A Self-Fulfilling Prophecy

Verma, Subodh; Wang, Chao-Hung; Li, Shuhong; Dumont, Aaron S.; Fedak, Paul W.M.; Badiwala, Mitesh; Dhillon, Bikramjit; Weisel, Richard D.; Li, Ren‐Ke; Mickle, Donald A.G.; Stewart, Duncan J.

doi:10.1161/01.cir.0000029802.88087.5e

Cited by 903 publications

(351 citation statements)

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“…Several other inflammatory markers for prediction of coronary accidents in healthy men and women and in patients with stable angina, acute coronary diseases and in follow up of cardiovascular accident have been studied. These markers include Values are mean ± SD; P [ 0.05 not significant; P \ 0.0001 highly significant interleukin (IL-6) [20,21], serum amyloid A (SAA) [22], Tumour necrosis factor-a (TNF-a) [23], CD40 ligand [24]. Among these markers CRP has emerged as most powerful inflammatory marker of future cardiovascular risk [25][26][27].…”

Section: Discussionmentioning

confidence: 99%

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

Datta¹,

Iqbal²,

Prasad³

2011

Ind J Clin Biochem

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Acute myocardial Infarction is one of the major causes of morbidity & mortality in world and atherosclerosis is the major cause of ischemic heart disease. In order to determine the better clinical marker of atherosclerosis, we estimated serum low-density lipoprotein (LDL-C) and high sensitivity C-reactive protein (hsCRP). Hundred patients of myocardial infarction and 100 controls irrespective of age and sex were studied for these parameters over a period of 2 years. The statistical analysis showed that the serum hsCRP was significantly raised in myocardial infarction cases than controls (P \ 0.01) but LDL-C was not (P [ 0.05). We conclude that the serum hsCRP has better predictive value for risk of atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

Datta¹,

Iqbal²,

Prasad³

2011

Ind J Clin Biochem

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“…Yet, as most of the experiments were in tissue culture with cause-effect exhibited following the use of commercial CRP preparations concern has been raised for spurious effects of contaminants. When impurities, in particular the preservative sodium azide and the contaminant endotoxin, are removed from commercial CRP preparations the putative direct endothelial activity is questioned [23][24][25][26][27][28]. Transgenic animals that express human CRP, or mice that express rabbit CRP [20], can be used to resolve the issue of this suspected spurious artifactual results.…”

Section: Discussionmentioning

confidence: 99%

“…Our studies, both in the injured artery and the distant lung tissue, indicate that CRP exerts an opposite effect, with suppression of p38 MAPK. These contradictory findings may result from the in vitro methodology which exposes the study to the risk of contamination with preservatives and endotoxin [23][24][25][26][27][28]. Another explanation is a possible differential effect of CRP on blood mononuclear cells and arterial and alveolar cells.…”

Section: Discussionmentioning

confidence: 99%

Neointimal formation is reduced after arterial injury in human crp transgenic mice

et al. 2008

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Objectives/Methods-Elevated CRP levels predict increased incidence of cardiovascular events and poor outcomes following interventions. There is the suggestion that CRP is also a mediator of vascular injury. Transgenic mice carrying the human CRP gene (CRPtg) are predisposed to arterial thrombosis post-injury. We examined whether CRP similarly modulates the proliferative and hyperplastic phases of vascular repair in CRPtg when thrombosis is controlled with daily aspirin and heparin at the time of trans-femoral arterial wire-injury.Results-Complete thrombotic arterial occlusion at 28 days was comparable for wild-type and CRPtg mice (14 and 19%, respectively). Neointimal area at 28d was 2.5 fold lower in CRPtg (4190 ± 3134 μm 2 , n = 12) compared to wild-types (10,157 ± 8890 μm 2 , n = 11, p < 0.05). Likewise, neointimal/media area ratio was 1.10 ± 0.87 in wild-types and 0.45 ± 0.24 in CRPtg (p < 0.05). Seven days post-injury, cellular proliferation and apoptotic cell number in the intima were both less pronounced in CRPtg than wild-type. No differences were seen in leukocyte infiltration or endothelial coverage. CRPtg mice had significantly reduced p38 MAPK signaling pathway activation following injury.Conclusions-The pro-thrombotic phenotype of CRPtg mice was suppressed by aspirin/ heparin, revealing CRP's influence on neointimal growth after trans-femoral arterial wire-injury. Signaling pathway activation, cellular proliferation, and neointimal formation were all reduced in CRPtg following vascular injury. Increasingly we are aware of CRP multipotent effects. Once considered only a risk factor, and recently a harmful agent, CRP is a far more complex regulator of vascular biology.

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“…In cell culture, proinflammatory factors such as TNF-α, CRP, and ox-LDL downregulate expression of endothelial nitric oxide synthase (eNOS) and thus decrease nitric oxide production (Vallance et al 1997, Verma et al 2002. This effect appears to be mediated via a decrease in the stability of eNOS messenger RNA (Verma et al 2002). Whereas it is clear that cytokines such as TNF-α activate endothelial cells, recent studies have raised the possibility that the reported effects of the acute phase reactant CRP might be attributable to contaminants in commercially available preparations.…”

Section: Experimental Studies Of Endothelial Activation By Proinflammmentioning

confidence: 99%

“…An important consequence of endothelial activation is a decrease in the bioavailability of endothelium-derived nitric oxide. In cell culture, proinflammatory factors such as TNF-α, CRP, and ox-LDL downregulate expression of endothelial nitric oxide synthase (eNOS) and thus decrease nitric oxide production (Vallance et al 1997, Verma et al 2002. This effect appears to be mediated via a decrease in the stability of eNOS messenger RNA (Verma et al 2002).…”

mentioning

confidence: 99%

Effects of Systemic Inflammation on Endothelium-Dependent Vasodilation

Huang

Vita

2006

Trends in Cardiovascular Medicine

118

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The importance of inflammation in the pathogenesis of atherosclerosis is well established. The vascular endothelium contributes to and is affected by the inflammatory process. For example, a variety of cytokines have the ability to "activate" the endothelium and thereby promote expression of adhesion molecules and chemotactic factors that accelerate the inflammatory process and direct accumulation of leukocytes to specific sites in the arterial tree. In experimental systems, activation of endothelial cells is also associated with a loss of the biologic activity of endothelium-derived nitric oxide, an effect that accelerates the inflammatory process and also promotes local thrombosis and impairs local control of vasomotor tone. Consistent with these experimental studies, recent studies have provided evidence that inflammation is associated with an impairment of nitric oxide-dependent responses in human subjects. This article will review the experimental and clinical studies that support the relevance of inflammation to nitric oxide bioactivity in human atherosclerosis.It is now well recognized that atherosclerosis is an inflammatory disease (Ross 1999). Systemic risk factors induce a state of inflammation that contributes to all stages of atherosclerosis from the initiating events in lesion formation to the latest phase when plaques rupture, thrombose, and produce clinical syndromes such as myocardial infarction or stroke (Libby et al. 2002). The importance of inflammation in atherosclerosis is supported by recent studies showing that elevated levels of inflammatory markers identify individuals with increased risk for cardiovascular events (Pearson et al. 2003). In particular, the acute phase reactant C-reactive protein (CRP) shows promise as a clinically useful marker of cardiovascular risk (Ridker 2003).The vascular endothelium is both affected by and contributes to the inflammatory process that leads to atherosclerosis. For example, proinflammatory factors "activate" endothelial cells to promote an atherogenic phenotype. The activated endothelium, in turn, expresses adhesion molecules and chemotactic factors that accelerate and localize the inflammatory process. An important consequence of endothelial activation is loss of the biologic activity of endotheliumderived nitric oxide. Investigators have argued that a broad alteration of endothelial function, including loss of nitric oxide under proinflammatory conditions, might be a critical mechanism that links systemic states of inflammation to atherosclerosis (Vallance et al. 1997). This article will review the recent studies that support the relevance of systemic inflammation to nitric oxide bioactivity in human subjects. The Endothelium as a Regulator of Vascular HomeostasisThe endothelium regulates vasomotor tone, blood fluidity, growth of vascular smooth muscle cells, and local inflammation by elaborating a number of paracrine factors, including nitric oxide (Widlansky et al. 2003a). Endothelium-derived nitric oxide is a potent vasodilator and acts ...

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A Self-Fulfilling Prophecy

Cited by 903 publications

References 43 publications

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

Neointimal formation is reduced after arterial injury in human crp transgenic mice

Effects of Systemic Inflammation on Endothelium-Dependent Vasodilation

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