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We sought to assess the impact of smoking status, cumulative pack-years, and time since cessation (the latter in former smokers only) on 3 important domains of cardiovascular disease: inflammation, vascular dynamics and function, and subclinical atherosclerosis. These findings expand our understanding of the harmful effects of smoking and help explain the cardiovascular benefits of smoking cessation.
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The newly released 2013 ACC/AHA Guideline for Assessing Cardiovascular Risk was a major advance over prior guidelines, but the new risk equations do not appear to lead to significantly better discrimination than older models. Since the same risk factors are incorporated, using the new risk estimators may lead to inaccurate assessment of atherosclerotic cardiovascular risk in certain groups of patients. There also is likely an overestimation of risk when applied to modern populations. Future guidelines could provide clearer direction on which individuals would benefit from additional testing for more personalized preventive therapies.
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There was a strong association between the baseline burden and regional distribution of CAC and the risk and type of future coronary revascularization among asymptomatic subjects.
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This analysis looks at the strengths and limitations of two large trials of statin therapy based on persons with an elevated hsCRP, CAC score, or both.
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This editorial examines the shortcomings of traditional cardiovascular risk assessment scores.
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CAC scoring can help match statin therapy to absolute atherosclerotic CVD risk.
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The presence of a high CAC burden, even among individuals without risk factors, is associated with an elevated event rate, whereas the absence of CAC, even among those with many risk factors, is associated with a low event rate. CAC scoring can further risk-stratify asymptomatic individuals at the extremes of risk factor burden.
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Although high-sensitivity C-reactive protein (hsCRP) is involved in the immunologic process that triggers vascular remodeling and plaque deposition and is associated with increased cardiovascular disease (CVD) risk, definitive randomized evidence for its role as a causative factor in atherothrombosis is lacking. This article reviews four distinct points from the literature to better understand the current state and application of hsCRP in clinical practice, and we highlight recommendations from societies and important considerations when using hsCRP to guide treatment decisions in the primary prevention setting.
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Unhealthy lifestyle habits are a major contributor to coronary artery disease (CAD). The purpose of the study was to investigate the associations of smoking, weight maintenance, physical activity, and Mediterranean-style diet with coronary calcium, cardiovascular events, and mortality. We discovered that, over the course of nearly 8 years, a combination of regular exercise, healthy diet, smoking avoidance, and weight maintenance contributed to lower coronary calcium incidence, slower calcium progression, and lower all-cause mortality.
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The aim of this study was to further explore the interplay between smoking status, coronary artery calcium (CAC), and all-cause mortality. Smoking is a risk factor for death across the entire spectrum of subclinical coronary atherosclerosis. Smokers with any CAC had significantly higher mortality than smokers without CAC, a finding with implications for smokers undergoing lung cancer CT-based screening. However, the absence of CAC might not be as useful a "negative risk factor" in active smokers, because this group has mortality rates similar to nonsmokers with mild-to-moderate atherosclerosis.
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The value of coronary artery calcium for predicting mortality extends to both elderly patients and those <45 years old. Elderly persons with no CAC have a lower mortality rate than younger persons with high CAC.
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In this featured debate in JAMA, we reviewed the extensive data from randomized clinical trials and observational studies supporting the selective use of lipid lowering therapy in a middle-aged man with hyperlipidemia.
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We conclude that CAC can help risk stratify individuals with diabetes and may aid in selection of patients who may benefit from therapies such as low-dose aspirin for primary prevention of CVD.
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Much attention has been directed toward lifestyle modifications as effective means of reducing cardiovascular disease risk. We review recent observational and interventional trials investigating the effects of physical activity on markers of (or causal factors for) atherosclerotic burden and vascular disease. There is a strong correlation between physical activity and triglyceride reduction, apolipoprotein B reduction, HDL increase, change in LDL particle size, increase in tissue plasminogen activator activity, and decrease in CAC. Further research is needed to elucidate the effect on inflammatory markers and intima-media thickness.
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This innovative study found that the Reynolds Risk Score was modestly better than the traditional Framingham risk score in predicting the incidence of new coronary calcification and the progression of existing calcification. This observation also applied to clinical events.
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The goal of this study was to assess the independent and collective associations of hepatic steatosis, obesity, and the metabolic syndrome with elevated hsCRP levels. We evaluated 2,388 individuals without clinical cardiovascular disease between December 2004 and December 2006. Hepatic steatosis was diagnosed by ultrasound, and the metabolic syndrome was defined using National Heart, Lung, and Blood Institute criteria. We concluded that hepatic steatosis, obesity, and the metabolic syndrome are independently and additively associated with increased odds of high hsCRP levels.
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The landmark Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) trial showed that some patients with LDL-cholesterol (LDL-C) <130 mg/dL and high-sensitivity C-reactive protein (hsCRP) concentrations of >2 mg/L benefit from treatment with rosuvastatin, although the absolute rates of cardiovascular events were low. In a population eligible for JUPITER, we established whether coronary artery calcium (CAC) might further stratify risk; additionally we compared hsCRP with CAC for risk prediction across the range of low and high hsCRP values. CAC further stratifies risk in patients eligible for JUPITER, and could be used to target subgroups of patients who are expected to derive the most, and the least, absolute benefit from statin treatment. Focusing of treatment on the subset of individuals with normal LDL-C and at least moderate subclinical atherosclerosis should allow for more appropriate allocation of resources.
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Levels of hsCRP are closely associated with abdominal obesity, metabolic syndrome, and atherosclerotic cardiovascular disease. The JUPITER trial has encouraged using hsCRP greater than or equal to 2 mg/L to guide statin therapy; however, the association of hsCRP and atherosclerosis, independent of obesity, remains unknown. We concluded that high hsCRP, as defined by JUPITER, was not associated with CAC and was mildly associated with carotid intima-media thickness (cIMT) in the absence of obesity. In contrast, obesity was associated with both measures of subclinical atherosclerosis independently of hsCRP status.
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Baseline CAC accurately identifies coronary atherosclerosis and improves prediction of future cardiac events. However, whether knowledge of progression of CAC scores over time further improves risk prediction is unclear. We conducted a comprehensive review of published reports on CAC progression and found that CAC progression correlates with worsening atherosclerosis and may facilitate prediction of future cardiac events. These findings support the notion that slowing CAC progression with therapeutic interventions might provide prognostic benefit. However, despite promising early data, such interventions (most notably with statin therapy) have not been shown to slow the progression of CAC in any randomized controlled trial to date, outside of post hoc subgroup analyses. Thus, routine quantification of CAC progression cannot currently be recommended in clinical practice.
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It is important to note that the conclusion in the editorial that the Gottlieb et al. paper presents a “starkly contrasting picture” to a prior systematic review is based on a statistical error.Once again, Bayes’ theorem is critical. Although CAC = 0 may not definitively exclude important coronary artery disease (CAD) in patients referred for coronary angiography, there may be potential applications in lower-risk patients presenting with atypical chest pain features.
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In this observational study, we examined whether high baseline CACS were associated with the initiation as well continuation of new lipid-lowering medication (LLM), blood pressure-lowering medication (BPLM), and regular aspirin (ASA) use in a multi-ethnic population-based cohort. Findings indicate that CACS >400 was associated with a higher likelihood of initiation and continuation of LLM, BPLM, and ASA. The association was weaker for continuation than for initiation of these preventive therapies.
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