 | This article needs more medical references for verification or relies too heavily on primary sources .(November 2021) |  |
| Vertical auto profile | |
|---|---|
| Purpose | lipoprotein test |
The vertical auto profile (VAP) test is a cholesterol, lipid and lipoprotein test.
| This article needs more medical references for verification or relies too heavily on primary sources .(November 2021) | |
| Vertical auto profile | |
|---|---|
| Purpose | lipoprotein test |
The vertical auto profile (VAP) test is a cholesterol, lipid and lipoprotein test.
The name "VAP test" uses a technology, the vertical auto profile, to measure and report risk factors for patients who are at increased risk for cardiovascular disease that are not captured by routine cholesterol testing. Its accuracy is unaffected by triglycerides and can be performed in a non-fasting state.
The VAP test has a unique ability to identify far more areas of risk to patients than the standard lipid panel, specifically because it reports 15 separate components versus four in the standard cholesterol test. Studies report that this comprehensive test is able to identify more than twice the number of patients with lipid abnormalities than the standard lipid panel (cholesterol and triglyceride test).
The VAP test directly measures and routinely reports all five lipoprotein classes and sub-classes, including LDL, HDL, intermediate-density lipoprotein (IDL), very low density lipoprotein (VLDL), and lipoprotein (a) [Lp(a)]. In routine cholesterol testing, LDL-cholesterol (LDL-C) is not directly measured, rather it is estimated using the Friedewald equation, is generally inaccurate when patients are not fasting because of its dependence on triglycerides levels in the calculation. Also, estimated LDL-C is falsely low when directly measured LDL-C is < 100 mg/dL or when triglycerides are elevated. The VAP technology also measures and reports LDL particle concentration (LDL-P).
The test meets the American Diabetes Association and American College of Cardiology (ADA-ACC) cholesterol guidelines for people at high risk of heart attack and stroke (including people with Type 2 diabetes mellitus). The ADA-ACC consensus statement establishes measurement and treatment guidelines for Apolipoprotein B|apoB in addition to LDL and non-HDL in high-risk patients. The VAP test was the first cholesterol profile to comply with updated National Cholesterol Education Program ATP III recommendations for LDL measurement.
The VAP technology is currently owned and operated by VAP Diagnostics Lab, an international company.
Summary of studies:
• In a Johns Hopkins study of 1.34 million patients, up to 60% of patients assessed were misclassified using the Friedewald estimated basic lipid panel, potentially leading to undertreatment of those patients most at risk.1
• Fasting remnant lipoprotein cholesterol is independently associated with subclinical atherosclerosis: The ELSA-BRASIL Study.2
• Smaller, denser HDL3-C levels are primarily responsible for the inverse association between HDL-C and incident CHD in this diverse group of primary prevention subjects: Jackson Heart Study & Framingham Offspring Cohort Study.3
• Remnant Lipoprotein cholesterol (RLP-C) levels are an independent predictor of the incidents of CHD in two primary prevention cohorts: Jackson Heart Study & Framingham Offspring Cohort Study.4
• Low HDL3-C, but not HDL2-C or HDL-C, independently increased the risk for long-term hard clinical events in secondary prevention patients: TRIUMPH.5
• The apo A1 remnant ratio was a significant predictor of short and intermediate-term death/myocardial infarction risk among women over 50.6
Cholesterol is any of a class of certain organic molecules. A cholesterol is a sterol, a type of lipid. Cholesterol is biosynthesized by all animal cells and is an essential structural component of animal cell membranes. When chemically isolated, 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 (LDL) 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 role.
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, hyperlipoproteinemia, and dyslipidemia.
Dyslipidemia is an abnormal amount of lipids in the blood. Dyslipidemia is a risk factor for the development of atherosclerotic cardiovascular disease (ASCVD). ASCVD includes coronary artery disease, cerbrovascular disease, and peripheral artery disease. Although dyslipidemia is a risk factor for ASCVD, abnormal levels doesn't mean that lipid lowering agents need to be started. Other factors, such as comorbid conditions and lifestyle in addition to dyslipidemia, is considered in a cardiovascular risk assessment. In developed countries, most dyslipidemias are hyperlipidemias; that is, an elevation of lipids in the blood. This is often due to diet and lifestyle. Prolonged elevation of insulin resistance can also lead to dyslipidemia. Likewise, increased levels of O-GlcNAc transferase (OGT) may cause dyslipidemia.
Combined hyperlipidemia is a commonly occurring form of hypercholesterolemia characterised by increased LDL and triglyceride concentrations, often accompanied by decreased HDL. On lipoprotein electrophoresis it shows as a hyperlipoproteinemia type IIB. It is the most commonly inherited lipid disorder, occurring in around one in 200 persons. In fact, almost one in five individuals who develop coronary heart disease before the age of 60 have this disorder.
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 triglycerides 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. The term hyperlipidemia refers to the laboratory finding itself and is also used as an umbrella term covering any of various acquired or genetic disorders that result in that finding. Hyperlipidemia represents a subset of dyslipidemia and a superset of hypercholesterolemia. Hyperlipidemia 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.
Hepatic lipase (HL), also called hepatic triglyceride lipase (HTGL) or LIPC, is a form of lipase, catalyzing the hydrolysis of triacylglyceride. Hepatic lipase is coded by chromosome 15 and its gene is also often referred to as HTGL or LIPC. Hepatic lipase is expressed mainly in liver cells, known as hepatocytes, and endothelial cells of the liver. The hepatic lipase can either remain attached to the liver or can unbind from the liver endothelial cells and is free to enter the body's circulation system. When bound on the endothelial cells of the liver, it is often found bound to HSPG, heparan sulfate proteoglycans (HSPG), keeping HL inactive and unable to bind to HDL or IDL. When it is free in the bloodstream, however, it is found associated with HDL to maintain it inactive. This is because the triacylglycerides in HDL serve as a substrate, but the lipoprotein contains proteins around the triacylglycerides that can prevent the triacylglycerides from being broken down by HL.
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.
Lomitapide, sold under the brand name Juxtapid in the US and as Lojuxta in the EU) is a medication used as a lipid-lowering agent for the treatment of familial hypercholesterolemia, developed by Aegerion Pharmaceuticals. It has been tested in clinical trials as single treatment and in combinations with atorvastatin, ezetimibe and fenofibrate.
Familial dysbetalipoproteinemia or type III hyperlipoproteinemia is a condition characterized by increased total cholesterol and triglyceride levels, and decreased HDL levels.
A lipid profile or lipid panel is a panel of blood tests used to find 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.
Evacetrapib was a drug under development by Eli Lilly & Company that inhibits cholesterylester transfer protein. CETP collects triglycerides from very low-density lipoproteins (VLDL) or low-density lipoproteins (LDL) and exchanges them for cholesteryl esters from high-density lipoproteins (HDL), and vice versa, but primarily increasing high-density lipoprotein and lowering low-density lipoprotein. It is thought that modifying lipoprotein levels modifies the risk of cardiovascular disease. The first CETP inhibitor, torcetrapib, was unsuccessful because it increased levels of the hormone aldosterone and increased blood pressure, which led to excess cardiac events when it was studied. Evacetrapib does not have the same effect. When studied in a small clinical trial in people with elevated LDL and low HDL, significant improvements were noted in their lipid profile.
Remnant cholesterol, also known as remnant lipoprotein, is a very atherogenic lipoprotein composed primarily of very low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL). Stated another way, remnant cholesterol is all plasma cholesterol that is not LDL cholesterol or HDL cholesterol, which are triglyceride-rich lipoproteins. Nonetheless, remnant cholesterol is primarily chylomicron and VLDL from which most triglyceride has been removed, such that each remnant particle contains about 40 times more cholesterol than LDL.
1. Friedewald-estimated versus directly measured low-density lipoprotein cholesterol and treatment implications. J Am Coll Cardiol. 2013 Aug 20;62(8):732-9.
2. Fasting remnant lipoprotein cholesterol is independently associated with subclinical atherosclerosis: The ELSA-BRASIL Study. JACC 5 April 2016 Volume 67, Issue 12.
3. Association of high-density lipoprotein subclasses and incident coronary heart disease: The Jackson Heart and Framingham Offspring Cohort Studies. Eur J Prev Cardiol. 2016 Jan;23(1):41-9.
4. Remnant lipoprotein cholesterol and incident coronary heart disease: The Jackson Heart and Framingham Offspring Cohort Studies. J Am Heart Assoc. 2016 Apr 29;5(5).
5. HDL cholesterol subclasses, myocardial infarction, and mortality in secondary prevention: the Lipoprotein Investigators Collaborative. Eur Heart J. 2015 Jan 1;36(1):22-30.
6. A new ratio for better predicting future death/myocardial infarction than standard lipid measurements in women >50 years undergoing coronary angiography: the apolipoprotein A1 remnant ratio (Apo A1/ [VLDL₃+IDL]). Lipids Health Dis. 2013 Apr 26;12:55.