Atherosclerosis

2014

DOI: 10.1016/j.atherosclerosis.2014.05.917

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Markers of atherosclerotic development in children with familial hypercholesterolemia: A literature review

Ingunn Narverud¹,

Kjetil Retterstøl²,

Per Ole Iversen³

et al.

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Lp(a) and Cardiometabolic And Vascular Disease: A Unique Ins1

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Cited by 94 publications

(72 citation statements)

References 94 publications

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“…Fatty streaks, which represent the earliest sign of atherosclerosis, have been observed in fetal aortas and in children as young as 3 years of age [3–5]. To determine the degree of atherosclerosis, several surrogate biomarkers have evolved to represent the major characteristics of atherogenesis, namely endothelial activation, inflammation, oxidative stress and prothrombogenesis.…”

Section: Introductionmentioning

confidence: 99%

“…Heterozygous forms of FH have inherited one mutation from one parent and are characterized by a 2-fold increase in both plasma total cholesterol (TC) and LDL-c concentrations [3, 10, 11]. It has been well established that patients with FH have higher risk of developing CAD compared to those with polygenic hypercholesterolaemia.…”

Section: Introductionmentioning

confidence: 99%

“…It has been well established that patients with FH have higher risk of developing CAD compared to those with polygenic hypercholesterolaemia. Approximately 5% of patients suffering myocardial infarction below the age of 60 years have heterozygous FH [3, 10], which resorted to current guidelines determining FH patients as high risk for developing CAD without undergoing risk stratification algorithms such as the Framingham Risk Score as they do not predict the 10-year CHD risk in these cohort.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Enhanced status of inflammation and endothelial activation in subjects with familial hypercholesterolaemia and their related unaffected family members: a case control study

¹

,

²

,

³

et al. 2017

Lipids Health Dis

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BackgroundFamilial hypercholesterolaemia (FH) leads to premature coronary artery diseases (CAD) which pathophysiologically can be measured by inflammation, endothelial activation and oxidative stress status. However, the status of these biomarkers among related unaffected relatives of FH cases and whether FH is an independent predictor of these biomarkers have not been well established. Thus, this study aims to (1) compare the biomarkers of inflammation, endothelial activation and oxidative stress between patients with FH, their related unaffected relatives (RUC) and normolipaemic subjects (NC) (2)determine whether FH is an independent predictor of these biomarkers.MethodsOne hundred thirty-one FH patients, 68 RUC and 214 matched NC were recruited. Fasting lipid profile, biomarkers of inflammation (hsCRP), endothelial activation (sICAM-1 and E-selectin) and oxidative stress [oxidized LDL (oxLDL), malondialdehyde (MDA) and F2-isoprostanes (ISP)] were analyzed and independent predictor was determined using binary logistic regression analysis.ResultshsCRP was higher in FH and RUC compared to NC (mean ± SD = 1.53 ± 1.24 mg/L and mean ± SD = 2.54 ± 2.30 vs 1.10 ± 0.89 mg/L, p < 0.05). sICAM-1 and E-selectin were higher in FH compared to NC (mean ± SD = 947 ± 742 vs 655 ± 191 ng/mL, p < 0.001 and 175 ± 131 vs 21.6 ± 10.7 ng/mL, p < 0.001 respectively) while sICAM-1 concentration was higher in RUC compared to NC (mean ± SD = 945 ± 379 vs 655 ± 191 ng/mL, p < 0.01). Biomarkers of oxidation (ox-LDL, MDA and ISP) were elevated in FH compared to NC [mean ± SD = (48.2 ± 26.8 vs 27.3 ± 13.2 mU/L, p < 0.001), (2.57 ± 1.3 vs 1.20 ± 0.30 nmol/mL, p < 0.001) and (645 ± 396 vs 398 ± 20.5 pg/L, p < 0.001) respectively], but no significant differences were observed between RUC and NC (p > 0.05). FH was an independent predictor for sICAM-1 (p = 0.007), ox-LDL (p < 0.001) and MDA (p < 0.001) while RUC independently predicted for sICAM-1 (p < 0.001).ConclusionThe screening for FH is vital as all biomarkers associated with atherogenesis are higher in these subjects and FH also independently predict biomarkers of endothelial activation and oxidative stress. Furthermore, despite not fulfilling the diagnostic criteria for FH, related unaffected family members that may not phenotypically express the mutation may still be at risk of developing CAD as reflected from the enhanced inflammatory and endothelial activation status observed in this group. This highlights the need to not only conduct family tracing in indexed FH cases, but also assess the coronary risk among family members that do not fulfil the FH diagnostic criteria.

“…Fatty streaks, which represent the earliest sign of atherosclerosis, have been observed in fetal aortas and in children as young as 3 years of age [3–5]. To determine the degree of atherosclerosis, several surrogate biomarkers have evolved to represent the major characteristics of atherogenesis, namely endothelial activation, inflammation, oxidative stress and prothrombogenesis.…”

Section: Introductionmentioning

confidence: 99%

“…Heterozygous forms of FH have inherited one mutation from one parent and are characterized by a 2-fold increase in both plasma total cholesterol (TC) and LDL-c concentrations [3, 10, 11]. It has been well established that patients with FH have higher risk of developing CAD compared to those with polygenic hypercholesterolaemia.…”

Section: Introductionmentioning

confidence: 99%

“…It has been well established that patients with FH have higher risk of developing CAD compared to those with polygenic hypercholesterolaemia. Approximately 5% of patients suffering myocardial infarction below the age of 60 years have heterozygous FH [3, 10], which resorted to current guidelines determining FH patients as high risk for developing CAD without undergoing risk stratification algorithms such as the Framingham Risk Score as they do not predict the 10-year CHD risk in these cohort.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Enhanced status of inflammation and endothelial activation in subjects with familial hypercholesterolaemia and their related unaffected family members: a case control study

¹

,

²

,

³

et al. 2017

Lipids Health Dis

View full text Add to dashboard Cite

BackgroundFamilial hypercholesterolaemia (FH) leads to premature coronary artery diseases (CAD) which pathophysiologically can be measured by inflammation, endothelial activation and oxidative stress status. However, the status of these biomarkers among related unaffected relatives of FH cases and whether FH is an independent predictor of these biomarkers have not been well established. Thus, this study aims to (1) compare the biomarkers of inflammation, endothelial activation and oxidative stress between patients with FH, their related unaffected relatives (RUC) and normolipaemic subjects (NC) (2)determine whether FH is an independent predictor of these biomarkers.MethodsOne hundred thirty-one FH patients, 68 RUC and 214 matched NC were recruited. Fasting lipid profile, biomarkers of inflammation (hsCRP), endothelial activation (sICAM-1 and E-selectin) and oxidative stress [oxidized LDL (oxLDL), malondialdehyde (MDA) and F2-isoprostanes (ISP)] were analyzed and independent predictor was determined using binary logistic regression analysis.ResultshsCRP was higher in FH and RUC compared to NC (mean ± SD = 1.53 ± 1.24 mg/L and mean ± SD = 2.54 ± 2.30 vs 1.10 ± 0.89 mg/L, p < 0.05). sICAM-1 and E-selectin were higher in FH compared to NC (mean ± SD = 947 ± 742 vs 655 ± 191 ng/mL, p < 0.001 and 175 ± 131 vs 21.6 ± 10.7 ng/mL, p < 0.001 respectively) while sICAM-1 concentration was higher in RUC compared to NC (mean ± SD = 945 ± 379 vs 655 ± 191 ng/mL, p < 0.01). Biomarkers of oxidation (ox-LDL, MDA and ISP) were elevated in FH compared to NC [mean ± SD = (48.2 ± 26.8 vs 27.3 ± 13.2 mU/L, p < 0.001), (2.57 ± 1.3 vs 1.20 ± 0.30 nmol/mL, p < 0.001) and (645 ± 396 vs 398 ± 20.5 pg/L, p < 0.001) respectively], but no significant differences were observed between RUC and NC (p > 0.05). FH was an independent predictor for sICAM-1 (p = 0.007), ox-LDL (p < 0.001) and MDA (p < 0.001) while RUC independently predicted for sICAM-1 (p < 0.001).ConclusionThe screening for FH is vital as all biomarkers associated with atherogenesis are higher in these subjects and FH also independently predict biomarkers of endothelial activation and oxidative stress. Furthermore, despite not fulfilling the diagnostic criteria for FH, related unaffected family members that may not phenotypically express the mutation may still be at risk of developing CAD as reflected from the enhanced inflammatory and endothelial activation status observed in this group. This highlights the need to not only conduct family tracing in indexed FH cases, but also assess the coronary risk among family members that do not fulfil the FH diagnostic criteria.

“…Increased cIMT is seen in children and adolescents with known cardiovascular risk factors such as familial hypercholesterolemia or obesity …”

Section: Discussionmentioning

confidence: 99%

Extracardial Vasculopathy After Kawasaki Disease: A Long‐Term Follow‐up Study

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et al. 2016

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BackgroundKawasaki disease (KD) is a pediatric vasculitis with coronary artery aneurysm (CAA) as a major complication. Controversy exists about cardiovascular risk later in life. The aim of our study was to evaluate whether KD patients are at increased risk, as assessed by carotid intima‐media thickness (cIMT).Methods and ResultsWe measured cIMT over 15 years by B‐mode ultrasonography in KD patients during follow‐up and in unaffected controls (mostly siblings). A multilevel, repeated‐measures, linear mixed‐effects model was used to evaluate the association between KD and cIMT. A total of 319 patients with 528 measurements were compared with 150 controls. In KD patients, the mean cIMT was increased compared with controls (0.375 mm [95% CI 0.372–0.378 mm] versus 0.363 mm [95% CI 0.358–0.368 mm]; P<0.001). Furthermore, mean cIMT of CAA‐negative patients was 0.373 mm (P<0.01 compared with controls), of patients with small–medium CAA was 0.374 mm (P<0.05 compared with controls), and of patients with giant CAA was 0.381 mm (P<0.01 compared with controls). Compared with controls, CAA‐negative participants started with an increased cIMT (+0.0193±0.0053 mm, P<0.001) but showed slower progression (−0.0014±0.0006 mm/year, P=0.012). Patients with giant CAA showed a trend toward increased cIMT progression (0.0013±0.0007 mm/year, P=0.058).ConclusionsWe observed a positive correlation between cIMT and KD severity of coronary arteritis at the acute stage. Although initially increased, the cIMT in CAA‐negative patients normalized at a later age. In contrast, patients with a history of KD complicated by giant CAA showed a trend toward persistently increased cIMT. These patients may need cardiovascular counseling and follow‐up beyond the heart.

“…Finally, a systematic review comprising 6 observational studies, described the relationship between Lp(a) and familiar hypercholesterolemia (FH) in children 9 between Lp(a) and FH in children was noticed 44 . The levels of Lp(a) were found to be higher in FH children, but this association remains controversial 45,46 .…”

Section: Lp(a) and Cardiometabolic And Vascular Disease: A Unique Insmentioning

confidence: 99%

Evidence-based assessment of lipoprotein(a) as a risk biomarker for cardiovascular diseases – Some answers and still many questions

¹

,

²

,

³

et al. 2016

Critical Reviews in Clinical Laboratory Sciences

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The present article is aimed to outline the current state of knowledge regarding the effects of lipoprotein(a) (Lp(a)) on cardiovascular disease (CVD) risk by summarizing the recent results of studies, meta-analyses and systematic reviews. The literature supports the predictive value of Lp(a) on CVD outcomes, although the effect size is modest. Lp(a) would also appear to have an effect on cerebrovascular outcomes, with the effect appearing even smaller than that for CVD outcomes. Consideration of apolipoprotein apolipoprotein(a) (apo (a)) isoforms and LPA genetics in relation to the simple assessment of Lp(a) concentration may enhance improving clinical practice in vascular medicine. We also describe recent advances in Lp(a) research (including therapies) and highlight areas where further research is needed such as the measurement of Lp(a) and its involvement in additional pathophysiological processes.

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