Comparison of C-Reactive Protein and Low-Density Lipoprotein Cholesterol Levels in the Prediction of First Cardiovascular Events

2002 ◽  
Vol 347 (20) ◽  
pp. 1557-1565 ◽  
Author(s):  
Paul M. Ridker ◽  
Nader Rifai ◽  
Lynda Rose ◽  
Julie E. Buring ◽  
Nancy R. Cook
Keyword(s):  
Cardiovascular Events ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
C Reactive Protein ◽  
Low Density Lipoprotein Cholesterol ◽  
Reactive Protein ◽  
Cholesterol Levels

scholarly journals Comparison of interleukin-6, C-reactive protein, and low-density lipoprotein cholesterol as biomarkers of residual risk in contemporary practice: secondary analyses from the Cardiovascular Inflammation Reduction Trial

2020 ◽  
Vol 41 (31) ◽  
pp. 2952-2961 ◽  
Author(s):  
Paul M Ridker ◽  
Jean G MacFadyen ◽  
Robert J Glynn ◽  
Gary Bradwin ◽  
Ahmed A Hasan ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Cardiovascular Events ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
C Reactive Protein ◽  
Low Density Lipoprotein Cholesterol ◽  
Reactive Protein ◽  
All Cause Mortality

Abstract Aims In epidemiologic cohorts initiated >30 years ago, inflammatory biomarkers, such as interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hsCRP) were shown to independently predict future cardiovascular events with a magnitude of effect comparable to that of low-density lipoprotein cholesterol (LDLC). Whether aggressive contemporary therapy for atherosclerosis has altered these relationships is unknown yet has major implications for future drug development. Methods and results Interleukin-6, hsCRP, and LDLC were measured at baseline in up to 4168 North American patients enrolled in the contemporary Cardiovascular Inflammation Reduction Trial with prior myocardial infarction or multivessel coronary disease who additionally had diabetes or metabolic syndrome and were followed for a period of up to 5 years for incident major recurrent cardiovascular events and all-cause mortality. Three-quarters of the cohort were previously revascularized and the great majority was taking statins, angiotensin blocking agents, beta-blockers, and antithrombotic agents. Participants were randomly allocated to low-dose methotrexate 15 mg weekly or to placebo. Randomized use of methotrexate had no effect on event rates nor plasma levels of IL-6, hsCRP, or LDL over time. Yet, baseline levels of IL-6, hsCRP, and LDLC were all predictors of major recurrent cardiovascular events; adjusted hazard ratios [HR; 95% confidence interval (CI)] for the lowest to highest baseline quartiles of IL-6 were 1.0 (referent), 1.66 (1.18–2.35), 1.92 (1.36–2.70), and 2.11 (1.49–2.99; P < 0.0001), while adjusted HRs for increasing quartiles of hsCRP were 1.0 (referent), 1.28 (0.92–1.79), 1.73 (1.25–2.38), and 1.79 (1.28–2.50; P < 0.0001) and adjusted HRs for increasing quartiles of LDLC were 1.0 (referent), 1.12 (0.78–1.62), 1.25 (0.87–1.79), and 2.38 (1.72–3.30; P < 0.0001). Effect estimates were not statistically different in these analyses for comparisons between IL-6, hsCRP, or LDLC, although IL-6 was the strongest predictor of all-cause mortality. The highest absolute risks were observed among those with elevated levels of both cholesterol and inflammation [HR 6.4 (95% CI 2.9–14.1) for those in the top quartiles of baseline IL-6 and LDLC, HR 4.9 (95% CI 2.6–9.4) for those in the top quartiles of baseline hsCRP and LDLC, both P < 0.0001]. Conclusion Despite aggressive contemporary secondary prevention efforts, the relationships between inflammation, cholesterol, and cardiovascular risk are largely unchanged from those described two decades ago. These data are consistent with the hypothesis that future treatments for atherosclerosis may require a combination of inflammation inhibition and additional cholesterol reduction. Clinical trial ClinicalTrials.gov NCT01594333.

scholarly journals Influence of lipid-lowering drugs on inflammation: what is yet to be done?

2021 ◽  
Author(s):  
Sabina Ugovšek ◽  
Janja Zupan ◽  
Andreja Rehberger Likozar ◽  
Miran Sebestjen
Keyword(s):  
Cardiovascular Events ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Lipid Lowering ◽  
Low Density ◽  
C Reactive Protein ◽  
Low Density Lipoprotein Cholesterol ◽  
Reactive Protein ◽  
Lipid Lowering Drugs

Atherosclerosis is a chronic inflammatory disease that is associated with risk of cardiovascular events. The best-characterised and well-standardised clinical indicator of inflammation is C-reactive protein. Current evidence-based drug therapies for prevention and treatment of cardiovascular diseases are mainly focused on reduction of low-density lipoprotein cholesterol. However, these drugs do not provide sufficient protection against recurrent cardiovascular events. One of the possible mechanisms behind this recurrence might be the persistence of residual inflammation. For the most commonly used lipid-lowering drugs, the statins, their reduction of cardiovascular events goes beyond lowering of low-density lipoprotein cholesterol. Here, we review the effects of these lipid-lowering drugs on inflammation, in terms of statins, ezetimibe, fibrates, niacin, proprotein convertase subtilisin/kexin type 9 inhibitors, bempedoic acid, ethyl eicosapentaenoic acid and antisense oligonucleotides. We focus in particular on C-reactive protein, and discuss how the effects of the statins might be related to reduced rates of cardiovascular events.

scholarly journals From lipoprotein apheresis to proprotein convertase subtilisin/kexin type 9 inhibitors: Impact on low-density lipoprotein cholesterol and C-reactive protein levels in cardiovascular disease patients

2018 ◽  
Vol 25 (17) ◽  
pp. 1843-1851 ◽  
Author(s):  
Maria G Zenti ◽  
Anna Altomari ◽  
Maria G Lupo ◽  
Margherita Botta ◽  
Enzo Bonora ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Proprotein Convertase ◽  
C Reactive Protein ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein Apheresis ◽  
Reactive Protein ◽  
Cholesterol Levels

In this observational study, we compared the effect of lipoprotein apheresis and evolocumab or alirocumab on levels of lipoprotein cholesterol, triglycerides and inflammatory markers (C reactive protein and interleukin 6) in cardiovascular patients ( n = 9). Patients were monitored during the last year of lipoprotein apheresis followed by six months of treatment with proprotein convertase subtilisin/kexin type 9 inhibitors. The biochemical parameters were determined pre- and post- every apheresis procedure for 12 months and then after one, three and six months of treatment with evolocumab (140 mg every two weeks [Q2W]) or alirocumab (75 mg or 150 mg every two weeks [Q2W]). Lipoprotein apheresis significantly reduced low-density lipoprotein cholesterol levels from 138 ± 32 mg/dl to 46 ± 16 mg/dl ( p < 0.001), with an inter-apheresis level of 114 ± 26 mg/dl. Lipoprotein(a) was also reduced from a median of 42 mg/dl to 17 mg/dl ( p < 0.01). Upon anti-proprotein convertase subtilisin/kexin type 9 therapy, low-density lipoprotein cholesterol levels were similar to post-apheresis (59 ± 25, 41 ± 22 and 42 ± 21mg/dl at one, three and six months, respectively) as well as those of lipoprotein(a) (18 mg/dl). However, an opposite effect was observed on high-density lipoprotein cholesterol levels: –16.0% from pre- to post-apheresis and +34.0% between pre-apheresis and proprotein convertase subtilisin/kexin type 9 inhibitors. Apheresis significantly reduced high-sensitivity C-reactive protein levels (1.5 ± 1.2 mg/l pre-apheresis to 0.6 ± 0.6 mg/l post-apheresis), while no changes were found upon proprotein convertase subtilisin/kexin type 9 mAbs administration. In conclusion, our study demonstrated that, by switching from lipoprotein apheresis to anti-proprotein convertase subtilisin/kexin type 9 therapies, patients reached similar low-density lipoprotein cholesterol and lipoprotein(a) levels, increased those of high-density lipoprotein cholesterol, and showed no changes on high-sensitivity C-reactive protein.

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