Relevant bibliographies by topics / Hypercholesterolaemia

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Hypercholesterolaemia'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 April 2022

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Journal articles on the topic "Hypercholesterolaemia"

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

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Dissertations / Theses on the topic "Hypercholesterolaemia"

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Sharifi, Mahtab. "Preclinical atherosclerosis in monogenic familial hypercholesterolaemia and polygenic hypercholesterolaemia." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10054674/.

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Familial Hypercholesterolaemia (FH) is an autosomal dominant disorder with a frequency of 1 in 250 to 500 in most European populations. It is characterised by a raised low density lipoprotein-cholesterol (LDL-C) and a high incidence of premature coronary heart disease (CHD). There are three genes where mutations are known to cause FH: the low-density lipoprotein receptor (LDLR) gene, the apolipoprotein B (APOB) gene and the pro-protein convertase subtilisin/kexin type 9 (PCSK9) gene. An FH-causing mutation can be found in around 40% of patients with a possible diagnosis of FH. It has been suggested that the patients with a clinical diagnosis of FH where no mutation were found might have a polygenic cause for their raised LDL-C. FH disorder is an under-diagnosed condition in many countries such as Poland. An analysis of a Polish FH cohort in this thesis, demonstrated the heterogeneous aetiology of FH. We found 39 different pathogenic mutations in the LDLR gene with 10 of them being novel and an overall detection rate of 43.4%. The aim of this thesis was to compare preclinical atherosclerosis between patients with monogenic FH and subjects with polygenic hypercholesterolaemia by means of a neck ultrasound to measure carotid Intima Media Thickness and a cardiac CT scan to assess coronary artery calcification. This study showed that preclinical atherosclerosis was greater in patients with monogenic FH. Lipoprotein(a) [Lp(a)] is a well-known biomarker for CHD risk prediction. The Lp(a) concentration and its association with two LPA single nucleotide polymorphisms (rs3798220 and rs6919346) were assessed in FH patients participating in the Simon Broome registry and a group of the general population participating in the Northwick Park Heart Study II. The results showed that the Lp(a) concentration and the frequency of rs3798220 was significantly higher in the FH patients compared to the general population.
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Hollman, Gunilla. "Living with familial hypercholesterolaemia /." Linköping : Univ, 2003. http://www.bibl.liu.se/liupubl/disp/disp2003/med810s.pdf.

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Bharaj, Harnovdeep Singh. "Studies in primary hypercholesterolaemia." Thesis, University of Leicester, 1996. http://hdl.handle.net/2381/34134.

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Cholesterol is an integral part of the cell membrane and influences both its fluidity and activity. Furthermore membrane lipids are influenced by plasma lipid levels. In familial hypercholesterolaemia (FH) red cell rheology and platelet aggregation is abnormal. These effects could be due to changes in plasma lipids since they are improved by cholesterol reduction. Section A Fasting lipid profile, membrane cholesterol, red cell ghost and platelet fluidity [using diphenyl hexatriene (DPH) and trimethylamino-diphenyl hexatriene (TMA-DPH) fluorescence anisotropy] and Ca2+ -Mg2+ -ATPase activity (using [32P] ATP hydrolysis) in 30 patients with heterozygous FH and 19 controls were compared before and after treatment with colestipol (10g) , simvastatin (10mg) and maxepa (10g). The two groups were generally comparable with respect to age, sex, BMI and blood pressure. In FH plasma cholesterol, membrane cholesterol, TMA-DPH anisotropy and red cell Ca2+ -Mg2+ -ATPase were increased whilst platelet Ca2+ -Mg2+ -ATPase was reduced (p<0.05). Colestipol and simvastatin reversed these changes toward controls. Maxepa increased DPH anisotropy and reduced Ca2+-Mg2+ -ATPase. In FH membrane fluidity and activity is altered and normalised by cholesterol lowering. This may account for the abnormal cell function in this condition. Section B A double blind, randomized, placebo controlled trial in hypercholesterolaemia (cholesterol 6.5-10 mmol/l, triglycerides <3 mmol/l). After 8 weeks of an AHA step I diet, patients were randomized to A: placebo; B: 5g colestipol + 10mg simvastatin; or C: 10g colestipol + 10mg simvastatin for 8 weeks. Patients were assessed 4 weekly. 44 patients were screened, 32 completed the study. Groups were generally comparable (group C patients were older p<0.02). Active treatment resulted in a 38% reduction in LDL cholesterol (p0.8). Mild gastro-intestinal upset was the commonest adverse event. Low dose combinations are effective and well tolerated. There is no apparent advantage of 10g over 5g colestipol when combined with l0mg simvastatin. HDL cholesterol and triglycerides were unchanged.
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Mendes, Ribeiro Antonio Claudio. "L-arginine in hypercholesterolaemia and uraemia." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320665.

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Futema, M. "The genetic architecture of familial hypercholesterolaemia." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1417767/.

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Familial Hypercholesterolaemia (FH) is a common autosomal dominant disorder of the defective plasma clearance of LDL-cholesterol. Mutations in three genes, LDLR/APOB/PCSK9, can be detected in 60-90% of definite FH patients. DNA-based testing for FH mutations has important clinical utility and is recommended by the UK and European guidelines to identify affected relatives. This thesis aimed to determine the frequency and spectrum of FH mutations in two independent cohorts of FH patients (from one Oxford lipid clinic, and of Indian background). The FH mutation spectrum was shown to be highly heterogeneous and the mutation detection rate was significantly dependent on the pre-treatment total cholesterol and triglyceride levels. This project also validated the findings that a proportion of clinically diagnosed FH patients have a polygenic cause of hypercholesterolaemia due to an accumulation of common mild LDL-C-raising alleles by analysing LDL-C gene score in 88 mutation negative and 21 mutation positive FH patients, and by replicating the results in further 231 FH patients. A high-throughput DNA sequencing method was assessed as a novel diagnostic tool for detection of FH mutations, and compared it with the currently used methods. This highlighted the need for updating the current FH mutation screening methods as well as the need for more efficient bioinformatics for the next generation sequencing data analysis. Lastly, whole exome sequencing of 125 definite FH patients with no mutations detected in known genes was performed to identify novel monogenic causes of FH. Variants in two genes, CH25H and INSIG2, were identified as potential novel FH mutations. Overall, the results of this thesis demonstrate the heterogeneous FH aetiology and help to understand the genetic architecture of the disease.
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Marks, Dalya. "An evaluation of strategies for detecting familial hypercholesterolaemia." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408037.

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Burden, Joanne Jemima Ellen. "Identification and characterisation of a novel intracellular protein that binds the low density lipoprotein (LDL) receptor." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271420.

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Nield, Heather S. "Control by cyclic AMP of the activity and gene expression of the low density lipoprotein receptor." Thesis, University of Nottingham, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240540.

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Backlund, Lars. "General practitioners' decision-making on drug treatment of hypercholesterolaemia /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-672-3/.

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Ward, Alana Jane. "The molecular genetics of familial hypercholesterolaemia in Northern Ireland." Thesis, Queen's University Belfast, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295435.

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Books on the topic "Hypercholesterolaemia"

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Drummond, M. F. Economic evaluation of drug therapy for hypercholesterolaemia in the United Kingdom. York: Centre for Health Economics, University of York, 1993.

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Drummond, Michael. Economic evaluation of drug therapy for Hypercholesterolaemia in the United Kingdom. York: York University, Centre for Health Economics, 1993.

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Latta, Eleanor Katrin. Effects on platelet function of chronic administration of ethanol to normo- and hypercholesterolaemic rabbits. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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D, Marks, and National Co-ordinating Centre for HTA (Great Britain), eds. Screening for hypercholesterolaemia versus case finding for familial hypercholesterolaemia: A systematic review and cost-effectiveness analysis. Alton: Core Research on behalf of the NCCHTA, 2000.

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Helen, Cook, and Centre for Pharmacy Postgraduate Education. Distance Learning., eds. Hypertension and hypercholesterolaemia: A distance learning pack for community pharmacists. [London]: HMSO, 1994.

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Limited, Quaker Oats, ed. Lowering blood cholesterol: A dietary approach : hypercholesterolaemia - what can be done?.... Quaker Oats Limited, 1986.

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Reiner, Željko, Olov Wiklund, and John Betteridge. Lipids. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0015.

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Dyslipidaemia, particularly elevated low-density lipoprotein (LDL) cholesterol, is one of the most important risk factors for cardiovascular disease (CVD). Low concentrations of high-density lipoprotein (HDL) cholesterol are independently associated with high CVD risk, while moderately elevated triglycerides are considered to be a marker of increased CVD risk. The presence of dyslipidaemias secondary to other conditions must be excluded before beginning treatment. All patients with familial hypercholesterolaemia are at high risk and should be treated by lipid-lowering therapy. Lifestyle changes are the backbone of treatment for dyslipidaemia. Statins are recommended as the first-line drugs for hypercholesterolaemia while fibrates are used primarily to decrease elevated triglycerides. If the treatment targets cannot be reached by monotherapy with lipid-lowering drugs, combination treatment may be needed.
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Banerjee, Amitava, and Kaleab Asrress. Risk factors for cardiovascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0086.

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The most prevalent cardiovascular diseases (CVDs) are atherosclerotic, affecting all arterial territories. Epidemiologic studies such as the Framingham and INTERHEART studies have firmly established the commonest or ‘traditional’ risk factors for CVD; namely, smoking, hypertension, diabetes mellitus, hypercholesterolaemia, and a family history of CVD. The ‘risk-factors approach’ to CVD looks at these factors, individually and in combination, in the causation of disease. The complex causation pathways involve interplay of individual factors, whether genetic or environmental. More recently, there has been increasing interest in ‘epigenetics’ or the way in which the environment interacts with genes in the process underlying CVD. This chapter presents an analysis of the traditional and novel risk factors for CVD.
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Bell, Robert M. Pathophysiology of coronary syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0145.

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The pathophysiology of acute coronary syndromes is characterized by an acute mismatch of blood supply to the myocardium to meet the prevailing metabolic need. By far the commonest aetiology of myocardial ischaemia is coronary artery disease . An inflammatory process that evolves over the period of many decades, coronary artery disease is characterized by the deposition of cholesterol and cholesterol laden macrophages within the intima of the vessel wall. This process can be accelerated by a number of cardiovascular risk factors (smoking, hypertension, hyperlipidaemia, hypercholesterolaemia, diabetes), which can culminate in the formation of the unstable plaque responsible for the emergent presentation of ST-elevation myocardial infarction. This chapter reviews the prolonged inflammatory process responsible for atheroma formation, along with rarer, non-atheroma-related causes of acute coronary syndromes.
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Book chapters on the topic "Hypercholesterolaemia"

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Goode, G. K., and A. M. Heagerty. "Hypercholesterolaemia and Vascular Function." In The Resistance Arteries, 339–46. Totowa, NJ: Humana Press, 1994. http://dx.doi.org/10.1007/978-1-4757-2296-3_32.

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Pottle, Alison. "Lipid Disorders and Familial Hypercholesterolaemia." In Advanced Practice in Endocrinology Nursing, 1101–20. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-99817-6_57.

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Horstman, Klasien, and Carin Smand. "Detecting Familial Hypercholesterolaemia: Escaping the Family History?" In Genetics from Laboratory to Society, 90–117. London: Palgrave Macmillan UK, 2008. http://dx.doi.org/10.1057/9780230598775_5.

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Attie, Alan D., Matthew T. Flowers, Jessica B. Flowers, Albert K. Groen, Folkert Kuipers, and James M. Ntambi. "Stearoyl-CoA Desaturase Deficiency, Hypercholesterolaemia, Cholestasis and Diabetes." In Novartis Foundation Symposia, 47–57. Chichester, UK: John Wiley & Sons, Ltd, 2007. http://dx.doi.org/10.1002/9780470985571.ch5.

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Woditsch, I., Th Hohlfeld, H. Strobach, and K. Schrör. "Oral Cicaprost Protects from Hypercholesterolaemia-Induced Impairment of Coronary Vasodilation." In Prostaglandins in the Cardiovascular System, 297–304. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7262-1_41.

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Cicero, Arrigo F. G. "Clinical Case 3: Patient with Essential Hypertension and Familial Hypercholesterolaemia." In Practical Case Studies in Hypertension Management, 33–50. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39504-3_3.

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Humphries, S., R. Taylor, M. Jeenah, and M. Seed. "The Use of Recombinant DNA Techniques for the Diagnosis of Familial Hypercholesterolaemia." In Studies in Inherited Metabolic Disease, 33–44. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1259-5_4.

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Shoulders, C. C., M. J. Ball, J. I. Mann, and F. E. Baralle. "A Genetic Marker in the Apolipoprotein AI/CIII Gene Complex Associated with Hypercholesterolaemia." In Drugs Affecting Lipid Metabolism, 56–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71702-4_10.

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Schuster, H., G. Wolfram, Ch Keller, and N. Zöllner. "Use of RFLPs of the LDL Receptor Gene in Diagnosis of Familial Hypercholesterolaemia." In Recent Developments in Lipid and Lipoprotein Research, 53–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83665-7_6.

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Gautschi, Matthias, Mladen Pavlovic, and Jean-Marc Nuoffer. "Fatal Myocardial Infarction at 4.5 Years in a Case of Homozygous Familial Hypercholesterolaemia." In JIMD Reports, 45–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/8904_2011_45.

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Conference papers on the topic "Hypercholesterolaemia"

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Sáez Rodríguez, MI, JJ Arenas Villafranca, B. Montero Salgado, PA Chinchurreta Capote, and B. Tortajada Goitia. "4CPS-119 Real-world experience with PCSK9 inhibitors protocol for hypercholesterolaemia." In 26th EAHP Congress, Hospital pharmacists – changing roles in a changing world, 23–25 March 2022. British Medical Journal Publishing Group, 2022. http://dx.doi.org/10.1136/ejhpharm-2022-eahp.146.

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2

Nikola, Christos. "32 Prevalence and characteristics of non –lipid risk factors in familial hypercholesterolaemia – a study based in the population registered in the latvian registry of familial hypercholesterolaemia." In Irish Cardiac Society Annual Scientific Meeting & AGM, Thursday October 17th – Saturday October 19th 2019, Galway, Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-ics.32.

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3

Laustiola, K., R. Lassila, P. Koskinen, and V. Manninen. "GEMFIBROZIL HAS ANTI-PLATELET EFFECTS IN PATIENTS WITH HYPERCHOLESTEROLAEMIA DURING PHYSICAL STRESS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643462.

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Abstract:
Earlier studies indicate an increased platelet reactivity in patients with hypercholesterolaemia. Physical and mental stress have also been reported to cause increased reactivity. The present study was undertaken to evaluate the effect of gemfibrozil (G) a new lipid lowering drug on platelet reactivity during physical stress. Ten otherwise healthy male subjects with serum cholesterol levels above 7 mmol/l were involved in a double-blind study. It consisted of two treatment periods of 8 weeks during which the patients were given either G (600 mg b.i.d.) or placebo (PI) and an 8 weeks wash-out period before the cross-over. At the end of the treatment periods an exercise test was carried out and platelet reactivity tested. Adrenaline, ADP and collagen were used to induce aggregation and 5-HT and T×B2 release measured. Plasma beta-TG and fibrinogen were also determined.The treshold concentration of adrenaline necessary to evoke secondary aggregation was increased in 8/10 patients during exercise after G treatment and in 2/10 after PI. When the lowest ADP concentration to cause secondary aggregation (2-4 uM) was used there was a significant decrease in the 5-HT (− 44%) and T×B2 (− 48%) secretion and a significant decrease in the area under the aggregation curve (− 28%). A decrease in 5-HT secretion was also seen after G treatment when a fixed ADP concentration of 10 uM was used. During collagen stimulation no changes were seen between the two groups. Beta-TG remained unchanged irrespective of treatment and fibrinogen showed a modest increase during exercise in both treatment groups. These results indicate a new anti-platelet effect of gemfibrozil which might be of importance in prevention of acute thrombotic events in hypercho1estero1aemic patients.
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4

Díez, B. Cancela, C. Muñoz, R. Claramunt, S. Guijarro, MJ Barbero, and F. Horno. "5PSQ-026 Efficacy and safety of evolocumab in hypercholesterolaemia and mixed dyslipidaemia." In Abstract Book, 23rd EAHP Congress, 21st–23rd March 2018, Gothenburg, Sweden. British Medical Journal Publishing Group, 2018. http://dx.doi.org/10.1136/ejhpharm-2018-eahpconf.380.

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5

Butt, Hafiz Shafiq, Lubna Mahmood, and Alfonso Herrera. "P66 A case of pseudohyponatremia due to hypercholesterolaemia in a patient with cholestasis." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.421.

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6

Duff, James, Robin Wang, John Graby, and Moya O’Doherty. "188 Identification of familial hypercholesterolaemia in patients presenting with premature acute coronary syndrome." In British Cardiovascular Society Virtual Annual Conference, ‘Cardiology and the Environment’, 7–10 June 2021. BMJ Publishing Group Ltd and British Cardiovascular Society, 2021. http://dx.doi.org/10.1136/heartjnl-2021-bcs.185.

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7

Garreffa, MR, C. Zito, S. Esposito, C. Monopoli, MD Naturale, and AE de Francesco. "5PSQ-028 The governance of PCSK9-inhibitors for the treatment of primary hypercholesterolaemia: appropriateness analysis." In 24th EAHP Congress, 27th–29th March 2019, Barcelona, Spain. British Medical Journal Publishing Group, 2019. http://dx.doi.org/10.1136/ejhpharm-2019-eahpconf.461.

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8

Aguilar-Valle, E., C. Estaun-Martinez, I. Moya-Carmona, M. Pedrosa-Ruiz, R. Mora-Santiago, and JM Fernández-Ovies. "CP-197 Protocol compliance in the treatment of hypercholesterolaemia with protein convertase SUBTILISIN-LIKE/KEXIN type 9 inhibitors (PCSK9 inhibitors)." In 22nd EAHP Congress 22–24 March 2017 Cannes, France. British Medical Journal Publishing Group, 2017. http://dx.doi.org/10.1136/ejhpharm-2017-000640.195.

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9

Elgerray, Samir, Gregory Oleszkiewicz, Zuhaina Noor Haque, and Akhlaque Uddin. "67 Are we missing patients with familial hypercholesterolaemia? assessment of lipid profile in patients referred via the primary PCI pathway." In British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.67.

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10

Ambel, H. Quiros, C. Donoso Rengifo, AA García Sacristán, JM Martinez Sesmero, A. Dominguez Barahona, S. González Suarez, P. Moya Gomez, and C. Blazquez Romero. "4CPS-034 Effectiveness and safety of monoclonal antibodies against proprotein convertase subtilisin/kexin 9 (pcsk9 inhibitors) for the treatment of hypercholesterolaemia." In Abstract Book, 23rd EAHP Congress, 21st–23rd March 2018, Gothenburg, Sweden. British Medical Journal Publishing Group, 2018. http://dx.doi.org/10.1136/ejhpharm-2018-eahpconf.125.

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