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Circulation. 1999;100:230-235

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(Circulation. 1999;100:230-235.)
© 1999 American Heart Association, Inc.


Clinical Investigation and Reports

Long-Term Effects of Pravastatin on Plasma Concentration of C-reactive Protein

Paul M. Ridker, MD; Nader Rifai, PhD; Marc A. Pfeffer, MD; Frank Sacks, MD; Eugene Braunwald, MD; for the Cholesterol and Recurrent Events (CARE) Investigators

From the Department of Medicine, Brigham and Women's Hospital and Harvard Medical School (P.M.R., M.A.P., F.S., E.B.), and the Children's Hospital Medical Center (N.R.), Boston, Mass.

Correspondence to Dr Paul M. Ridker, Cardiovascular Diseases, Brigham and Womens' Hospital, 75 Francis St, Boston, MA 02115. E-mail pridker{at}rics.bwh.harvard.edu


*    Abstract
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*Abstract
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Background—Elevated plasma concentrations of C-reactive protein (CRP) are associated with increased cardiovascular risk. We evaluated whether long-term therapy with pravastatin, an agent that reduces cardiovascular risk, might alter levels of this inflammatory parameter.

Methods and Results—CRP levels were measured at baseline and at 5 years in 472 randomly selected participants in the Cholesterol and Recurrent Events (CARE) trial who remained free of recurrent coronary events during follow-up. Overall, CRP levels at baseline and at 5 years were highly correlated (r=0.60, P<0.001). However, among those allocated to placebo, median CRP levels and the mean change in CRP tended to increase over time (median change, +4.2%; P=0.2 and mean change, +0.07 mg/dL; P=0.04). By contrast, median CRP levels and the mean change in CRP decreased over time among those allocated to pravastatin (median change, -17.4%; P=0.004 and mean change, -0.07 mg/dL; P=0.002). Thus, statistically significant differences were observed at 5 years between the pravastatin and placebo groups in terms of median CRP levels (difference, -21.6%; P=0.007), mean CRP levels (difference, -37.8%; P=0.002), and absolute mean change in CRP (difference, -0.137 mg/dL; P=0.003). These effects persisted in analyses stratified by age, body mass index, smoking status, blood pressure, and baseline lipid levels. Attempts to relate the magnitude of change in CRP to the magnitude of change in lipids in both the pravastatin and placebo groups did not reveal any obvious relationships.

Conclusions—Among survivors of myocardial infarction on standard therapy plus placebo, CRP levels tended to increase over 5 years of follow-up. In contrast, randomization to pravastatin resulted in significant reductions in this inflammatory marker that were not related to the magnitude of lipid alterations observed. Thus, these data further support the potential for nonlipid effects of this agent.


Key Words: myocardial infarction • proteins • pravastatin • atherosclerosis


*    Introduction
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up arrowAbstract
*Introduction
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Plasma concentrations of C-reactive protein (CRP), a sensitive marker of underlying systemic inflammation, are elevated among men and women at risk for future cardiovascular events.1 Specifically, prospective studies indicate that baseline levels of CRP are associated with increased risk of myocardial infarction and stroke among apparently healthy individuals,2 3 those at increased risk because of older age or smoking status,4 5 and those with symptomatic angina pectoris6 or prior myocardial infarction.7 8 Furthermore, the predictive value of high-sensitivity testing for CRP (hs-CRP) appears to be additive to that of total and HDL cholesterol,9 data that suggest that screening for hs-CRP may have a role in cardiovascular risk prediction.

To date, few therapeutic modalities have been shown to influence CRP levels. However, in a nested case-control analysis of post–myocardial infarction patients randomly assigned to pravastatin or placebo in the Cholesterol and Recurrent Events (CARE) trial, those with elevated levels of CRP at baseline were found to have an increased risk of recurrent coronary events (RR=1.77, P=0.02).7 Moreover, in that study, the association between CRP and subsequent risk was significant among those randomized to placebo (RR=2.1, P=0.048) but was attenuated and no longer significant among those assigned to pravastatin (RR=1.29, P=0.5). These effects were present even though those with and without elevated levels of CRP had virtually identical baseline lipid levels. This observation, as well as experimental data demonstrating that therapy with pravastatin10 11 and cerivastatin12 reduces the number and activity of inflammatory cells present within atherosclerotic plaques, raises the possibility that HMG-CoA reductase inhibition may have clinically important anti-inflammatory actions.

Despite these data, it is unknown whether long-term HMG-CoA reductase inhibition affects plasma concentration of CRP. The availability of baseline and 5-year follow-up blood samples in the CARE study afforded us the opportunity to directly address this issue for pravastatin, a potent HMG-CoA reductase inhibitor that has been shown in several large-scale trials to significantly reduce rates of myocardial infarction, stroke, and cardiovascular mortality in both high-risk and moderate-risk populations.13 14 15


*    Methods
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*Methods
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down arrowDiscussion
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The CARE study was a secondary prevention trial of cardiovascular disease conducted among 4159 patients with a prior history of MI who had total cholesterol levels <240 mg/dL and LDL cholesterol levels between 115 and 175 mg/dL. As described previously,14 patients were eligible for inclusion if they had had an acute myocardial infarction between 3 and 20 months before randomization, were 21 to 75 years of age, had a left ventricular ejection fraction of >=25%, and had no evidence of congestive heart failure. The primary end point of the CARE trial was death from coronary heart disease (including fatal myocardial infarction, either definite or probable; sudden death; death during a coronary intervention; and death from other coronary causes) or a symptomatic (unless during noncardiac surgery) nonfatal myocardial infarction confirmed by serum creatine kinase measurements. Overall, the randomized use of pravastatin in the CARE trial was associated with a 24% reduction in risk of this primary end point.14

Blood samples were collected in CARE during prerandomization clinic visits designed in part to determine baseline lipid levels for study eligibility. On average, these visits occurred 8.9 months after the qualifying acute myocardial infarction. Samples were collected in EDTA, shipped to a central collection site on cooled gel packs, and frozen at -80°C for future analyses. Follow-up blood samples were also obtained in the CARE trial at the 60-month (5-year) visit after randomization. Details of the blood collection and storage procedures used in the CARE trial are outlined elsewhere.16

For this analysis, we evaluated the effects of pravastatin on CRP levels among a randomly selected group of 477 participants in the CARE trial in whom both baseline and 5-year blood samples were available and who had remained free of recurrent vascular events during the trial follow-up. To avoid the potential for misclassification because of any elevation of CRP that might be due to the presence of an exogenous acute-phase stimulus, patients with either a baseline or 5-year CRP value >3 SD above the mean value were excluded from analysis on an a priori basis; in total, 5 patients (2 on placebo, 3 on pravastatin) were thus excluded. Of the remaining 472 patients, 258 had been randomly assigned in the CARE trial to receive pravastatin (40 mg PO QD), and 214 had been assigned to matching placebo. None of the study participants had previously been selected to serve as case or control subjects in an earlier analysis of inflammation within the CARE trial.7

Stored frozen blood samples from both baseline and 60-month visits were analyzed simultaneously by hs-CRP performed according to methods described by the manufacturer (Dade Behring).17 Baseline and 60-month samples were assayed in pairs to minimize interassay variation and eliminate the possibility of drift over the course of the study. All assays were performed without knowledge of treatment assignment.

Means or proportions for baseline clinical characteristics were computed for those allocated to pravastatin or placebo, and the significance of any difference in means was tested with Student's t test; differences in proportions were tested with the {chi}2 statistic. Because the distribution of CRP levels are skewed rightward, median concentrations were computed for those allocated to pravastatin and to placebo both at baseline and at 5 years, and log-normalized values of CRP were used to evaluate correlations over time. The significance of any differences in medians between drug groups was assessed by the Wilcoxon rank-sum test, and the significance of any differences in medians over time within each drug stratum was evaluated with the sign test for paired data. We also computed the absolute change in CRP level over time for each study subject, a process that resulted in a normal distribution of values. Thus, paired t tests were used to evaluate the significance of any differences in mean CRP changes over time within each drug stratum. Correlation coefficients were computed to assess for any evidence of association between the change in CRP observed over time with any change observed for total cholesterol, LDL cholesterol, HDL cholesterol, or triglycerides. These latter analyses were performed both on absolute change values for CRP and lipid levels and after categorization of the lipid data. Finally, linear regression models were used to compute ß-coefficients associated with pravastatin use and the observed change in CRP. All probability values are 2-tailed.


*    Results
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*Results
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Table 1Down shows baseline clinical characteristics of the study participants according to placebo or pravastatin allocation. There were no significant differences between study groups in terms of age, blood pressure, body mass index, smoking status, prevalence of diabetes, or measured baseline levels of total cholesterol, LDL cholesterol, HDL cholesterol, or triglycerides. Overall, baseline clinical characteristics among patients in this analysis were similar to those reported in the CARE trial as a whole.14 Aspirin use at study entry was 83%. In ongoing safety analyses, pravastatin use in the CARE trial has had no effects on hepatic function.


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Table 1. Baseline Clinical Characteristics of Study Participants According to Pravastatin or Placebo Assignment

As shown in Figure 1Down, log-normalized CRP levels were highly correlated over time among individuals allocated to placebo (r=0.60, P<0.001). Indeed, despite its being an acute-phase reactant, the absolute magnitude of the correlation coefficient for CRP in these data was similar to that observed for total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides over the 5-year follow-up period (Table 2Down).



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Figure 1. Relationship of log-normalized levels of CRP at baseline and at 60 months among study participants allocated to placebo. Dotted lines represent 95% CIs.


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Table 2. Age-Adjusted Correlation Coefficients for Log-Normalized CRP Levels and for Lipid Parameters at Baseline and After 5-Year Follow-Up Among Study Participants Randomly Allocated to Placebo

Although baseline and follow-up CRP levels were correlated, median CRP concentrations tended to increase over time among patients allocated to placebo (median change, +4.2%; P=0.2). By contrast, among those allocated to pravastatin, median CRP concentrations decreased significantly after 5 years of active treatment (median change, -17.4%; P=0.004) (Table 3Down). Thus, as shown in Figure 2Down (bottom, solid lines), whereas no difference in medians was observed between those allocated to pravastatin or placebo at baseline (P=0.8), the median CRP level was 21.6% lower at 5 years for those allocated to pravastatin (P=0.007).


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Table 3. Median and Mean Concentrations of CRP at Baseline and After 5 Years of Follow-Up According to Pravastatin or Placebo Assignment



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Figure 2. Median (solid lines) and mean (dotted lines) levels of CRP at baseline and at 60 months, according to placebo or pravastatin assignment.

Similarly, among those allocated to placebo, mean CRP levels tended to increase over the 5-year follow-up period (mean change, +0.065 mg/dL; P=0.04). By contrast, among those allocated to pravastatin, mean CRP levels decreased (mean change, -0.072 mg/dL; P=0.002). Thus, as shown in Figure 2Up (top, dotted lines), although no difference in means was observed between those allocated to pravastatin or placebo at baseline (P=0.5), the mean CRP level was 37.8% lower at 5 years for those allocated to pravastatin (P=0.002).

This difference between pravastatin and placebo groups in terms of the absolute mean change in CRP over time persisted in analyses stratified by age, body mass index, smoking status, blood pressure, and baseline levels of total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides (Table 4Down).


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Table 4. Change in Mean CRP Concentration Over 5 Years of Follow-Up According to Pravastatin or Placebo Assignment

We performed several additional analyses designed to assess whether the change in CRP observed over time might be related to changes in lipid levels associated with each treatment group. Overall, no significant correlation was observed in these data between the magnitude of change in CRP and the magnitude of change in LDL cholesterol among those allocated to pravastatin (r=0.10, P=0.1) or to placebo (r=0.02, P=0.8). A similar lack of correlation between the change in CRP and changes in total cholesterol (r=0.10, P=0.1 for pravastatin and r=0.02, P=0.8 for placebo) and triglycerides (r=0.06, P=0.3 for pravastatin and r=0.05, P=0.4 for placebo) was observed. Finally, no correlation was observed between the change in CRP and the change in HDL cholesterol among those on pravastatin (r=-0.09, P=0.2), whereas a modest correlation was observed among those on placebo (r=-0.15, P=0.03).

We explored this issue further in analyses that categorized absolute LDL changes observed at the end of the treatment period into increments of 25 mg/dL. As shown in Figure 3Down, allocation to pravastatin tended to reduce CRP levels at all LDL change increments, whereas placebo allocation tended to be associated with elevations of CRP. This appeared to be the case even among those individuals who, despite placebo allocation, experienced a reduction in LDL levels over the 5-year follow-up period. For example, in a subgroup analysis limited to study participants with a 0- to 50-mg/dL decrease in LDL cholesterol during trial follow-up, a 0.05-mg/dL decrease in CRP was observed among those assigned to pravastatin (n=144) compared with a 0.10-mg/dL increase among those assigned to placebo (n=102) (P=0.01) (Figure 3Down).



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Figure 3. Mean change in CRP levels over time according to observed changes in LDL cholesterol. Data are shown for those allocated to pravastatin (solid bars) or to placebo (open bars).

Finally, in linear regression models, pravastatin use was a significant predictor of change in CRP over time (P=0.001). However, in linear regression models that included change in LDL as well as pravastatin use, change in LDL was not a predictor of change in CRP (P=0.2), whereas the effect of pravastatin remained statistically significant (P=0.02). Moreover, the ß-coefficient for pravastatin use in models including change in LDL was similar to that in models excluding change in LDL (ß-coefficients, -0.11 and -0.14, respectively). Thus, these latter findings indicate that the effect of pravastatin on change in CRP over time is only slightly attenuated in analyses controlled for change in LDL.


*    Discussion
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
In this study of post–myocardial infarction patients enrolled in the CARE trial and followed up for 5 years, we found that CRP levels tended to increase among those treated with standard therapy plus placebo. In contrast, randomization to pravastatin resulted in significant reductions in this inflammatory marker, such that those allocated to active therapy had median CRP levels 21.6% lower than those on placebo at the end of the treatment period (P=0.007). This effect was present in the total study cohort as well as in analyses stratified by age, body mass index, smoking status, blood pressure, and baseline lipid levels. Moreover, the magnitude of change in CRP associated with randomized treatment assignment did not correlate with the magnitude of change in lipid levels observed during follow-up. For example, allocation to placebo was associated with increased CRP levels (and allocation to pravastatin was associated with decreased CRP levels) regardless of the magnitude of LDL reduction achieved. This appeared to be the case even among those individuals who, despite placebo allocation, experienced a reduction in LDL levels over the 5-year follow-up period. Finally, in linear regression analyses that controlled for change in LDL, pravastatin use remained a statistically significant predictor of change in CRP over time (P=0.02), and the ß-coefficient associated with pravastatin use was minimally altered.

Previous data evaluating the effects of HMG-CoA reductase inhibition on plasma concentrations of CRP are scant.18 However, the possibility that statin therapy might have clinically relevant anti-inflammatory effects has been suggested previously in both experimental and clinical settings. For example, HMG-CoA reductase inhibitors, such as pravastatin, have been shown to inhibit endogenous cholesterol synthesis in macrophages, a process that may reduce macrophage activation.19 Similarly, treatment with pravastatin as well as cerivastatin has been shown to reduce the number of inflammatory cells present within atherosclerotic plaques, possibly in a cholesterol-independent manner.10 11 12 Recent experimental data also indicate that lipid-lowering reduces matrix metalloproteinase activity, an effect mediated in part by inhibition of macrophage function.20 21 These latter data thus suggest that part of the plaque-stabilizing effects of statin therapy may relate to reduced inflammatory-cell function.

With regard to previous clinical evidence, a previous report from the CARE trial has shown that elevated levels of CRP after myocardial infarction were associated with increased risk of recurrent coronary events,7 data that extend evidence indicating that this inflammatory marker is a potent cardiovascular risk factor among low-risk individuals2 3 as well as those with significant preclinical atherosclerosis4 5 or angina pectoris.6 8 However, in the CARE trial, the association between elevated levels of CRP and risk was significant only among those randomized to placebo (RR=2.11, P=0.048) but was attenuated and nonsignificant among those randomized to pravastatin (RR=1.29, P=0.5). Furthermore, the risk reduction attributable to pravastatin in the CARE trial was substantially greater among those with evidence of inflammation (54%) than among those without evidence of inflammation (25%); this effect was present even though baseline lipid levels were similar in these 2 groups.7 Thus, the current finding that pravastatin reduces CRP levels supports previous observations regarding interrelations between inflammation, pravastatin, and the risk of recurrent coronary events.

The observation in these data that the magnitude of CRP reduction associated with pravastatin use did not correlate with the magnitude of LDL reduction achieved is intriguing and merits further investigation. Several large-scale randomized trials demonstrate that therapy with HMG-CoA reductase inhibitors significantly reduces the risk of subsequent myocardial infarction, stroke, and cardiovascular mortality.13 14 15 22 23 However, it has also been suggested that these risk reductions are greater than that expected on the basis of LDL reduction alone.24 Furthermore, in the West of Scotland Coronary Prevention Study trial, those on pravastatin fared better than those on placebo even when matched for LDL levels achieved.25 Thus, in this context, the present data also provide mechanistic support for the possibility that therapy with pravastatin may have important nonlipid effects.

Potential limitations of these data require consideration. For example, the magnitude of change in median CRP levels observed over time in our study were modest (+4.2% for placebo, -17.4% for pravastatin), and there was variation in both the degree and direction of change observed for individuals within each treatment stratum. However, the mean changes observed in these data were stable in analyses stratified by all available baseline variables as well as in analyses stratified by LDL change over time, an observation that suggests that our sample size was more than adequate to discern important small to moderate effects. In addition, because CRP is an acute-phase reactant, it is at least theoretically possible that the differences observed over time might have been the result of an unanticipated exogenous anti-inflammatory stimulus rather than an effect of pravastatin. We believe, however, that the randomization of our study subjects between pravastatin and placebo and the consistency of effects across subgroups makes such a possibility highly unlikely. Finally, to limit any potentially misleading effects due to outlying values, we chose prospectively to exclude from our analysis individuals with CRP levels >3 SD above the mean at either baseline or 60 months. This decision proved to have minimal impact on our analysis, because only 5 individuals were excluded on this basis (2 on placebo, 3 on pravastatin). Furthermore, post hoc inclusion of these individuals did not result in any change in median CRP levels, the analyses we believe to be most informative given the skewed nature of this inflammatory parameter.

In sum, the present data support several conclusions. First, among patients on standard therapy plus placebo followed up over a 5-year period, CRP levels were correlated, median CRP levels were stable, and the mean change in CRP over time tended to increase. The general stability of CRP over long follow-up periods thus supports the use of this inflammatory marker as a novel means for cardiovascular risk detection.

Second, long-term HMG-CoA reductase therapy with pravastatin appears to result in significantly reduced levels of CRP. These data suggest that CRP may be a modifiable marker of risk, an important observation in that previous studies indicate that individuals with elevations of CRP but normal lipid levels are at significantly increased risks of developing cardiovascular disease.9

Finally, previous studies of inflammation in the CARE trial indicate that the efficacy of pravastatin is greater among those with elevated levels of CRP, an effect that is independent of baseline lipid levels.7 In the present analysis, we found that pravastatin resulted in changes in CRP that also did not correlate with changes in LDL cholesterol. Thus, taken together, these data provide additional insights into the role of inflammation in atherogenesis and the mechanisms by which HMG-CoA reductase therapy reduces the risk of recurrent coronary events.


*    Acknowledgments
 
This study was supported by HL-58755 from the National Heart, Lung, and Blood Institute. Dr Ridker is additionally supported by an Established Investigator Award from the American Heart Association.

Received January 18, 1999; revision received April 12, 1999; accepted April 22, 1999.


*    References
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up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
up arrowDiscussion
*References
 
1. Ridker PM, Haughie P. Prospective studies of C-reactive protein as a risk factor for cardiovascular disease. J Invest Med. 1988;46:391–395.[Medline] [Order article via Infotrieve]

2. Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and risks of cardiovascular disease in apparently healthy men. N Engl J Med. 1997;336:973–979.[Abstract/Free Full Text]

3. Ridker PM, Buring JE, Shih J, Matias M, Hennekens CH. Prospective study of C-reactive protein and the risk of future cardiovascular events among apparently healthy women. Circulation. 1998;98:731–733.[Abstract/Free Full Text]

4. Tracy RP, Lemaitre RN, Psaty BM, Ives DG, Evans RW, Cushman M, Meilahn EN, Kuller LH. Relationship of C-reactive protein to risk of cardiovascular disease in the elderly: results from the Cardiovascular Health Study and the Rural Health Promotion Project. Arterioscler Thromb Vasc Biol. 1997;17:1121–1127.[Abstract/Free Full Text]

5. Kuller LH, Tracy RP, Shaten J, Meilahn EN, for the MRFIT Research Group. Relationship of C-reactive protein and coronary heart disease in the MRFIT nested case-control study. Am J Epidemiol. 1996;144:537–547.[Abstract/Free Full Text]

6. Haverkate F, Thompson SG, Pyke SDM, Gallimore JR, Pepys MB, for the European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. Production of C-Reactive protein and risk of coronary events in stable and unstable angina. Lancet. 1997;349:462–466.[Medline] [Order article via Infotrieve]

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9. Ridker PM, Glynn RJ, Hennekens CH. C-reactive protein adds to the predictive value of total and HDL cholesterol in determining risk of first myocardial infarction. Circulation. 1998;97:2007–2011.[Abstract/Free Full Text]

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11. Williams JK, Sukhova GK, Herrington DM, Libby P. Pravastatin has cholesterol-lowering independent effects on the artery wall of atherosclerotic monkeys. J Am Coll Cardiol. 1998;31:684–691.[Abstract/Free Full Text]

12. Aikawa M, Voglic SJ, Rabkin E, Shiomi M, Libby P. An HMG-CoA reductase inhibitor (cerivastatin) supresses accumulation of macrophages expressing matrix metalloproteinases and tissue factor in atheroma of WHHL rabbits. Circulation. 1998;98(suppl I):I-47. Abstract.

13. Shepard J, Cobb SM, Ford I, Isles CG, Lorimer AR, Macfarlane PW, McKillop JH, Packard CJ, for the West of Scotland Coronary Prevention Study Group. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med. 1995;333:1301–1307.[Abstract/Free Full Text]

14. Sacks FM, Pfeffer MA, Moye LA, Rouleau JL, Rutherford JD, Cole TG, Brown L, Warnica JW, Arnold JMO, Wun C, Davis BR, Braunwald E, for the Cholesterol and Recurrent Events Trial Investigators. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N Engl J Med. 1996;335:1001–1009.[Abstract/Free Full Text]

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16. Sacks FM, Pfeffer MA, Moyé L, Brown LE, Hamm P, Cole TG, Hawkins CM, Braunwald E, for the CARE Investigators. Rationale and design of a secondary prevention trial of lowering normal plasma cholesterol levels after acute myocardial infarction: the Cholesterol and Recurrent Events Trial. Am J Cardiol. 1991;68:1436–1446.[Medline] [Order article via Infotrieve]

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19. Keidar S, Aviram M, Maor I, Oiknine J, Brook JG. Pravastatin inhibits cellular cholesterol synthesis and increases low density lipoprotein receptor activity in macrophages: in vitro and in vivo studies. Br J Clin Pharmacol. 1994;38:513–519.[Medline] [Order article via Infotrieve]

20. Aikawa M, Rabkin E, Okada Y, Voglic SJ, Clinton SK, Brinckerhoff CE, Sukhova GK, Libby P. Lipid lowering by diet reduces matrix metalloproteinase activity and increases collagen content of rabbit atheroma: a potential mechanism of lesion stabilization. Circulation. 1998;97:2433–2444.[Abstract/Free Full Text]

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Clin. Chem.Home page
T. Shemesh, K. G. Rowley, A. J. Jenkins, J. D. Best, and K. O'Dea
C-Reactive Protein Concentrations Are Very High and More Stable over Time Than the Traditional Vascular Risk Factors Total Cholesterol and Systolic Blood Pressure in an Australian Aboriginal Cohort
Clin. Chem., February 1, 2009; 55(2): 336 - 341.
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Clin. Chem.Home page
S. Mora, K. Musunuru, and R. S. Blumenthal
The Clinical Utility of High-Sensitivity C-Reactive Protein in Cardiovascular Disease and the Potential Implication of JUPITER on Current Practice Guidelines
Clin. Chem., February 1, 2009; 55(2): 219 - 228.
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Clin. Chem.Home page
R. J. Glynn, J. G. MacFadyen, and P. M Ridker
Tracking of High-Sensitivity C-Reactive Protein after an Initially Elevated Concentration: The JUPITER Study
Clin. Chem., February 1, 2009; 55(2): 305 - 312.
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Clin. Chem.Home page
P. M Ridker
C-Reactive Protein: Eighty Years from Discovery to Emergence as a Major Risk Marker for Cardiovascular Disease
Clin. Chem., February 1, 2009; 55(2): 209 - 215.
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Clin. Chem.Home page
A. D. Hingorani, T. Shah, J. P. Casas, S. E. Humphries, and P. J. Talmud
C-Reactive Protein and Coronary Heart Disease: Predictive Test or Therapeutic Target?
Clin. Chem., February 1, 2009; 55(2): 239 - 255.
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Psychosom. Med.Home page
M. B. Howren, D. M. Lamkin, and J. Suls
Associations of Depression With C-Reactive Protein, IL-1, and IL-6: A Meta-Analysis
Psychosom Med, February 1, 2009; 71(2): 171 - 186.
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Cleveland Clinic Journal of MedicineHome page
M. H. SHISHEHBOR and S. L. HAZEN
JUPITER to Earth: A statin helps people with normal LDL-C and high hs-CRP, but what does it mean?
Cleveland Clinic Journal of Medicine, January 1, 2009; 76(1): 37 - 44.
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VASC ENDOVASCULAR SURGHome page
A. Gottsater, D. Flondell-Site, T. Kolbel, and B. Lindblad
Associations Between Statin Treatment and Markers of Inflammation, Vasoconstriction, and Coagulation in Patients With Abdominal Aortic Aneurysm
Vascular and Endovascular Surgery, January 1, 2009; 42(6): 567 - 573.
[Abstract] [PDF]


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Circ Cardiovasc Qual OutcomesHome page
E. S. Spatz, M. E. Canavan, and M. M. Desai
From Here to JUPITER: Identifying New Patients for Statin Therapy Using Data From the 1999-2004 National Health and Nutrition Examination Survey
Circ Cardiovasc Qual Outcomes, January 1, 2009; 2(1): 41 - 48.
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J. Thorac. Cardiovasc. Surg.Home page
V. A. Mannacio, D. Iorio, V. De Amicis, F. Di Lello, and F. Musumeci
Effect of rosuvastatin pretreatment on myocardial damage after coronary surgery: a randomized trial.
J. Thorac. Cardiovasc. Surg., December 1, 2008; 136(6): 1541 - 1548.
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NEJMHome page
P. M Ridker, E. Danielson, F. A.H. Fonseca, J. Genest, A. M. Gotto Jr., J. J.P. Kastelein, W. Koenig, P. Libby, A. J. Lorenzatti, J. G. MacFadyen, et al.
Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein
N. Engl. J. Med., November 20, 2008; 359(21): 2195 - 2207.
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Circ Cardiovasc Qual OutcomesHome page
P. W.F. Wilson, M. Pencina, P. Jacques, J. Selhub, R. D'Agostino Sr, and C. J. O'Donnell
C-Reactive Protein and Reclassification of Cardiovascular Risk in the Framingham Heart Study
Circ Cardiovasc Qual Outcomes, November 1, 2008; 1(2): 92 - 97.
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QJMHome page
J. Sanchez-Quinones, F. Marin, V. Roldan, and G.Y.H. Lip
The impact of statin use on atrial fibrillation
QJM, November 1, 2008; 101(11): 845 - 861.
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ANGIOLOGYHome page
N. Isma, J. Barani, I. Mattiasson, B. Lindblad, and A. Gottsater
Lipid-Lowering Therapy is Related to Inflammatory Markers and 3-Year Mortality in Patients With Critical Limb Ischemia
Angiology, October 1, 2008; 59(5): 542 - 548.
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VASC ENDOVASCULAR SURGHome page
A. L. Hogh, J. Joensen, J. S. Lindholt, M. R. Jacobsen, and L. Ostergaard
C-Reactive Protein Predicts Future Arterial and Cardiovascular Events in Patients With Symptomatic Peripheral Arterial Disease
Vascular and Endovascular Surgery, August 1, 2008; 42(4): 341 - 347.
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Arterioscler. Thromb. Vasc. Bio.Home page
H. Nabi, A. Singh-Manoux, M. Shipley, D. Gimeno, M. G. Marmot, and M. Kivimaki
Do Psychological Factors Affect Inflammation and Incident Coronary Heart Disease: The Whitehall II Study
Arterioscler Thromb Vasc Biol, July 1, 2008; 28(7): 1398 - 1406.
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Ther Adv Cardiovasc DisHome page
M. Rodriguez-Yanez, J. Agulla, R. Rodriguez-Gonzalez, T. Sobrino, and J. Castillo
Review: Statins and stroke
Therapeutic Advances in Cardiovascular Disease, June 1, 2008; 2(3): 157 - 166.
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VASC ENDOVASCULAR SURGHome page
E. Debing, E. Peeters, C. Demanet, M. De Waele, and P. Van den Brande
Markers of Inflammation in Patients With Symptomatic and Asymptomatic Carotid Artery Stenosis: A Case-Control Study
Vascular and Endovascular Surgery, May 1, 2008; 42(2): 122 - 127.
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Proc Am Thorac SocHome page
J. A. Falk, S. Kadiev, G. J. Criner, S. M. Scharf, O. A. Minai, and P. Diaz
Cardiac Disease in Chronic Obstructive Pulmonary Disease
Proceedings of the ATS, May 1, 2008; 5(4): 543 - 548.
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Hum Mol GenetHome page
B. S. Sutton, D. R. Crosslin, S. H. Shah, S. C. Nelson, A. Bassil, A. B. Hale, C. Haynes, P. J. Goldschmidt-Clermont, J. M. Vance, D. Seo, et al.
Comprehensive genetic analysis of the platelet activating factor acetylhydrolase (PLA2G7) gene and cardiovascular disease in case-control and family datasets
Hum. Mol. Genet., May 1, 2008; 17(9): 1318 - 1328.
[Abstract] [Full Text] [PDF]


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Journals of Gerontology Series A: Biological Sciences and Medical SciencesHome page
A. Z. LaCroix, S. L. Gray, A. Aragaki, B. B. Cochrane, A. B. Newman, C. L. Kooperberg, H. Black, J. D. Curb, P. Greenland, and N. F. Woods
Statin Use and Incident Frailty in Women Aged 65 Years or Older: Prospective Findings From the Women's Health Initiative Observational Study
J. Gerontol. A Biol. Sci. Med. Sci., April 1, 2008; 63(4): 369 - 375.
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Br J AnaesthHome page
F. Gao, L. Linhartova, A. McD. Johnston, and D. R. Thickett
Statins and sepsis
Br. J. Anaesth., March 1, 2008; 100(3): 288 - 298.
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HeartHome page
D Conen, B M Everett, R J Glynn, and P M Ridker
Effect of valsartan compared with valsartan/hydrochlorothiazide on plasma levels of cellular adhesion molecules: the Val-MARC trial
Heart, March 1, 2008; 94(3): e13 - e13.
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Mayo Clin Proc.Home page
P. Dandona
Effects of Antidiabetic and Antihyperlipidemic Agents on C-Reactive Protein
Mayo Clin. Proc., March 1, 2008; 83(3): 333 - 342.
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Clin. Chem.Home page
R. R. S. Packard and P. Libby
Inflammation in Atherosclerosis: From Vascular Biology to Biomarker Discovery and Risk Prediction
Clin. Chem., January 1, 2008; 54(1): 24 - 38.
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Am J EpidemiolHome page
J. M. Catov, L. M. Bodnar, R. B. Ness, S. J. Barron, and J. M. Roberts
Inflammation and Dyslipidemia Related to Risk of Spontaneous Preterm Birth
Am. J. Epidemiol., December 1, 2007; 166(11): 1312 - 1319.
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NeurologyHome page
S. J. Szwast, H. C. Hendrie, K. A. Lane, S. Gao, S. E. Taylor, F. Unverzagt, J. Murrell, M. Deeg, A. Ogunniyi, M. R. Farlow, et al.
Association of statin use with cognitive decline in elderly African Americans
Neurology, November 6, 2007; 69(19): 1873 - 1880.
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Am J Health Syst PharmHome page
J. S. Gortney and R. M. Sanders
Impact of C-reactive protein on treatment of patients with cardiovascular disease
Am. J. Health Syst. Pharm., October 1, 2007; 64(19): 2009 - 2016.
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Arch OphthalmolHome page
S. S. Boekhoorn, J. R. Vingerling, J. C. M. Witteman, A. Hofman, and P. T. V. M. de Jong
C-reactive Protein Level and Risk of Aging Macula Disorder: The Rotterdam Study
Arch Ophthalmol, October 1, 2007; 125(10): 1396 - 1401.
[Abstract] [Full Text] [PDF]


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Eur Heart JHome page
N. Tahara, H. Kai, H. Nakaura, M. Mizoguchi, M. Ishibashi, H. Kaida, K. Baba, N. Hayabuchi, and T. Imaizumi
The prevalence of inflammation in carotid atherosclerosis: analysis with fluorodeoxyglucose positron emission tomography
Eur. Heart J., September 2, 2007; 28(18): 2243 - 2248.
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Eur J EndocrinolHome page
F. Anan, T. Masaki, Y. Umeno, T. Iwao, H. Yonemochi, N. Eshima, T. Saikawa, and H. Yoshimatsu
Correlations of high-sensitivity C-reactive protein and atherosclerosis in Japanese type 2 diabetic patients
Eur. J. Endocrinol., September 1, 2007; 157(3): 311 - 317.
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Diabetes and Vascular Disease ResearchHome page
M. Hatunic, F. Finucane, N. Burns, D. Gasparro, and J. J Nolan
Vascular inflammatory markers in early-onset obese and type 2 diabetes subjects before and after three months' aerobic exercise training
Diabetes and Vascular Disease Research, September 1, 2007; 4(3): 231 - 234.
[Abstract] [PDF]


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J Am Coll CardiolHome page
K. M. Maki-Petaja, A. D. Booth, F. C. Hall, S. M.L. Wallace, J. Brown, C. M. McEniery, and I. B. Wilkinson
Ezetimibe and Simvastatin Reduce Inflammation, Disease Activity, and Aortic Stiffness and Improve Endothelial Function in Rheumatoid Arthritis
J. Am. Coll. Cardiol., August 28, 2007; 50(9): 852 - 858.
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J Am Coll CardiolHome page
P. M. Ridker
C-Reactive Protein and the Prediction of Cardiovascular Events Among Those at Intermediate Risk: Moving an Inflammatory Hypothesis Toward Consensus
J. Am. Coll. Cardiol., May 29, 2007; 49(21): 2129 - 2138.
[Abstract] [Full Text] [PDF]


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CirculationHome page
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, and R. H. Christenson
National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes
Circulation, April 3, 2007; 115(13): e356 - e375.
[Full Text] [PDF]


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ANGIOLOGYHome page
H. Oren, A. R. Erbay, M. Balci, and S. Cehreli
Role of Novel Biomarkers of Inflammation in Patients With Stable Coronary Heart Disease
Angiology, April 1, 2007; 58(2): 148 - 155.
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Journal of Pharmacy PracticeHome page
S. C. Fagan, H. F. Elewa, and D. J. Rychly
Statin Therapy for Secondary Stroke Prevention: Evidence Catches Up to Practice
Journal of Pharmacy Practice, April 1, 2007; 20(2): 117 - 122.
[Abstract] [PDF]


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Clin. Chem.Home page
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.
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CirculationHome page
K. K. Khush, D. D. Waters, V. Bittner, P. C. Deedwania, J. J.P. Kastelein, S. J. Lewis, and N. K. Wenger
Effect of High-Dose Atorvastatin on Hospitalizations for Heart Failure: Subgroup Analysis of the Treating to New Targets (TNT) Study
Circulation, February 6, 2007; 115(5): 576 - 583.
[Abstract] [Full Text] [PDF]


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Arch Intern MedHome page
G. Schett, S. Kiechl, S. Weger, A. Pederiva, A. Mayr, M. Petrangeli, F. Oberhollenzer, R. Lorenzini, K. Redlich, R. Axmann, et al.
High-Sensitivity C-Reactive Protein and Risk of Nontraumatic Fractures in the Bruneck Study
Arch Intern Med, December 11, 2006; 166(22): 2495 - 2501.
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Arterioscler. Thromb. Vasc. Bio.Home page
C. L. Carty, P. Heagerty, K. Nakayama, E. C. McClung, J. Lewis, D. Lum, E. Boespflug, C. McCloud-Gehring, B. R. Soleimani, J. Ranchalis, et al.
Inflammatory Response After Influenza Vaccination in Men With and Without Carotid Artery Disease
Arterioscler Thromb Vasc Biol, December 1, 2006; 26(12): 2738 - 2744.
[Abstract] [Full Text] [PDF]


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StrokeHome page
R. Schmidt, H. Schmidt, M. Pichler, C. Enzinger, K. Petrovic, K. Niederkorn, S. Horner, S. Ropele, N. Watzinger, M. Schumacher, et al.
C-Reactive Protein, Carotid Atherosclerosis, and Cerebral Small-Vessel Disease: Results of the Austrian Stroke Prevention Study
Stroke, December 1, 2006; 37(12): 2910 - 2916.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
N. Tahara, H. Kai, M. Ishibashi, H. Nakaura, H. Kaida, K. Baba, N. Hayabuchi, and T. Imaizumi
Simvastatin Attenuates Plaque Inflammation: Evaluation by Fluorodeoxyglucose Positron Emission Tomography
J. Am. Coll. Cardiol., November 7, 2006; 48(9): 1825 - 1831.
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J Am Coll CardiolHome page
P. Libby and P. M. Ridker
Inflammation and Atherothrombosis: From Population Biology and Bench Research to Clinical Practice
J. Am. Coll. Cardiol., October 27, 2006; 48(9_Suppl_A): A33 - A46.
[Abstract] [Full Text] [PDF]


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Arterioscler. Thromb. Vasc. Bio.Home page
M. Juonala, J. S.A. Viikari, T. Ronnemaa, L. Taittonen, J. Marniemi, and O. T. Raitakari
Childhood C-Reactive Protein in Predicting CRP and Carotid Intima-Media Thickness in Adulthood: The Cardiovascular Risk in Young Finns Study
Arterioscler Thromb Vasc Biol, August 1, 2006; 26(8): 1883 - 1888.
[Abstract] [Full Text] [PDF]


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StrokeHome page
B. A.N. Verhoeven, F. L. Moll, J. A.F. Koekkoek, A. C. van der Wal, D. P.V. de Kleijn, J. P. P.M. de Vries, J. H. Verheijen, E. Velema, E. Busser, A. Schoneveld, et al.
Statin Treatment Is Not Associated With Consistent Alterations in Inflammatory Status of Carotid Atherosclerotic Plaques: A Retrospective Study in 378 Patients Undergoing Carotid Endarterectomy
Stroke, August 1, 2006; 37(8): 2054 - 2060.
[Abstract] [Full Text] [PDF]


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CirculationHome page
M. A. Albert and P. M Ridker
C-Reactive Protein as a Risk Predictor: Do Race/Ethnicity and Gender Make a Difference?
Circulation, August 1, 2006; 114(5): e67 - e74.
[Full Text] [PDF]


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Journals of Gerontology Series A: Biological Sciences and Medical SciencesHome page
G. Onder, S. Volpato, R. Liperoti, C. D'Arco, C. Maraldi, R. Fellin, R. Bernabei, F. Landi, and on Behalf of the GIFA Investigators
Total serum cholesterol and recovery from disability among hospitalized older adults.
J. Gerontol. A Biol. Sci. Med. Sci., July 1, 2006; 61(7): 736 - 742.
[Abstract] [Full Text] [PDF]


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RadiologyHome page
K. Groschel, U. Ernemann, J. B. Schulz, T. Nagele, C. Terborg, and A. Kastrup
Statin Therapy at Carotid Angioplasty and Stent Placement: Effect on Procedure-related Stroke, Myocardial Infarction, and Death.
Radiology, July 1, 2006; 240(1): 145 - 151.
[Abstract] [Full Text] [PDF]


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CirculationHome page
B. M. Scirica, D. A. Morrow, S. Verma, S. Devaraj, I. Jialal, B. M. Scirica, D. A. Morrow, S. Verma, S. Devaraj, and I. Jialal
The Verdict Is Still Out
Circulation, May 2, 2006; 113(17): 2128 - 2151.
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J Am Coll CardiolHome page
S. Tsimikas, J. T. Willerson, and P. M. Ridker
C-reactive protein and other emerging blood biomarkers to optimize risk stratification of vulnerable patients.
J. Am. Coll. Cardiol., April 18, 2006; 47(8 Suppl): C19 - C31.
[Abstract] [Full Text] [PDF]


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Eur J EndocrinolHome page
J. Bollerslev, T. Ueland, A. P Jorgensen, K. J Fougner, R. Wergeland, T. Schreiner, and P. Burman
Positive effects of a physiological dose of GH on markers of atherogenesis: a placebo-controlled study in patients with adult-onset GH deficiency.
Eur. J. Endocrinol., April 1, 2006; 154(4): 537 - 543.
[Abstract] [Full Text] [PDF]


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Journals of Gerontology Series A: Biological Sciences and Medical SciencesHome page
H.-K. Kuo, J. F. Bean, C.-J. Yen, and S. G. Leveille
Linking C-Reactive Protein to Late-Life Disability in the National Health and Nutrition Examination Survey (NHANES) 1999-2002.
J. Gerontol. A Biol. Sci. Med. Sci., April 1, 2006; 61(4): 380 - 387.
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CirculationHome page
S. Kathiresan, M. G. Larson, R. S. Vasan, C.-Y. Guo, P. Gona, J. F. Keaney Jr, P. W.F. Wilson, C. Newton-Cheh, S. L. Musone, A. L. Camargo, et al.
Contribution of Clinical Correlates and 13 C-Reactive Protein Gene Polymorphisms to Interindividual Variability in Serum C-Reactive Protein Level
Circulation, March 21, 2006; 113(11): 1415 - 1423.
[Abstract] [Full Text] [PDF]


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Eur Heart JHome page
K. Iwakura, H. Ito, S. Kawano, A. Okamura, T. Kurotobi, M. Date, K. Inoue, and K. Fujii
Chronic pre-treatment of statins is associated with the reduction of the no-reflow phenomenon in the patients with reperfused acute myocardial infarction
Eur. Heart J., March 1, 2006; 27(5): 534 - 539.
[Abstract] [Full Text] [PDF]


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Cancer Res.Home page
M. J. Gunter, R. Stolzenberg-Solomon, A. J. Cross, M. F. Leitzmann, S. Weinstein, R. J. Wood, J. Virtamo, P. R. Taylor, D. Albanes, and R. Sinha
A Prospective Study of Serum C-Reactive Protein and Colorectal Cancer Risk in Men
Cancer Res., February 15, 2006; 66(4): 2483 - 2487.
[Abstract] [Full Text] [PDF]


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Eur Heart JHome page
N. Eldrup, H. Sillesen, E. Prescott, and B. G. Nordestgaard
Ankle brachial index, C-reactive protein, and central augmentation index to identify individuals with severe atherosclerosis
Eur. Heart J., February 1, 2006; 27(3): 316 - 322.
[Abstract] [Full Text] [PDF]


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Eur Heart JHome page
C. J. Boos, R. A. Anderson, and G. Y.H. Lip
Is atrial fibrillation an inflammatory disorder?
Eur. Heart J., January 2, 2006; 27(2): 136 - 149.
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ANGIOLOGYHome page
J.-J. Li, C.-H. Fang, H.-Y. Qian, and W.-L. Hu
Time Course of Rapid C-Reactive Protein Reduction by Pravastatin in Patients with Stable Angina
Angiology, January 1, 2006; 57(1): 1 - 7.
[Abstract] [PDF]


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J Am Coll CardiolHome page
G. S. Ginsburg, M. P. Donahue, and L. K. Newby
Prospects for Personalized Cardiovascular Medicine: The Impact of Genomics
J. Am. Coll. Cardiol., November 1, 2005; 46(9): 1615 - 1627.
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Cancer Epidemiol. Biomarkers Prev.Home page
D. Il'yasova, L. H. Colbert, T. B. Harris, A. B. Newman, D. C. Bauer, S. Satterfield, and S. B. Kritchevsky
Circulating Levels of Inflammatory Markers and Cancer Risk in the Health Aging and Body Composition Cohort
Cancer Epidemiol. Biomarkers Prev., October 1, 2005; 14(10): 2413 - 2418.
[Abstract] [Full Text] [PDF]


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ChestHome page
R. S. Finkelhor, G. Cater, A. Qureshi, D. Einstadter, M. T. Hecker, and G. Bosich
Seasonal Diagnosis of Echocardiographically Demonstrated Endocarditis
Chest, October 1, 2005; 128(4): 2588 - 2592.
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Am. J. Pathol.Home page
H. Sun, T. Koike, T. Ichikawa, K. Hatakeyama, M. Shiomi, B. Zhang, S. Kitajima, M. Morimoto, T. Watanabe, Y. Asada, et al.
C-Reactive Protein in Atherosclerotic Lesions: Its Origin and Pathophysiological Significance
Am. J. Pathol., October 1, 2005; 167(4): 1139 - 1148.
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Arch Intern MedHome page
R. E. Scranton, M. Young, E. Lawler, D. Solomon, D. Gagnon, and J. M. Gaziano
Statin Use and Fracture Risk: Study of a US Veterans Population
Arch Intern Med, September 26, 2005; 165(17): 2007 - 2012.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
P. Calabro, D. W. Chang, J. T. Willerson, and E. T.H. Yeh
Release of C-Reactive Protein in Response to Inflammatory Cytokines by Human Adipocytes: Linking Obesity to Vascular Inflammation
J. Am. Coll. Cardiol., September 20, 2005; 46(6): 1112 - 1113.
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Antimicrob. Agents Chemother.Home page
L. Erkkila, M. Jauhiainen, K. Laitinen, K. Haasio, T. Tiirola, P. Saikku, and M. Leinonen
Effect of Simvastatin, an Established Lipid-Lowering Drug, on Pulmonary Chlamydia pneumoniae Infection in Mice
Antimicrob. Agents Chemother., September 1, 2005; 49(9): 3959 - 3962.
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Clin. Chem.Home page
J.-J. Li and C.-H. Fang
Effects of 4 Weeks of Atorvastatin Administration on the Antiinflammatory Cytokine Interleukin-10 in Patients with Unstable Angina
Clin. Chem., September 1, 2005; 51(9): 1735 - 1738.
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CirculationHome page
L. G. Best, Y. Zhang, E. T. Lee, J.-L. Yeh, L. Cowan, V. Palmieri, M. Roman, R. B. Devereux, R. R. Fabsitz, R. P. Tracy, et al.
C-Reactive Protein as a Predictor of Cardiovascular Risk in a Population With a High Prevalence of Diabetes: The Strong Heart Study
Circulation, August 30, 2005; 112(9): 1289 - 1295.
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QJMHome page
H.T. Ong
The statin studies: from targeting hypercholesterolaemia to targeting the high-risk patient
QJM, August 1, 2005; 98(8): 599 - 614.
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Eur Heart JHome page
H. Lorenz, C. Junger, K. Seidl, A. Gitt, S. Schneider, R. Schiele, H. Wienbergen, R. Winkler, M. Gottwik, W. Delius, et al.
Do statins influence the prognostic impact of non-sustained ventricular tachycardia after ST-elevation myocardial infarction?
Eur. Heart J., June 1, 2005; 26(11): 1078 - 1085.
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J Am Coll CardiolHome page
P. M. Ridker, D. A. Morrow, L. M. Rose, N. Rifai, C. P. Cannon, and E. Braunwald
Relative Efficacy of Atorvastatin 80 mg and Pravastatin 40 mg in Achieving the Dual Goals of Low-Density Lipoprotein Cholesterol <70 mg/dl and C-Reactive Protein <2 mg/l: An Analysis of the PROVE-IT TIMI-22 Trial
J. Am. Coll. Cardiol., May 17, 2005; 45(10): 1644 - 1648.
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J. Pharmacol. Exp. Ther.Home page
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