(Circulation. 2001;103:1933.)
© 2001 American Heart Association, Inc.
Brief Rapid Communication |
Effect of Hydroxymethyl Glutaryl Coenzyme A Reductase Inhibitor Therapy on High Sensitive C-Reactive Protein Levels
Presented in part at the 73rd Scientific Sessions of the American Heart Association, New Orleans, La, November 12–15, 2000, and published in abstract form (Circulation. 2000;102[suppl II]:II-833).
From the University of Texas Southwestern Medical Center at Dallas, Tex (I.J., D.B., S.M.G., B.A.H. S.D.), and Albert Einstein College of Medicine, Bronx, NY (D.S.).
Correspondence to I. Jialal, MD, PhD, Director, Division of Clinical Biochemistry and Human Metabolism, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-9073. E-mail jialal.i{at}pathology.swmed.edu
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Abstract |
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Background—Prospective studies indicate that baseline levels of C-reactive protein (CRP), the prototypic marker of inflammation, are associated with an increased risk for cardiovascular events. Limited studies have examined therapies that influence high-sensitive CRP (hs-CRP) levels, especially in hyperlipidemic patients. Thus, we tested the effects of 3 hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins), simvastatin (20 mg/d), pravastatin (40 mg/d), and atorvastatin (10 mg/d), on levels of hs-CRP in a randomized, double-blind, crossover trial of 22 patients with combined hyperlipidemia (LDL cholesterol >130 mg/dL and triglycerides of 200 to 600 mg/dL).
Methods and Results—After 6 weeks of an American Heart Association Step 1 diet, fasting blood samples were drawn at baseline and after 6 weeks of therapy with each drug. hs-CRP levels were significantly decreased after treatment with all 3 statins compared with baseline (median values: baseline, 2.6 mg/L; atorvastatin, 1.7 mg/L; simvastatin, 1.7 mg/L; and pravastatin, 1.9 mg/L; P<0.025). The reductions obtained with the 3 statins were similar. In addition, there was no significant effect on either plasma interleukin-6 or interleukin-6 soluble receptor levels. There was no relationship between reductions in hs-CRP and LDL cholesterol.
Conclusions—Pravastatin, simvastatin, and atorvastatin significantly decreased levels of hs-CRP. These data support an anti-inflammatory effect of these drugs.
Key Words: statins • inflammation • C-reactive protein
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Introduction |
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Recently, numerous trials with the hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins) demonstrated a significant reduction in cardiovascular events.1 Although the majority of the effect could be ascribed to a beneficial effect on the lipid profile, the statins might have additional effects that could confer benefit. Inflammation seems to be a pivotal final step in acute coronary syndromes.2 3 The advent of a highly sensitive assay for C-reactive protein (CRP) has led to a greater understanding of the role of inflammation in coronary artery disease. CRP, a prototypic marker of inflammation, is driven by the proinflammatory cytokines interleukin (IL)-1, tumor necrosis factor-
, and
IL-6.4 Numerous prospective
epidemiological studies have clearly demonstrated an increased risk
with increasing CRP
levels.2 3 In
addition, studies have demonstrated that CRP confers risk above that of
an abnormal lipid
profile.2 5 Thus,
modalities targeting inflammation and reducing proinflammatory
cytokines and CRP levels could be a potential additional strategy in
the prevention of cardiovascular disease. Regarding the statins, one study to date demonstrated that patients who have increased CRP levels (increased inflammation) have a greater benefit from pravastatin therapy6 and that median CRP levels were reduced 17.4% in the group that received pravastatin.7 Thus, it is important to determine whether this reduction in CRP is specific for pravastatin or if it also occurs with other commonly prescribed statins. The aim of the present study was to test if simvastatin and atorvastatin, at LDL-lowering doses similar to those of pravastatin (as determined by the CURVES study8 ), resulted in a significant reduction in high-sensitive CRP levels (hs-CRP).
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Methods |
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Patients
Patients were recruited from the Lipid Clinics at the University of Texas Southwestern Medical Center in Dallas. This protocol was approved by the Institutional Review Board, and all patients gave informed consent. Inclusion criteria for the subjects included an age of 18 to 70 years, a triglyceride level between 200 to 600 mg/dL, and an LDL cholesterol level
130 mg/dL. Exclusion criteria were as follows: use of lipid-lowering drugs or drugs known to affect lipid metabolism, use of antioxidant supplements, use of warfarin or heparin for the past 4 weeks, liver or renal dysfunction, diabetes, hypothyroidism, infection, cancer, and/or recent major surgery or illness.
Study Design
This was a randomized, double-blind, crossover study
design. A total of 22 patients were enrolled. There was a 6-week
lead-in dietary phase when the patients were instructed by the
dietitian to follow an American Heart Association Step 1 diet for the
study duration, followed by a 6-week drug therapy phase with a 3-week
washout period between drugs. The statins used included simvastatin (20
mg/d), atorvastatin (10 mg/d), and pravastatin (40
mg/d).8
Three fasting blood samples were obtained at baseline (7 days apart), and 2 fasting blood samples were obtained during therapy with each drug (5.5 and 6 weeks). Levels of total cholesterol, total triglycerides, and LDL and HDL cholesterol were assayed by routine laboratory techniques, as reported previously.9 If plasma triglycerides were >400 mg/dL, LDL cholesterol was assessed by a direct method.9 Levels of CRP were measured by a highly sensitive nephelometric assay using a monoclonal antibody to CRP coated on polystyrene beads (Dade Behring). This assay is referenced to the World Health Organization standard and is sensitive in the range of 0.175 to 60 mg/L. Both interassay and intra-assay coefficients of variation were <5%. IL-6 and IL-6 soluble receptor levels in serum were measured using a highly sensitive immunoassay (R&D Systems). The intra-assay coefficient of variation was <4%.
Statistical Analyses
All statistical analyses were performed using
SAS version 8.0. Because some variables were
skewed (triglycerides, hs-CRP), nonparametric tests were used for these
data. The number of replicates needed to achieve the validity
coefficient of cholesterol (0.91) with CRP was
2.10 Treatment order for
this crossover study was assessed with repeated measures ANOVA models
using log transformations for skewed data.
The 3 statin drugs were compared with Friedman’s test and Wilcoxon signed rank test for pairwise comparisons: the means of the 3 baseline levels were compared with the 2 levels obtained on therapy. Weighted correlation coefficients were computed to assess associations between variables of interest.11 The level of significance was set at P<0.05 (2-sided).
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Results |
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The salient characteristics of the participants in this study are as follows: age, 47.2±9.7 years; male/female ratio, 10/12; and body mass index, 24.5±4.9 kg/m2. As is evident in the Table
,
there was a significant reduction in total and LDL cholesterol with all
3 statins; a significant reduction in plasma triglycerides was only
seen with simvastatin and atorvastatin. None of the drugs had a
significant effect on HDL cholesterol levels in these patients. As
shown in the
Figure,
all 3 drugs resulted in a significant reduction in CRP levels. The
percentage of patients showing a reduction of CRP with pravastatin,
simvastatin, and atorvastatin was 72.7%, 81.8%, and 81.8%. A total
of 54.6% of patients responded to all 3 statins. There were no
significant differences in the median percent reduction in hs-CRP
levels with pravastatin, simvastatin, and atorvastatin (20.3%, 22.8%,
and 28.3%, respectively). Of the responders, 40% of the reduction
in CRP was seen in 31.3%, 38.8%, and 44.4% of patients receiving
pravastatin, simvastatin, and atorvastatin, respectively.
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Neither plasma IL-6 nor IL-6 soluble receptor levels were significantly reduced with any of the drugs (IL-6: baseline, 2.5±0.4 pg/mL; pravastatin, 2.6±0.5 pg/mL; simvastatin, 2.4±0.4 pg/mL; and atorvastatin, 2.8±0.5 pg/mL; P>0.4; IL-6 soluble receptor: baseline, 21.5±8.1 ng/mL; pravastatin, 21.0±7.5 ng/mL; simvastatin, 21.3±9.0 ng/mL; atorvastatin, 21.7±8.4 ng/mL; P>0.4). Although no significant correlation was found between changes in CRP levels and changes in LDL cholesterol (r=-0.1, P=0.7) or HDL cholesterol (r=0.04, P=0.9), the correlation with triglycerides was significant (r=0.59, P=0.005). Furthermore, while in the washout phase, LDL-cholesterol increased significantly (P<0.001) but, compared with the drug phase, there was no significant increase in CRP levels (P=0.21).
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Discussion |
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Whether CRP is a risk marker or risk factor will only be settled by future studies. To date, CRP has been localized to foam cells in atherosclerotic lesions, it colocalizes with activated complement fragments, and it induces adhesion molecule expression from the endothelium and tissue factor secretion from monocytes.3 12 13
Previously, Ridker et al6 showed that patients with hs-CRP levels in the upper quartile had a greater benefit (54% relative risk reduction) compared with those in the lowest quartile. Furthermore, they showed a significant reduction in hs-CRP with pravastatin therapy. In the present report, we confirm that pravastatin therapy results in a significant reduction in CRP levels. Furthermore, we show that simvastatin and atorvastatin also result in a significant reduction in CRP levels. There was no significant difference between the 3 statins regarding reductions in hs-CRP. Like the Cholesterol And Recurrent Events (CARE) study, we showed no significant correlations between total cholesterol, LDL cholesterol, or HDL cholesterol and hs-CRP levels. The increase in LDL-cholesterol but not CRP in the washout phase further underscores a divergence of statins on these 2 effects. However, we found a significant correlation between a reduction in triglycerides and hs-CRP levels. Because our sample size is small and pravastatin reduced CRP without having a significant effect on triglycerides, these findings need to be viewed with caution, and confirmation must await future studies.
This study explored a potential mechanism by which statins may result in a significant reduction in hs-CRP levels. IL-6 levels were measured, but statin drugs had no effect on IL-6 levels. Because there is a great circadian variation in IL-6 levels and our sample size is small, this finding needs to be viewed with caution. Plasma IL-6 may not be the best reflection of the IL-6 levels that bathe the liver. More meaningful data would have been obtained if IL-6 levels were measured after activation, because statin therapy resulted in a significant reduction in IL-6 in lipopolysaccharide-activated whole blood.14 Because IL-6 soluble receptor levels did not change, a decrease in IL-6 soluble receptor levels cannot explain the reduction in CRP.15 Another potential reason for a failure to see a reduction in IL-6 levels despite a reduction in CRP could be that statins are acting through IL-6–independent mechanisms.16
In conclusion, the present study makes the novel observation that pravastatin, atorvastatin, and simvastatin therapy result in a significant reduction in hs-CRP levels. Furthermore, all 3 statins reduced hs-CRP levels to a similar extent.
Recently, the present investigators showed that high-dose
RRR- tocopherol (1200 IU/d) resulted in a reduction in plasma hs-CRP
levels and monocyte IL-6 levels in both controls and type 2 diabetic
patients.17 In the
Physician’s Health Study, patients with the highest CRP levels
received the greatest benefit from aspirin
therapy.18 Although studies
with aspirin therapy are
conflicting,19 20
the benefit of statins in reducing hs-CRP levels is supported by at
least 2 studies to date. Further studies need to be directed toward
elucidating the mechanism of reduction in
CRP.
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Acknowledgments |
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Supported by Merck, Warner-Lambert, and the National Institutes of Health (grants K24 AT00596 and MO1-RR-00633).
Received January 16, 2001; revision received February 15, 2001; accepted February 16, 2001.
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References |
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1. Maron DJ, Fazio S, MacRae FL. Current perspectives on statins. Circulation. 2000;101:207–213.
2. Morrow DA, Ridker PM. C-reactive protein, inflammation, and coronary risk. Med Clin North Am. 2000;84:149–161.[Medline] [Order article via Infotrieve]
3. Tracy RP. Inflammation markers and coronary heart disease. Curr Opin Lipidol. 1999;10:435–551.[Medline] [Order article via Infotrieve]
4.
Gabay C, Kushner I.
Acute-phase proteins and other systemic responses to inflammation.
N Engl J Med. 1999;340:448–351.
5. Ridker PM, Hennekens CH, Buring JE, et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med. 2000;432:836–843.
6.
Ridker PM, Rifai N,
Pfeffer M, et al. Inflammation, pravastatin, and the risk of coronary
events after myocardial infarction in patients with average cholesterol
levels. Circulation. 1998;98:839–844.
7.
Ridker PM, Rifai N,
Pfeffer MA, et al. Long-term effects of pravastatin on plasma
concentration of C-reactive protein.
Circulation. 1999;100:230–235.
8. Jones P, Kafonek S, Laurora I, et al. Comparative dose efficacy study of atorvastatin versus simvastatin, pravastatin, lovastatin, and fluvastatin in patients with hypercholesterolemia (the CURVES study). Am J Cardiol. 1998;81:582–587.[Medline] [Order article via Infotrieve]
9.
Maitra A, Hirany S,
Jialal I. A comparison of two assays for the measurement of LDL
cholesterol. Clin Chem. 1997;43:1040–1047.
10.
Sakkinen P, Macy
EM, Callas PW, et al. Analytical and biologic variability in measures
of hemostasis, fibrinolysis, and inflammation: assessment and
implications for epidemiology. Am J
Epidemiol. 1999;149:261–267.
11.
Bland JM, Altman
DG. Calculating correlation coefficients with repeated observations,
part 2: correlation between subjects.
BMJ. 1995;310:633.
12.
Pasceri V,
Willerson JT, Yeh ETH. Direct proinflammatory effect of C-reactive
protein on human endothelial cells.
Circulation. 2000;102:2165–2168.
13.
Torzewski M, Rist
C, Mortensen RF, et al. C-reactive protein in the arterial intima: role
of C-reactive protein receptor-dependent monocyte recruitment in
atherogenesis. Arterioscler Thromb Vasc
Biol. 2000;20:2094–2099.
14. Rosenson RS, Tangney CC, Casey LC. Inhibition of proinflammatory cytokine production by pravastatin. Lancet. 1999;353:983–984.[Medline] [Order article via Infotrieve]
15. Mackiewicz A, Schooltink H, Heinrich PC. Complex of soluble human Il-6-Receptor/Il-6 up-regulates expression of acute-phase proteins. J Immunol. 1992;149:2021–2027.[Abstract]
16. Weinhold B, Rüther U. Interleukin-6-dependent and -independent regulation of the human C-reactive protein gene. Biochem J. 1997;327:425–429.
17. Devaraj S, Jialal I. Alpha tocopherol supplementation decreases C-reactive protein and monocyte interleukin-6 levels in type 2 diabetic patients. Free Radic Biol Med,. 2000;29:790–792.[Medline] [Order article via Infotrieve]
18.
Ridker PM,
Cushman M, Stampfer MJ, et al. Inflammation, aspirin, and risks of
cardiovascular disease in apparently healthy men.
N Engl J Med. 1997;336:973–979.
19.
Ikonomidis I,
Andreotti F, Economou E, et al. Increased proinflammatory cytokines in
patients with chronic stable angina and their reduction by aspirin.
Circulation. 1999;100:793–798.
20. Feng D-L, Tracy RP, Lipinska I, et al. Effect of short-term aspirin use on C-reactive protein. J Thromb Thrombolysis. 2000;9:37–41.[Medline] [Order article via Infotrieve]
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S. M. Grundy, J. I. Cleeman, S. R. Daniels, K. A. Donato, R. H. Eckel, B. A. Franklin, D. J. Gordon, R. M. Krauss, P. J. Savage, S. C. Smith Jr, et al. Diagnosis and Management of the Metabolic Syndrome: An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement Circulation, October 25, 2005; 112(17): 2735 - 2752. [Full Text] [PDF]
|
|
|
|
|
|
M. D.M. Engelmann and J. H. Svendsen Inflammation in the genesis and perpetuation of atrial fibrillation Eur. Heart J., October 2, 2005; 26(20): 2083 - 2092. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Bruni, A. L. Pasqui, M. Pastorelli, G. Bova, M. Cercignani, A. Palazzuoli, T. Sawamura, A. Auteri, and L. Puccetti Different Effect of Statins on Platelet Oxidized-LDLReceptor (CD36 and LOX-1) Expressionin Hypercholesterolemic Subjects Clinical and Applied Thrombosis/Hemostasis, October 1, 2005; 11(4): 417 - 428. [Abstract] [PDF]
|
|
|
|
 |
|
 M. B. Clearfield C-Reactive Protein: A New Risk Assessment Tool for Cardiovascular Disease J Am Osteopath Assoc, September 1, 2005; 105(9): 409 - 416. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. T. Bloomgarden Inflammation, Atherosclerosis, and Aspects of Insulin Action Diabetes Care, September 1, 2005; 28(9): 2312 - 2319. [Full Text] [PDF]
|
|
|
|
|
|
R. Tiruvoipati, M. Loubani, M. Lencioni, S. Ghosh, P. W. Jones, and R. L. Patel Coronary Endarterectomy: Impact on Morbidity and Mortality When Combined With Coronary Artery Bypass Surgery Ann. Thorac. Surg., June 1, 2005; 79(6): 1999 - 2003. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.P. Empana, D.H. Sykes, G. Luc, I. Juhan-Vague, D. Arveiler, J. Ferrieres, P. Amouyel, A. Bingham, M. Montaye, J.B. Ruidavets, et al. Contributions of Depressive Mood and Circulating Inflammatory Markers to Coronary Heart Disease in Healthy European Men: The Prospective Epidemiological Study of Myocardial Infarction (PRIME) Circulation, May 10, 2005; 111(18): 2299 - 2305. [Abstract] [Full Text] [PDF]
|
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|
|
 |
|
 The Diabetes Prevention Program Research Group Intensive Lifestyle Intervention or Metformin on Inflammation and Coagulation in Participants With Impaired Glucose Tolerance Diabetes, May 1, 2005; 54(5): 1566 - 1572. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Cohen, D. Singh, P. Greenland, D. M. Lloyd-Jones, A. J. Moss, B. L. Jaber, N. E. Madias, P. M Ridker, C. P. Cannon, and E. Braunwald C-Reactive Protein Levels and Outcomes after Statin Therapy N. Engl. J. Med., April 14, 2005; 352(15): 1603 - 1605. [Full Text] [PDF]
|
|
|
|
 |
|
 V. M. Campese, M. K. Nadim, and M. Epstein Are 3-Hydroxy-3-Methylglutaryl-CoA Reductase Inhibitors Renoprotective? J. Am. Soc. Nephrol., March 1, 2005; 16(3_suppl_1): S11 - S17. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. J. Kullo and C. M. Ballantyne Conditional Risk Factors for Atherosclerosis Mayo Clin. Proc., February 1, 2005; 80(2): 219 - 230. [Abstract] [PDF]
|
|
|
|
|
|
P. M Ridker, C. P. Cannon, D. Morrow, N. Rifai, L. M. Rose, C. H. McCabe, M. A. Pfeffer, E. Braunwald, and the Pravastatin or Atorvastatin Evaluation and Inf C-Reactive Protein Levels and Outcomes after Statin Therapy N. Engl. J. Med., January 6, 2005; 352(1): 20 - 28. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Ghayour-Mobarhan, D. J. Lamb, N. Vaidya, C. Livingstone, T. Wang, and G. A. A. Ferns Heat Shock Protein Antibody Titers Are Reduced by Statin Therapy in Dyslipidemic Subjects: A Pilot Study Angiology, January 1, 2005; 56(1): 61 - 68. [Abstract] [PDF]
|
|
|
|
|
|
L. M. Biasucci CDC/AHA Workshop on Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: Clinical Use of Inflammatory Markers in Patients With Cardiovascular Diseases: A Background Paper Circulation, December 21, 2004; 110(25): e560 - e567. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. Marz, H. Scharnagl, M. M. Hoffmann, B. O. Boehm, and B. R. Winkelmann The apolipoprotein E polymorphism is associated with circulating C-reactive protein (the Ludwigshafen risk and cardiovascular health study) Eur. Heart J., December 1, 2004; 25(23): 2109 - 2119. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Pleiner, G. Schaller, F. Mittermayer, S. Zorn, C. Marsik, S. Polterauer, S. Kapiotis, and M. Wolzt Simvastatin Prevents Vascular Hyporeactivity During Inflammation Circulation, November 23, 2004; 110(21): 3349 - 3354. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. O. Obisesan, C. Leeuwenburgh, T. Phillips, R. E. Ferrell, D. A. Phares, S. J. Prior, and J. M. Hagberg C-Reactive Protein Genotypes Affect Baseline, but not Exercise Training-Induced Changes, in C-Reactive Protein Levels Arterioscler Thromb Vasc Biol, October 1, 2004; 24(10): 1874 - 1879. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T.-S. Lee, C.-C. Chang, Y. Zhu, and J. Y.-J. Shyy Simvastatin Induces Heme Oxygenase-1: A Novel Mechanism of Vessel Protection Circulation, September 7, 2004; 110(10): 1296 - 1302. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Fliser, K. Buchholz, H. Haller, and for the EUropean Trial on Olmesartan and Pravastat Antiinflammatory Effects of Angiotensin II Subtype 1 Receptor Blockade in Hypertensive Patients With Microinflammation Circulation, August 31, 2004; 110(9): 1103 - 1107. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Beckman, J. K. Liao, S. Hurley, L. A. Garrett, D. Chui, D. Mitra, and M. A. Creager Atorvastatin Restores Endothelial Function in Normocholesterolemic Smokers Independent of Changes in Low-Density Lipoprotein Circ. Res., July 23, 2004; 95(2): 217 - 223. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C G Perry, S J Cleland, J M Connell, J R Petrie, and N Sattar Low grade inflammation is notably suppressed by conventional anti-inflammatory treatment: a randomised crossover trial Heart, July 1, 2004; 90(7): 804 - 805. [Full Text] [PDF]
|
|
|
|
 |
|
 C. Kluft Identifying patients at risk of coronary vascular disease: the potential role of inflammatory markers Eur. Heart J. Suppl., July 1, 2004; 6(suppl_C): C21 - C27. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D.D. Waters and K.K. Khush Management of the acute coronary syndrome patient Eur. Heart J. Suppl., July 1, 2004; 6(suppl_C): C49 - C57. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Jialal, S. Devaraj, and S. K. Venugopal C-Reactive Protein: Risk Marker or Mediator in Atherothrombosis? Hypertension, July 1, 2004; 44(1): 6 - 11. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Paoletti, A. M. Gotto Jr, and D. P. Hajjar Inflammation in Atherosclerosis and Implications for Therapy Circulation, June 15, 2004; 109(23_suppl_1): III-20 - III-26. [Abstract] [Full Text]
|
|
|
|
|
|
J. Davignon Beneficial Cardiovascular Pleiotropic Effects of Statins Circulation, June 15, 2004; 109(23_suppl_1): III-39 - III-43. [Abstract] [Full Text]
|
|
|
|
 |
|
 R. Kleemann, L. Verschuren, B.-J. de Rooij, J. Lindeman, M. M. de Maat, A. J. Szalai, H. M. G. Princen, and T. Kooistra Evidence for anti-inflammatory activity of statins and PPAR{alpha} activators in human C-reactive protein transgenic mice in vivo and in cultured human hepatocytes in vitro Blood, June 1, 2004; 103(11): 4188 - 4194. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. P.J. Halcox and J. E. Deanfield Beyond the Laboratory: Clinical Implications for Statin Pleiotropy Circulation, June 1, 2004; 109(21_suppl_1): II-42 - II-48. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. L. Brown, K. K. Desai, B. A. Vakili, C. Nouneh, H.-M. Lee, and L. M. Golub Clinical and Biochemical Results of the Metalloproteinase Inhibition with Subantimicrobial Doses of Doxycycline to Prevent Acute Coronary Syndromes (MIDAS) Pilot Trial Arterioscler Thromb Vasc Biol, April 1, 2004; 24(4): 733 - 738. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Kumagai, H. Nakashima, and K. Saku The HMG-CoA reductase inhibitor atorvastatin prevents atrial fibrillation by inhibiting inflammation in a canine sterile pericarditis model Cardiovasc Res, April 1, 2004; 62(1): 105 - 111. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. M. Sacks High-Intensity Statin Treatment for Coronary Heart Disease JAMA, March 3, 2004; 291(9): 1132 - 1134. [Full Text] [PDF]
|
|
|
|
 |
|
 V. Fonseca, C. Desouza, S. Asnani, and I. Jialal Nontraditional Risk Factors for Cardiovascular Disease in Diabetes Endocr. Rev., February 1, 2004; 25(1): 153 - 175. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M Backes, P. A Howard, and P. M Moriarty Role of C-Reactive Protein in Cardiovascular Disease Ann. Pharmacother., January 1, 2004; 38(1): 110 - 118. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Trovati and F. Cavalot Optimization of Hypolipidemic and Antiplatelet Treatment in the Diabetic Patient with Renal Disease J. Am. Soc. Nephrol., January 1, 2004; 15(90010): S12 - 20. [Abstract] [Full Text]
|
|
|
|
|
|
S. M. Grundy Inflammation, Hypertension, and the Metabolic Syndrome JAMA, December 10, 2003; 290(22): 3000 - 3002. [Full Text] [PDF]
|
|
|
|
 |
|
 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]
|
|
|
|
 |
|
 E. M. Balk, J. Lau, L. C. Goudas, H. S. Jordan, B. Kupelnick, L. U. Kim, and R. H. Karas Effects of Statins on Nonlipid Serum Markers Associated with Cardiovascular Disease: A Systematic Review Ann Intern Med, October 21, 2003; 139(8): 670 - 682. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Ferroni, F. Martini, C. M. Cardarello, P. P. Gazzaniga, G. Davi, and S. Basili Enhanced Interleukin-1{beta} in Hypercholesterolemia: Effects of Simvastatin and Low-Dose Aspirin Circulation, October 7, 2003; 108(14): 1673 - 1675. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Haffner and H. Taegtmeyer Epidemic Obesity and the Metabolic Syndrome Circulation, September 30, 2003; 108(13): 1541 - 1545. [Full Text] [PDF]
|
|
|
|
|
|
S. Kinlay, G. G. Schwartz, A. G. Olsson, N. Rifai, S. J. Leslie, W. J. Sasiela, M. Szarek, P. Libby, P. Ganz, and for the Myocardial Ischemia Reduction with Aggress High-Dose Atorvastatin Enhances the Decline in Inflammatory Markers in Patients With Acute Coronary Syndromes in the MIRACL Study Circulation, September 30, 2003; 108(13): 1560 - 1566. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. M. Blanco-Colio, B. Munoz-Garcia, J. L. Martin-Ventura, C. Lorz, C. Diaz, G. Hernandez, and J. Egido 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitors Decrease Fas Ligand Expression and Cytotoxicity in Activated Human T Lymphocytes Circulation, September 23, 2003; 108(12): 1506 - 1513. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Susic, J. Varagic, J. Ahn, M. Slama, and E. D. Frohlich Beneficial pleiotropic vascular effects of rosuvastatin in two hypertensive models J. Am. Coll. Cardiol., September 17, 2003; 42(6): 1091 - 1097. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. B. Rice, L. L. Stoll, W.-G. Li, G. M. Denning, J. Weydert, E. Charipar, W. E. Richenbacher, F. J. Miller Jr, and N. L. Weintraub Low-Level Endotoxin Induces Potent Inflammatory Activation of Human Blood Vessels: Inhibition by Statins Arterioscler Thromb Vasc Biol, September 1, 2003; 23(9): 1576 - 1582. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Hognestad, K. Endresen, R. Wergeland, O. Stokke, O. Geiran, T. Holm, S. Simonsen, J. K. Kjekshus, and A. K. Andreassen Plasma C-reactive protein as a marker of cardiac allograft vasculopathy in heart transplant recipients J. Am. Coll. Cardiol., August 6, 2003; 42(3): 477 - 482. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
C Abud-Mendoza, H de la Fuente, E Cuevas-Orta, L Baranda, J Cruz-Rizo, and R Gonzalez-Amaro Therapy with statins in patients with refractory rheumatic diseases: a preliminary study Lupus, August 1, 2003; 12(8): 607 - 611. [Abstract] [PDF]
|
|
|
|
 |
|
 Y. Almog Statins, Inflammation, and Sepsis: Hypothesis Chest, August 1, 2003; 124(2): 740 - 743. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. B. Ledue and N. Rifai Preanalytic and Analytic Sources of Variations in C-reactive Protein Measurement: Implications for Cardiovascular Disease Risk Assessment Clin. Chem., August 1, 2003; 49(8): 1258 - 1271. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. J. A. Jenkins, C. W. C. Kendall, A. Marchie, D. A. Faulkner, J. M. W. Wong, R. de Souza, A. Emam, T. L. Parker, E. Vidgen, K. G. Lapsley, et al. Effects of a Dietary Portfolio of Cholesterol-Lowering Foods vs Lovastatin on Serum Lipids and C-Reactive Protein JAMA, July 23, 2003; 290(4): 502 - 510. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Schachter Review: Lipid lowering drugs, inflammation and cardiovascular disease The British Journal of Diabetes & Vascular Disease, May 1, 2003; 3(3): 178 - 182. [Abstract] [PDF]
|
|
|
|
|
|
A. W. Chan, D. L. Bhatt, D. P. Chew, J. Reginelli, J. P. Schneider, E. J. Topol, and S. G. Ellis Relation of Inflammation and Benefit of Statins After Percutaneous Coronary Interventions Circulation, April 8, 2003; 107(13): 1750 - 1756. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Lesperance and N. Frasure-Smith Depression and coronary artery disease: time to move from observation to trials Can. Med. Assoc. J., March 4, 2003; 168(5): 570 - 571. [Full Text] [PDF]
|
|
|
|
|
|
G. J. Blake and P. M. Ridker C-reactive protein and other inflammatory risk markers in acute coronary syndromes J. Am. Coll. Cardiol., February 19, 2003; 41(4_Suppl_S): 37S - 42S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. D. Horne, J. B. Muhlestein, J. F. Carlquist, T. L. Bair, T. E. Madsen, N. I. Hart, J. L. Anderson, and for the Intermountain Heart Collaborative (IHC) St Statin Therapy Interacts With Cytomegalovirus Seropositivity and High C-Reactive Protein in Reducing Mortality Among Patients With Angiographically Significant Coronary Disease Circulation, January 21, 2003; 107(2): 258 - 263. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Schachinger and A. M. Zeiher Atherogenesis--recent insights into basic mechanisms and their clinical impact Nephrol. Dial. Transplant., December 1, 2002; 17(12): 2055 - 2064. [Full Text] [PDF]
|
|
|
|
|
|
N. Stone Combination therapy: its rationale and the role of ezetimibe Eur. Heart J. Suppl., December 1, 2002; 4(suppl_J): J19 - J22. [Abstract] [PDF]
|
|
|
|
|
|
S. Mathur, S. Devaraj, S. M. Grundy, and I. Jialal Cocoa Products Decrease Low Density Lipoprotein Oxidative Susceptibility but Do Not Affect Biomarkers of Inflammation in Humans J. Nutr., December 1, 2002; 132(12): 3663 - 3667. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. R. Mehra, P. A. Uber, K. Vivekananthan, S. Solis, R. L. Scott, M. H. Park, R. V. Milani, and C. J. Lavie Comparative beneficial effects of simvastatin and pravastatin on cardiac allograft rejection and survival J. Am. Coll. Cardiol., November 6, 2002; 40(9): 1609 - 1614. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Stefanadis, K. Toutouzas, M. Vavuranakis, E. Tsiamis, D. Tousoulis, D.B. Panagiotakos, S. Vaina, C. Pitsavos, and P. Toutouzas Statin treatment is associated with reduced thermal heterogeneity in human atherosclerotic plaques Eur. Heart J., November 1, 2002; 23(21): 1664 - 1669. [Abstract] [Full Text] [PDF]
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