Prevalence of conventional risk factors in patients with coronary heart disease

Khot, Umesh N.; Khot, Monica B.; Bajzer, Chris

doi:10.1016/j.accreview.2003.09.010

Cited by 348 publications

(436 citation statements)

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“…Consistent with this observation, several studies have demonstrated the efficacy of statin in lowering CRP, and further, that this is independent of cholesterol-lowering effects. 15,39 These data, combined with the realization that 20% of coronary events occur in patients with no major risk factors, 40 served as the impetus for using CRP to identify additional at-risk patients who might benefit from statin therapy. 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.…”

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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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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“…There is evidence that the disease might have its roots already in childhood [1]. Traditional risk factors such as smoking, diabetes, hypercholesterolemia and hypertension are not sufficient to explain the high incidence of CHD in the western world [2,3].…”

Section: Introductionmentioning

confidence: 99%

Dual role of infections as risk factors for coronary heart disease

et al. 2007

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“…As previously reported, established risk factors do associate with the risk of CAD in FH patients. 8,22 However, none of the tested CAD-associated SNPs significantly modified the risk of CAD in our FH cohort in analyses unadjusted or adjusted for established cardiovascular risk factors. The lowest observed P-value of association was for a SNP in the SMARCA44 gene, near the LDLR gene (in adjusted analysis; P ¼ 0.021 ); however, it showed a paradoxically protective effect.…”

Section: Discussionmentioning

confidence: 81%

Common genetic variants do not associate with CAD in familial hypercholesterolemia

et al. 2013

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In recent years, multiple loci dispersed on the genome have been shown to be associated with coronary artery disease (CAD). We investigated whether these common genetic variants also hold value for CAD prediction in a large cohort of patients with familial hypercholesterolemia (FH). We genotyped a total of 41 single-nucleotide polymorphisms (SNPs) in 1701 FH patients, of whom 482 patients (28.3%) had at least one coronary event during an average follow up of 66 years. The association of each SNP with event-free survival time was calculated with a Cox proportional hazard model. In the cardiovascular disease risk factor adjusted analysis, the most significant SNP was rs1122608:G4T in the SMARCA4 gene near the LDL-receptor (LDLR) gene, with a hazard ratio for CAD risk of 0.74 (95% CI 0.49-0.99; P-value 0.021). However, none of the SNPs reached the Bonferroni threshold. Of all the known CAD loci analyzed, the SMARCA4 locus near the LDLR had the strongest negative association with CAD in this high-risk FH cohort. The effect is contrary to what was expected. None of the other loci showed association with CAD.

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Prevalence of conventional risk factors in patients with coronary heart disease

Cited by 348 publications

References 0 publications

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

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

Dual role of infections as risk factors for coronary heart disease

Common genetic variants do not associate with CAD in familial hypercholesterolemia

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