(Circulation. 1999;99:855-860.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Elevated Levels of C-Reactive Protein at Discharge in Patients With Unstable Angina Predict Recurrent Instability
From the Institute of Cardiology and Institute of Microbiology Catholic University of the Sacred Heart (R.L.G., G.F.), Rome, Italy.
Correspondence to Luigi M. Biasucci, Istituto di Cardiologia, Universitá Cattolica del S Cuore, Largo Francesco Vito 1, 00168 Roma, Italy. E-mail biasucci{at}pelagus.it
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Abstract |
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Background—In a group of patients admitted for unstable angina, we investigated whether C-reactive protein (CRP) plasma levels remain elevated at discharge and whether persistent elevation is associated with recurrence of instability.
Methods and Results—We measured plasma levels of CRP, serum
amyloid A protein (SAA), fibrinogen, total cholesterol, and
Helicobacter pylori and
Chlamydia pneumoniae antibody titers in
53 patients admitted to our coronary care unit for Braunwald
class IIIB unstable angina. Blood samples were taken on admission, at
discharge, and after 3 months. Patients were followed for 1 year. At
discharge, CRP was elevated (>3 mg/L) in 49% of patients; of these,
42% had elevated levels on admission and at 3 months. Only 15% of
patients with discharge levels of CRP <3 mg/L but 69% of those with
elevated CRP (P<0.001) were readmitted because of
recurrence of instability or new myocardial infarction. New
phases of instability occurred in 13% of patients in the lower tertile
of CRP (
2.5 mg/L), in 42% of those in the intermediate tertile (2.6
to 8.6 mg/L), and in 67% of those in the upper tertile (
8.7 mg/L,
P<0.001). The prognostic value of SAA was similar to
that of CRP; that of fibrinogen was not significant.
Chlamydia pneumoniae but not
Helicobacter pylori antibody titers
significantly correlated with CRP plasma levels.
Conclusions—In unstable angina, CRP may remain elevated for at
3 months after the waning of symptoms and is associated with
recurrent instability. Elevation of acute-phase reactants in unstable
angina could represent a hallmark of subclinical persistent
instability or of susceptibility to recurrent instability and, at least
in some patients, could be related to chronic Chlamydia
pneumoniae infection.
Key Words: angina • prognosis • Chlamydia pneumoniae
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In patients with unstable angina, the common persistence of instability for weeks,1 together with evidence of a rebound phenomenon after reduction of the dose of heparin treatment,2 raises the possibility that a subclinical component of instability may persist after the waning of symptoms. In unstable patients, elevated levels of C-reactive protein (CRP), a nonspecific but sensitive marker of inflammation, were found to have a short-term prognostic value unrelated to myocardial cell damage, myocardial ischemia, or episodes of activation of the hemostatic system.3 4 5 More recently, evidence of a long-term prognostic value of elevated CRP levels was reported in patients with coronary artery disease6 7 8 and in healthy individuals with high9 and low10 levels of coronary risk factors. Evidence of persisting inflammation at the time of hospital discharge could represent either a subclinical hallmark of persistent instability or a marker of susceptibility to recurrent unstable phases, possibly related to Chlamydia pneumoniae (CP) or Helicobacter pylori (HP) infection as recently proposed.11 12 13 14 We have found that serum CRP levels may remain elevated at the time of discharge and at a 3-month follow-up in a substantial proportion of patients admitted with Braunwald class IIIB unstable angina and that such an elevation is associated with frequent hospital readmission for recurrent instability.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patients
Of 164 patients admitted to our institute with a diagnosis of unstable angina from November 1992 to March 1994, 53 were included in the study, 10 patients were also part of our previous study,4 and the remaining 111 patients were excluded because they did not fulfill the inclusion criteria on admission or at discharge.
Inclusion criteria on admission were angina at rest with >2 ischemic episodes or 1 episode lasting >20 minutes in the last 24 hours with diagnostic ST-segment shift. Patients were excluded if they had any ECG abnormalities that could affect the recognition of ST-segment ischemic changes (10) and elevation of creatine kinase or troponin T (32). Exclusion criteria were malignancy or inflammatory disease (4), surgery or major trauma in the previous month (5), known thrombotic disorders, dilated cardiomyopathy (1), valvular heart disease (5), previous myocardial infarction within 3 weeks or during the index hospitalization (28), and ejection fraction <40% (10) or age >75 years (16) because these latter conditions carry an additional risk independent of the severity of instability. Because of the severity of their symptoms, 55% of patients were secondary referrals.
This study was approved by the Ethics Committee of the university, and all patients gave written informed consent.
Study Protocol and Laboratory Assays
Blood samples were taken from all patients at entry to the
study, at discharge (mean, 12±5 days after admission), and 3 months
after admission (15 days after any acute event); all patients were
followed up regularly as outpatients for 1 year. In case of cardiac
surgery, discharge samples were collected before surgery. Plasma
concentrations of CRP and serum amyloid A protein (SAA) were measured
in a single batch at the end of the study (to avoid bias in the
evaluation of symptoms and in clinical decision making) except for the
first 10 patients; in all an automated monoclonal antibody solid-phase
sandwich enzyme immunoassay was used.15 16 Plasma
concentrations of fibrinogen were measured by use of the Clauss method,
and HP antibody titers were measured in all patients on admission with
a commercial ELISA for specific IgG (Dade-Behring). A titer >10 U/mL
was considered a sign of HP infection. CP antibody titers were also
measured in all patients on admission with a
microimmunofluorescence assay (MRL
Diagnostics Chlamydia MIF kit17 18 ). Samples
were diluted from 1:8 to 1:64. Seropositivity to CP was defined as
presence of specific antibodies at a dilution of 1:16; however,
seropositivity at a dilution of 1:32 was also considered.
Coronary angiography was performed before discharge in all but
2 patients (who refused) and during follow-up when clinically
indicated. Patients were classified into 2 groups according to CRP
levels at the time of discharge: individuals with normal values of CRP
(<3 mg/L) and those with levels >3 mg/L (ie, above the upper value
found in 90% of healthy individuals). Refractory angina was defined as
angina persisting despite full medical therapy, including
intravenous nitrates and heparin (at least 2 episodes
within 48 hours from institution of full medical therapy), requiring
urgent revascularization. During follow-up, the
recurrence of instability was defined as a new phase of
unstable angina, with documented ischemic changes on the ECG,
requiring readmission to hospital.
Statistical Analysis
Because CRP values were not normally distributed, data are
presented as median and range. Nonparametric tests
were used for comparison of CRP levels between groups (Mann-Whitney U
test) and correlations (Spearman's 
test); discontinuous
variables were tested by a contingency 
2
test. Event-free survival was analyzed by the Kaplan-Meier
method, and the log-rank test was used for comparison among curves. By
logistic regression analysis, we calculated the relative odds
ratio (OR) and 95% confidence intervals (CIs) for CRP and the
following confounding variables: occurrence of in-hospital events,
family history of ischemic heart disease,
cholesterol level >200 mg/dL, fibrinogen level >400
mg/dL, smoking, age, sex, and diabetes or systemic hypertension. For
comparison with recent studies,6 19 patients were also
grouped into tertiles according to CRP, fibrinogen, and
cholesterol levels, and differences in events among
tertiles were calculated by a contingency 2
test.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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At discharge, CRP levels were normal (<3 mg/L) in 27 of 53 patients (51%) (group 1) and elevated (>3 mg/L) in 26 patients (group 2). SAA levels at discharge were elevated in 28 of 53 patients and correlated closely with those of CRP (r=0.76, P<0.001). Because the results of SAA analysis were similar to those of CRP, the SAA data are not presented. The demographic data of patients are reported in Table 1
. Therapy before
hospitalization, during hospitalization in the
coronary care unit, and after discharge was not different
between the 2 groups because all patients took aspirin or ticlopidine
and a various combination of ß-blocking agents, calcium
antagonists, and nitrates; in the coronary care
unit, all patients were treated with intravenous heparin
(Table 2). No patient was discharged with
lipid-lowering drugs, but in 18 patients, these drugs were added at the
1-month follow-up visit. These patients were equally distributed
between the 2 groups.
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Group 1
In group 1, median CRP levels at discharge were 2.4 mg/L (range,
0.6 to 2.9 mg/L) and were normal on admission in 15 of 27 patients and
in 23 of 27 at 3 months. A total of 11 of the 27 patients had CRP
levels within the normal range throughout the initial 3-month follow-up
period. During hospitalization, coronary
revascularization was undertaken in 33% of
patients on an urgent basis and in 22% on an elective basis; 45% of
patients had an uneventful course. In this group, 20 of 27 patients
(75%) were positive to HP, and HP antibody titers were 35.3±79 UI/L;
10 of 27 patients (37%) were positive to CP, and 6 of 27 (22%) were
positive at a dilution 1:32. At discharge, blood levels of fibrinogen
and cholesterol were 319±164 and 220±49 mg/dL,
respectively. During follow-up, 4 of 27 patients (15%) had
coronary events: myocardial infarction in 1 and a new phase of
instability requiring readmission in 3.
Group 2
In group 2, median CRP levels at discharge were 9.9 mg/L (range,
3.3 to 9 mg/L; P<0.001 versus group 1) and were elevated in
24 of 26 patients on admission and in 22 of 26 at 3 months. A total of
21 of 26 patients (81%) had elevated CRP levels throughout the initial
3-month follow-up period. They represent 40% of the group of
53 total patients. During hospitalization, 58% of group 2 patients had
coronary events and underwent urgent coronary
revascularization; 19% underwent elective
revascularization. Of these patients, 23% (versus
45% in group 1) were treated medically, but the difference was not
significant. In group 2, 21 of 26 patients (81%) were positive to HP
(P=NS versus group 1); HP antibody titers were 28.9±53 UI/L
(P=NS versus group 1). In addition, 21 of 26 patients (81%)
were positive to CP (P=0.0014 versus group 1), and 13 of 26
(50%) were positive at a dilution 1:32 (P=0.035 versus
group 1). At discharge, blood levels of fibrinogen and
cholesterol were 395±152 and 207±51 mg/dL, respectively
(P=NS versus group 1 for both).
During follow-up, 18 of 26 patients (69%, versus 15% in group 1,
P<0.001) had coronary events: myocardial infarction
in 4 (1 patient died after the infarction) and a new phase of
instability requiring readmission in 14. The 1-year survival free from
readmission, myocardial infarction, and death was significantly higher
in group 1 than group 2 as assessed by the log-rank test
(P=0.0001, Figure 1A) and was
independent of in-hospital revascularization during
the first admission (Figure 1B). CRP values >3 mg/L at
discharge had an adjusted OR for recurrent instability of 8.57 (95%
CI, 1.66 to 44.2; Table 3). In all
patients, we carefully considered whether or not recurrent
ischemia or infarction was at same site as the index event, and
we found that the site of the recurrent event was the same as the
culprit site in 16 patients (73%) but was different in 6. Culprit site
was assessed by the analysis of ECG and
echocardiographic data; in 11 patients, this was
confirmed by coronary angiography.
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Recurrence of instability was due to post-PTCA restenosis in 5 of 22 patients (23%) and to saphenous vein graft stenosis in 2 of 22 (9%). PTCA was performed with the same technique in the 2 groups, and no stents were used. Procedure and vessel characteristics were similar; all but 2 patients were treated on a single vessel. In only 1 group 1 patient, a severe complication caused by abrupt vessel occlusion was observed and treated with emergency CABG. The procedure was successful in all other patients without acute or subacute coronary occlusion. The only difference that we observed was a more severe preprocedural stenosis in group 2 than in group 1 (82.3±10.5% versus 78.5±5%, P=0.03); however, residual stenosis after the procedure was not different in the 2 groups (33.4±9% in group 2 versus 29±7.9% in group 1, P=NS), with TIMI grade III flow in all patients.
Tertile Distribution of CRP, Fibrinogen, and Cholesterol
We also assessed the relation between the recurrence of
instability in the whole group and the distribution of patients into
tertiles according to levels of CRP, fibrinogen, and
cholesterol. A new phase of instability occurred in 13% of
patients in the lower tertile of CRP (with values 2.5 mg/L), in 42%
of those in the intermediate tertile (with values from 2.5 to 8.6
mg/L), and in 67% of those in the upper tertile (with values 8.7
mg/L, P<0.01, Figure 2A). A
similar trend, although not significant, was observed for fibrinogen
levels (22% versus 44% versus 59%, Figure 2B) but not for
total cholesterol. For patients in the upper tertile of
cholesterol but in the lower tertile of CRP, readmission
rate was lower than for those in the intermediate and upper tertiles of
CRP, but the difference was of borderline significance
(P=0.05, Figure 3A). A similar
trend was observed by a comparison of tertiles of
cholesterol with those of CRP and fibrinogen according to
the following distribution: low-low (first tertile), high-high (third),
and any different combination (intermediate) (Figure 3B).
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No correlation was found between CRP levels and HP antibody titers or seropositivity, but a significant correlation was found between seropositivity to CP and CRP at any time (P<0.005), and a trend was observed between CP dilution titers and CRP levels at entry (P=0.06). Seropositivity to CP was associated with recurrence of instability because seropositivity to CP was found in 17 of 22 patients (77%) with recurrent instability but in only 14 of 31 patients (45%) without events (P<0.05).
CRP Admission Levels and Follow-Up Prognosis
On admission, CRP levels were elevated in most group 2 patients
(24 of 26). Patients with elevated CRP levels at entry had
significantly more events at follow-up by the log-rank test compared
with patients with normal CRP levels (P=0.037), but the
difference was weaker than that observed for CRP discharge levels.
Positive predictive value of CRP at entry was 50%, but that of CRP at
discharge was 69%. Negative predictive value was 86% for CRP levels
at entry and 85% at discharge; diagnostic accuracy was
60% for CRP levels at entry and 77% at discharge.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Our study demonstrates that serum levels of CRP may remain elevated above the normal range after the waning of symptoms in nearly one half of patients admitted to hospital with a diagnosis of Braunwald class IIIB unstable angina and that such an elevation is associated with a significantly higher incidence of new phases of instability within 1 year. The recurrence of instability appears to be independent of coronary revascularization procedures performed during the initial hospitalization and cholesterol levels, which were of borderline significance only when associated with elevated CRP levels. Thus, recurrent instability may be associated with persisting inflammatory stimuli, the cause of which is still unknown. This observation, if confirmed, would have important implications for clinical practice and research because it could provide a useful marker for the separation of patients at low risk of recurrent instability from those at high risk for whom more careful clinical monitoring and more aggressive treatment are required. Moreover, the understanding of the causes of persistent inflammation may provide novel additional therapeutic tools.
Our study shows that although entry levels of CRP predict recurrence of instability at 1 year, this predictive value is lower than that of CRP levels at discharge because entry values may be affected by the acute phase of the disease and are better predictors of short-term occurrence of new ischemic episodes.3 20 Our findings confirm the primary role of an inflammatory component in unstable angina by showing that CRP levels remained elevated in 42% of our patients 3 months after hospital discharge, when causal roles of coronary thrombosis, myocardial necrosis, or ischemia and of in-hospital revascularization procedures are unlikely.
Elevated CRP levels are a marker of increased production of IL-1 and IL-6,21 22 2 proinflammatory cytokines that also have prothrombotic properties, and CRP itself can activate monocytes to produce tissue factor23 and induce monocyte and endothelial cell release of IL-1 and IL-6.22 However, the mechanisms that can lead to initiation of such inflammatory reaction may be multiple and to date are largely unexplained. The mechanisms that can lead to the persistence of this "acute-phase" reaction also are unexplained.24 It is possible that oxidized LDL25 or infections caused by CP, HP, and Cytomegalovirus (CMV) may cause a low-grade chronic inflammatory condition.26 Preliminary findings from our group failed to detect mRNA of CMV in endoartherectomy specimens of coronary plaques in unstable patients.27 We also failed to detect an association between CMV and HP serum antibody titers and acute myocardial infarction and unstable angina, although such an association was found with chronic atherosclerotic syndromes.28 29 In the present study, HP antibody titers were not correlated with the levels of CRP at discharge or with the recurrence of instability. Only seropositivity for CP correlated with CRP levels and was associated with recurrence of instability during follow-up. Thus, CP infection could be 1 stimulus responsible for the persistent inflammatory state or for the recurrence of instability. Although our study does not allow us to draw definitive conclusions on the role of CP in unstable angina, this possibility is supported by recent reports of a reduction in cardiovascular events (recurrence of angina, myocardial infarction, and death) in unstable angina and in survivors of myocardial infarction after antibiotic treatment for CP.12 13
We have also recently shown that patients with persistently elevated CRP levels have an exaggerated production of IL-6 after angioplasty,30 acute myocardial infarction,31 and lipopolysaccharide challenge.32 Collectively, these observations, together with the stronger correlation with recurrence of instability and myocardial infarction of elevated levels of CRP than of seropositivity to CP, suggest that the intensity of the individual inflammatory response may be an independent pathogenic component of unstable angina.
Conclusions
Our study has included a relatively small number of patients;
however, we adopted strict enrollment criteria to have a
homogeneous population: Not only were all patients in
Braunwald class IIIB, but they also were selected to avoid patients in
whom severity of angina was not necessarily the major determinant of
prognosis. Thus, our findings may not apply to the whole spectrum of
unstable patients.
If confirmed in larger studies, our findings may have relevant practical implications because low serum levels of CRP at the time of hospital discharge identify a group of patients at low risk, even in patients with severe unstable angina. Conversely, elevated CRP levels at discharge identify patients at high risk even after successful revascularization who therefore may benefit from a more careful clinical follow-up and appropriate antithrombotic and possibly anti-inflammatory treatment. Precise knowledge of the possible triggers of the inflammation and the determinants of its individual response may open novel therapeutic avenues.
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Acknowledgments |
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This study was supported by research grant 94.00518.PF41 from the National Research Council targeted project Prevention and Control Disease Factors, Rome, Italy, and in part by the European Community (Biomed 2 research grant PL 951502) and the Associazione Ricerche Coronariche.
Received July 28, 1998; revision received November 9, 1998; accepted November 11, 1998.
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32. Liuzzo G, Angiolillo DJ, Ginnetti F, Caligiuri G, Rizzello V, Petrone E, Kol A, Sperti G, Biasucci LM, Maseri A. Monocytes of patients with recurrent unstable angina are hyper-responsive to lipopolysaccaride challenge. J Am Coll Cardiol. 1998;31(suppl A):272A. Abstract.We measured the plasma concentrations of C-reactive protein (CRP), fibrinogen, total cholesterol, and Helicobacter pylori and Chlamydia pneumoniae antibody titers in 53 patients admitted to our coronary care unit with a diagnosis of unstable angina. At the time of discharge, CRP was elevated (>3 mg/L) in 49% of patients, 42% of whom presented elevated levels in all blood samples. Fifteen percent of patients with discharge levels of CRP <3 mg/L and 69% of those with elevated CRP (P<0.001) were readmitted because of recurrence of symptoms, independent of in-hospital course. Measurements of CRP levels at the time of hospital discharge could identify unstable patients at risk of recurrent instability who therefore require a more aggressive treatment.
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H. O. Caymaz and G. Yuksel Fate of Incidental, Asymptomatic Lesions Discovered During Percutaneous Coronary Intervention Angiology, May 1, 2008; 59(2): 193 - 197. [Abstract] [PDF]
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M. L. Narducci, A. Grasselli, L. M. Biasucci, A. Farsetti, A. Mule, G. Liuzzo, G. La Torre, G. Niccoli, R. Mongiardo, A. Pontecorvi, et al. High Telomerase Activity in Neutrophils From Unstable Coronary Plaques J. Am. Coll. Cardiol., December 18, 2007; 50(25): 2369 - 2374. [Abstract] [Full Text] [PDF]
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G. Liuzzo, L. M. Biasucci, G. Trotta, S. Brugaletta, M. Pinnelli, G. Digianuario, V. Rizzello, A. G. Rebuzzi, C. Rumi, A. Maseri, et al. Unusual CD4+CD28null T Lymphocytes and Recurrence of Acute Coronary Events J. Am. Coll. Cardiol., October 9, 2007; 50(15): 1450 - 1458. [Abstract] [Full Text] [PDF]
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B. M. Scirica, D. A. Morrow, C. P. Cannon, J. A. de Lemos, S. Murphy, M. S. Sabatine, S. D. Wiviott, N. Rifai, C. H. McCabe, E. Braunwald, et al. Clinical Application of C-Reactive Protein Across the Spectrum of Acute Coronary Syndromes Clin. Chem., October 1, 2007; 53(10): 1800 - 1807. [Abstract] [Full Text] [PDF]
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NACB WRITING GROUP MEMBERS, D. A. Morrow, C. P. Cannon, R. L. Jesse, L. K. Newby, J. Ravkilde, A. B. Storrow, A. H.B. Wu, R. H. Christenson, NACB COMMITTEE MEMBERS, et al. National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes Clin. Chem., April 1, 2007; 53(4): 552 - 574. [Full Text] [PDF]
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R. S. Vasan Biomarkers of Cardiovascular Disease: Molecular Basis and Practical Considerations Circulation, May 16, 2006; 113(19): 2335 - 2362. [Full Text] [PDF]
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T. Lenderink, C. Heeschen, S. Fichtlscherer, S. Dimmeler, C. W. Hamm, A. M. Zeiher, M. L. Simoons, E. Boersma, and for the CAPTURE Investigators Elevated Placental Growth Factor Levels Are Associated With Adverse Outcomes at Four-Year Follow-Up in Patients With Acute Coronary Syndromes J. Am. Coll. Cardiol., January 17, 2006; 47(2): 307 - 311. [Abstract] [Full Text] [PDF]
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D. Feinbloom and K. A. Bauer Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events Arterioscler Thromb Vasc Biol, October 1, 2005; 25(10): 2043 - 2053. [Abstract] [Full Text] [PDF]
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C. Monaco, E. Rossi, D. Milazzo, F. Citterio, F. Ginnetti, G. D'Onofrio, D. Cianflone, F. Crea, L. M. Biasucci, and A. Maseri Persistent systemic inflammation in unstable angina is largely unrelated to the atherothrombotic burden J. Am. Coll. Cardiol., January 18, 2005; 45(2): 238 - 243. [Abstract] [Full Text] [PDF]
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R. Glaser, F. Selzer, D. P. Faxon, W. K. Laskey, H. A. Cohen, J. Slater, K. M. Detre, and R. L. Wilensky Clinical Progression of Incidental, Asymptomatic Lesions Discovered During Culprit Vessel Coronary Intervention Circulation, January 18, 2005; 111(2): 143 - 149. [Abstract] [Full Text] [PDF]
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M. J. Zibaeenezhad, A. Amanat, A. Alborzi, and A. Obudi Relation of Chlamydia Pneumoniae Infection to Documented Coronary Artery Disease in Shiraz, Southern Iran Angiology, January 1, 2005; 56(1): 43 - 48. [Abstract] [PDF]
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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]
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S. Fichtlscherer, S. Breuer, and A. M. Zeiher Prognostic Value of Systemic Endothelial Dysfunction in Patients With Acute Coronary Syndromes: Further Evidence for the Existence of the "Vulnerable" Patient Circulation, October 5, 2004; 110(14): 1926 - 1932. [Abstract] [Full Text] [PDF]
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L. M. Biasucci and G. G.L. Biondi-Zoccai Preprocedural C-Reactive Protein for Risk Prediction Before Percutaneous Coronary Intervention (PCI): A European Perspective Clin. Chem., September 1, 2004; 50(9): 1492 - 1494. [Full Text] [PDF]
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B. Schieffer, C. Bunte, J. Witte, K. Hoeper, R. H. Boger, E. Schwedhelm, and H. Drexler Comparative effects of AT1-antagonism and angiotensin-converting enzyme inhibition on markers of inflammation and platelet aggregation in patients with coronary artery disease J. Am. Coll. Cardiol., July 21, 2004; 44(2): 362 - 368. [Abstract] [Full Text] [PDF]
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A. Abbate, E. Bonanno, A. Mauriello, R. Bussani, G. G.L. Biondi-Zoccai, G. Liuzzo, A. M. Leone, F. Silvestri, A. Dobrina, F. Baldi, et al. Widespread Myocardial Inflammation and Infarct-Related Artery Patency Circulation, July 6, 2004; 110(1): 46 - 50. [Abstract] [Full Text] [PDF]
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A. Lombardo, L. M. Biasucci, G. A. Lanza, S. Coli, P. Silvestri, D. Cianflone, G. Liuzzo, F. Burzotta, F. Crea, and A. Maseri Inflammation as a Possible Link Between Coronary and Carotid Plaque Instability Circulation, June 29, 2004; 109(25): 3158 - 3163. [Abstract] [Full Text] [PDF]
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S. Verma, P. E. Szmitko, and E. T.H. Yeh C-Reactive Protein: Structure Affects Function Circulation, April 27, 2004; 109(16): 1914 - 1917. [Full Text] [PDF]
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R. V. Milani, C. J. Lavie, and M. R. Mehra Reduction in C-reactive protein through cardiac rehabilitation and exercise training J. Am. Coll. Cardiol., March 17, 2004; 43(6): 1056 - 1061. [Abstract] [Full Text] [PDF]
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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]
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H C Routledge, J G Ayres, and J N Townend Why cardiologists should be interested in air pollution Heart, December 1, 2003; 89(12): 1383 - 1388. [Abstract] [Full Text] [PDF]
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M. Cesari, B. W.J.H. Penninx, A. B. Newman, S. B. Kritchevsky, B. J. Nicklas, K. Sutton-Tyrrell, S. M. Rubin, J. Ding, E. M. Simonsick, T. B. Harris, et al. Inflammatory Markers and Onset of Cardiovascular Events: Results From the Health ABC Study Circulation, November 11, 2003; 108(19): 2317 - 2322. [Abstract] [Full Text] [PDF]
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R. Wolk, P. Berger, R. J. Lennon, E. S. Brilakis, and V. K. Somers Body Mass Index: A Risk Factor for Unstable Angina and Myocardial Infarction in Patients With Angiographically Confirmed Coronary Artery Disease Circulation, November 4, 2003; 108(18): 2206 - 2211. [Abstract] [Full Text] [PDF]
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G.M. Hirschfield and M.B. Pepys C-reactive protein and cardiovascular disease: new insights from an old molecule QJM, November 1, 2003; 96(11): 793 - 807. [Abstract] [Full Text] [PDF]
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D.J. Brull, N. Serrano, F. Zito, L. Jones, H.E. Montgomery, A. Rumley, P. Sharma, G.D.O. Lowe, M.J. World, S.E. Humphries, et al. Human CRP Gene Polymorphism Influences CRP Levels: Implications for the Prediction and Pathogenesis of Coronary Heart Disease Arterioscler Thromb Vasc Biol, November 1, 2003; 23(11): 2063 - 2069. [Abstract] [Full Text] [PDF]
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H S Gurm, D L Bhatt, A M Lincoff, J E Tcheng, D J Kereiakes, N S Kleiman, G Jia, and E J Topol Impact of preprocedural white blood cell count on long term mortality after percutaneous coronary intervention: insights from the EPIC, EPILOG, and EPISTENT trials Heart, October 1, 2003; 89(10): 1200 - 1204. [Abstract] [Full Text] [PDF]
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O. Manfrini, C. Pizzi, D. Trere, F. Fontana, and R. Bugiardini Parasympathetic failure and risk of subsequent coronary events in unstable angina and non-ST-segment elevation myocardial infarction Eur. Heart J., September 1, 2003; 24(17): 1560 - 1566. [Abstract] [Full Text] [PDF]
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D. G. Hackam and S. S. Anand Emerging Risk Factors for Atherosclerotic Vascular Disease: A Critical Review of the Evidence JAMA, August 20, 2003; 290(7): 932 - 940. [Abstract] [Full Text] [PDF]
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H. O. Ventura and M. R. Mehra C-Reactive protein and cardiac allograft vasculopathy: is inflammation the critical link? J. Am. Coll. Cardiol., August 6, 2003; 42(3): 483 - 485. [Full Text] [PDF]
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A. Maseri and V. Fuster Is There a Vulnerable Plaque? Circulation, April 29, 2003; 107(16): 2068 - 2071. [Full Text] [PDF]
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C. Heeschen, S. Dimmeler, C. W. Hamm, S. Fichtlscherer, E. Boersma, M. L. Simoons, A. M. Zeiher, and for the CAPTURE Study Investigators Serum Level of the Antiinflammatory Cytokine Interleukin-10 Is an Important Prognostic Determinant in Patients With Acute Coronary Syndromes Circulation, April 29, 2003; 107(16): 2109 - 2114. [Abstract] [Full Text] [PDF]
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G. G. L. Biondi-Zoccai, A. Abbate, G. Liuzzo, and L. M. Biasucci Atherothrombosis, inflammation, and diabetes J. Am. Coll. Cardiol., April 2, 2003; 41(7): 1071 - 1077. [Abstract] [Full Text] [PDF]
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D. J. Angiolillo, G. Liuzzo, S. Pelliccioni, E. De Candia, R. Landolfi, F. Crea, A. Maseri, and L. M. Biasucci Combined role of the Lewis antigenic system, Chlamydia pneumoniae, and C-reactive protein in unstable angina J. Am. Coll. Cardiol., February 19, 2003; 41(4): 546 - 550. [Abstract] [Full Text] [PDF]
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E. T.H. Yeh and J. T. Willerson Coming of Age of C-Reactive Protein: Using Inflammation Markers in Cardiology Circulation, January 28, 2003; 107(3): 370 - 371. [Full Text] [PDF]
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L.K Newby, M.V Bhapkar, H.D White, E.J Topol, F.C Dougherty, R.A Harrington, M.C Smith, L.F Asarch, R.M Califf, and for the SYMPHONY and 2nd SYMPHONY Investigators Predictors of 90-day outcome in patients stabilized after acute coronary syndromes Eur. Heart J., January 2, 2003; 24(2): 172 - 181. [Abstract] [Full Text] [PDF]
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T Lenderink, E Boersma, C Heeschen, A Vahanian, M.-J de Boer, V Umans, M.J.B.M van den Brand, C.W Hamm, M.L Simoons, and for the CAPTURE investigators Elevated troponin T and C-reactive protein predict impaired outcome for 4 years in patients with refractory unstable angina, and troponin T predicts benefit of treatment with abciximab in combination with PTCA Eur. Heart J., January 1, 2003; 24(1): 77 - 85. [Abstract] [Full Text] [PDF]
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N.T. Mulvihill, B. Foley, P. Crean, and M. Walsh Prediction of cardiovascular risk using soluble cell adhesion molecules Eur. Heart J., October 2, 2002; 23(20): 1569 - 1574. [Full Text] [PDF]
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A. D. Pradhan, J. E. Manson, J. E. Rossouw, D. S. Siscovick, C. P. Mouton, N. Rifai, R. B. Wallace, R. D. Jackson, M. B. Pettinger, and P. M Ridker Inflammatory Biomarkers, Hormone Replacement Therapy, and Incident Coronary Heart Disease: Prospective Analysis From the Women's Health Initiative Observational Study JAMA, August 28, 2002; 288(8): 980 - 987. [Abstract] [Full Text] [PDF]
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J. F. Keaney Jr. and J. A. Vita The Value of Inflammation for Predicting Unstable Angina N. Engl. J. Med., July 4, 2002; 347(1): 55 - 57. [Full Text] [PDF]
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D. L. Bhatt and E. J. Topol Need to Test the Arterial Inflammation Hypothesis Circulation, July 2, 2002; 106(1): 136 - 140. [Full Text] [PDF]
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E. Ronner, E. Boersma, G.-J. Laarman, G. A. Somsen, R. A. Harrington, J. W. Deckers, E. J. Topol, R. M. Califf, and M. L. Simoons Early angioplasty in acute coronary syndromes without persistent st-segment elevation improves outcome but increases the need for six-month repeat revascularization: An analysis of the pursuit trial J. Am. Coll. Cardiol., June 19, 2002; 39(12): 1924 - 1929. [Abstract] [Full Text] [PDF]
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R.J. de Winter, G.S. Heyde, K.T. Koch, J. Fischer, J.P. van Straalen, M. Bax, C.E. Schotborgh, K.J. Mulder, G.T. Sanders, J.J. Piek, et al. The prognostic value of pre-procedural plasma C-reactive protein in patients undergoing elective coronary angioplasty Eur. Heart J., June 2, 2002; 23(12): 960 - 966. [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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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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G. J. Blake and P. M. Ridker Novel Clinical Markers of Vascular Wall Inflammation Circ. Res., October 26, 2001; 89(9): 763 - 771. [Abstract] [Full Text] [PDF]
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A. Galante, A. Pietroiusti, M. Vellini, P. Piccolo, G. Possati, M. De Bonis, R. L. Grillo, C. Fontana, and C. Favalli C-reactive protein is increased in patients with degenerative aortic valvular stenosis J. Am. Coll. Cardiol., October 1, 2001; 38(4): 1078 - 1082. [Abstract] [Full Text] [PDF]
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S. Blankenberg, H. J. Rupprecht, C. Bickel, D. Peetz, G. Hafner, L. Tiret, and J. Meyer Circulating Cell Adhesion Molecules and Death in Patients With Coronary Artery Disease Circulation, September 18, 2001; 104(12): 1336 - 1342. [Abstract] [Full Text] [PDF]
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D.J. Brull, H.E. Montgomery, J. Sanders, S. Dhamrait, L. Luong, A. Rumley, G.D.O. Lowe, and S.E. Humphries Interleukin-6 Gene -174G>C and -572G>C Promoter Polymorphisms Are Strong Predictors of Plasma Interleukin-6 Levels After Coronary Artery Bypass Surgery Arterioscler Thromb Vasc Biol, September 1, 2001; 21(9): 1458 - 1463. [Abstract] [Full Text] [PDF]
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P. Bogaty, P. Poirier, S. Simard, L. Boyer, S. Solymoss, and G. R. Dagenais Biological Profiles in Subjects With Recurrent Acute Coronary Events Compared With Subjects With Long-Standing Stable Angina Circulation, June 26, 2001; 103(25): 3062 - 3068. [Abstract] [Full Text] [PDF]
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N T Mulvihill, J B Foley, R T Murphy, R Curtin, P A Crean, and M Walsh Risk stratification in unstable angina and non-Q wave myocardial infarction using soluble cell adhesion molecules Heart, June 1, 2001; 85(6): 623 - 627. [Abstract] [Full Text]
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V. Pasceri, J. Chang, J. T. Willerson, and E. T. H. Yeh Modulation of C-Reactive Protein-Mediated Monocyte Chemoattractant Protein-1 Induction in Human Endothelial Cells by Anti-Atherosclerosis Drugs Circulation, May 29, 2001; 103(21): 2531 - 2534. [Abstract] [Full Text] [PDF]
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G. Liuzzo, D. J. Angiolillo, A. Buffon, V. Rizzello, C. Colizzi, F. Ginnetti, L. M. Biasucci, and A. Maseri Enhanced Response of Blood Monocytes to In Vitro Lipopolysaccharide-Challenge in Patients With Recurrent Unstable Angina Circulation, May 8, 2001; 103(18): 2236 - 2241. [Abstract] [Full Text] [PDF]
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P. M. Ridker High-Sensitivity C-Reactive Protein : Potential Adjunct for Global Risk Assessment in the Primary Prevention of Cardiovascular Disease Circulation, April 3, 2001; 103(13): 1813 - 1818. [Abstract] [Full Text] [PDF]
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M. Di Napoli, F. Papa, and V. Bocola C-Reactive Protein in Ischemic Stroke : An Independent Prognostic Factor Stroke, April 1, 2001; 32(4): 917 - 924. [Abstract] [Full Text] [PDF]
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G.J. Blake and P.M. Ridker High sensitivity C-reactive protein for predicting cardiovascular disease: an inflammatory hypothesis Eur. Heart J., March 1, 2001; 22(5): 349 - 352. [PDF]
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N. Rifai and P. M. Ridker High-Sensitivity C-Reactive Protein: A Novel and Promising Marker of Coronary Heart Disease Clin. Chem., March 1, 2001; 47(3): 403 - 411. [Abstract] [Full Text] [PDF]
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W. L. Roberts, L. Moulton, T. C. Law, G. Farrow, M. Cooper-Anderson, J. Savory, and N. Rifai Evaluation of Nine Automated High-Sensitivity C-Reactive Protein Methods: Implications for Clinical and Epidemiological Applications. Part 2 Clin. Chem., March 1, 2001; 47(3): 418 - 425. [Abstract] [Full Text] [PDF]
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 K. Yasojima, C. Schwab, E. G. McGeer, and P. L. McGeer Generation of C-Reactive Protein and Complement Components in Atherosclerotic Plaques Am. J. Pathol., March 1, 2001; 158(3): 1039 - 1051. [Abstract] [Full Text] [PDF]
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U. Stenestrand, L. Wallentin, and for the Swedish Register of Cardiac Intensive Care Early Statin Treatment Following Acute Myocardial Infarction and 1-Year Survival JAMA, January 24, 2001; 285(4): 430 - 436. [Abstract] [Full Text] [PDF]
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R.R Azar, S Rinfret, P Theroux, P.H Stone, R Dakshinamurthy, Y.-J Feng, A.H.B Wu, G Range, and D.D Waters A randomized placebo-controlled trial to assess the efficacy of antiinflammatory therapy with methylprednisolone in unstable angina (MUNA trial) Eur. Heart J., December 2, 2000; 21(24): 2026 - 2032. [Abstract] [PDF]
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 A. Manhapra and S. Borzak Regular review: Treatment possibilities for unstable angina BMJ, November 18, 2000; 321(7271): 1269 - 1275. [Full Text]
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