Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events

Ridker, Paul M.; Rifai, Nader; Clearfield, Michael

doi:10.1016/s1062-1458(01)00460-3

Cited by 445 publications

(453 citation statements)

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“…In this study, CRP levels improved in both groups over the study period by amounts that have a clinically significant benefit [39], despite regain of all the fat lost in the initial intervention. Thus the CRP and HDL-C changes mirror each other and may represent better overall health status in the volunteers.…”

Section: Discussionmentioning

confidence: 54%

Long-term effects of advice to consume a high-protein, low-fat diet, rather than a conventional weight-loss diet, in obese adults with Type 2 diabetes: one-year follow-up of a randomised trial

et al. 2004

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Aims/hypothesis. This study compared the long-term weight loss and health outcomes at 1-year follow-up, after a 12-week intensive intervention consisting of two low-fat, weight-loss diets, which differed in protein content. Methods. We randomly assigned 66 obese patients (BMI: 27-40 kg/m 2 ) with Type 2 diabetes to either a low-protein (15% protein, 55% carbohydrate) or high-protein diet (30% protein, 40% carbohydrate) for 8 weeks of energy restriction (~6.7 MJ/day) and 4 weeks of energy balance. Subjects were asked to maintain the same dietary pattern for a further 12 months of follow-up. Results. The study was completed by 38 of the subjects, with equal dropouts in each group. At Week 64, weight reductions against baseline were −2.2±1.1 kg (low protein) and −3.7±1.0 kg (high protein), p<0.01, with no diet effect. Fat mass was not different from baseline in either group. At Week 12, both diets reduced systolic and diastolic blood pressure by 6 and 3 mm Hg respectively, but blood pressure increased more with weight regain during follow-up in the lowprotein group (p≤0.04). At Week 64, both diets significantly increased HDL cholesterol and lowered C-reactive protein concentrations. There was no difference in the urinary urea : creatinine ratio at baseline between the two groups, but this ratio increased at Week 12 (in the high-protein group only, p<0.001, diet effect), remaining stable during follow-up in both diets. Conclusions/interpretation. A high-protein weightreduction diet may in the long term have a more favourable cardiovascular risk profile than a lowprotein diet with similar weight reduction in people with Type 2 diabetes.

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Section: Discussionmentioning

confidence: 54%

Long-term effects of advice to consume a high-protein, low-fat diet, rather than a conventional weight-loss diet, in obese adults with Type 2 diabetes: one-year follow-up of a randomised trial

et al. 2004

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“…Post hoc analysis from the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TEXCAPS) trial, a study randomizing patients without cardiovascular disease with average LDL and low high-density lipoprotein (HDL) levels to lovastatin or placebo, found that patients with a high CRP (defined as a CRP level above the median value of 1.6 mg/L) benefited from statin therapy whereas those with a low CRP (defined as a CRP level below the median value of 1.6 mg/L) did not. 16 Post hoc analysis from the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) trial comparing pravastatin (40 mg) to atorvastatin (80 mg) in patients following acute coronary syndromes, demonstrated that patients who achieved low levels of LDL (<70 mg/dL) and low CRP levels (<2 mg/dL) after statin therapy had less recurrent events than those who achieved low levels of LDL without a concomitant decrease in CRP. 41 The authors concluded that elevated CRP, irrespective of LDL level, was a marker of increased cardiovascular risk.…”

Section: C-reactive Proteinmentioning

confidence: 99%

Should We Measure C‐reactive Protein on Earth or Just on JUPITER?

Bajpai

Goyal

Sperling

2010

Clinical Cardiology

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Evidence for the role of inflammation in the pathogenesis of atherosclerosis is compelling and has generated interest in high‐sensitivity C‐reactive protein (hs‐CRP) as a marker of cardiovascular risk. Data regarding hs‐CRP and cardiovascular risk, though largely consistent, is of unclear clinical relevance. Most recently, the Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) trial has led to further debate regarding the utility of hs‐CRP. This article provides a comprehensive review of the data regarding cardiovascular risk and hs‐CRP with an emphasis on the JUPITER trial and concludes with an evidence‐based analysis of the current role of hs‐CRP in cardiovascular risk assessment. Copyright © 2010 Wiley Periodicals, Inc.

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“…For example, statins have been shown to reduce levels of C-reactive protein, which results in a decreased risk of coronary events independent of lipid lowering. 81,82 Unlike coronary artery disease, there is surprisingly little evidence to support a correlation between elevated serum cholesterol levels and overall cerebrovascular events. Prospective observational cohorts, with 450 000 patients, demonstrated no correlation except among patients under the age of 45.…”

Section: Lipid-lowering Agentsmentioning

confidence: 99%

Current and future concepts in stroke prevention

O’Rourke

Dean

Akhtar

et al. 2004

Canadian Medical Association Journal

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STROKE IS A MAJOR CAUSE OF MORBIDITY and mortality in an aging population. The current understanding of the pathophysiology of atherosclerotic diseases, the most common cause of stroke, and the evidence for existing therapeutic interventions for the prevention of stroke are presented. Specifically, we review the evidence for antiplatelet agents, anticoagulants, antihypertensive medications, lipidlowering agents and carotid endarterectomy for stroke prevention. primary preventive measure, antiplatelet agents do not reduce the risk of ischemic stroke among patients without vascular disease. They are associated with an increased risk of intracranial hemorrhage (odds ratio [OR] 1.35, 95% confidence interval [CI] 0.88-2.10) 23 and major noncerebral hemorrhage (OR 1.73, 95% CI 1.14-2.63 ). 24 The benefits of ASA in the secondary prevention of stroke have been well documented in the period immediately after a stroke 25 (Table 1). Long-term antiplatelet treatment after stroke shows an even more impressive reduction of 25 nonfatal strokes and 36 serious vascular events per 1000 treated over a 29-month follow-up period. 25 There appears to be no difference in efficacy between low (50 mg) and higher doses (up to 1500 mg) of ASA. 29,30 The combination of dipyridamole and ASA has been shown to reduce the relative risk of recurrent stroke compared with ASA alone 26 (Table 1). Dipyridamole inhibits platelet aggregation by increasing levels of cyclic adenosine monophosphate and cyclic guanosine monophosphate. The limiting factor in the use of the ASAdipyridamole combination is the latter's potential effects on coronary perfusion. Dipyridamole can cause coronary vasodilation, which results in increased blood flow to nonstenosed coronary arteries. The result is that myocardial ischemia may be provoked during exercise. As such, the current American College of Cardiology/American Heart Association guidelines recommend that dipyridamole not be used in patients with chronic stable angina. 31 However, this recommendation was based on shortacting dipyridamole, which also reduced myocardial ischemia in a similar number of patients in the study quoted by these guidelines. 32 With the use of sustained-release dipyridamole, no increase in cardiac events was observed in subjects with prior coronary artery disease. 33 Thienopyridines block adenosine-diphosphate-mediated platelet aggregation. Ticlopidine was the first of this class of drug to be studied for stroke prevention. One clinical trial demonstrated that patients treated with ticlopidine had similar rates of stroke as those treated with ASA 28 (Table 1). However, serious granulocytopenia associated with ticlo- Leukocytes localize in the earliest atherosclerotic lesions, binding to vascular cell adhesion molecules (VCAM-1) on the vascular endothelium and migrating into the intima. This initiates and perpetuates a local inflammatory response. Monocytes mature into lipid-scavenging macrophages and subsequently foam cells. T-lymphocytes express inflammatory cytokines, which cont...

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Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events

Cited by 445 publications

References 0 publications

Long-term effects of advice to consume a high-protein, low-fat diet, rather than a conventional weight-loss diet, in obese adults with Type 2 diabetes: one-year follow-up of a randomised trial

Long-term effects of advice to consume a high-protein, low-fat diet, rather than a conventional weight-loss diet, in obese adults with Type 2 diabetes: one-year follow-up of a randomised trial

Should We Measure C‐reactive Protein on Earth or Just on JUPITER?

Current and future concepts in stroke prevention

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