Endothelial activation, inflammation and premature atherosclerosis in children with familial dyslipidemia

Guardamagna, Ornella; Abello, Francesca; Saracco, Paola; Baracco, V.; Rolfo, E.; Pirro, Matteo

doi:10.1016/j.atherosclerosis.2009.06.006

Cited by 61 publications

(43 citation statements)

References 39 publications

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“…In favor of such an interpretation, studies of patients with heterozygous familial hypercholesterolemia, which is an inherited condition with very high levels of LDL cholesterol caused by a defect in the LDL receptor, found either no difference in CRP levels between patients and control subjects [18][19][20][21] or only slightly higher levels of CRP in patients compared with control subjects. [22][23][24] Even patients with homozygous familial hypercholesterolemia, who have extremely high levels of LDL cholesterol and therefore have a very high risk of early atherosclerosis, had only slightly increased levels of CRP compared with control subjects. 25 In addition, it has always been puzzling that LDL particles need to be oxidized before they can be taken up by macrophages, whereas triglyceride-rich lipoproteins or remnants can be taken up by macrophages without oxidation.…”

Section: Discussionmentioning

confidence: 99%

Elevated Remnant Cholesterol Causes Both Low-Grade Inflammation and Ischemic Heart Disease, Whereas Elevated Low-Density Lipoprotein Cholesterol Causes Ischemic Heart Disease Without Inflammation

et al. 2013

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Background-Elevated nonfasting remnant cholesterol and low-density lipoprotein (LDL) cholesterol are causally associated with ischemic heart disease (IHD), but whether elevated nonfasting remnant cholesterol and LDL cholesterol both cause low-grade inflammation is currently unknown. Methods and Results-We studied 60 608 individuals from the Copenhagen General Population Study, the Copenhagen City Heart Study, and the Copenhagen Ischemic Heart Disease study, of whom 10 668 had IHD diagnosed between 1977 and 2011. We genotyped for variants affecting levels of nonfasting remnant cholesterol, LDL cholesterol, C-reactive protein by CRP alleles, and C-reactive protein by IL6R alleles. Using a multidirectional mendelian randomization design, we investigated possible causal associations between the lipoproteins and C-reactive protein and between the lipoproteins and IHD. A 1-mmol/L(39 mg/dL) higher level of nonfasting remnant cholesterol was associated observationally with a 37% (95% confidence interval, 35-39) higher C-reactive protein level and causally with a 28% (95% confidence interval, 10-48) higher level. For LDL cholesterol, a 1-mmol/L (39-mg/dL) higher level was associated observationally with a 7% (95% confidence interval, 6-7) higher C-reactive protein level, but we found no causal association. Likewise, higher levels of C-reactive protein did not associate causally with elevated nonfasting remnant cholesterol or LDL cholesterol. Finally, the causal risk ratio for IHD for a 1-mmol/L (39-mg/dL) higher level was 3.3 (95% confidence interval, 2.1-5.2) for nonfasting remnant cholesterol and 1.8 (95% confidence interval, 1.5-2.2) for LDL cholesterol. The causal associations for remnant cholesterol were present even in those without diabetes mellitus and obesity. Conclusions-Elevated nonfasting remnant cholesterol is causally associated with low-grade inflammation and with IHD, whereas elevated LDL cholesterol is associated causally with IHD without inflammation. (Circulation. 2013;128:1298-1309.)

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Section: Discussionmentioning

confidence: 99%

Elevated Remnant Cholesterol Causes Both Low-Grade Inflammation and Ischemic Heart Disease, Whereas Elevated Low-Density Lipoprotein Cholesterol Causes Ischemic Heart Disease Without Inflammation

et al. 2013

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“…The distance between the leading edge of the first bright line on the far wall (lumen-intima interface) and the leading edge of the second bright line (media-adventitia interface) indicates the IMT of the far wall, as previously described. 19 Three measurements of the left and right common carotid were taken, and the mean for the higher measures of each side, representing the IMT, was used 11 for statistical analysis.…”

Section: Measurements Of Carotid Artery Imtmentioning

confidence: 99%

Improvement in HOMA-IR is an independent predictor of reduced carotid intima-media thickness in obese adolescents participating in an interdisciplinary weight-loss program

et al. 2010

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The aim of this study was to verify whether a 1-year interdisciplinary weight-loss program improved common carotid artery intima-media thickness (IMT) and whether insulin resistance and/or inflammation (as measured by the markers plasminogen activator inhibitor type-1 and adiponectin) might underlie obesity in adolescents. A group of 29 post-pubescent obese adolescents were submitted to an interdisciplinary intervention over the course of 1 year. Common carotid artery IMT was determined ultrasonographically. Body composition, blood pressure (BP), glycemia, insulinemia, homeostasis model assessment of insulin resistance (HOMA-IR), lipid profile and adipokine concentrations were analyzed before and after the intervention. The interdisciplinary weight-loss program promoted a significant improvement in body composition, insulin concentration, HOMA-IR, lipid profile, BP and inflammatory state, in addition to significantly decreasing the common carotid artery IMT. Furthermore, this study demonstrated that the difference between baseline and final values of HOMA-IR (DHOMA-IR) was negatively correlated with concomitant changes in the adiponectin concentration (Dadiponectin; r¼À0.42; P¼0.02) and positively correlated with changes in common carotid artery IMT (Dcarotid IMT; r¼0.41; P¼0.03). Multiple regression analysis adjusted by age, cardiovascular risk factors and inflammatory markers showed that DHOMA-IR was an independent predictor of significant changes in common carotid artery IMT. This investigation demonstrated that an interdisciplinary weight-loss program promoted a reduction of the common carotid artery IMT in obese Brazilian adolescents, and the improvement of HOMA-IR was an independent predictor of carotid IMT changes in this population.

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“…17,18 In obese children, increased plasma volume also increases cardiac output, which enhances the work of the left ventricle, causing an increase in left ventricular mass. 19,20 In our study, the mean hs-CRP of obese adolescents was 3.60 mg/dL. Pearson's correlation analysis showed that there was no significant correlation between hs-CRP and left ventricular mass (r=0.083;P=0.305).…”

Section: Discussionmentioning

confidence: 80%

“…21 In susceptible individuals, the release of adipokines, such as tumor necrosis factor α and interleukin-6 (IL-6) produced by macrophages and adipocytes, can directly stimulate production of CRP in the liver. 20 A cross-sectional study showed that CRP levels correlated with atherogenic dyslipidemia, obesity, hypertension, and insulin resistance. 21 The continuous production of CRP can aggravate chronic inflammation by means of endothelial cell activation.…”

Section: Discussionmentioning

confidence: 99%

High sensitivity C-reactive protein, left ventricular mass, and systolic function in obese adolescents

Kaunang

As’ad

Warouw

et al. 2016

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Endothelial activation, inflammation and premature atherosclerosis in children with familial dyslipidemia

Cited by 61 publications

References 39 publications

Elevated Remnant Cholesterol Causes Both Low-Grade Inflammation and Ischemic Heart Disease, Whereas Elevated Low-Density Lipoprotein Cholesterol Causes Ischemic Heart Disease Without Inflammation

Elevated Remnant Cholesterol Causes Both Low-Grade Inflammation and Ischemic Heart Disease, Whereas Elevated Low-Density Lipoprotein Cholesterol Causes Ischemic Heart Disease Without Inflammation

Improvement in HOMA-IR is an independent predictor of reduced carotid intima-media thickness in obese adolescents participating in an interdisciplinary weight-loss program

High sensitivity C-reactive protein, left ventricular mass, and systolic function in obese adolescents

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