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Nature of Flow of a Liquid
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Both low high-density (Stamos and Rosenson, 1999) and high low-density (Rosenson and Lowe, 1998) lipoprotein levels are associated with elevated plasma viscosity. In patients with hyperlipoproteinemia, the risk can be reduced by aggressive lipid-lowering therapy (Braunwald, 1997a; Braunwald, 1997b). Low-density lipoprotein (LDL) immunophoresis is an excellent therapeutic option in patients with familial hypercholesterolemia: long-term LDL apheresis treatment is known to reduce plasma LDL cholesterol and plasma viscosity (Otto et al., 2002). Agents such as statins and gembibrozil that lower LDL and triglycerides, respectively, improve cardiovascular risk and may lower plasma viscosity (Stein and Rosenson, 1998; Banyai et al., 2001). C-reactive protein, a sensitive indicator of inflammation and cardiovascular risk, is positively associated with plasma fibrinogen and viscosity (Mendall et al., 2000) and is significantly reduced by pravastatin (Ridker et al., 1999). Also, hormone replacement therapy improves cardiovascular risk by lowering plasma viscosity in postmenopausal women (Rosenson et al., 1998).
Lipoprotein lipase deficiency/type I hyperlipoproteinemia
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
Lipoprotein electrophoresis yields a characteristic chylomicron band at the origin. The type I pattern can be demonstrated by electrophoresis or ultracentrifugation as consisting exclusively, or nearly so, of chylomicrons (Table 86.1). The very low-density lipoproteins (VLDL) are normal or slightly increased and the LDL and HDL are usually depressed. Treatment with a low-fat, high-carbohydrate diet usually leads, as chylomicrons fall, to an increase toward normal of LDL and increased levels of VLDL, but those of HDL remain low. The diagnosis of type I hyperlipoproteinemia is often confirmed by the elimination of fat from the diet, after which the chylomicrons disappear from the blood within a few days and triglyceride concentrations fall to 200–400 mg/dL. Most pediatric patients with hyperchylomicronemia have type I hyperlipoproteinemia. Most patients with type V are adults. However, childhood type V hyperlipoproteinemia has been reported [32], and patients with classic lipoprotein lipase deficiency sometimes have a type V pattern with time. Incubation of plasma in 3 percent polyvinylpyrrolidone will separate chylomicrons from other lipoproteins and is thus useful for the diagnosis of hyperchylomicronemia.
The Cardiovascular System and its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Pharmacists studying cardiovascular terminology should not ignore the disorders that seemed to come to the fore of American consciousness in the 1990s as a major risk factor in a large number of other cardiovascular disorders—dyslipidemias. Formerly, the term hyperlipidemia was the most commonly used since it describes an excess lipid level in the blood, which was the distinguishing characteristic of the entire group or disorders; then hypercholesterolemia became the more common term since cholesterol seemed to be the most significant chemical involved in the negative sequelae. Even the more specific term hyperlipoproteinemia has been used extensively since the excessive components are lipoproteins.
The clinical and laboratory investigation of dysbetalipoproteinemia
Published in Critical Reviews in Clinical Laboratory Sciences, 2020
Christopher S. Boot, Ahai Luvai, Robert D. G. Neely
Another suggested approach to distinguishing hyperlipoproteinemia sub-types, including FDBL, with straightforward laboratory tests is to use a stepwise algorithm incorporating apo B, TC and TG. One algorithm uses a total TG cutoff followed by a TC/apo B ratio cutoff and finally a TG/apo B ratio to identify cases of FDBL. This algorithm was applied to patients with a range of hyperlipoproteinemia subtypes (38 dysbetalipoproteinemia, 16 type I, 736 type IIa, 371 type IIb, 509 type IV, 101 type V). If TG was lower than the 75th percentile for gender and age, subjects were designated as type IIa. If TG was greater than the 75th percentile, the TC/apo B ratio was determined: if the TC/apo B ratio was less than 6.2 mmol/g, subjects were designated as type IIb or type IV, while if it was greater than 6.2 mmol/g, subjects were separated according to their TG/apo B ratio. Those with TG/apo B greater than 10 were classified as type I or type V and those with TG/apo B less than 10 were classified as having FDBL. Using this approach, the ROC area under the curve as a diagnostic test for FDBL was very high at 0.988. A second algorithm, designed to identify all hyperlipoproteinemia phenotypes including FDBL, used cutoffs for apo B followed by TG, TG/apo B then TC/apo B [50]. In this algorithm the following criteria were applied stepwise to identify dysbetalipoproteinemia: apo B < 1.2 g/L, TG ≥1.5 mmol/L, TG/apo B < 10 mmol/g, then TC/apo B ≥ 6.2 mmol/g.
Optimization and evaluation of lyophilized fenofibrate nanoparticles with enhanced oral bioavailability and efficacy
Published in Pharmaceutical Development and Technology, 2018
Ahmed H. Ibrahim, Hany M. Ibrahim, Hatem R. Ismael, Ahmed M. Samy
Hyperlipidemia is a medical condition associated with abnormal elevation in the level of any or all lipids in the blood including cholesterol (hypercholesterolemia), triglyceride (hypertriglyceridemia) and lipoprotein (hyperlipoproteinemia) focused on low-density lipoprotein (LDL), or “bad” cholesterol. Hyperlipidemia is considered as one of the major risk factors in developing hepatic failure, atherosclerosis and atherosclerosis-associated disease including coronary heart disease, cerebrovascular disease and peripheral vascular disease. About 73.5 million adults (31.7%) in the United States have high level of bad cholesterol which necessitate patients to receive treatments (Keating & Croom 2007).
Lipoprotein(a) in atherosclerosis: from pathophysiology to clinical relevance and treatment options
Published in Annals of Medicine, 2020
Andreja Rehberger Likozar, Mark Zavrtanik, Miran Šebeštjen
Higher plasma levels of Lp(a) have been linked to increased risk of CVD, and especially of MI, stroke, and aortic valve stenosis due to calcification [46]. This risk is usually increased two-fold for patients who have mostly small apo(a) isoforms (which are smaller due to the lower levels of KIV subtype 2), as this leads to rapid production of, and thus higher levels of, Lp(a). Also, patients who have FH have greater risk of developing CVD [62]. According to the 2019 European Society of Cardiology/European Atherosclerosis Society guidelines, Lp(a) measurements should be considered at least once in the lifetime of each adult, to identify those with very high inherited Lp(a) levels (>180 mg/dL; >430 nmol/L). These people might have a lifetime risk of atherosclerotic CVD that is equivalent to that associated with heterozygous FH [10]. The 2016, the Canadian Cardiovascular Society guidelines for the management of dyslipidemia suggested that Lp(a) might aid risk assessment in subjects at intermediate Framingham risk or with a family history of premature CAD. Particular attention should be given to individuals with Lp(a) levels >30 mg/dL, for whom CVD risk is increased by approximately two-fold [63]. The 2018 American College of Cardiology/American Heart Association guidelines on blood cholesterol defined Lp(a) ≥50 mg/dL, or ≥125 nmol/L, as a risk-enhancing factor; according to their guidelines, this is a relative indication for its measurement with a family history of premature CVD. HEART UK recommended that Lp(a) is only measured in specific cohorts, rather than in all adults, to identify those with a lower Lp(a) threshold than 430 nmol/L. They recommended the management of Lp(a)-associated risk in those with Lp(a) levels >90 nmol/L. They also recommend measuring Lp(a) levels in patients with personal or family history of premature atherosclerotic CVD (<60 years of age), in those with FH or other genetic dyslipidemias (e.g. familial combined hyperlipidaemia, familial dysbetalipoproteinemia, familial hypertriglyceridaemia), in those whose first-degree relative has Lp(a) levels >200 nmol/L, in those who have calcific aortic valve stenosis, and in those with borderline increased (but <15%) 10-year risk of CV events [13]. A single measurement of serum Lp(a) appears sufficient for cardiovascular risk assessment [13, 63], as for most patients repeat measurement is only indicated if a secondary cause is suspected (e.g. chronic kidney disease, nephrotic proteinuria, hypothyroidism, liver disease) or if therapeutic measures to lower levels have been introduced [13]. Hyperlipoproteinemia(a) should be considered as a hereditary and quantitative risk factor that can be mitigated by controlling the CV risk factors, and in particular by reduction of Lp(a) levels by treatment [64].