Academic literature on the topic 'Remnant cholesterol'
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Journal articles on the topic "Remnant cholesterol"
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Sultan, F., D. Lagrange, X. Le Liepvre, and S. Griglio. "Chylomicron-remnant uptake by freshly isolated hepatocytes. Effect of heparin and of hepatic triacylglycerol lipase." Biochemical Journal 258, no. 2 (March 1, 1989): 587–94. http://dx.doi.org/10.1042/bj2580587.
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Chylomicron remnants labelled biologically with [3H]cholesterol were efficiently taken up by freshly isolated hepatocytes during a 3 h incubation in Krebs bicarbonate medium. Their [3H]cholesteryl ester was hydrolysed (74% net hydrolysis), and 0.1 mM-chloroquine could partially inhibit this hydrolysis, provided that hepatocytes were first preincubated for 2 h 30 min at 37 degrees C. This hydrolysis was also measured in preincubated cells with remnants double-labelled (3H and 14C) on their free cholesterol moiety; [3H]cholesterol arising from [3H]cholesteryl ester hydrolysis was recovered in the free [3H]cholesterol pool. A dose-response study showed saturation of remnant uptake at 180 micrograms of remnant protein/10(7) cells. Heparin (10 units/ml) increased remnant uptake by 63% (P less than 0.01), [3H]cholesteryl ester accumulation in the cell pellet by 110% (P less than 0.025) and hepatic lipase activity secreted in the medium by 2.4-fold (P less than 0.01) and by 3.3-fold (P less than 0.01) at the end of the preincubation and incubation periods respectively. Addition of 100 munits of semi-purified hepatic lipase preparation/flask stimulated remnant uptake by 44-69%, and [3H]cholesteryl ester accumulation in the presence of chloroquine by 2.1-fold (P less than 0.025). When hepatic lipase was incubated solely with the remnants, it decreased their triacylglycerol and phospholipid contents by 24% and 26% respectively. Thus freshly isolated hepatocytes may be used to study chylomicron-remnant uptake. Hepatic lipase, which seems to underly the stimulating effect of heparin, facilitates remnant uptake in vitro, and this could be mediated by at least one (or both) of its hydrolytic properties.
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Redgrave, T. G., C. L. Elsegood, J. C. L. Mamo, and M. J. Callow. "Effects of hypothyroidism on the metabolism of lipid emulsion models of triacylglycerol-rich lipoproteins in rats." Biochemical Journal 273, no. 2 (January 15, 1991): 375–81. http://dx.doi.org/10.1042/bj2730375.
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Methimazole-treated hypothyroid rats were injected intravenously with triacylglycerol/cholesteryl oleate/cholesterol/phospholipid emulsions designed to model the composition of chylomicrons. Compared with controls, hypothyroidism decreased the clearance rates of emulsion cholesteryl oleate. Clearance of emulsion triolein was affected much less and could be accounted for by residual triolein in remnants, suggesting that triacylglycerol lipolysis by lipoprotein lipase was unaffected by hypothyroidism but that clearance of remnants from plasma was decreased. Assays in vitro showed increased activities of lipoprotein lipase and hepatic lipase in hypothyroid rats. Emulsions were incubated with post-heparin plasma lipoprotein lipase to prepare remnants in vitro. The clearance from plasma of pre-formed remnants was slower after injection into hypothyroid rats than in control rats. Uptake of remnant cholesteryl oleate by the liver was significantly decreased in the hypothyroid rats. Treatment of hypothyroid rats for 7 days with 3,3′,5′-tri-iodo-L-thyronine (T3) reversed the inhibition of hepatic remnant uptake and normalized plasma cholesterol. A thyroid hormone analogue with decreased hypermetabolic side-effects, L-94901, attenuated plasma cholesterol and improved but did not normalize remnant clearance. Emulsions incubated with plasma from hypothyroid rats had a decreased ratio of apolipoprotein E/apolipoprotein C compared with control rats or hypothyroid rats treated with T3. The change in the apolipoprotein E/apolipoprotein C ratio probably accounts for the defect in remnant clearance in hypothyroidism.
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WATTS, G. F., D. C. F. CHAN, P. H. R. BARRETT, I. J. MARTINS, and T. G. REDGRAVE. "Preliminary experience with a new stable isotope breath test for chylomicron remnant metabolism: a study in central obesity." Clinical Science 101, no. 6 (November 20, 2001): 683–90. http://dx.doi.org/10.1042/cs1010683.
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We aimed to investigate the metabolism of chylomicron remnants in the postabsorptive state employing a new stable isotope breath test in centrally obese men without overt hyperlipidaemia. Groups of 12 centrally obese and 12 non-obese men of similar age and with similar plasma cholesterol and triacylglycerol (triglyceride) levels were studied. The catabolism of chylomicron remnants was measured using an intravenous injection of a remnant-like emulsion containing cholesteryl [13C]oleate. Isotopic enrichment of 13CO2 in breath was determined using isotope-ratio mass spectrometry, and a multi-compartmental model (SAAM II program) was used to estimate the fractional catabolic rate (FCR) of the chylomicron remnant-like particles. The plasma concentrations of low-density lipoprotein (LDL)-cholesterol, non-high-density lipoprotein (HDL)-cholesterol and insulin were significantly higher (P < 0.05) in the obese than the control subjects. The obese subjects had significantly lower HDL-cholesterol (P < 0.05) and, in particular, a decreased FCR of the remnant-like particles compared with lean subjects (0.061±0.014 and 0.201±0.048pools/h respectively; P = 0.016). In the obese group, the FCR of remnant-like particles was inversely associated with the waist/hip ratio, and with plasma triacylglycerol, cholesterol, LDL-cholesterol and non-HDL-cholesterol levels. In multiple regression analysis, the waist/hip ratio was the best predictor of the FCR of the emulsion. In conclusion, this new test suggests that postabsorptive chylomicron remnant catabolism is impaired in centrally obese subjects without overt hyperlipidaemia. This defect may be due to the degree of adiposity.
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Chan, Dick C., Gerald F. Watts, P. Hugh Barrett, John CL Mamo, and Trevor G. Redgrave. "Markers of Triglyceride-rich Lipoprotein Remnant Metabolism in Visceral Obesity." Clinical Chemistry 48, no. 2 (February 1, 2002): 278–83. http://dx.doi.org/10.1093/clinchem/48.2.278.
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Abstract Background: Triglyceride-rich lipoprotein remnants are atherogenic, and this may be particularly important in visceral obesity. We investigated remnant metabolism in obese men by measuring remnant-like particle-cholesterol (RLP-C), apolipoprotein (apo) B-48, apoC-III, and the clearance of a labeled remnant-like emulsion. Methods: Fasting RLP-C, apoB-48, and apoC-III concentrations were measured in 48 viscerally obese men and 10 lean controls. RLP-C was determined by immunoseparation assay, apoB-48 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and enhanced chemiluminescence, and apoC-III by immunoturbidimetric assay. The catabolism of chylomicron remnants was measured by intravenous injection of a remnant-like emulsion containing cholesteryl [13C]oleate, with isotopic enrichment of 13CO2 in breath determined by isotope-ratio mass spectrometry and a multicompartmental model to estimate fractional catabolic rate (FCR) of the emulsion. Results: Compared with controls, obese men had significantly increased plasma concentrations of RLP-C, apoB-48, and apoC-III (P <0.001 for all). Plasma total apoB-100, non-HDL-cholesterol, LDL-cholesterol, triglycerides, and insulin resistance (HOMA score) were also significantly higher in the obese group (P <0.001 for all). Obese men had a significantly lower FCR of the remnant-like emulsion compared with controls (P = 0.020). Conclusions: Viscerally obese individuals have insulin resistance and increased plasma concentrations of triglyceride-rich lipoprotein remnants, which may be attributable to decreased catabolism of these particles.
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McPherson, Ruth. "Remnant Cholesterol." Journal of the American College of Cardiology 61, no. 4 (January 2013): 437–39. http://dx.doi.org/10.1016/j.jacc.2012.11.009.
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Bowler, A., T. G. Redgrave, and J. C. L. Mamo. "Chylomicron-remnant clearance in homozygote and heterozygote Watanabe-heritable-hyperlipidaemic rabbits is defective. Lack of evidence for an independent chylomicron-remnant receptor." Biochemical Journal 276, no. 2 (June 1, 1991): 381–86. http://dx.doi.org/10.1042/bj2760381.
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Lymph chylomicrons radiolabelled in triacylglycerol and cholesteryl ester were injected into control and Watanabe heritable-hyperlipidaemic (WHHL) rabbits. Clearance of chylomicrons was slower in heterozygote and homozygote WHHL rabbits. Slower remnant clearance in WHHL rabbits was confirmed by monitoring the clearance from plasma of preformed chylomicron remnants. Use of chylomicron-like lipid emulsions injected into control and WHHL rabbits also confirmed the defect in remnant clearance in heterozygote WHHL and homozygote WHHL groups. Clearance from plasma of emulsion triolein was delayed in both WHHL groups compared with controls, owing to slower remnant clearance. The clearance from plasma of radioiodinated rabbit low-density lipoproteins (LDL) in heterozygote WHHL rabbits was the same as control rabbits. Defective chylomicron-remnant removal but normal LDL clearance in the heterozygote WHHL corresponded to elevated concentrations of plasma triacylglycerol and normal concentrations of plasma cholesterol. Receptor versus non-receptor clearances of chylomicron remnants were studied by comparing the clearance of emulsions with and without unesterified cholesterol respectively. Unlike control rabbits, there were no significant differences in the clearances of the two emulsion types in either the homozygote or heterozygote WHHL rabbits, indicating that the apolipoprotein-B100/E receptor is the primary route for clearance of chylomicron remnants from plasma.
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Langsted, Anne, Anne Marie Reimer Jensen, Anette Varbo, and Børge G. Nordestgaard. "Low High-Density Lipoprotein Cholesterol to Monitor Long-Term Average Increased Triglycerides." Journal of Clinical Endocrinology & Metabolism 105, no. 4 (December 11, 2019): e1657-e1666. http://dx.doi.org/10.1210/clinem/dgz265.
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Abstract Context Increased triglyceride-rich remnants represent a causal risk factor for ischemic cardiovascular disease. Objective We tested the hypothesis that low high-density lipoprotein (HDL) cholesterol can be used to monitor long-term high triglycerides/remnant cholesterol, just as high hemoglobin A1c (HbA1c) can be used to monitor long-term high glucose levels. Design, Setting, Participants, and Interventions We studied cross-sectionally 108 731 individuals, dynamically 1313 individuals with lipid measurement at 10 repeated visits, short-term 305 individuals during a fat load, and long-term 10 479 individuals with 2 lipid measurements 10 years apart. Main Outcome Measures Levels of HDL cholesterol and triglycerides. Results Cross-sectionally, HDL cholesterol was inversely associated with triglycerides (R2 = 0.26) and remnant cholesterol (R2 = 0.26). Dynamically, major changes in triglyceride levels from measurement to measurement were mimicked by corresponding modest changes in HDL cholesterol. In the short-term after a fat load, median triglycerides increased 96% while HDL cholesterol decreased only 1%. Long-term, in individuals with measurements 10 years apart, those who initially had the highest triglycerides and corresponding lowest HDL cholesterol, still had highest triglycerides and lowest HDL cholesterol 10 years later. Prospectively, individuals with increased triglycerides/remnant cholesterol had increased risk of myocardial infarction; however, when the HDL cholesterol monitoring was removed, increased triglycerides/remnant cholesterol were largely no longer associated with increased risk of myocardial infarction. Conclusions Low HDL cholesterol is a stable marker of average high triglycerides/remnant cholesterol. This suggests that low HDL cholesterol can be used to monitor long-term average high triglycerides and remnant cholesterol, analogous to high HbA1c as a long-term monitor of average high glucose levels.
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Lambert, M. S., K. M. Botham, and P. A. Mayes. "Variations in composition of dietary fats affect hepatic uptake and metabolism of chylomicron remnants." Biochemical Journal 310, no. 3 (September 15, 1995): 845–52. http://dx.doi.org/10.1042/bj3100845.
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The hepatic metabolism of [1-14C]oleate- and [1,2-3H]cholesterol-dual-labelled chylomicron remnants derived from olive, corn, palm and fish oil and butter fat was compared by adding each lipoprotein separately to the perfusate of isolated livers from rats fed on a normal diet. Labelled remnants from butter fat and fish oil were removed more rapidly from the perfusate than remnants derived from olive, corn and palm oil. The oxidation of labelled remnant fatty acid from olive oil, fish oil or butter fat was four to seven times greater than that from corn and palm oil. Labelled fatty acid in fish oil remnants was incorporated into phospholipid significantly more efficiently than the labelled fatty acid in olive, corn or palm oil remnants, with butter fat giving an intermediate value. For all the remnants, there was a significant amount of hydrolysis of labelled esterified cholesterol by the liver which was dependent on the magnitude of hepatic uptake of each type of remnant. The recovery of remnant [3H]cholesterol label in the bile was 50% less with palm oil remnants than with all the other remnants studied. The results indicate that the fatty acid composition of chylomicron remnants has a major impact on their uptake and metabolism by the liver.
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Miyauchi, Kazuhito, Norihiko Kayahara, Masato Ishigami, Hideyuki Kuwata, Hideharu Mori, Hiroyuki Sugiuchi, Tetsumi Irie, Akira Tanaka, Shizuya Yamashita, and Taku Yamamura. "Development of a Homogeneous Assay to Measure Remnant Lipoprotein Cholesterol." Clinical Chemistry 53, no. 12 (December 1, 2007): 2128–35. http://dx.doi.org/10.1373/clinchem.2007.092296.
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Abstract Background: Quantification of triglyceride-rich lipoprotein (TRL) remnants is useful for risk assessment of coronary artery disease and the diagnosis of type III hyperlipoproteinemia. Although an immunoseparation procedure for remnant-like particle cholesterol has been evaluated extensively in recent years, available methods for measuring TRL remnants have not achieved wide use in routine laboratory practice, suggesting a need for a homogeneous assay that can measure TRL remnant cholesterol in serum or plasma without pretreatment. Methods: We screened for suitable surfactants that exhibited favorable selectivity toward the VLDL remnant (VLDLR) fraction, including intermediate-density lipoproteins (IDLs). We investigated the principal characteristics of this assay by gel filtration of lipoproteins and their particle size distribution. We developed a simple assay and evaluated its performance with the Hitachi-7170 analyzer. Results: Polyoxyethylene-polyoxybutylene block copolymer (POE-POB) exhibited favorable selectivity toward VLDLR and IDL fractions. POE-POB removed apolipoprotein (apo) E and apo C-III from IDL particles in the presence of cholesterol esterase (CHER), and the particle size distribution of IDLs became smaller after the reaction. These results revealed that IDL particles are specifically modified in the presence of CHER and POE-POB, making their component cholesterol available for enzymatic assay. Addition of phospholipase D improved the reactivity toward chylomicron remnants (CMRs). We found a high correlation [y = 1.018x− 0.01 mmol/L, r = 0.962 (n = 160)] between the proposed assay and the immunoseparation assay in serum from healthy individuals. Conclusion: The homogeneous assay described in this report can measure TRL remnant cholesterol, including CMRs, VLDLRs, and IDLs, with high sensitivity and specificity.
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CHAN, Dick C., Gerald F. WATTS, P. Hugh R. BARRETT, Frans H. O'NEILL, Trevor G. REDGRAVE, and Gilbert R. THOMPSON. "Relationships between cholesterol homoeostasis and triacylglycerol-rich lipoprotein remnant metabolism in the metabolic syndrome." Clinical Science 104, no. 4 (March 14, 2003): 383–88. http://dx.doi.org/10.1042/cs1040383.
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The dysmetabolic syndrome of insulin resistance and visceral obesity is characterized by elevated plasma concentration of triacylglycerol-rich lipoprotein (TRL) remnants that may be related to increased cardiovascular risk. Perturbed hepato-intestinal cholesterol metabolism may play a contributory role in this abnormality. We therefore investigated the association between plasma markers of cholesterol absorption and synthesis with TRL remnant metabolism in 35 men with the metabolic syndrome (MS). Plasma campesterol:cholesterol and lathosterol:cholesterol ratios were measured as estimates of cholesterol absorption and synthesis respectively. Remnant metabolism was assessed by measuring remnant-like particle-cholesterol (RLP-C), apolipoprotein (apo)B-48 and the fractional catabolic rate (FCR) of a labelled remnant-like emulsion. Compared with controls, subjects with the MS had significantly lower plasma campesterol:cholesterol ratio, but higher lathosterol:cholesterol ratio (P<0.05). Plasma RLP-C and apoB-48 concentrations were also higher (P<0.01) and the remnant-like emulsion FCR was lower (P<0.05). The plasma campesterol:cholesterol ratio was inversely correlated (P<0.05) with plasma triacylglycerols (r =-0.346), RLP-C (r =-0.443), apoB-48 (r =-0.427) and plasma lathosterol:cholesterol ratio (r =-0.366); the campesterol:cholesterol ratio was also positively correlated with the remnant-like emulsion FCR (r = 0.398, P<0.05). In multiple regression analysis, the significant correlations between plasma campesterol:cholesterol ratio and plasma triacylglycerols, RLP-C, apoB-48 and FCR of the remnant-like emulsion were independent of age, dietary energy and plasma lathosterol. Our findings suggest that in subjects with the MS alterations in cholesterol absorption and synthesis may be closely linked with the kinetic defects in TRL metabolism.
Dissertations / Theses on the topic "Remnant cholesterol"
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SULTAN, FABRICE. "Lipase hepatique chez le rat : role dans le metabolisme des remnants de chylomicrons et regulation par le cholesterol alimentaire." Paris 7, 1990. http://www.theses.fr/1990PA077097.
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Le role de la lipase hepatique (lh) dans le metabolisme des lipoproteines et plus particulierement dans celui des remnants de chylomicrons (rm) est encore mal compris. La premiere partie de cette etude a ete de rechercher si la lh etait impliquee dans le metabolisme des rm. Les rm marques au cholesterol (#3h) ou au cholesteryl-ether (#1#4c) puis co-incubes avec la lh, sont plus efficacement captes par des hepatocytes que les rm temoins (+50% a 100%). L'utilisation d'un anticorps anti-lh nous a permis de confirmer la specificite de la lh dans ce processus. Des rm traites par de la lh, puis injectes a des rats, subissent un captage majore (+36%). Apres immuno-inhibition de la lh, l'epuration des rm est diminuee (t 1/2=5,55 vs 2,98 min) et leur captation hepatique est abaisse (22,8 vs 45%). Le traitement des rm par la lh, s'accompagne d'une baisse des triglycerides (24%) et des phospholipides (36%). L'apo e, principal determinant de la liaison des rm, n'est pas modifiee apres hydrolyse. La liaison de rm traites par la lh, a des membranes plasmiques de foie est majoree (2 a 3 fois) mais avec une plus faible affinite. Ces resultats indiquent clairement que la lh est active dans le captage des rm par le foie. Dans la seconde partie de ce travail, nous avons recherche les effets d'un regime cholesterol sur la regulation de la lh. Apres un tel regime, sont diminuees: l'activite (1,4 fois), la proteine-enzyme (1,7 fois) et les arnm (2 a 4 fois). Ces donnees originales indiquent un effet regulateur du cholesterol alimentaire sur la lh
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Warnakula, Samantha. "The role of ezetimibe and simvastatin in modulating intestinal cholesterol transport, chylomicron profile and chylomicron-remnant uptake by the arterial wall in a rodent model of the metabolic syndrome." Master's thesis, 2010. http://hdl.handle.net/10048/1374.
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Intestinally derived chylomicron remnants (CM-r) may contribute to atherogenic dyslipidemia during the Metabolic Syndrome (Mets). However, the combined effects of ezetimibe (EZ) and simvastatin (SV) on post-prandial (PP) dyslipidemia during MetS remains unclear, nor is it known whether the combination has a synergistic anti-atherogenic effect on CM-r arterial retention. The first objective was to delineate the effects of EZ+SV therapy on intestinal cholesterol flux and CM PP metabolism in the JCR:LA-cp rat, a model of MetS. The second objective was to quantify the impact of EZ+SV therapy on arterial retention of CM-r and subsequent myocardial lesion development in the JCR:LA-cp rat. EZ+SV therapy decreased net intestinal cholesterol absorption in MetS rats. Furthermore, EZ+SV therapy reduced arterial retention of CM-r and frequency of myocardial lesions in MetS rats. In conclusion, EZ+SV therapy reduces arterial retention of CM-r and myocardial lesion development possibly through its beneficial effects on cholesterol transport and PP-metabolism.Nutrition and Metabolism
Books on the topic "Remnant cholesterol"
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Wiklund, Olov, and Jan Borén. Pathogenesis of atherosclerosis: lipid metabolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0011.
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Lipids are carried in plasma as microparticles, lipoproteins, composed of a core of hydrophobic lipids and a surface of amphipathic lipids. In addition, the particles carry proteins (i.e. apolipoproteins). The proteins have key functions in the metabolism as receptor ligands, enzymes or activators. Lipoproteins are classified based on density into: chylomicrons, VLDL, IDL, LDL, and HDL. Retention of apoB-containing lipoproteins (LDL, IDL, and VLDL) in the arterial intima is the initiating event in the development of atherosclerosis. Retention is mediated by binding of apoB to structural proteoglycans in the intima. Increased plasma concentration of apoB-containing lipoproteins is the main risk factor for atherosclerotic cardiovascular disease (CVD) and the causative role of LDL has been demonstrated in several studies. Lp(a) is a subclass of LDL and elevated Lp(a) is an independent risk-factor, primarily genetically mediated. Genetic data support that high Lp(a) causes atherosclerosis. Elevated triglycerides in plasma are associated with increased risk for CVD. Whether triglycerides directly induce atherogenesis is still unclear, but current data strongly support that remnant particles from triglyceride-rich lipoproteins are causal. HDL are lipoproteins that have been considered to be important for reversed cholesterol transport. Low HDL is a strong risk-factor for CVD. However, the causative role of HDL is debated and intervention studies to raise HDL have not been successful. Reduction of LDL is the main target for prevention and treatment, using drugs that inhibit the enzyme HMG-CoA reductase, i.e. statins. Other drugs for LDL reduction and to modify other lipoproteins may further reduce risk, and new therapeutic targets are explored.
Book chapters on the topic "Remnant cholesterol"
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Nordestgaard, Børge G., and Anette Varbo. "Triglyceride-rich Lipoprotein Cholesterol (Remnant Cholesterol) as a Therapeutic Target for Cardiovascular Disease Risk." In Contemporary Cardiology, 139–58. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-56514-5_8.
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Wadström, Benjamin Nilsson, Anders Berg Wulff, Kasper Mønsted Pedersen, and Børge Grønne Nordestgaard. "Triglyceride- and Cholesterol-Rich Remnant Lipoproteins in Risk of Cardiovascular Disease in Diabetes Mellitus." In Contemporary Diabetes, 195–222. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-26681-2_8.
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Cegla, Jaimini, and James Scott. "Lipid disorders." In Oxford Textbook of Medicine, edited by Timothy M. Cox, 2055–97. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0232.
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High blood cholesterol and high blood triglycerides are causal risk factors for atherosclerotic cardiovascular disease, which remains the leading cause of death in the developed world. Lipid and lipoprotein metabolism—cholesterol, triglycerides, and fat-soluble vitamins are transported with specific proteins in the blood as multimeric complexes called lipoproteins. Lipid and lipoprotein metabolism are effected by three principal physiological processes: (1) intestinal absorption of dietary lipid and transport in the blood of dietary lipid and lipids, principally derived from the liver (as triglyceride-rich lipoproteins) to peripheral tissues for catabolism by skeletal and cardiac muscle or storage in adipose tissue; (2) return of triglyceride-rich lipoprotein remnants to the liver, hepatic synthesis of low-density lipoprotein, and the transport of cholesterol between peripheral tissues and the liver; and (3) reverse cholesterol transport by high-density lipoprotein (HDL) between peripheral tissues and the liver. Dyslipidaemias are disorders of lipoprotein metabolism in which there is elevation of total cholesterol and/or triglycerides, often accompanied by reduced levels of HDL cholesterol. Causes of dyslipidaemia—particular lipid disorders including polygenic hypercholesterolaemia, familial hypercholesterolaemia, combined hypercholesterolaemia and hypertriglyceridaemia, familial combined hyperlipidaemia, familial dysbetalipoproteinaemia (also called type 3 hyperlipoproteinaemia), and severe hypertriglyceridaemia, as well as secondary or aggravating factors. Management of dyslipidaemia—the key questions are: (1) what classes of lipoproteins and lipids are increased or decreased in the patient’s plasma? (2) Does the patient has a primary (genetic) or secondary (acquired) dyslipidaemia (often contributions from both influences)? (3) Is the patient at risk of atherosclerotic cardiovascular disease or acute pancreatitis? (4) What other risk factors (e.g. hypertension or diabetes) are present? (5) What treatments might be used to address these abnormalities?
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Joner, Michael, Maria Isabel Castellanos, Anna Bulin, and Kristin Steigerwald. "Pathology of stable coronary artery disease." In ESC CardioMed, edited by William Wijns, 1315–20. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0325.
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Coronary artery disease remains the major cause of morbidity and mortality on a global scale. Intimal thickening and fatty streaks represent early adaptive vascular changes, which are often regressive. Pathological intimal thickening represents the earliest progressive atherosclerotic lesion characterized by a focal accumulation of smooth muscle cells and acellular areas, often associated with lipid pools. Fibroatheroma is characterized by a necrotic core and can be split into early and late fibroatheroma, where macrophage apoptosis and defective efferocytosis play important roles in lesion progression. Intraplaque hypoxia is believed to result in neovascularization with subsequent intraplaque haemorrhage because of immature and leaky microvessels. Due to excessive cholesterol in remnants of erythrocyte membranes, intraplaque haemorrhage may result in rapid progression of necrotic core and plaque destabilization. Healed plaque rupture has been well delineated as an important mechanism of gradual luminal narrowing, where changes in collagen deposition allow recognition of rupture and healing sites. Calcification results from apoptosis of smooth muscle cells and macrophages or may also be caused by active release of cellular vesicles involved in calcium haemostasis. Extracellular matrix changes are associated with progression of atherosclerosis, while integrin signalling has been recognized as an important outside-in transcellular target of the inflammatory response.
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Joner, Michael, Maria Isabel Castellanos, Anna Bulin, and Kristin Steigerwald. "Pathology of stable coronary artery disease." In ESC CardioMed, edited by William Wijns, 1315–20. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0325_update_001.
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Coronary artery disease remains the major cause of morbidity and mortality on a global scale. Intimal thickening and fatty streaks represent early adaptive vascular changes, which are often regressive. Pathological intimal thickening represents the earliest progressive atherosclerotic lesion characterized by a focal accumulation of smooth muscle cells and acellular areas, often associated with lipid pools. Fibroatheroma is characterized by a necrotic core and can be split into early and late fibroatheroma, where macrophage apoptosis and defective efferocytosis play important roles in lesion progression. Intraplaque hypoxia is believed to result in neovascularization with subsequent intraplaque haemorrhage because of immature and leaky microvessels. Due to excessive cholesterol in remnants of erythrocyte membranes, intraplaque haemorrhage may result in rapid progression of necrotic core and plaque destabilization. Healed plaque rupture has been well delineated as an important mechanism of gradual luminal narrowing, where changes in collagen deposition allow recognition of rupture and healing sites. Calcification results from apoptosis of smooth muscle cells and macrophages or may also be caused by active release of cellular vesicles involved in calcium haemostasis. Extracellular matrix changes are associated with progression of atherosclerosis, while integrin signalling has been recognized as an important outside-in transcellular target of the inflammatory response.
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Erbel, Raimund. "Aortic sclerosis: therapy." In ESC CardioMed, edited by Raimund Erbel, 2583–89. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0613.
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Aortic sclerosis is a very common disease and is related to the atherosclerotic process which can start in young adulthood. The loss of compliance of the aortic ‘Windkessel’ is a major drawback of the disease, leading to enhanced blood pressure amplitude—elevated pulse pressure—due to a higher systolic and a lower diastolic blood pressure. The pressure pulse wave augmentation index and the pulse wave velocity increase. Ultrasound is able to visualize only limited aortic segments, whereas computed tomography and magnetic resonance imaging are the best tools to detect and quantify aortic atheromas. Nevertheless, transoesophageal echocardiography can image the descending thoracic aorta down to the coeliac trunk. An aortic atheroma, particularly one greater than 4 mm in size in the aortic arch, indicates an increased risk of stroke and other cardiovascular events. A grading is helpful. Plaque rupture is quite frequent and often found in multiple segments of the aorta indicating an increased risk of cholesterol emboli due to the wash-out of debris with or without thrombotic material. Free-floating structures, possible remnants of fibrous cap, are found as well as mobile thrombi. Calcification of the thoracic aorta is often found when coronary artery calcification is present, but may be present when coronary artery calcification is absent. Risk prediction of events is, however, not improved. Therapy for aortic sclerosis is based on common and recent guidelines for prevention and treatment of risk factors. Endovascular or surgical interventions are limited to rare situation in which blood flow is not preserved.