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Coronary artery disease (CAD), also called coronary heart disease (CHD), ischemic heart disease (IHD), or simply heart disease, involves the reduction of blood flow to the heart muscle due to build-up of plaque (atherosclerosis) in the arteries of the heart. It is the most common of the cardiovascular diseases. Types include stable angina, unstable angina, myocardial infarction, and sudden cardiac death. A common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw. Occasionally it may feel like heartburn. Usually symptoms occur with exercise or emotional stress, last less than a few minutes, and improve with rest. Shortness of breath may also occur and sometimes no symptoms are present. In many cases, the first sign is a heart attack. Other complications include heart failure or an abnormal heartbeat.
Cholesterol is an organic molecule. It is a sterol, a type of lipid. Cholesterol is biosynthesized by all animal cells and is an essential structural component of animal cell membranes. It is a yellowish crystalline solid.
High-density lipoprotein (HDL) is one of the five major groups of lipoproteins. Lipoproteins are complex particles composed of multiple proteins which transport all fat molecules (lipids) around the body within the water outside cells. They are typically composed of 80–100 proteins per particle and transporting up to hundreds of fat molecules per particle.
Low-density lipoprotein (LDL) is one of the five major groups of lipoprotein which transport all fat molecules around the body in the extracellular water. These groups, from least dense to most dense, are chylomicrons, very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein and high-density lipoprotein (HDL). LDL delivers fat molecules to cells. LDL is involved in atherosclerosis, a process in which it is oxidized within the walls of arteries.
A lipoprotein is a biochemical assembly whose primary function is to transport hydrophobic lipid molecules in water, as in blood plasma or other extracellular fluids. They consist of a Triglyceride and Cholesterol center, surrounded by a phospholipid outer shell, with the hydrophilic portions oriented outward toward the surrounding water and lipophilic portions oriented inward toward the lipid center. A special kind of protein, called apolipoprotein, is embedded in the outer shell, both stabilising the complex and giving it a functional identity that determines its fate.
Very-low-density lipoprotein (VLDL), density relative to extracellular water, is a type of lipoprotein made by the liver. VLDL is one of the five major groups of lipoproteins that enable fats and cholesterol to move within the water-based solution of the bloodstream. VLDL is assembled in the liver from triglycerides, cholesterol, and apolipoproteins. VLDL is converted in the bloodstream to low-density lipoprotein (LDL) and intermediate-density lipoprotein (IDL). VLDL particles have a diameter of 30–80 nm. VLDL transports endogenous products, whereas chylomicrons transport exogenous (dietary) products. In the early 2010s both the lipid composition and protein composition of this lipoprotein were characterised in great detail.
Hypercholesterolemia, also called high cholesterol, is the presence of high levels of cholesterol in the blood. It is a form of hyperlipidemia, high blood lipids, and hyperlipoproteinemia.
Intermediate-density lipoproteins (IDLs) belong to the lipoprotein particle family and are formed from the degradation of very low-density lipoproteins as well as high-density lipoproteins. IDL is one of the five major groups of lipoproteins that enable fats and cholesterol to move within the water-based solution of the bloodstream. Each native IDL particle consists of protein that encircles various lipids, enabling, as a water-soluble particle, these lipids to travel in the aqueous blood environment as part of the fat transport system within the body. Their size is, in general, 25 to 35 nm in diameter, and they contain primarily a range of triacylglycerols and cholesterol esters. They are cleared from the plasma into the liver by receptor-mediated endocytosis, or further degraded by hepatic lipase to form LDL particles.
Hyperlipidemia is abnormally elevated levels of any or all lipids or lipoproteins in the blood. Hyperlipidemia is an umbrella term that refers to acquired or genetic disorders that result in high levels of lipids circulating in the blood. This disease is usually chronic and requires ongoing medication to control blood lipid levels.
The low-density lipoprotein (LDL) receptor (LDL-R) is a mosaic protein of 839 amino acids that mediates the endocytosis of cholesterol-rich LDL. It is a cell-surface receptor that recognizes the apoprotein B100, which is embedded in the outer phospholipid layer of LDL particles. The receptor also recognizes the apoE protein found in chylomicron remnants and VLDL remnants (IDL). In humans, the LDL receptor protein is encoded by the LDLR gene on chromosome 19. It belongs to the low density lipoprotein receptor gene family. It is most significantly expressed in bronchial epithelial cells and adrenal gland and cortex tissue.
Apolipoprotein B (ApoB) is a protein that in humans is encoded by the APOB gene.
Familial hypercholesterolemia (FH) is a genetic disorder characterized by high cholesterol levels, specifically very high levels of low-density lipoprotein, in the blood and early cardiovascular disease.The most common mutations diminish the number of functional LDL receptors in the liver. Since the underlying body biochemistry is slightly different in individuals with FH, their high cholesterol levels are less responsive to the kinds of cholesterol control methods which are usually more effective in people without FH. Nevertheless, treatment is usually effective.
Lecithin cholesterol acyltransferase deficiency is a disorder of lipoprotein metabolism. The disease has two forms: Familial LCAT deficiency, in which there is complete LCAT deficiency, and Fish-eye disease, in which there is a partial deficiency.
Lipoprotein(a) is a low-density lipoprotein variant containing a protein called apolipoprotein(a). Genetic and epidemiological studies have identified lipoprotein(a) as a risk factor for atherosclerosis and related diseases, such as coronary heart disease and stroke.
Blood lipids are lipids in the blood, either free or bound to other molecules. They are mostly transported in a protein capsule, and the density of the lipids and type of protein determines the fate of the particle and its influence on metabolism. The concentration of blood lipids depends on intake and excretion from the intestine, and uptake and secretion from cells. Hyperlipidemia is the presence of elevated or abnormal levels of lipids and/or lipoproteins in the blood, and is a major risk factor for cardiovascular disease.
Apolipoprotein A-V is a protein that in humans is encoded by the APOA5 gene on chromosome 11. It is significantly expressed in liver. The protein encoded by this gene is an apolipoprotein and an important determinant of plasma triglyceride levels, a major risk factor for coronary artery disease. It is a component of several lipoprotein fractions including VLDL, HDL, chylomicrons. It is believed that apoA-V affects lipoprotein metabolism by interacting with LDL-R gene family receptors. Considering its association with lipoprotein levels, APOA5 is implicated in metabolic syndrome. The APOA5 gene also contains one of 27 SNPs associated with increased risk of coronary artery disease.
James D. Otvos, Ph.D. is an academician/researcher/entrepreneur in nuclear magnetic resonance spectroscopy who has pioneered and published, since the later 1970s, extensive research on the roles of the various lipoproteins in cardiovascular disease and lead the company, LipoScience, which developed the Vantera Analyzer.
Familial dysbetalipoproteinemia or type III hyperlipoproteinemia is a condition characterized by increased total cholesterol and triglyceride levels, and decreased HDL levels.
Lipid profile or lipid panel is a panel of blood tests that serves as an initial screening tool for abnormalities in lipids, such as cholesterol and triglycerides. The results of this test can identify certain genetic diseases and can determine approximate risks for cardiovascular disease, certain forms of pancreatitis, and other diseases.
The vertical auto profile (VAP) test is a cholesterol, lipid and lipoprotein test.
References
- 1 2 Jørgensen AB, Frikke-Schmidt R, West AS, Grande P, Nordestgaard BG, Tybjærg-Hansen A (2013). "Genetically elevated non-fasting triglycerides and calculated remnant cholesterol as causal risk factors for myocardial infarction". European Heart Journal . 34 (24): 1826–1833. doi: 10.1093/eurheartj/ehs431 . PMID 23248205.
- 1 2 Nordestgaard BG (2016). "Triglyceride-Rich Lipoproteins and Atherosclerotic Cardiovascular Disease: New Insights From Epidemiology, Genetics, and Biology". Circulation Research . 118 (4): 547–563. doi: 10.1161/CIRCRESAHA.115.306249 . PMID 26892957.
- ↑ Dallinga-Thie GM, Kroon J, Borén J, Chapman MJ (2016). "Triglyceride-Rich Lipoproteins and Remnants: Targets for Therapy?". Current Cardiology Reports. 18 (7): 67. doi:10.1007/s11886-016-0745-6. PMC 4877422 . PMID 27216847.
- ↑ Goliasch G, Wiesbauer F, Blessberger H, Demyanets S, Wojta J, Huber K, Maurer G, Schillinger M, Speidl WS (2015). "Premature myocardial infarction is strongly associated with increased levels of remnant cholesterol". Journal of Clinical Lipidology. 9 (6): 801–6.e1. doi:10.1016/j.jacl.2015.08.009. PMID 26687701.
- ↑ Masuoka H, Kamei S, Wagayama H, Ozaki M, Kawasaki A, Tanaka T, Kitamura M, Katoh S, Shintani U, Misaki M, Sugawa M, Ito M, Nakano T (2000). "Association of remnant-like particle cholesterol with coronary artery disease in patients with normal total cholesterol levels". American Heart Journal . 139 ((2 Pt 1)): 305–310. doi:10.1016/j.atherosclerosis.2008.05.024. PMID 10650304.
- ↑ Nakamura T, Kugiyama K (2006). "Triglycerides and remnant particles as risk factors for coronary artery disease". Current Atherosclerosis Reports . 8 (2): 107–110. doi:10.1007/s11883-006-0047-3. PMID 16510044.
- ↑ Chapman MJ, Ginsberg HN, Amarenco P, Andreotti F, Borén J, Catapano AL, Descamps OS, Fisher E, Kovanen PT, Kuivenhoven JA, Lesnik P, Masana L, Nordestgaard BG, Ray KK, Reiner Z, Taskinen MR, Tokgözoglu L, Tybjærg-Hansen A, Watts GF, European Atherosclerosis Society Consensus Panel (2011). "Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management". European Heart Journal . 32 (11): 1345–1361. doi:10.1093/eurheartj/ehr112. PMC 3105250 . PMID 21531743.
- ↑ Fujioka Y, Ishikawa Y (2009). "Remnant lipoproteins as strong key particles to atherogenesis". Journal of Atherosclerosis and Thrombosis. 16 (3): 145–154. doi: 10.5551/jat.E598 . PMID 19556722.
- ↑ Varbo A, Benn M, Tybjærg-Hansen A, Jørgensen AB, Frikke-Schmidt R, Nordestgaard BG (2013). "Remnant cholesterol as a causal risk factor for ischemic heart disease". Journal of the American College of Cardiology . 61 (4): 427–436. doi: 10.1016/j.jacc.2012.08.1026 . PMID 23265341.
- ↑ Varbo A, Freiberg JJ, Nordestgaard BG (2018). "Remnant Cholesterol and Myocardial Infarction in Normal Weight, Overweight, and Obese Individuals from the Copenhagen General Population Study". Clinical Chemistry . 64 (1): 219–230. doi: 10.1373/clinchem.2017.279463 . PMID 29021326.
- ↑ Varbo A, Nordestgaard BG (2014). "Remnant cholesterol and ischemic heart disease". Current Opinion in Lipidology. 25 (4): 266–273. doi:10.1097/MOL.0000000000000093. PMID 24977981.