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Journal articles on the topic 'Hypercholesterolaemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 April 2022

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1

Wang, Zheng, Ya Yang, Zhi'an LI, Xiaoshan Zhang, Jie Lin, and Lvya Wang. "Analysis of coronary flow haemodynamics in homozygous familial hypercholesterolaemic adolescents with aortic supravalvular stenosis." Cardiology in the Young 23, no. 2 (May 30, 2012): 219–24. http://dx.doi.org/10.1017/s1047951112000704.

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AbstractObjectiveTo study coronary artery haemodynamics in adolescents with homozygous familial hypercholesterolaemia and aortic supravalvular stenosis.MethodsPatients diagnosed with familial hypercholesterolaemia who were younger than 16 years and who had undergone transthoracic echocardiography from 2007 to 2010 were included in this study. We included patients with homozygous familial hypercholesterolaemia and aortic supravalvular stenosis and those with heterozygous familial hypercholesterolaemia. All patients underwent stress echocardiography, and left anterior descending coronary artery flow was successfully detected. Coronary flow velocity reserve was calculated as the ratio of hyperaemic mean diastolic flow velocity after injection of adenosine to basal mean diastolic flow velocity. Changes in coronary haemodynamics and the relationship between lipid concentrations were determined.ResultsA total of 11 patients with homozygous familial hypercholesterolaemia were enrolled in this study. Lipid concentrations were measured, and the mean coronary flow velocity reserve was 1.97 plus or minus 0.51. Seven children were included in the group of patients with heterozygous familial hypercholesterolaemia. In these children, the mean coronary flow velocity reserve was 3.08 plus or minus 0.84.ConclusionThe coronary flow velocity reserve of homozygous familial hypercholesterolaemic patients is lower than that of heterozygous familial hypercholesterolaemic patients, and it is associated with a high concentration of low-density lipoprotein cholesterol. Aortic stenosis and plaques compromised the ostia of the coronary artery and caused increased basal mean diastolic coronary velocity with blunted increase in peak velocity, which decreased the coronary flow velocity reserve.

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2

Smith, C. C. T., B. N. C. Prichard, and D. J. Betteridge. "Plasma and platelet free catecholamine concentrations in patients with familial hypercholesterolaemia." Clinical Science 82, no. 1 (January 1, 1992): 113–16. http://dx.doi.org/10.1042/cs0820113.

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1. Plasma and platelet free catecholamine concentrations were measured in 22 normal subjects and in 10 treated and 11 untreated patients with heterozygous familial hypercholesterolaemia. 2. Plasma noradrenaline concentrations were significantly higher in both treated and untreated hypercholesterolaemic patients than in normal subjects. Adrenaline concentrations did not differ. 3. Platelet noradrenaline levels were higher in untreated hypercholesterolaemic patients than in normal subjects. 4. Positive correlations between the plasma noradrenaline concentration and the platelet noradrenaline concentration were observed in both normal subjects and hypercholesterolaemic patients. 5. Combining the data for normal subjects and hypercholesterolaemic patients revealed that the plasma noradrenaline concentration correlated positively with the plasma cholesterol concentration. The platelet noradrenaline concentration was also found to correlate with the plasma cholesterol concentration. 6. Our results suggest that an increased plasma cholesterol concentration may be associated with increased sympathetic nervous system activity as indicated by elevated plasma and platelet noradrenaline levels. Increases in circulating catecholamines may contribute to the platelet hyperaggregability seen in familial hypercholesterolaemia.

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3

Chan, Y., A. Mcgill, R. Kanwar, G. Krissansen, N. Haggarty, L. Xin, and S. Poppitt. "Bovine Peptic Casein Hydrolysate Ameliorates Cardiovascular Risk Factors in a Model of ApoE-deficient Mice but not Overweight, Mildly Hypercholesterolaemic Men." Current Research in Nutrition and Food Science Journal 2, no. 1 (April 28, 2014): 08–19. http://dx.doi.org/10.12944/crnfsj.2.1.02.

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Associations have been shown between consumption of bovine dairy and decreased prevalence of metabolic related disorders. Milk peptides may promote both angiotensin-I- converting enzyme (ACE) inhibition for blood pressure (BP) lowering and insulin action for better glycaemic control. Less is known of other metabolic parameters. The aim of this study was to investigate effects of dairy peptic casein hydrolysate (CH) on markers of cardiovascular disease (CVD) risk in (1) an apolipoproteinE (ApoE) - deficient mouse model of high-fat fed hypercholesterolaem- ia, and, (2) a clinical study of moderate overweight and hypercholesterolaemia. In Trial 1, ApoE-deficient mice were supplemented with high dose CH (~1g/kg body weight) in a randomised, 9-wk, parallel design intervention, and blood and tissue samples harvested. In Trial 2, 24 mildly hypercholesterolaemic men were supplemented with lower dose CH (~0.1g/kg body weight, 10g/day, 3-wks) and matched whey protein control (WP, 10g/day, 3-wks) in a randomised, 9-wk, cross-over design intervention. Diets were separated by a 3-wk washout. Fasting blood and urine samples were collected, and blood pressure (BP) measured weekly. Clinical trial registration number, ACTRN 12611001013954. In ApoE-deficient mice, administration of CH significantly inhibited circulating total cholesterol concentrations by 37% (TC, P<0.01) and decreased aorta atherosclerotic lesion score by 25% (P<0.01). In the clinical study there were no significant differential effects of CH supplementation on CV markers, including serum lipids (TC, LDL-C, HDL-C, triglyceride), glucose and BP. Whilst high dose bovine peptic CH attenuated CVD risk in a murine ApoE deficient model of aggressive hypercholesterolaemia, no evidence of amelioration of risk by supplementation with a lower dose of CH in an overweight population of mildly hypercholesterolaemic men was found.

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4

Taylor, A. J. "Erythrocyte Membrane Fatty Acid Composition in Hypercholesterolemia." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 31, no. 4 (July 1994): 351–54. http://dx.doi.org/10.1177/000456329403100408.

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The fatty acid composition of the erythrocyte membrane was determined in 22 hypercholesterolaemic patients managed by dietary restriction, and compared with that of 22 normocholesterolaemic controls, roughly matched for age and sex with the patient group. The patients exhibited higher relative proportions of palmitic ( P<0·01) and stearic ( P<0·005) acids and lower relative proportions of linoleic acid ( P<0·05) in the erythrocyte membrane, compared with controls, which could be due to presumed dietary differences between the groups. In the patients, the degree of hypercholesterolaemia was poorly correlated with erythrocyte linoleic acid. Measurement of erythrocyte linoleic acid might prove useful in the routine management of hypercholesterolaemia.

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5

Wenham, Philip R., Peter Bloomfield, Gillian Blundell, Michael D. Penney, Peter W. H. Rae, and Simon W. Walker. "Familial Defective Apolipoprotein B-100: A Study of Patients from Lipid Clinics in Scotland and Wales." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 33, no. 5 (September 1996): 443–50. http://dx.doi.org/10.1177/000456329603300508.

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Familial defective apolipoprotein (apo) B-100 (FDB) is an autosomal codominant disorder, which may be associated with hypercholesterolaemia. The defect is caused by the substitution of glutamine for arginine at amino acid residue 3500 of apo B-100. A total of 357 hypercholesterolaemic patients, 48 with a clinical diagnosis of familial hypercholesterolaemia attending lipid clinics in Scotland and Wales, were screened for the presence of FDB. Seven unrelated individuals, five of whom had a family history of coronary heart disease, and a further 11 first-degree relatives, were shown to be heterozygous for the mutation. Pedigree analysis demonstrated the mutation to be present on a single haplotype, suggesting that in Britain it is inherited from a common ancestor. Treatment of 11 heterozygous individuals with lipid-lowering medication showed falls in total and low density lipoprotein cholesterol ranging from 11·6 to 38·8% and 5·3 to 49·5%, respectively. In view of the condition's association with coronary heart disease and hypercholesterolaemia, it may be worthwhile identifying carriers attending lipid clinics, so that affected siblings can be offered cholesterol-lowering treatment where necessary.

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6

Martino, Francesco, Fabrizio Carlomosti, Daniele Avitabile, Luca Persico, Mario Picozza, Francesco Barillà, Marcello Arca, et al. "Circulating miR-33a and miR-33b are up-regulated in familial hypercholesterolaemia in paediatric age." Clinical Science 129, no. 11 (September 10, 2015): 963–72. http://dx.doi.org/10.1042/cs20150235.

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Circulating miR-33a and miR-33b are up-regulated in familial hypercholesterolaemic children. miR-33a and miR-33b positively correlate with total cholesterol, LDL-cholesterol, LDL-cholesterol/HDL-cholesterol ratio, apolipoprotein B, C-reactive protein and glycaemia. miR-33 could be a novel prognostic marker and therapeutic target for cardiovascular diseases associated with paediatric hypercholesterolaemia.

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7

Pengnet, Sirinat, Sakdina Prommaouan, Phinsuda Sumarithum, and Wachirawadee Malakul. "Naringin Reverses High-Cholesterol Diet-Induced Vascular Dysfunction and Oxidative Stress in Rats via Regulating LOX-1 and NADPH Oxidase Subunit Expression." BioMed Research International 2019 (October 24, 2019): 1–11. http://dx.doi.org/10.1155/2019/3708497.

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Hypercholesterolaemia is associated with oxidative stress and endothelial dysfunction and leads to the development of atherosclerosis. Naringin exhibits cardiovascular protective and antioxidant properties. Therefore, the aim of this study was to assess the effect of naringin administration on vascular oxidative stress and endothelial dysfunction in hypercholesterolaemic rats and to elucidate its underlying mechanism. Sprague Dawley rats were fed a diet with 1.5% cholesterol (HCD) for 8 weeks to induce hypercholesterolaemia. Naringin (100 mg/kg body weight) was orally administrated to rats during the last 4 weeks of the diet treatment. After 8 weeks, the thoracic aorta was isolated to determine vascular function and nitric oxide (NO) levels. The aortic superoxide anion (O2−) level was detected using dihydroethidium (DHE) fluorescence staining. Protein expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits, and inducible nitric oxide synthase (iNOS), as well as oxidative damage markers, was also evaluated in aortae. Naringin treatment of hypercholesterolaemic rats enhanced aortic NO levels, restored endothelium-dependent responses to acetylcholine (ACh), and reduced aortic O2− levels. Furthermore, naringin treatment decreased LOX-1, NADPH oxidase subunits (p47phox, Nox2, and Nox4), and iNOS as well as oxidative damage markers (3-nitrotyrosine (3-NT) and 4-hydroxynonenal (4-HNE)) expression in aortic tissues from hypercholesterolaemic rats. These results demonstrate that naringin treatment improves endothelium dysfunction in hypercholesterolaemic rats, at least partially by decreasing oxidative stress via downregulation of LOX-1 and NADPH oxidase.

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8

Stefanutti, Claudia, and Maria Grazia Zenti. "Lipoprotein Apheresis and PCSK9-Inhibitors. Impact on Atherogenic Lipoproteins and Anti-Inflammatory Mediators in Familial Hypercholesterolaemia." Current Pharmaceutical Design 24, no. 31 (January 2, 2019): 3634–37. http://dx.doi.org/10.2174/1381612824666181025115658.

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Background: A combination therapy with PCSK9-inhibitors (PCSK9-I) and lipoprotein-apheresis (LA) may have synergistic effects on circulating lipid and lipoprotein levels, in particular in Homozygous Familial Hypercholesterolaemic (HoFH) subjects. The relationships between the above mentioned novel therapeutic approaches as highly effective treatment option for Dyslipidemia in Heterozygous Familial Hypercholesterolaemic (HeFH) patients deserve further investigation in larger datasets. Objective: This review aims to present the role of lipoprotein apheresis in the management of familial hypercholesterolaemia and discuss the potential advantages and disadvantages of its combination with PCSK9 inhibitors. Methods: A comprehensive literature search regarding lipoprotein apheresis in patients with familial hypercholesterolaemia and its combination with PCSK9 inhibitors has been performed. Results: LA is also a potent therapeutic player having impact on inflammation and related mediators. A large body of evidence on this is available. On the contrary, only few observations are available on PCSK9-I effects on inflammation. Conclusions: It is quite clear that further investigation on possible direct and/or indirect pleiotropic effects of PCSK9-I on inflammatory molecules is necessary and to be expected. Evidence on both arguments with regard to HoFH and HeFH, are reported in short.

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9

Choudhary, Ferrah, Huda Al-Hadithy, and Chantal Simon. "Hypercholesterolaemia." InnovAiT: Education and inspiration for general practice 2, no. 12 (November 17, 2009): 721–31. http://dx.doi.org/10.1093/innovait/inp180.

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10

Thelle, Dag S. "Hypercholesterolaemia." Drug Investigation 2, S2 (January 1990): 1–8. http://dx.doi.org/10.1007/bf03258188.

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11

Mariano, Cibelle, Ana Catarina Alves, Ana Margarida Medeiros, Joana Rita Chora, Marília Antunes, Marta Futema, Steve E. Humphries, and Mafalda Bourbon. "The familial hypercholesterolaemia phenotype: Monogenic familial hypercholesterolaemia, polygenic hypercholesterolaemia and other causes." Clinical Genetics 97, no. 3 (February 16, 2020): 457–66. http://dx.doi.org/10.1111/cge.13697.

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12

Wald, David S., and Nicholas J. Wald. "Integration of child–parent screening and cascade testing for familial hypercholesterolaemia." Journal of Medical Screening 26, no. 2 (October 14, 2018): 71–75. http://dx.doi.org/10.1177/0969141318796856.

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Objective To integrate child–parent screening and cascade testing into a single pathway-child-parent cascade screening (CPCS), for the identification of familial hypercholesterolaemia in the population and to estimate the number of new familial hypercholesterolaemia cases identified per child screened and the associated costs. Methods We applied the results from the published MRC Child–Parent Screening Study to 10,000 children, together with cascade testing first degree relatives of parents with a familial hypercholesterolaemia mutation identified by child–parent screening. We estimated the number of familial hypercholesterolaemia cases identified per child screened, the median cost per familial hypercholesterolaemia case identified and the median cost per child screened to identify one case using a range of cholesterol and familial hypercholesterolaemia mutation testing costs. We present a case study to illustrate the application of CPCS in practice. Results CPCS identifies one new familial hypercholesterolaemia case per 70 children screened at a median estimated cost of £960 per new familial hypercholesterolaemia case or £4 per child screened. CPCS identifies an average of four new familial hypercholesterolaemia cases per family. In the case study, six new familial hypercholesterolaemia cases were identified, and preventive treatment started in five, with the index child expected to start when older. Conclusion CPCS for familial hypercholesterolaemia are complementary strategies. The sustainability of cascade testing relies on identifying new unrelated index cases. This is achieved with population-wide child–parent screening. Integrated CPCS is currently better than either method of familial hypercholesterolaemia detection alone. It has the potential to identify all, or nearly all, individuals with familial hypercholesterolaemia in the population at low cost.

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13

Bergelson, Bruce A., Tse-Kuan Yu, and Nicholas A. Ruocco. "Effects of Hypercholesterolaemia on Physiological Recruitment of Coronary Vascular Reserve in Swine." Clinical Science 90, no. 4 (April 1, 1996): 261–68. http://dx.doi.org/10.1042/cs0900261.

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1. The endothelium participates in the regulation of coronary vascular tone. As evidence exists from studies performed on epicardial vessels that hypercholesterolaemia impairs endothelial function, we tested the hypothesis that hypercholesterolaemia impairs coronary vascular reserve in an intact animal. 2. Domestic swine, maintained on a regular (n = 9) or a 2% high-cholesterol (n = 9) diet for 3 months were instrumented with a catheter in the left atrium for microsphere injection, a catheter in the anterior interventricular vein for venous sampling and an 82% stenosis in the left anterior descending artery. Papaverine was used to determine coronary vascular reserve. Regional coronary flow as reflected by perfusion (microsphere measurement), lactate consumption, oxygen consumption and haemodynamics were obtained at baseline, after 10 mg of papaverine and after atrial pacing at a rate of 120 beats/min and 150 beats/min. 3. Cholesterol was elevated in animals on the high cholesterol diet (350 ± 50 mg/dl versus 99 ± 10 mg/dl, P<0.001). Baseline haemodynamics were similar between groups. Baseline transmural flow and its augmentation with papaverine were comparable in the two groups in the control (circumflex) and stenosed (left anterior descending artery) zones. In both groups, perfusion increased in the control zone in response to increased oxygen demand, whereas in the stenosis zone no increase was observed in either group (P not significant for normal versus high cholesterol diet). Endocardial flow reserve in the stenosis zone was exhausted in both groups. Epicardial flow in the stenosis zone increased significantly in the normal (P<0.02) but not in the hypercholesterolaemic animals (P not significant). 4. The endocardial/epicardial ratio in the control zone at baseline revealed greater endocardial dominance in the normal compared with the hypercholesterolaemic animals (1.35 versus 1.10, P<0.01). With papaverine, similar ratios indicated a similar reserve potential in both groups. During increased oxygen demand, normal animals continued to demonstrate endocardial dominance whereas it diminished in the hypercholesterolaemic group. In the stenosis zone, endocardial blood flow dominated at baseline in the normal animals and to a lesser extent in the hypercholesterolaemic animals (1.30 versus 1.10, P = 0.10). During increased oxygen demand, endocardial dominance decreased significantly in both groups of animals; however, it remained greater than 1.0 only in the normal animals. 5. Exposure to elevated cholesterol levels did not impair an animal's ability to augment coronary blood flow in response to an increase in oxygen demand. In contrast to this lack of effect on recruitment of coronary reserve, regional coronary blood flow was altered in the hypercholesterolaemic animals.

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14

Kempaiah, Rayavara K., and Krishnapura Srinivasan. "Influence of dietary spices on the fluidity of erythrocytes in hypercholesterolaemic rats." British Journal of Nutrition 93, no. 1 (January 2005): 81–91. http://dx.doi.org/10.1079/bjn20041317.

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In rats rendered hypercholesterolaemic by maintaining them on a cholesterol-enriched diet (0·5 %) for 8 weeks, as a result of alteration in membrane structural lipids, erythrocytes were observed to be deformed and become more fragile. This deformity and fragility was partially reversed by the two dietary spice principles, curcumin and capsaicin, and the spice, garlic, by virtue of their ability to lower the extent of hypercholesterolaemia. A further insight into the factors that might have reduced the fluidity of erythrocytes in hypercholesterolaemic rats revealed changes in fatty acid profile of the membranes, phospholipid composition of the membrane bilayer, reduced Ca2+, Mg2+-ATPase, and reduction in the sensitivity of erythrocytes to concanavaline A. Dietary capsaicin appeared to counter these changes partially in hypercholesterolaemic rats. Electron spin resonance (ESR) spectra and fluorescence anisotropy parameters also revealed altered fluidity of erythrocytes in hypercholesterolaemic rats. Dietary capsaicin and curcumin significantly reversed this alteration. Scanning electron microscopic examination revealed that the echinocyte population was increased in the erythrocytes of hypercholesterolaemic rats, and this was significantly countered by dietary capsaicin. The membrane protein profile and the active cation efflux appeared to be unaffected in the hypercholesterolaemic situation.

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15

Manning, Serena, and Pippa Oakeshott. "Familial hypercholesterolaemia." British Journal of General Practice 59, no. 569 (December 1, 2009): 944.2–945. http://dx.doi.org/10.3399/bjgp09x473213.

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16

Vohnout, Branislav, Katarina Rašlová, Juraj Gašvparovič, Maria Benedetta Donati, and Licia Lacoviello. "Familial hypercholesterolaemia." Lancet 357, no. 9269 (May 2001): 1712. http://dx.doi.org/10.1016/s0140-6736(00)04847-9.

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17

Umans-Eckenhausen, Marina AW, Joep C. Defesche, Eric GJ Sijbrands, and John JP Kastelein. "Familial hypercholesterolaemia." Lancet 357, no. 9269 (May 2001): 1712. http://dx.doi.org/10.1016/s0140-6736(00)04848-0.

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18

Phillips, T., and I. M. Leigh. "Familial hypercholesterolaemia." Journal of the Royal Society of Medicine 80, no. 10 (October 1987): 649–51. http://dx.doi.org/10.1177/014107688708001019.

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19

Wierzbicki, A. "Familial hypercholesterolaemia." Coronary Health Care 4, no. 4 (November 2000): 192–97. http://dx.doi.org/10.1054/chec.2000.0094.

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20

Gill, P. J., A. Harnden, and F. Karpe. "Familial hypercholesterolaemia." BMJ 344, may11 1 (May 11, 2012): e3228-e3228. http://dx.doi.org/10.1136/bmj.e3228.

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21

Nair, Devaki R., Mahtab Sharifi, and Khalid Al-Rasadi. "Familial hypercholesterolaemia." Current Opinion in Cardiology 29, no. 4 (July 2014): 381–88. http://dx.doi.org/10.1097/hco.0000000000000083.

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22

Gray, D. P., R. Steele, K. Sweeney, and P. Evans. "Asymptomatic hypercholesterolaemia." BMJ 302, no. 6783 (April 27, 1991): 1022. http://dx.doi.org/10.1136/bmj.302.6783.1022-a.

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23

Fogarty, A. J. "Asymptomatic hypercholesterolaemia." BMJ 302, no. 6789 (June 8, 1991): 1402. http://dx.doi.org/10.1136/bmj.302.6789.1402-b.

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24

Sharifi, M., A. Gallivan, D. Harvey, K. Wah Li, M. Futema, J. Cooper, S. Humphries, and D. Nair. "Atherosclerosis in monogenic Familial Hypercholesterolaemia versus polygenic hypercholesterolaemia." Atherosclerosis 245 (February 2016): e246-e247. http://dx.doi.org/10.1016/j.atherosclerosis.2015.10.036.

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25

Wah-Suarez, Martin I., Christopher J. Danford, Vilas R. Patwardhan, Z. Gordon Jiang, and Alan Bonder. "Hyperlipidaemia in primary biliary cholangitis: treatment, safety and efficacy." Frontline Gastroenterology 10, no. 4 (January 9, 2019): 401–8. http://dx.doi.org/10.1136/flgastro-2018-101124.

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Primary biliary cholangitis (PBC) is an autoimmune liver disease associated with altered lipoprotein metabolism, mainly cholesterol. Hypercholesterolaemia, a major modifiable risk factor for cardiovascular disease in the general population, occurs in 75%–95% of individuals with PBC. The impact of hypercholesterolaemia on cardiovascular risk in PBC, however, is controversial. Previous data have shown that hypercholesterolaemia in PBC is not always associated with an increase in cardiovascular events. However, patients with PBC with cardiovascular risk factors may still warrant cholesterol-lowering therapy. Treatment of hypercholesterolaemia in PBC poses unique challenges among primary care providers due to concerns of hepatotoxicity associated with cholesterol-lowering medications. This review summarises the current understanding of the pathophysiology of hypercholesterolaemia in PBC and its pertinent cardiovascular risk. We will also discuss indications for treatment and the efficacy and safety of available agents for hypercholesterolaemia in PBC.

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LORENZO, F. DE, M. MUKHERJEE, Z. KADZIOLA, R. SHERWOOD, and V. V. KAKKAR. "Central cooling effects in patients with hypercholesterolaemia." Clinical Science 95, no. 2 (August 1, 1998): 213–17. http://dx.doi.org/10.1042/cs0950213.

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1.A prospective study has been carried out, and 68 patients with hypercholesterolaemia have been investigated to study the effects of central cooling on serum lipid levels. 2.Central cooling was obtained by the exposure of the whole body to cold water. All patients were trained to gradually reduce the water temperature from 22 to 14 ;°C and to increase the time of exposure from 5 to 20 ;min over a period of 90 days. The 33 male and 35 female patients were aged between 40 and 60 years at entry with total cholesterol of 6.0 ;mmol/l or greater and low-density lipoprotein (LDL)-cholesterol of 4.0 ;mmol/l or greater. Thyroid-stimulating hormone, free thyroxine (FT4), total T3, total cholesterol, LDL-cholesterol, high-density lipoprotein (HDL)-cholesterol, triacylglycerols and total fat mass (determined by dual-energy X-ray absorptiometry scan) were obtained at baseline and after 3 months treatment with hydrotherapy. 3.Central cooling obtained by hydrotherapy results in a median fall in tympanic temperature from 0.2 ;°C (P< 0.001) to 0.8 ;°C (P< 0.001). We have observed in these patients a significant reduction in total cholesterol (-0.2 ;mmol/l, P = 0.006) and LDL-cholesterol (-0.2 ;mmol/l, P = 0.004). Serum FT4 level was higher than baseline results in 30 of these hypercholesterolaemic patients (15.5 ;pmol/l to 17.3 ;pmol/l) and there was no significant change in serum thyroid-stimulating hormone and total T3. 4.In conclusion, in our patients with hypercholesterolaemia we have observed a significant reduction of total cholesterol and LDL-cholesterol after body temperature regulation.

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Yu, Kenneth C. W., Darrin Smith, Akira Yamamoto, Akito Kawaguchi, Mariko Harada-Shiba, Taku Yamamura, and John C. L. Mamo. "Phagocytic Degradation of Chylomicron Remnants by Fibroblasts from Subjects with Homozygous Familial Hypercholesterolemia." Clinical Science 92, no. 2 (February 1, 1997): 197–203. http://dx.doi.org/10.1042/cs0920197.

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1. Familial hypercholesterolaemia is a common genetic abnormality in man characterized by premature atherogenesis as a consequence of disturbed lipoprotein metabolism. Chylomicrons, which represent intestinally derived lipoproteins, are cleared poorly in familial hypercholesterolaemia which may explain the increased retention of chylomicron remnants in arterial fatty lesions. However, cellular uptake of chylomicron remnants in familial hypercholesterolaemia remains unclear. This study determined the quantitative significance of non-low-density lipoprotein receptor-mediated uptake in fibroblasts from subjects with homozygous familial hypercholesterolaemia. 2. The metabolism of chylomicron remnants was assessed in fibroblasts from subjects with homozygous familial hypercholesterolaemia who lack low-density lipoprotein receptors. Compared with fibroblasts from normolipidaemic subjects, binding and degradation of chylomicron remnants was reduced by about two-thirds. Nevertheless, degradation of chylomicron remnants in cells from subjects with familial hypercholesterolaemia persisted in the absence of functioning low-density lipoprotein receptors. 3. Binding of chylomicron remnants to fibroblasts from subjects with familial hypercholesterolaemia was saturable. Unlabelled chylomicron remnants competed efficiently for binding but unlabelled low-density lipoprotein or a monoclonal antibody specific to the human low-density lipoprotein receptor had little effect on binding or degradation. 4. Polyinosinic acid did not alter binding and degradation of chylomicron remnants by fibroblasts from subjects with familial hypercholesterolaemia, ruling out involvement of the scavenger receptor. Lactoferrin was found to inhibit binding and degradation of chylomicron remnants by fibroblasts from subjects with familial hypercholesterolaemia by approximately 50%, implicating involvement of the α2-macroglobulin receptor. 5. Cytochalasin D blocked degradation of chylomicron remnants at 37°C in fibroblasts from subjects with familial hypercholesterolaemia by more than 80% but had no effect on binding at 4°C, consistent with a phagocytic uptake pathway. Collectively, the data suggest that chylomicron remnants bind to a cell-surface protein which initiates phagocytosis and that lactoferrin interferes with binding to this putative cell-surface protein. Phagocytic uptake of chylomicron remnants provides an additional mechanism whereby cells from subjects with familial hypercholesterolaemia can accumulate lipid.

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Pederiva, Cristina, Maria Elena Capra, Claudia Viggiano, Valentina Rovelli, Giuseppe Banderali, and Giacomo Biasucci. "Early Prevention of Atherosclerosis: Detection and Management of Hypercholesterolaemia in Children and Adolescents." Life 11, no. 4 (April 14, 2021): 345. http://dx.doi.org/10.3390/life11040345.

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Coronary heart disease (CHD) is the main cause of death and morbidity in the world. There is a strong evidence that the atherosclerotic process begins in childhood and that hypercholesterolaemia is a CHD major risk factor. Hypercholesterolaemia is a modifiable CHD risk factor and there is a tracking of hypercholesterolaemia from birth to adulthood. Familial hypercholesterolaemia (FH) is the most common primitive cause of hypercholesterolaemia, affecting 1:200–250 individuals. Early detection and treatment of hypercholesterolaemia in childhood can literally “save decades of life”, as stated in the European Atherosclerosis Society Consensus. Multiple screening strategies have been proposed. In 2008, the American Academy of Pediatrics published the criteria for targeted screening, while some expert panels recommend universal screening particularly in the young, although cost effectiveness has not been fully analysed. Blood lipid profile evaluation [total cholesterol, Low-Density Lipoprotein Cholesterol (LDL-C), High-Density Lipoprotein Cholesterol (HDL-C) and triglycerides] is the first step. It has to be ideally performed between two and ten years of age. Hypercholesterolaemia has to be confirmed with a second sample and followed by the detection of family history for premature (before 55 years in men and 60 years in women) or subsequent cardio-vascular events and/or hypercholesterolaemia in 1st and 2nd degree relatives. The management of hypercholesterolaemia in childhood primarily involves healthy lifestyle and a prudent low-fat diet, emphasising the benefits of the Mediterranean diet. Statins are the cornerstone of the drug therapy approved in USA and in Europe for use in children. Ezetimibe or bile acid sequestrants may be required to attain LDL-C goal in some patients. Early identification of children with severe hypercholesterolaemia or with FH is important to prevent atherosclerosis at the earliest stage of development, when maximum benefit can still be obtained via lifestyle adaptations and therapy. The purpose of our review is to highlight the importance of prevention and treatment of hypercholesterolaemia starting from the earliest stages of life.

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Sharifi, Mahtab, Anjly Jain, Jahm Persaud, Steve E. Humphries, and Devaki Nair. "Cardiovascular biomarkers in monogenic familial hypercholesterolaemia and polygenic hypercholesterolaemia." Atherosclerosis 255 (December 2016): 4. http://dx.doi.org/10.1016/j.atherosclerosis.2016.09.055.

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Office, Editorial. "Serum melatonin concentrations in coronary heart disease patients with hypercholesterolaemia." Suid-Afrikaanse Tydskrif vir Natuurwetenskap en Tegnologie 20, no. 1 (September 28, 2001): 22–23. http://dx.doi.org/10.4102/satnt.v20i1.246.

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This investigation was undertaken to determine the serum melatonin concentrations in coronary heart disease patients (CHD) with hypercholesterolaemia. Hypercholesterolaemia is a contributing factor to atherogenesis in CHD. Melatonin suppresses cholesterol synthesis. The preliminary results indicate that melatonin levels seem to be suppressed in CHD patients with hypercholesterolaemia.

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Park, Jeong Euy, Chern-En Chiang, Muhammad Munawar, Gia Khai Pham, Apichard Sukonthasarn, Anastacio R. Aquino, Kah Lin Khoo, and Hon Wah Raymond Chan. "Lipid-lowering treatment in hypercholesterolaemic patients: the CEPHEUS Pan-Asian survey." European Journal of Preventive Cardiology 19, no. 4 (March 7, 2011): 781–94. http://dx.doi.org/10.1177/1741826710397100.

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Background: Treatment of hypercholesterolaemia in Asia is rarely evaluated on a large scale, and data on treatment outcome are scarce. The Pan-Asian CEPHEUS study aimed to assess low-density lipoprotein cholesterol (LDL-C) goal attainment among patients on lipid-lowering therapy. Methods: This survey was conducted in eight Asian countries. Hypercholesterolaemic patients aged ≥18 years who had been on lipid-lowering treatment for ≥3 months (stable medication for ≥6 weeks) were recruited, and lipid concentrations were measured. Demographic and other clinically relevant information were collected, and the cardiovascular risk of each patient was determined. Definitions and criteria set by the updated 2004 National Cholesterol Education Program guidelines were applied. Results: In this survey, 501 physicians enrolled 8064 patients, of whom 7281 were included in the final analysis. The mean age was 61.0 years, 44.4% were female, and 85.1% were on statin monotherapy. LDL-C goal attainment was reported in 49.1% of patients overall, including 51.2% of primary and 48.7% of secondary prevention patients, and 36.6% of patients with familial hypercholesterolaemia. The LDL-C goal was attained in 75.4% of moderate risk, 55.4% of high risk, and only 34.9% of very high-risk patients. Goal attainment was directly related to age and inversely related to cardiovascular risk and baseline LDL-C. Conclusion: A large proportion of Asian hypercholesterolaemic patients on lipid-lowering drugs are not at recommended LDL-C levels and remain at risk for cardiovascular disease. Given the proven efficacy of lipid-lowering drugs in the reduction of LDL-C, there is room for further optimization of treatments to maximize benefits and improve outcomes.

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&NA;. "Update on hypercholesterolaemia." Inpharma Weekly &NA;, no. 885 (May 1993): 16. http://dx.doi.org/10.2165/00128413-199308850-00034.

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Olsson, AndersG, Jorgen Mölgaard, and Henning Von Schenk. "SYNVINOLIN IN HYPERCHOLESTEROLAEMIA." Lancet 328, no. 8503 (August 1986): 390–91. http://dx.doi.org/10.1016/s0140-6736(86)90070-x.

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Bilheimer, David. "4 Familial hypercholesterolaemia." Baillière's Clinical Endocrinology and Metabolism 1, no. 3 (August 1987): 581–601. http://dx.doi.org/10.1016/s0950-351x(87)80024-1.

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Macchiaiolo, Marina, Maria Giulia Gagliardi, Alessandra Toscano, Paolo Guccione, and Andrea Bartuli. "Homozygous familial hypercholesterolaemia." Lancet 379, no. 9823 (April 2012): 1330. http://dx.doi.org/10.1016/s0140-6736(11)61476-1.

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36

Oelbaum, R. S., and D. J. Galton. "Management of hypercholesterolaemia." Current Opinion in Cardiology 3, no. 2 (March 1988): 255–63. http://dx.doi.org/10.1097/00001573-198803000-00015.

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Gagné, Claude, Sital Moorjani, AnaL Torres, Daniel Brun, and Paul-J. Lupien. "Homozygous familial hypercholesterolaemia." Lancet 343, no. 8890 (January 1994): 177. http://dx.doi.org/10.1016/s0140-6736(94)90968-7.

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&NA;. "Antacids treat hypercholesterolaemia." Inpharma Weekly &NA;, no. 821 (January 1992): 9. http://dx.doi.org/10.2165/00128413-199208210-00021.

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Abrantes, L. B., A. C. Alves, A. M. Medeiros, S. Correia, A. Cruz, A. Ferreira, G. Lobarinhas, et al. "Pediatric Familial Hypercholesterolaemia." Atherosclerosis 287 (August 2019): e216. http://dx.doi.org/10.1016/j.atherosclerosis.2019.06.658.

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Schofield, Jonathan, Michael France, Ruth Eatough, See Kwok, and Handrean Soran. "Familial hypercholesterolaemia knowledge." Atherosclerosis 231, no. 2 (December 2013): e4-e5. http://dx.doi.org/10.1016/j.atherosclerosis.2013.07.019.

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Suades, Rosa, Teresa Padró, Rodrigo Alonso, José López-Miranda, Pedro Mata, and Lina Badimon. "Circulating CD45+/CD3+ lymphocyte-derived microparticles map lipid-rich atherosclerotic plaques in familial hypercholesterolaemia patients." Thrombosis and Haemostasis 111, no. 01 (2014): 111–21. http://dx.doi.org/10.1160/th13-07-0612.

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SummaryCirculating microparticles (cMPs) seem to play important roles in vascular function. Beyond markers of activated cells, cMPs may have potential paracrine functions and influence atherosclerosis. Here, our objective was to characterise a) the abundance and phenotype of cMPs in stable statin-treated heterozygous familial hypercholesterolaemia (FH) patients exposed to life-long hypercholesterolaemia and b) the principal phenotype associated to lipid-rich atherosclerotic plaques in hFHpatients with significant atherosclerotic plaque burden. An age/gender/ treatment-matched group of adult-onset non-FH hypercholesterolaemic patients (n=37/group) was comparatively analysed. cMPs were characterised by flow cytometry using annexin-V and cell surface-specific antibodies. Our study shows that LLT-FH patients had higher overall cMP-numbers (p<0.005) than LLT-non-FH patients. Endothelial cellshed cMPs were also significantly higher in FH (p<0.0005). Within the leukocyte-derived cMP-subpopulations, FH-patients had significantly higher lymphocyte- and monocyte-derived cMP-numbers as well as cMPs carrying leukocyte-activation markers. Normalisation of cMPs by LDL levels did not affect cMP number or phenotype, indicating that the proinflammatory effect was derived from chronic vascular damage. Levels of AV+-total, CD45+-pan-leukocyte and CD45+/CD3+-lymphocyte-derived cMPs were significantly higher in FH-patients with subclinical lipid-rich atherosclerotic plaques than fibrous plaques. Levels of CD45+/CD3+-lymphocyte-MPs above 20,000/ml could differentiate between FH-patients with lipidic or non-lipidic plaques (area under the ROC curve of 0.803, 95%CI: 0.641–0.965, p=0.008). In summary, in this snapshot cross-sectional study cMP concentration and phenotype in FH differed markedly from non-FH hypercholesterolaemia. Patients with life-long high LDL exposure have higher endothelial activation and higher proinflammatory profile, even under current state-of-the-art LLT. cMPs carrying lymphocyte-epitopes appear as markers of lipid-rich atherosclerotic plaques in FH.

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Klinke, J. A., S. C. Shapira, E. Akbari, and D. T. Holmes. "Quetiapine-associated cholestasis causing lipoprotein-X and pseudohyponatraemia." Journal of Clinical Pathology 63, no. 8 (August 2010): 741–43. http://dx.doi.org/10.1136/jcp.2008.064063.

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A case of intrahepatic cholestasis secondary to treatment with quetiapine in combination with lamotrigine and zopiclone, resulting in severe hypercholesterolaemia without overt lactescence of the plasma, is presented. Abundant lipoprotein-X was seen on lipoprotein electrophoresis. The patient was diagnosed and treated for hyponatraemia which was likely factitious and caused by hypercholesterolaemia. Cholestasis and hypercholesterolaemia resolved over a period of several months after the discontinuation of quetiapine.

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Ashfield-Watt, Pauline, Kate Haralambos, Rhiannon Edwards, Delyth Townsend, Rob Gingell, Kah Wa Li, Steve E. Humphries, and Ian McDowell. "Estimation of the prevalence of cholesteryl ester storage disorder in a cohort of patients with clinical features of familial hypercholesterolaemia." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 56, no. 1 (August 8, 2018): 112–17. http://dx.doi.org/10.1177/0004563218793165.

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Background and aim Familial hypercholesterolaemia is caused by variants in the low-density lipoprotein cholesterol metabolic pathway involving LDLR, APOB and PCSK9 genes. A national genetic testing service in Wales, UK has observed that no familial hypercholesterolaemia variant is found in almost 80% patients with the familial hypercholesterolaemia phenotype. It has recently been suggested that some adult patients with a familial hypercholesterolaemia phenotype may have cholesteryl ester storage disease which can also present as a mixed hyperlipidaemia. The commonest genetic cause of cholesteryl ester storage disease is an exon 8 splice junction variant in the LIPA gene (rs116928232, c.894G>A; E8SJM) previously found to have an allele frequency of 0.0011 (1 in 450 individuals) in a large European population. This study investigated the prevalence of the E8SJM in patients with a familial hypercholesterolaemia phenotype in Wales, UK. Method A total of 1203 patients with a clinical suspicion of familial hypercholesterolaemia but no familial hypercholesterolaemia variant were invited to participate. Of these, 668 patients provided informed written consent. Stored DNA samples from 663 patients were genotyped for the E8SJM variant. Results Three heterozygotes were identified (allele frequency 0.0023). Whole gene sequencing of the LIPA gene was undertaken in these three individuals, but no other variants were found. Therefore, there were no cholesteryl ester storage disease patients (homozygote or compound heterozygote) identified in this cohort. Conclusion The allele frequency 0.0023 (1 in 221 individuals) for the E8SJM variant was more prevalent in this cohort than in a European population study; however, no cholesteryl ester storage disease homozygotes were identified. We found no evidence to support routine testing for cholesteryl ester storage disease in adult patients with a familial hypercholesterolaemia phenotype.

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JILMA, Bernd, Christian JOUKHADAR, Ulla DERHASCHNIG, Fausi RASSOUL, Volker RICHTER, Michael WOLZT, Guido T. DORNER, Vanessa PETTERNEL, and Oswald F. WAGNER. "Levels of adhesion molecules do not decrease after 3 months of statin therapy in moderate hypercholesterolaemia." Clinical Science 104, no. 2 (January 17, 2003): 189–93. http://dx.doi.org/10.1042/cs1040189.

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Studies in animals and humans indicate a pivotal role for adhesion molecules (AMs) in the pathogenesis of atherosclerosis. Whereas an association between hypercholesterolaemia and AM expression has been suggested, it is unclear whether lowering cholesterol decreases AM expression and release. We compared the effects of a 3-month treatment with standard doses of three different statins (atorvastatin, simvastatin and pravastatin) on plasma levels of circulating AM (cAM) in 75 hypercholesterolaemic patients in a randomized clinical trial. Plasma levels of circulating (c)E-selectin, circulating intercellular adhesion molecule-1 (cICAM-1) and circulating vascular cell adhesion molecule-1 (cVCAM-1) were measured before and after 3 months of therapy. None of the statins lowered plasma cAM levels and pooled analyses of all patients showed a 1.7% [95% confidence interval (CI), -1.4–4.9%] increase in cE-selectin, a 2.1% (95% CI, -0.2–4.4%) increase in cICAM-1, and a 2.7% (95% CI, -0.6–6.1%) increase in cVCAM-1 levels. cAM levels did not decrease, even in patients with a >50% decrease (n = 19) in low-density lipoprotein cholesterol levels. This study provides strong evidence that 3 months of therapy with three different statins does not decrease cAM levels, despite normalization of cholesterol levels, and a minor decrease in C-reactive protein levels in patients with moderate hypercholesterolaemia.

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Tesoriere, Luisa, Alessandro Attanzio, Mario Allegra, and Maria A. Livrea. "Dietary indicaxanthin from cactus pear (Opuntia ficus-indicaL. Mill) fruit prevents eryptosis induced by oxysterols in a hypercholesterolaemia-relevant proportion and adhesion of human erythrocytes to endothelial cell layers." British Journal of Nutrition 114, no. 3 (July 14, 2015): 368–75. http://dx.doi.org/10.1017/s0007114515002111.

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Toxic oxysterols in a hypercholesterolaemia-relevant proportion cause suicidal death of human erythrocytes or eryptosis. This process proceeds through early production of reactive oxygen species (ROS), release of prostaglandin (PGE2) and opening of PGE2-dependent Ca channels, membrane phosphatidylserine (PS) externalisation, and cell shrinkage. The present study was the first to reveal that a bioavailable phytochemical, indicaxanthin (Ind) from cactus pear fruit, in a concentration range (1·0–5·0 μM) consistent with its plasma level after a fruit meal, prevents PS externalisation and cell shrinkage in a dose-dependent manner when incubated with isolated healthy human erythrocytes exposed to an oxysterol mixture for 48 h. Dietary Ind inhibited ROS production, glutathione (GSH) depletion, PGE2 release and Ca2+entry. Ind alone did not modify the erythrocyte redox environment or affect other parameters.Ex vivospiking of normal human blood with the oxysterol mixture for 48 h induced eryptosis, resulting in the production of ROS and decreased levels of GSH, which was prevented by concurrent exposure to 5 μm-Ind. The adherence of eryptotic erythrocytes to the endothelium causes vascular tissue injury. Erythrocytes isolated from blood incubated with the oxysterol mixture plus 5 μm-Ind did not adhere to endothelial cell monolayers. Eryptotic erythrocytes may contribute to thrombotic complications in hypercholesterolaemia. Our findings suggest the positive effects of diets containing Ind on erythrocytes in hypercholesterolaemic subjects.

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Holliday, M. P., A. F. Winder, and A. P. Wojciechowski. "Apoprotein, lipoprotein & receptor studies in non-familial hypercholesterolaemia heritable hypercholesterolaemia." Atherosclerosis 68, no. 3 (December 1987): 273. http://dx.doi.org/10.1016/0021-9150(87)90215-2.

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Dutta, B., AKMM Islam, M. Ullah, A. Zaman, KK Karmakar, MZ Rahman, and SK Kundu. "Homozygous Familial Hypercholesterolaemia with Valvular Aortic Stenosis and Significant Coronary Artery Disease: A Case Report." Cardiovascular Journal 6, no. 2 (March 17, 2014): 180–83. http://dx.doi.org/10.3329/cardio.v6i2.18365.

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Homozygous Familial Hypercholesterolaemia is a genetic disorder which usually presents with early cardiovascular disease ranging from premature ischaemic disease, including myocardial infarction to aortic root stenosis. A 21 year old Bangladeshi male presented with exertional chest pain and breathlessness. He was diagnosed as a case of Homozygous Familial Hypercholesterolaemia. His angina symptoms were due to underlying valvular aortic stenosis which is a rare presentation of Homozygous Familial Hypercholesterolaemia. DOI: http://dx.doi.org/10.3329/cardio.v6i2.18365 Cardiovasc. j. 2014; 6(2): 180-183

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Jones, Jane L., Edin Lakasing, and Stefanos Archontakis. "Familial hypercholesterolaemia: different perspectives." Nursing Standard 23, no. 50 (August 19, 2009): 35–38. http://dx.doi.org/10.7748/ns2009.08.23.50.35.c7212.

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Češka, Richard, Michaela Šnejdrlová, Michal Vrablík, Tereza Altschmiedová, and Tomáš Štulc. "Treating hypercholesterolaemia with evolocumab." Intervenční a akutní kardiologie 17, no. 4 (December 1, 2018): 212–17. http://dx.doi.org/10.36290/kar.2018.057.

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Jones, L. Jane, Edin Lakasing, and Stefanos Archontakis. "Familial hypercholesterolaemia: different perspectives." Nursing Standard 23, no. 50 (August 19, 2009): 35–38. http://dx.doi.org/10.7748/ns.23.50.35.s49.

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