Reynolds Risk Score Research Articles

Reynolds Risk Score as a Risk Assessment Tool for Cardiovascular Disease After 10 Years: Its Strong Relationship With Blood Pressure

Reynolds Risk Score as a Risk Assessment Tool for Cardiovascular Disease After 10 Years: Its Strong Relationship With Blood Pressure

Reduction in Estimated 10-Year Coronary Heart Disease Risk Using Reynolds Risk Score: A Post-Hoc Analysis of Exenatide-Treated Patients with Diabetes

Reduction in Estimated 10-Year Coronary Heart Disease Risk Using Reynolds Risk Score: A Post-Hoc Analysis of Exenatide-Treated Patients with Diabetes

Usefulness of Risk Scores to Estimate the Risk of Cardiovascular Disease in Patients With Rheumatoid Arthritis

Patients with rheumatoid arthritis (RA) have an excess burden of cardiovascular (CV) disease (CVD). CV risk scores for the general population may not accurately predict CV risk for patients with RA. A population-based inception cohort of patients who fulfilled 1987 American College of Rheumatology criteria for RA from 1988 to 2007 was followed until death, migration, or December 31, 2008. CV risk factors and CVD (myocardial infarction, CV death, angina, stroke, intermittent claudication, and heart failure) were ascertained by medical record review. Ten-year predicted CVD risk was calculated using the general Framingham and the Reynolds risk scores. Standardized incidence ratios were calculated to compare observed and predicted CVD risks. The study included 525 patients with RA aged ≥30 years without previous CVD. The mean follow-up period was 8.4 years, during which 84 patients developed CVD. The observed CVD risk was 2-fold higher than the Framingham risk score predicted in women and 65% higher in men, and the Reynolds risk score revealed similar deficits. Patients aged ≥75 years had observed CVD risk >3 times the Framingham-predicted risk. Patients with positive rheumatoid factor or persistently elevated erythrocyte sedimentation rates also experienced more CVD events than predicted. In conclusion, the Framingham and Reynolds risk scores substantially underestimated CVD risk in patients with RA of both genders, especially in older ages and in patients with positive rheumatoid factor. These data underscore the need for more accurate tools to predict CVD risk in patients with RA.

Risk Models and Patient-Centered Evidence

A FUNDAMENTAL CONTRADICTION OF EVIDENCEbased medicine (EBM) is that evidence is derived from groups, whereas medicine is applied to individuals. Inferring individual effects from average group effects is an example of the fallacy of division. Even in a randomized trial, benefit in a summary result does not imply that the probability of benefitting outweighs the risk of harm for all (or even most) patients within the trial. Use of risk models, which estimate the probability of a health outcome in an individual based on patient-specific characteristics, has been proposed as a way to make evidence more “patient-centered”—permitting, for example, the targeting of risky or costly therapies to higher-risk patients with more opportunity for benefit or the disaggregation of the “average” effect reported in trials to reveal riskgroup–specific effects. In this Viewpoint, we discuss some fundamental limits of evidence individualization using risk models. Consider the use of antiplatelet medication for primary prevention of coronary heart disease (CHD). Based on a comprehensive pooled analysis of 6 trials including more than 90 000 patients, guidelines agree that use of aspirin is helpful for high-risk patients but not for low-risk patients. American Heart Association (AHA) guidelines recommend targeting aspirin to patients with a 10-year risk of CHD higher than 10%. The Framingham Risk Score (FRS), the Atherosclerosis in Communities (ARIC) risk score, and the Reynolds Risk Score (RRS) are validated models that estimate CHD risk. Although all incorporate similar cardiac risk factors, the FRS and ARIC score were developed using population-based cohorts; the RRS was derived from the Physicians’ Health Study (for men) and the Women’s Health Study (for women). However, applying each of these 3 risk models in a nationally representative population showed that 39% of men and 21% of women exceeded the AHA threshold for aspirin therapy in at least 1 score, but only 13% of men and 10% of women exceeded this threshold in all 3 risk scores. Thus, for more than 60% of patients who might receive aspirin, the recommendation was conditional on which tool was applied. To better understand this, consider an example: one of us (D.M.K.) halved his 10-year CHD risk (from 7% to 3%) simply by applying the RRS instead of the FRS. This is explainable in part by the lower risk of the Reynolds population (in which all men were physicians) and by his favorable C-reactive protein and family history (variables omitted from the FRS). Which model is correct for D.M.K.? The fact is that he either will or will not develop CHD in 10 years so, arguably, both models are wrong; a perfectly accurate model would make only 2 kinds of predictions: 0% and 100%. Although proponents might have strong arguments favoring their model (and while D.M.K. has a clear preference based on the results), all arguments are based on measures of aggregate performance, not accuracy in the individual. Even given the same large derivation sample, because there are many ways to define, select, and code variables and many statistical approaches to relate the expected value to the predictor variables and to optimize model fit, risk models are fundamentally underdetermined by data, meaning there is no unique “best” model. Competing models fitting the data equally well nonetheless shuffle individuals between risk groups considerably. Since uncertainty at the individual level derives in part from the fact that estimates come from different models, not from statistical imprecision alone, some of this uncertainty is irreducible; more data to improve each model’s precision would not necessarily cause predictions in individuals to converge. This discussion has presented only one part of the complex decision to initiate a therapy because there is rarely complete agreement on the risk threshold at which therapy should start. Experts can disagree about where a treatment threshold should lie and about the credibility of subgroup effects. Indeed, based on the results of the Women’s Health Study, which showed a reduction in first stroke but not first

Application of Reynolds Risk Score for younger generation with different ethnicities

Application of Reynolds Risk Score for younger generation with different ethnicities

Abstract MP074: High-sensitivity C-reactive Protein and Family History in the Prediction of Risk for Coronary Heart Disease: The Atherosclerosis Risk in Communities Study

Background: Reynolds Risk Score (RRS) has been proposed as an improved tool for prediction of coronary heart disease (CHD), adding high sensitivity C-reactive protein (hsCRP) and family history of premature coronary heart disease (FH) to traditional risk factors (TRF). RRS was developed in 2 studies of predominantly Caucasian health professionals and has not been validated in other cohorts. Aim: To assess whether FH and hsCRP improve risk prediction for CHD beyond TRF in the Atherosclerosis Risk in Communities (ARIC) study. Methods: hsCRP was measured using an immunonephelometric assay in 7240 Caucasian and African-American adults during ARIC visit 4 (1996-1998). FH was defined as parental history of myocardial infarction (MI) before age 60. CHD was defined as hospitalized MI, CHD death or coronary revascularization. Adults with diabetes, known CHD or stroke before visit 4 were excluded. 10-yr risk of incident CHD was estimated using a Cox proportional hazards model and categorized as 0-5%, >5%-10%, >10%-20%, or >20%. Two baseline models were described: model 1, that included age, sex, systolic blood pressure, total and HDL cholesterol, and current smoking; and model 2, which included model 1 + antihypertensive medication use and race. We calculated area under the ROC curve (AUC), Bayes Information Criterion (BIC), Gronnesby & Borgan goodness of fit test, and net reclassification improvement (NRI) for both models with and without log (hsCRP) and FH. Confidence intervals were calculated using bootstrapping. Analyses were stratified by sex. Results: Over a median of 11.04 years, 430/2945 men (14.6%) and 253/4295 women (5.9%) experienced events. Addition of hsCRP and FH to baseline model 1 was associated with a modest improvement in AUC and BIC (Table). The NRI was not significant. Further, results were attenuated when antihypertensive medication and race were included in the model. Conclusions: Addition of hsCRP and FH to a model based on TRF resulted in only modest improvements in CHD risk prediction in the ARIC cohort. Table. Prediction of Risk for Coronary Heart Disease in the Atherosclerosis Risk in Communities Study, 1996-2008 Statistical measure Model 1 * Model 1 * + log(hsCRP) and FH Model 2 † Model 2 † + log(hsCRP) and FH Men BIC 6627.88 6619.63 6658.82 6651.20 AUC (95% CI) 0.65 (0.62-0.68) 0.66 (0.64-0.69) 0.66 (0.64-0.69) 0.67 (0.65-0.70) GB p value 0.74 0.61 0.69 0.85 NRI (95% CI) --- 0.067 (-0.015-0.133) --- 0.035 (-0.012-0.133) Women BIC 4075.33 4071.97 4108.08 4105.00 AUC (95% CI) 0.68 (0.65-0.72) 0.69 (0.66-0.73) 0.68 (0.65-0.72) 0.69 (0.67-0.73) GB p value 0.98 0.38 0.79 0.37 NRI (95% CI) --- 0.033 (-0.039-0.137) --- 0.014 (-0.044-0.128) * Includes age, total and HDL cholesterol, SBP, current smoking † Includes age, total and HDL cholesterol, SBP, current smoking, antihypertensive medication use and race BIC: Bayes information criterion; AUC: area under the ROC curve; GB: Gronnesby & Borgan goodness-of-fit test; NRI: net reclassification improvement; CI: confidence interval

How Accurate Are 3 Risk Prediction Models in US Women?

Cardiovascular disease (CVD) is the leading cause of death for US women, and nearly two thirds who died suddenly of CVD had no previous symptoms.1 Therefore, it is of great importance to identify “at-risk” women early, so that effective primary prevention strategies can be instituted. A universal recommendation of prevention guidelines is that all asymptomatic women should undergo a global risk assessment.2 Article see p 1748 The Adult Treatment Panel III (ATP-III) of the National Cholesterol Education Program set thresholds for lipid treatment based on one's predicted 10-year risk for a hard coronary heart disease (CHD) event (myocardial infarction or CHD death) using a modified Framingham risk score (FRS).3 There are limitations, however, with use of the ATP-III model for CVD prediction in women. The ATP-III version predicts “hard” CHD events but not angina or revascularizations, even if such revascularizations are performed to manage an acute coronary syndrome. Yet women are more likely to experience “soft” CHD events or strokes than men. Moreover, a single laboratory measurement does not reflect lipid values over a woman's lifetime. The FRS does not take into account family history of premature CHD, a well-established independent risk factor for CHD events.4 Also, because stroke accounts for a higher proportion of CVD events than CHD in women before age 75 years,1 we believe that total CVD risk should be the outcome for prediction and preventive strategies. Indeed, that is the conclusion of the 2011 American Heart Association CVD prevention guidelines for women.5 Furthermore, the FRS only predicts 10-year risk, whereas for women, the issue is most often “lifetime” risk. The Third National Health and Nutrition Examination Survey found that among women without a history of CHD or diabetes, 92% of those aged 60 to 69 years and >98% aged <59 …

RECLASSIFICATION OF CARDIOVASCULAR RISK WITH CORONARY CALCIUM SCORING IN SUBJECTS WITHOUT DOCUMENTED CORONARY HEART DISEASE: COMPARISON WITH RISK ASSESSMENT BASED ON REYNOLDS RISK SCORE

Unlike Framingham risk score (FRS), Reynolds risk score (RRS) predicts future coronary heart disease (CHD) while incorporating C-reactive protein (CRP) & family history. Coronary calcium scoring (CAC) has shown additive value over FRS but not RRS. We investigated if CAC leads to reclassification of

Cardiovascular disease, statins and vitamin D

Cardiovascular disease is the number one killer in the UK, causing more than 50 000 premature deaths per year, at a cost of over £30 billion to the economy (British Heart Foundation, 2010). Reducing this burden is a priority of the Government and health professionals (Department of Health, 2000). The aim of this paper is to inform and update nurses on four aspects. Firstly, to examine a more accurate test than cholesterol to predict cardiovascular risk that used C-reactive protein (CRP), an inflammatory marker, called the Reynold's Risk Score. Use of this score reclassified almost half of women, and one-fifth of men, into lower or higher risk categories, more accurately compared to conventional tools (Ridker et al, 2007; Ridker et al, 2008b). Secondly, to highlight a potential change to the indications for statin-therapy; an indication for those who ordinarily would not receive a statin: healthy middle-aged adults with normal or low cholesterol, but elevated CRP. This includes discussion of the JUPITER trial and its sub-analyses. This large, multicentre, double-blind randomized, placebo-controlled trial in apparently healthy men over the age of 50 years and women over 60 years, with normal or low cholesterol but elevated CRP, demonstrated significant benefit. Rosuvastatin 20 mg per day compared to a placebo reduced myocardial infarction and stroke by half, and reduced venous thromboembolism by almost half (Ridker et al, 2008a; Glynn et al. 2009; Everett, et al, 2010). Thirdly, to discuss the pleiotropic effects of statins, which include reduction of CRP (Ridker et al, 2008a), increases in endothelial repair cells (Spiel, et al, 2008), alteration of clotting factors (Glynn, et al, 2009), and enhancement of vitamin D metabolism (Yavuz et al, 2009). Fourthly, to discuss evidence that the pleiotropic effects of statins may be attributable to the vitamin D effect. This paper therefore evaluates the evidence suggesting that vitamin D supplementation may attain the same benefit as statins (Grimes, 2006), in addition to reducing statinassociated side-effects when co-administered (Ahmed et al, 2009).

The Association of Framingham and Reynolds Risk Scores With Incidence and Progression of Coronary Artery Calcification in MESA (Multi-Ethnic Study of Atherosclerosis)

The purpose of this study was to compare the association of the Framingham risk score (FRS) and Reynolds risk score (RRS) with subclinical atherosclerosis, assessed by incidence and progression of coronary artery calcium (CAC). The comparative effectiveness of competing risk algorithms for identifying subclinical atherosclerosis is unknown. MESA (Multi-Ethnic Study of Atherosclerosis) is a prospective cohort study of 6,814 participants free of baseline cardiovascular disease. All participants underwent risk factor assessment, as well as baseline and follow-up CAC testing. We assessed the performance of the FRS and RRS to predict CAC incidence and progression using relative risk and robust linear regression. The study population included 5,140 individuals (mean age 61 ± 10 years, 47% males, mean follow-up: 3.1 ± 1.3 years). Among 53% of subjects (n = 2,729) with no baseline CAC, 18% (n = 510) developed incident CAC. Both the FRS and RRS were significantly predictive of incident CAC (relative risk: 1.40 [95% confidence interval (CI): 1.29 to 1.52] and 1.41 [95% CI: 1.30 to 1.54] per 5% increase in risk, respectively) and CAC progression (mean CAC score change: 6.92 [95% CI: 5.31 to 8.54] and 6.82 [95% CI: 5.51 to 8.14] per 5% increase). Discordance in risk category classification (<10% or >10% per 10-year coronary heart disease risk) occurred in 13.7%, with only the RRS consistently adding predictive value for incidence and progression of CAC. These subclinical atherosclerosis findings are supported by a coronary heart disease events analysis over a mean follow-up of 5.6 ± 0.7 years. Both the RRS and FRS predict onset and progression of subclinical atherosclerosis. However, the RRS may provide additional predictive information when discordance between the scoring systems exists.

Novel cardiovascular risk prediction models in patients with systemic lupus erythematosus

Women with systemic lupus erythematosus (SLE) have increased risk for coronary heart disease (CHD) which is underestimated by the Framingham risk score (FRS). We hypothesized that new risk scores that include inflammation or vascular age in the risk calculation would better identify women with SLE at risk for CHD, particularly in those with subclinical coronary atherosclerosis. We calculated the FRS and Reynolds risk score (RRS) in 121 women with SLE and 65 age-matched female controls; coronary age-modified risk scores (camFRS, camRRS) were calculated using coronary age derived from the coronary artery calcium (CAC) score. Risk scores were compared in SLE and controls, and in SLE patients with and without CAC. Although CAC was present in 21 SLE patients (17%) and four controls (6%) (p = 0.033); the FRS, camFRS, RRS, and camRRS, did not differ significantly among SLE and controls (p > 0.05), but were all significantly higher in SLE patients with CAC compared with those without (p < 0.001 for all). The camFRS (8%, p = 0.016) but not camRRS (5%, p = 0.221) assigned significantly more SLE patients to a category of ≥ 10% risk than conventional FRS (1%) and RRS (2%). The RRS was of limited use but coronary age may improve CHD risk prediction in SLE.

Gender-specific association between carotid intima-media thickness and Reynolds risk score

Appropriate assessment and prevention of cardiovascular (CV) disease is one of the most important medical tasks worldwide. Carotid artery intima-media thickness (CIMT) is a marker of atherosclerosis, which has been associated with CV events. We examined the associations of a panel of different clinical, laboratory, and ultrasound variables simultaneously and individually with CIMT; to reveal the presence of additional surrogate markers of atherosclerosis to CIMT. 407 Consecutive non-diabetic individuals (220 men) who underwent comprehensive CV evaluation were included. The maximum IMT of the common and internal carotid artery on the right and left side of the neck were recorded by ultrasonography, and CIMT was calculated as the average of the four measurements. Ten-year Reynolds risk score (RRS) for CV events was calculated online for men and women. CAVI was measured using a VaSera vascular screening system, and the averages of the right and left CAVI were used for analysis after being adjusted for age. Univariate linear regression models were constructed to test the association of each of the independent variables with the log-transformed CIMT values [Ln (average CIMT) + 2] separately for men and women. Only the variables with non-adjusted p ⩽ 0.1 were included in the final multivariately-adjusted stepwise linear regression model. After multivariate adjustment, only two variables were significantly and independently associated with log-transformed CIMT values in males (the log-transformed Reynolds risk score and the average age-matched CAVI) and females (the average age-matched CAVI and systolic blood pressure). RRS could be a candidate marker of atherosclerosis in men but not in women, while age-adjusted CAVI could be considered a marker of atherosclerosis in both genders.

Should C-Reactive Protein Be a Target of Therapy?

Multiple studies have demonstrated that elevated levels of high-sensitivity C-reactive protein (hs-CRP) are associated with increased cardiovascular (CV) risk. Newer CV risk stratification strategies incorporating hs-CRP (e.g., Reynolds Risk Score) have also been shown to improve risk stratification better than algorithms incorporating only traditional risk factors. There is also evidence from several landmark statin trials that on-treatment hs-CRP levels predict the likelihood of CV events. Although there is increasing evidence that CRP may be directly involved in the pathogenesis of atherosclerosis, the question of whether reduction in CRP levels and/or its associated downstream effects will provide novel therapeutic avenues to reduce CV risk requires further investigation. CV diseases are the number one cause of mortality worldwide (1). Recent efforts directed at primary prevention of atherosclerosis have significantly reduced the incidence of initial clinical presentation of atherosclerosis. It is well established that patients with known diabetes or other traditional CV risk factors have an increased risk of atherosclerosis. Nonetheless, 15–20% of major CV events occur in patients with no major traditional CV risk factors (2). As a result, recent preventive efforts have been directed at finding newer, nontraditional, biomarkers to improve risk stratification, particularly in otherwise apparently low-risk individuals. hs-CRP, previously considered to be an indicator of systemic inflammation, has recently received much attention in the scientific literature, not only as a potential marker of increased atherosclerotic risk, but also as a potential target of therapy for the prevention of atherosclerotic CV disease. In this review, we discuss whether hs-CRP should indeed be a target for therapy in the prevention of CV disease as well as other potential clinical implications related to hs-CRP. Multiple studies have demonstrated that elevated levels of hs-CRP are clearly associated with increased CV risk (3,4). However, considerable controversy exists on whether CRP itself is …

Fibrinogen concentration and its role in CVD risk in black South Africans – effect of urbanisation

The aim of this study was to investigate correlates of fibrinogen concentration in black South Africans, as well as its association with cardiovascular disease (CVD) risk and whether urbanisation influences this association. A total of 1,006 rural and 1,004 urban black South Africans from the PURE study were cross-sectionally analysed. The association of fibrinogen with CVD risk was determined by investigating the association of fibrinogen with other CVD risk markers as well as with predicted CVD risk using the Reynolds Risk score. The rural group had a significantly higher fibrinogen concentration than the urban group, despite higher levels of risk factors and increased predicted CVD risk in the urban group. Increased levels of CVD risk factors were, however, still associated with increased fibrinogen concentration. Fibrinogen correlated significantly, but weakly, with overall predicted CVD risk. This correlation was stronger in the urban than in the rural group. Multiple regression analysis showed that a smaller percentage of the variance in fibrinogen is explained by the traditional CVD risk factors in the rural than in the urban group. In conclusion, fibrinogen is weakly associated with CVD risk (predicted overall risk as well with individual risk factors) in black South Africans, and is related to the degree of urbanisation. Increased fibrinogen concentration, in black South Africans, especially in rural areas, is largely unexplained, and likely not strongly correlated with traditional CVD-related lifestyle and pathophysiological processes. This does, however, not exclude the possibility that once increased, the fibrinogen concentration contributes to future development of CVD.

C-Reactive Protein and High-Sensitivity C-Reactive Protein: An Update for Clinicians

The measurement of C-reactive protein (CRP) using both standard and high-sensitivity CRP (hs-CRP) assays is becoming common in clinical practice. This article addresses the causes of CRP elevation and the use of different CRP assays in internal medicine, including cardiology, gastroenterology, rheumatology, infectious diseases, and oncology. We focus on the recent medical literature on the use of hs-CRP in cardiovascular disease risk stratification and management, including updated screening guidelines on the use of hs-CRP, such as those issued in 2009 by the Canadian Cardiovascular Society. We also discuss the Reynolds Risk Score, which incorporates hs-CRP and family history with more standard cardiovascular risk factors (eg, tobacco use, hypertension, and dyslipidemia) and frequently leads to improved recategorization of cardiovascular disease risk levels. As the recently completed Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) trial indicated that statin therapy decreases the vascular events among persons with elevated hs-CRP by half, even when cholesterol levels are low, the inclusion of information on hs-CRP values with other cardiovascular risk factors may assist physicians in medical decision making for patients.

Most of the patients presenting myocardial infarction would not be eligible for intensive lipid-lowering based on clinical algorithms or plasma C-reactive protein

ObjectiveThe study we assessed how often patients who are manifesting a myocardial infarction (MI) would not be considered candidates for intensive lipid-lowering therapy based on the current guidelines. MethodsIn 355 consecutive patients manifesting ST elevation MI (STEMI), admission plasma C-reactive protein (CRP) was measured and Framingham risk score (FRS), PROCAM risk score, Reynolds risk score, ASSIGN risk score, QRISK, and SCORE algorithms were applied. Cardiac computed tomography and carotid ultrasound were performed to assess the coronary artery calcium score (CAC), carotid intima-media thickness (cIMT) and the presence of carotid plaques. ResultsLess than 50% of STEMI patients would be identified as having high risk before the event by any of these algorithms. With the exception of FRS (9%), all other algorithms would assign low risk to about half of the enrolled patients. Plasma CRP was <1.0mg/L in 70% and >2mg/L in 14% of the patients. The average cIMT was 0.8±0.2mm and only in 24% of patients was ≥1.0mm. Carotid plaques were found in 74% of patients. CAC ≥100 was found in 66% of patients. Adding CAC ≥100 plus the presence of carotid plaque, a high-risk condition would be identified in 100% of the patients using any of the above mentioned algorithms. ConclusionMore than half of patients manifesting STEMI would not be considered as candidates for intensive preventive therapy by the current clinical algorithms. The addition of anatomical parameters such as CAC and the presence of carotid plaques can substantially reduce the CVD risk underestimation.

Cardiovascular risk scores in the prediction of subclinical atherosclerosis in young adults: evidence from the cardiovascular risk in a young Finns study

To study the utility of risk scores in the prediction of subclinical atherosclerosis in young adults. Participants were 2204 healthy Finnish adults aged 24-39 years in 2001 from a population-based follow-up study Cardiovascular Risk in Young Finns. We examined the performance of the Framingham, Reynolds, Systematic Coronary Risk Evaluation (SCORE), PROCAM, and Finrisk cardiovascular risk scores to predict subclinical atherosclerosis, that is carotid artery intima-media thickness (IMT) and plaque, carotid artery distensibility (CDist), and brachial artery flow-mediated dilatation (FMD) 6 years later. In a 6-year prediction of high IMT (highest decile or plaque), areas under the receiver operating characteristic curves (AUC) for baseline Finrisk (0.733), SCORE (0.726), PROCAM (0.712), and Reynolds (0.729) risk scores were similar as for Framingham risk score (0.728, P always ≥0.15). All risk scores had a similar discrimination in predicting low CDist (lowest decile) (0.652, 0.642, 0.639, 0.658, 0.652 respectively, P always ≥0.41). In the prediction of low FMD (lowest decile), Finrisk, PROCAM, Reynolds, and Framingham scores had similar AUCs (0.578, 0.594, 0.582, 0.568, P always ≥0.08) and SCORE discriminated slightly better (AUC=0.596, P<0.05). The prediction of subclinical outcomes was consistent when estimated from other statistical measures of discrimination, reclassification, and calibration. Cardiovascular disease risk scores had equal value in predicting subclinical atherosclerosis measured by IMT and CDist in young adults. SCORE was more accurate in predicting low FMD than Framingham risk score.

Rosuvastatin for Primary Prevention Among Individuals With Elevated High-Sensitivity C-Reactive Protein and 5% to 10% and 10% to 20% 10-Year Risk

Recent primary prevention guidelines issued in Canada endorse the use of statin therapy among individuals at "intermediate risk" who have elevated levels of high-sensitivity C-reactive protein (hsCRP). However, trial data directly addressing whether this recommendation defines a patient population in which statin therapy is effective have not previously been published. In the Justification for Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) trial, which demonstrated a 44% reduction in first vascular events when rosuvastatin 20 mg was compared with placebo among 17 802 primary prevention patients with LDL cholesterol <130 mg/dL and hsCRP ≥2 mg/L, 6091 participants (2525 women, 3566 men) had baseline estimated 10-year Framingham risks of 5% to 10% and 7340 participants (1404 women, 5936 men) had baseline estimated Framingham risk of 11% to 20%. In these 2 "intermediate risk" subgroups, relative risk reductions consistent with the overall trial treatment effect were observed (hazard ratio, 0.55; 95% confidence interval, 0.36 to 0.84; 5-year number needed to treat=40, P=0.005 for those with 5% to 10% risk; hazard ratio, 0.51; 95% confidence interval, 0.39 to 0.68, 5-year number needed to treat=18, P<0.0001 for those with 11% to 20% risk). Use of the Reynolds Risk Score to stratify the study population gave similar results but reclassified large numbers of individuals into lower- or higher-risk groups. The majority of women with elevated hsCRP who benefited from rosuvastatin were at 5% to 10% 10-year risk at study entry using either global risk scoring system. Consistent with recent evidence-based Canadian Cardiovascular Society guidelines for primary prevention, the JUPITER trial demonstrates that rosuvastatin 20 mg significantly reduces major cardiovascular events among men and women with elevated hsCRP and "intermediate risk" defined either as 5% to 10% or 10% to 20% 10-year risk.

The Case for C-Reactive Protein as a Risk Marker for Coronary Heart Disease

Letters16 March 2010The Case for C-Reactive Protein as a Risk Marker for Coronary Heart DiseaseNancy R. Cook, ScDNancy R. Cook, ScDFrom Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-152-6-201003160-00020 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Buckley and colleagues (1) state that the utility of measuring C-reactive protein (CRP) is uncertain and conclude that routine screening by CRP levels cannot be recommended. The reasoning behind this conclusion, however, seems flawed. First, since the literature review in 2007, additional articles have been published, particularly ones featuring risk reclassification (including the Reynolds Risk Score for men [2] and the analysis of high-sensitivity CRP in the Framingham cohort [3]). The latter work should replace the cited negative study from Framingham, which did not use the high-sensitivity assay.Second, the authors cite a lack of evidence that ...

Coronary Atherosclerosis in Rheumatoid Arthritis: Could Endothelial Progenitor Cells Be the Missing Link?

Patients with rheumatoid arthritis (RA) have a reduced life expectancy of 5–10 years1, largely driven by its association with an increased risk of cardiovascular disease (CVD), which accounts for about half of all deaths in patients with RA2. The reasons for such a disproportionately high risk compared to the general population are not yet fully understood, but conventional risk factors alone do not appear to fully account for the difference3. It follows that conventional CV risk stratification tools, such as the Framingham risk score, used so widely in primary prevention in the general population, may not be as well suited for use in patients with RA. Arguably the most appropriate algorithm of CV risk assessment for this cohort of patients may be the Reynolds risk score, which includes the measurement of high sensitivity C-reactive protein (CRP), reflecting the underlying inflammatory nature to atherosclerosis4. Another tool to improve coronary risk stratification is coronary artery calcium (CAC) scoring by computed tomography, which has gained popularity in recent years. High CAC scores have been associated with an increase in all-cause mortality5, and patients with RA have a higher prevalence and a greater burden of coronary calcification than non-RA controls. Therefore, its application for measuring subclinical atherosclerosis in this patient cohort could be utilized. However, pathophysiological links between arterial calcium deposition and atherosclerotic plaque formation are not completely clear, and clinical utility of CAC as well as the Reynolds risk score as a risk stratification tool has not been well validated in RA patients; therefore, the challenge of trying to predict patients who are most at risk continues6. The process of atherogenesis has been fundamentally linked to endothelial injury unbalanced by appropriate endothelial recovery, which appears to be at least partly attributable … Address correspondence to Dr. Shantsila; E-mail: shantsila{at}yandex.ru