outcome. Some of our results are therefore consistent with those of the recently presented substudy of the Thrombolysis in Myocardial Infarction (TIMI) IIIB trial, in which elevated fibrinogen levels were associated with spontaneous, in-hospital ischemic episodes in the subgroup of patients with unstable angina.27 However, in the TIMI IIIB trial, increased fibrinogen levels were not associated with an increased risk of death or myocardial infarction during a 42-day follow-up. In contrast, in the present study, we found that even during the first 40 days, there was an increased probability of death or myocardial infarction in patients with increased fibrinogen levels. The discrepancy between the findings of the two investigations could, at least in part, be accounted for by different study designs. In the TIMI IIIB trial, the "natural course" of the disease may be less easy to observe because of the randomized interventions with immediate thrombolytic treatment and/or early coronary angioplasty in a 2x2 factorial design.
In addition, there have been a few other previous reports of the association between fibrinogen levels and outcome in acute coronary artery syndromes. In acute myocardial infarction, a trend toward more frequent ischemic events was found in patients with a fibrinogen level of >4.0 g/L at admission.11 Haines et al12 described an increased 1-year mortality rate in patients with an elevated level of fibrinogen measured on the days after a myocardial infarction, which could not be confirmed in a study of patients treated with thrombolytics.13 However, in these trials, unspecified, and probably larger, acute myocardial infarctions were included, and the influence of the myocardial damage on the fibrinogen levels was not controlled for.
Elevated C-reactive protein levels were associated with an increased mortality in the present investigation. In a recent study of 31 patients with severe unstable angina, an increased C-reactive protein level was linked to an increased frequency of recurrent angina and ischemic episodes on Holter monitoring, although there was no relation to harder end points, such as death or myocardial infarction.20 Because the present study embraced a considerably larger patient sample, with a wider spectrum of unstable coronary artery disease and an extended follow-up period, the chances of demonstrating relations to hard end points were proportionally increased. However, there was no relation between increased C-reactive protein levels and the risk of myocardial infarctions in our investigation. Furthermore, increased fibrinogen levels turned out to also be an independent risk factor for death after exclusion of C-reactive protein levels from the multiple regression model. Thus, C-reactive protein levels might be of less importance than has been suggested from previous experiences in limited patient populations. Because there are close relations between acute phase proteins, it might be suggested that fibrinogen, rather than C-reactive protein, contributes to the increased risk of new events in unstable coronary artery disease.
We could not confirm the previous findings of a worse outcome in terms of death, myocardial infarction, or revascularization in patients with unstable angina with an increased C-reactive protein level but no sign of minor myocardial damage.20 To increase the sensitivity for identifying patients with minor myocardial damage, we used a lower discrimination limit of 0.1 µg/L. This, together with a tn-T assay, with both increased sensitivity and increased specificity, might have increased the proportion of individuals with signs of myocardial damage.
tn-T level determined early in unstable coronary artery disease is a strong prognostic marker.28 Increased fibrinogen levels might in part reflect the acute phase response induced by myocardial damage and, hence, a worse prognosis related to left ventricular dysfunction. However, in the present study, there was only a weak correlation between fibrinogen and tn-T levels. Furthermore, increased fibrinogen levels were associated with an increased risk of new coronary events after control for tn-T concentrations. This indicates that increased fibrinogen levels have additive prognostic value in unstable coronary artery disease.
The Braunwald classification system has been found to be a useful prognostic tool in patients with unstable angina.29 Because we also included individuals with signs of minor myocardial damage, a modified Braunwald classification system was constructed.22 An increased, modified Braunwald class was associated with an increased risk of death as well as with the combined end point (death and/or myocardial infarction) but not when controlling for other risk factors. This difference compared with previous findings could be attributed to a different classification system but also to differences in inclusion criteria and end point definitions.
Unstable coronary artery disease is a heterogeneous syndrome. A plaque fissure could be visualized by angioscopy in ~65% of the individuals with unstable angina.30,31 Increased tn-T levels might be a tool for selecting individuals at greater risk28 (ie, patients with plaque fissure and subsequent thrombus formation) and hence with a greater susceptibility to increased fibrinogen concentrations. In our investigation, >50% of deaths or new myocardial infarctions occurred during the first 4 weeks in individuals with a fibrinogen concentration level of >4.0 g/L. This early susceptibility to increased fibrinogen concentrations, in the time period with an active plaque fissure, is in line with findings of enhanced platelet aggregation in humans32 and of more extensive thrombus formation in animals33 with elevated fibrinogen levels. Furthermore, increased plasma viscosity, which is mainly determined by fibrinogen levels, indicates an unfavorable outcome in patients with unstable angina.34 This negative influence of increased viscosity might be more pronounced in patients with a decreased vessel lumen because of a mural thrombus.
One limitation of the study was that the venous blood samples were obtained at inclusion, a median of 25 hours after the onset of the latest episode of chest pain. However, inclusion of the delay from onset of pain to time of blood sampling had no major influence on the results in regression analysis. Furthermore, we did not determine the blood lipid levels in the study. An increased risk of subsequent events has been described in individuals with a combination of elevated fibrinogen and cholesterol.21 However, the prognostic influence of an increased cholesterol level would probably be of minor importance in this short-term perspective.35
In conclusion, increased fibrinogen levels and, less convincingly, elevated C-reactive protein levels are associated with a guarded short-term prognostic significance in unstable coronary artery disease. This influence is independent from, and additive to, the prognostic influence of increased tn-T levels. Fibrinogen levels should be measured as a baseline characteristic and used in subgroup analysis in future studies of interventions in unstable coronary artery disease to help refine the choice of therapy.
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Acknowledgments |
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This study was supported by grants from the Swedish National Association against Heart and Lung Disease and from Uppsala County Association Against Heart and Lung Diseases. We thank the clinical and laboratory staff at each center for skillful assistance and excellent technical assistance.
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Footnotes |
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Participating clinical centers and investigators of the research group on Fragmin during Instability in Coronary Artery Disease (FRISC) are given in "Appendix."
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Appendix 1 |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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The following are participating investigators of the FRISC research group: chairman and coordinator, Lars Wallentin; cochairman and coordinator, Eva Swahn; and Steering Committee members, Erling Karlsson, Lennart Lundin, Finn Landgren, Helge Sætre, Bertil Andrén, and Jan Ohlsson.
The following are participating centers and investigators of FRISC: Uppsala: Lennart Lundin, Bertil Lindahl, Henrik Toss, Gunilla Lindström, Eva Svensson, Gerd Ålsjö; Falun: Helge Sætre, Greger Ahlberg, Lars Hagström, Christina Sundqvist, Eva Pihl; Gävle: Gunnar Gustafsson, Lotta Larsson, Per-Erik Gustavsson, Rurik Löfmark, Ing-Britt Lundqvist; Sandviken, ; Hudiksvall, ; Bollnäs, Eskil Hammarström, Hamid Bastani, Erland Eng; Danderyd, Peter Lundin, Nina Rehnqvist, Björn Ambrant, Pia Oblack, Martin Holmstrand; Mora, Björn Fjelstad, Dic Aronsson, Solveig Østberg; Ludvika, John Eric Frisell, Anders Hedman, Marianne Sandström; Avesta, Göran Perers, Per Irving, Irene Andersson; South Hospital, Stockholm, Johan Hulting, Jonas Höjier, Aman Amanullah, Bassem Samad, Ingemar Steinbruck, Mona Ekblom; Linköping, Eva Swahn, Erling Karlsson, Niels Nielsen, Kåge Säfström, Elisabeth Logander; Norrköping, Stig-Åke Falk, Jan Fridén, Ove Nilsson, Katarina Rönnhagen, Lena Abou-Zeid; Oskarshamn, Bo Hedbäck, Joep Perk, Lotta Ossiansson-Pettersson; Kalmar, Bengt Holmberg, Finn Landgren, Stefan Rydén, Eva Bjurling; Jönköping, Jan-Erik Karlsson, Claes Malmberg, Olof Svensson, Eira Svensson; Eksjö, Sten Ekdahl, Ingvar Nyman, Yvonne Pantzar; Västervik, ; Karlstad, End Point Classification Committee, Ebba Enghoff, Torbjörn Lundström; ECG evaluation, Bertil Andren, Jan Ohlsson; Data Center, Lars Wallentin, Jan Ohlsson; and research nurses and monitors, Gunilla Lindström, Eva Svensson, Gerd Ålsjö.
Received April 30, 1997; revision received July 29, 1997; accepted August 2, 1997.
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P. M. Ridker, C. H. Hennekens, J. E. Buring, and N. Rifai C-Reactive Protein and Other Markers of Inflammation in the Prediction of Cardiovascular Disease in Women N. Engl. J. Med., March 23, 2000; 342(12): 836 - 843. [Abstract] [Full Text] [PDF]
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D. A. Morrow, N. Rifai, E. M. Antman, D. L. Weiner, C. H. McCabe, C. P. Cannon, and E. Braunwald Serum amyloid A predicts early mortality in acute coronary syndromes: a TIMI 11A substudy J. Am. Coll. Cardiol., February 1, 2000; 35(2): 358 - 362. [Abstract] [Full Text] [PDF]
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B. W. Walsh, S. Paul, R. A. Wild, R. A. Dean, R. P. Tracy, D. A. Cox, and P. W. Anderson The Effects of Hormone Replacement Therapy and Raloxifene on C-Reactive Protein and Homocysteine in Healthy Postmenopausal Women: A Randomized, Controlled Trial J. Clin. Endocrinol. Metab., January 1, 2000; 85(1): 214 - 218. [Abstract] [Full Text]
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E. R. Ferreiros, C. P. Boissonnet, R. Pizarro, P. F. G. Merletti, G. Corrado, A. Cagide, and O. O. Bazzino Independent Prognostic Value of Elevated C-Reactive Protein in Unstable Angina Circulation, November 9, 1999; 100(19): 1958 - 1963. [Abstract] [Full Text] [PDF]
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 K. J. Harjai Potential New Cardiovascular Risk Factors: Left Ventricular Hypertrophy, Homocysteine, Lipoprotein(a), Triglycerides, Oxidative Stress, and Fibrinogen Ann Intern Med, September 7, 1999; 131(5): 376 - 386. [Abstract] [Full Text] [PDF]
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W. K. Lagrand, C. A. Visser, W. T. Hermens, H. W. M. Niessen, F. W. A. Verheugt, G.-J. Wolbink, and C. E. Hack C-Reactive Protein as a Cardiovascular Risk Factor : More Than an Epiphenomenon? Circulation, July 6, 1999; 100(1): 96 - 102. [Abstract] [Full Text] [PDF]
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 J. F. KEANEY JR., D. I. SIMON, and J. E. FREEDMAN Vitamin E and vascular homeostasis: implications for atherosclerosis FASEB J, June 1, 1999; 13(9): 965 - 975. [Abstract] [Full Text]
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G. Maresca, A. Di Blasio, R. Marchioli, and G. Di Minno Measuring Plasma Fibrinogen to Predict Stroke and Myocardial Infarction : An Update Arterioscler Thromb Vasc Biol, June 1, 1999; 19(6): 1368 - 1377. [Abstract] [Full Text] [PDF]
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M. H. Moghadasian, B. M. McManus, D. V. Godin, B. Rodrigues, and J. J. Frohlich Proatherogenic and Antiatherogenic Effects of Probucol and Phytosterols in Apolipoprotein E–Deficient Mice : Possible Mechanisms of Action Circulation, April 6, 1999; 99(13): 1733 - 1739. [Abstract] [Full Text] [PDF]
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P. W. H. M. Verheggen, M. P. M. de Maat, V. M. Cats, F. Haverkate, A. H. Zwinderman, C. Kluft, and A. V. G. Bruschke Inflammatory status as a main determinant of outcome in patients with unstable angina, independent of coagulation activation and endothelial cell function Eur. Heart J., April 2, 1999; 20(8): 567 - 574. [Abstract] [PDF]
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R. J de Winter, R. Bholasingh, J. G Lijmer, R. W Koster, J. P.M.C Gorgels, Y. Schouten, F. J Hoek, and G. T Sanders Independent prognostic value of C-reactive protein and troponin I in patients with unstable angina or non-Q-wave myocardial infarction Cardiovasc Res, April 1, 1999; 42(1): 240 - 245. [Abstract] [Full Text] [PDF]
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R. Rabbani and E. J. Topol Strategies to achieve coronary arterial plaque stabilization Cardiovasc Res, February 1, 1999; 41(2): 402 - 417. [Abstract] [Full Text] [PDF]
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R. Ross Atherosclerosis -- An Inflammatory Disease N. Engl. J. Med., January 14, 1999; 340(2): 115 - 126. [Full Text] [PDF]
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G. Montalescot, F. Philippe, A. Ankri, E. Vicaut, E. Bearez, J. E. Poulard, D. Carrie, D. Flammang, A. Dutoit, A. Carayon, et al. Early Increase of von Willebrand Factor Predicts Adverse Outcome in Unstable Coronary Artery Disease : Beneficial Effects of Enoxaparin Circulation, July 28, 1998; 98(4): 294 - 299. [Abstract] [Full Text] [PDF]
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J. Danesh, R. Collins, P. Appleby, and R. Peto Association of Fibrinogen, C-reactive Protein, Albumin, or Leukocyte Count With Coronary Heart Disease: Meta-analyses of Prospective Studies JAMA, May 13, 1998; 279(18): 1477 - 1482. [Abstract] [Full Text] [PDF]
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