Noncommunicable diseases (NCDs), diseases not caused by infectious agents, are responsible for a significant portion of deaths worldwide. Cardiovascular disease (CVD) accounts for the highest rates of NCD deaths, responsible for 17.5 million deaths worldwide. A lipid panel is a blood test that measures the amount of lipids, or fat molecules, in the blood. Elevated levels of lipids in the bloodstream may result in the accumulation of deposits within blood vessels. This buildup can inflict damage and increase the likelihood of cardiovascular complications.Β
Healthcare professionals utilize lipid panels to assess the susceptibility to cardiovascular diseases such as heart disease, myocardial infarction (heart attack), and stroke. Globally, hyperlipidemia high lipid levels, is associated with more than half of ischemic heart disease cases and more than 4 million deaths per year. This article will increase understanding of lipid panel results and how to use them to make informed decisions, implement proactive changes, and enhance cardiovascular health.
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What Does A Lipid Panel Test For?Β
Lipids are fat-like substances found in blood and body tissues. They serve as energy stores, structural components of cell membranes, and signaling molecules. The main types of lipids include triglycerides, phospholipids, and sterols.Β
A lipid panel analyzes cholesterol, triglycerides, and lipoprotein levels. Triglycerides are a fundamental component of the body's energy storage system, serving as a concentrated source of energy. Cholesterol, a sterol, is an essential component of cell membranes and is a precursor for the synthesis of hormones, vitamin D, and bile acids. Because lipids are insoluble in plasma, they must be bound to lipoproteins for transport. Lipoproteins consist of lipids (cholesterol, triglycerides, phospholipids) and a protein component known as apolipoproteins. Lipoproteins are classified based on characteristics like size/density, the types of lipids they carry, and the apolipoproteins they possess. The most commonly measured lipoproteins are low-density (LDL), high-density (HDL), and very-low-density (VLDL).
Generally, a lipid panel will include:
- Total cholesterol (TC)
- LDL cholesterol (LDL-C)
- VLDL cholesterol (VLDL-C)
- HDL cholesterol (HDL-C)
- Triglycerides (TG)
Preparing for a Lipid Panel Test
The lipid panel requires a blood sample. A phlebotomist draws the sample from a vein and sends it to the lab to be analyzed. In most cases, patients will need to be fasting for 10-12 hours prior to the sample being drawn.
Healthcare providers use lipid panels for both screening and monitoring purposes. Several risk factors for cardiovascular disease might prompt a healthcare provider to order a lipid panel:
- Men over the age of 45 or women over the age of 50
- Previous high cholesterol level
- Smoking
- Obesity
- Little physical activity
- High blood pressure (hypertension)
- Diabetes or prediabetes
- First-degree relative with heart disease
Certain health conditions can also cause high lipid levels, including pancreatitis, hypothyroidism, and chronic kidney disease (CKD). If a patient has been diagnosed with any of these conditions, the provider might also routinely monitor lipid levels using a lipid panel.
Understanding Normal and Abnormal Lipid Levels
Dyslipidemia refers to an abnormal concentration of lipids in the blood. Dyslipidemias can be primary, genetic conditions that cause abnormally high lipid levels, or secondary, resulting from medications or other conditions, such as diabetes mellitus, hypothyroidism, liver disease, or renal failure. According to the Adult Treatment Panel III (ATP III) guidelines, normal lipid levels are as follows:Β
Dyslipidemias can be categorized as high total cholesterol (TC), high LDL cholesterol, high non-HDL cholesterol, high triglycerides, and low HDL cholesterol.Β
LDL Cholesterol: βBadβ Cholesterol Explained
LDL-C is a measurement of the amount of cholesterol carried by low-density lipoproteins. It is often considered the βbadβ cholesterol because elevated LDL-C is associated with an increased risk of atherosclerosis, plaque build-up in the arteries, and cardiovascular diseases such as coronary artery disease (CAD), and myocardial infarction (heart attack), ischemic stroke, and peripheral artery disease (PAD).Β
Low-density lipoproteins have several characteristics that contribute to the development of atherosclerosis. Firstly, they carry high amounts of cholesterol, with most of our serum cholesterol transported by low-density lipoproteins. If they are produced in excess or are not recycled efficiently, low-density lipoproteins can cause cholesterol to build up in the arteries.Β
Secondly, they can vary in size. Smaller, dense LDL particles can easily penetrate the artery walls, initiating the process of atherosclerosis. Finally, they are also susceptible to oxidative modifications. This oxidation makes LDL more likely to be recognized as a foreign or damaged substance by the immune system, leading to the recruitment of immune cells and the release of inflammatory molecules. This exacerbates the atherosclerotic process.Β
HDL Cholesterol: βGoodβ Cholesterol ExplainedΒ
HDL-C is a measurement of the amount of cholesterol carried by high-density lipoproteins in the blood. HDL cholesterol is known as βgoodβ cholesterol because of its anti-atherogenic and anti-inflammatory effects. Cells in peripheral tissues are not able to break down accumulated cholesterol and instead rely upon a reverse transport mechanism to remove it. The primary lipoprotein on HDL particles is ApoA-1. It encourages the removal of cholesterol from cells so that HDL can redistribute cholesterol. Thanks to its uptake of cholesterol from plaques, it can reduce plaque size and its associated inflammation.Β
High-density lipoproteins have additional protective functions beyond their role in plasma lipid transport. They contain antioxidant enzymes that can neutralize free radicals, preventing the oxidation of LDL. HDL reduces the expression of adhesion molecules and inhibits the recruitment of inflammatory cells to the vessel walls, preventing the initiation of inflammation seen in atherosclerosis. HDL can also inhibit blood clot formation by modulating platelet activity. Uncontrolled platelet activation can lead to inflammation and thrombosis (6, 17).Β
The Significance of TriglyceridesΒ
Triglycerides are derived from the fats we consume in our diet or are produced by the body through the conversion of excess calories, especially from carbohydrates. Although they are not considered to be directly atherogenic, elevated triglyceride levels are associated with an increased risk of atherosclerosis and CVD. This is due to its apolipoprotein (apo-CIII) and its association with other atherogenic particles, like VLDL. Triglycerides are packaged into very low-density lipoprotein (VLDL) particles and released into the bloodstream. As VLDL travels in the bloodstream, it undergoes a series of changes.Β
Enzymes break down triglycerides within VLDL, releasing free fatty acids. As a result, VLDL is transformed into smaller, denser particles known as intermediate-density lipoprotein (IDL). Further processing converts IDL into LDL particles. Lipoproteins with apo-CIII activate immune cells in the blood vessels that stimulate inflammation, promote the formation of blood clots, and reduce the production of nitric oxide (NO), causing vascular dysfunction. High triglycerides are often seen in conjunction with low levels of high-density lipoprotein (HDL) cholesterol and the formation of small, dense, low-density lipoprotein (LDL) particles, which are more atherogenic. This pattern is common in conditions like metabolic syndrome and type 2 diabetes (32, 41, 44).Β
Factors Influencing Lipid LevelsΒ
Lipid levels are influenced by a combination of genetic, lifestyle, and environmental factors. Understanding these influences is crucial in assessing cardiovascular risk and developing effective strategies for lipid management.
One notable genetic cause is familial hypercholesterolemia (FH), an inherited disorder that significantly elevates cholesterol levels from an early age. FH is primarily associated with mutations in genes involved in cholesterol metabolism. The most common forms of FH result from mutations in the LDL receptor (LDLR) gene, which encodes a protein responsible for removing low-density lipoprotein (LDL) cholesterol from the bloodstream. Mutations in the apolipoprotein B (APOB) gene, which is involved in the formation of LDL particles, and the proprotein convertase subtilisin/kexin type 9 (PCSK9) gene, which regulates LDL receptor activity, can also contribute to FH.
Medical conditions such as diabetes, hypothyroidism, and kidney disease can all cause dyslipidemia. Furthermore, hormonal changes, like those experienced during pregnancy and menopause, can also affect lipid levels.
The amount and type of fat in oneβs diet also influences lipid levels. Diets high in saturated fat and trans fats tend to raise LDL cholesterol, while diets rich in unsaturated fats tend to lower LDL and raise HDL cholesterol. Avoiding excessive alcohol consumption, carbohydrate and sugar intake, and calories in general prevents high triglyceride levels.
Regular physical activity is associated with a more favorable lipid profile, including lower triglyceride levels, lower LDL-C, higher HDL-C, and larger LDL and HDL particle sizes. Obesity, especially abdominal obesity, is linked to elevated triglycerides and lower HDL. Regular physical activity can help to prevent excessive weight gain.
Smoking is associated with increased TC, VLDL, LDL, and TG concentrations and reduced HDL levels. It also activates the immune system, increasing inflammation, and increases platelet activation, which increases the risk of clotting.
Psychological stress is also associated with dyslipidemia, as chronic stress triggers a cascade of physiological responses. Chronic elevations in cortisol increase glucose availability and visceral fat deposits. Stress can also negatively influence lifestyle factors, such as diet and lifestyle choices, ultimately impacting lipid levels.
Next Steps After Receiving Your Lipid Panel Test ResultsΒ
After receiving abnormal lipid panel results, it is important to consult with a healthcare provider to take appropriate action to mitigate potential cardiovascular risks. The healthcare provider will conduct a comprehensive risk assessment to determine overall cardiovascular risk. Often, the atherosclerotic cardiovascular disease (ASCVD) calculator is used to estimate the 10-year ASCVD risk. This assessment considers factors such as age, gender, blood pressure, smoking status, family history, and the presence of other medical conditions. Cardiac risk calculators give a heart disease risk score as a percentage. The lower the percentage, the lower your chances of developing heart disease in the next ten years. The higher the rate, the greater your chances of developing cardiovascular problems. They also show how specific treatments might improve your risk status. Depending on the results of the lipid panel and the patientβs overall risk, the healthcare provider can help to determine what lifestyle and/or medication options are in the patientβs best interest.Β
Additional labs can also be ordered to help further assess cardiovascular risk. The apoB/apoA-I ratio sets the balance between apolipoprotein B (ApoB) and apolipoprotein A1 (ApoA) in the blood. ApoB is the apolipoprotein on lipoproteins that carry cholesterol out into the periphery and are considered atherogenic, while ApoA1 is the apolipoprotein associated with HDL and reverse cholesterol transport. High apoB and a high apoB/apoA-I ratio are strongly related to increased coronary risk, while high apoA-I is inversely associated with risk. The apoB/apoA-I ratio is considered to be superior to other cholesterol markers in predicting risk. Apolipoprotein E (Apo E) is involved in the production, transport, and use of cholesterol in the body. Variants in the ApoE gene are associated with lipid metabolism differences.Β
There are three different common variations of the APOE gene: E2, E3, and E4. The E4 variant is associated with an increased risk of dementia and hypercholesterolemia. Lp(a) is a type of LDL cholesterol that contains apolipoprotein(A) on its surface. It is genetically determined and considered to be more atherogenic. It can penetrate the arterial walls more efficiently, contributing to plaque formation. It is regarded as an independent and causal risk factor for atherosclerotic cardiovascular diseases. Oxidized LDL (OxLDL) measures oxidative protein damage to the ApoB subunit. This promotes atherosclerosis through inflammatory and immunologic mechanisms that lead to the formation of macrophage foam cells. Increased levels of circulating ox-LDL are significantly associated with the risk of clinical ASCVD events. Inflammation is related to the development of atherosclerosis and cardiovascular events. Inflammatory markers have a prognostic value for the result of cardiovascular events independent of conventional risk factors and may be helpful in identifying people who are at high risk of future cardiovascular events. hs-CRP is a well-studied marker in assessing cardiac-related inflammation.
A Coronary Artery Calcium (CAC) score measures the amount of calcium deposits in the coronary arteries, which can be detected through a specialized imaging test such as a coronary CT scan. This score provides an indication of the extent of atherosclerosis in the coronary arteries. While CAC scores are not typically used as a routine screening tool, they can be instrumental in the case of hyperlipidemia to assess the extent of atherosclerosis and guide treatment decisions. A high CAC score may benefit from more aggressive treatment strategies.
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Interpreting Your Lipid Panel: Final Thoughts
Lipid panels are indispensable tools in preventative healthcare, providing information regarding cholesterol levels and cardiovascular risk. Proactively managing cholesterol through regular testing, heart-healthy diet and lifestyle choices, and consulting with healthcare professionals is paramount for cardiovascular well-being. Lipid panels empower individuals to make informed decisions, implement lifestyle changes, and, when necessary, explore medical interventions to optimize heart health, reduce the risk of cardiovascular diseases, and enhance overall well-being.