When it comes to cholesterol, it's critical to understand your numbers. Hyperlipidemia is characterized by an excess of lipids (or fats) in the blood, such as cholesterol and triglycerides. These fats can penetrate the artery walls and raise your chance of developing atherosclerosis (artery hardening), which can lead to stroke, heart attack, and the need for amputation. If you smoke, or if you have or develop diabetes, high blood pressure, or renal failure, your risk of atherosclerosis increases.
What is hyperlipidemia?
Hyperlipidemia is a term used to describe a group of inherited and acquired illnesses characterized by high lipid levels in the human body. Hyperlipidemia is highly widespread, particularly in the Western hemisphere, but also globally.
A more objective definition of hyperlipidemia would include LDL, total cholesterol, triglyceride levels, or lipoprotein levels more than the 90th percentile in comparison to the general population, or an HDL level less than the 10th percentile in contrast to the general population. Cholesterol levels, lipoproteins, chylomicrons, VLDL, LDL, apolipoproteins, and HDL are all examples of lipids.
A wide range of trials and research have repeatedly proven that high levels of LDL cholesterol enhance a person's risk of developing atherosclerotic plaques and consequent vascular disease. In sharp contrast, high-density lipoprotein (HDL) cholesterol aids in the regulation of cholesterol levels, hence reducing the risk of atherosclerotic vascular disease.
Each patient's LDL cholesterol target is depending on their total cardiovascular risk, and medical therapy should be customized to the patient individually. "Primary prevention" refers to the management of risk factors such as hyperlipidemia in order to reduce the risk of atherosclerotic cardiovascular disease. The justification for decreasing LDL cholesterol stems from extensive epidemiologic evidence that shows a positive, continuous association between LDL cholesterol levels, cardiovascular events, and patient death.
Over three million persons in the United States and Europe today have hyperlipidemia, and the number is rapidly increasing. Hyperlipidemia is usually a chronic, progressive illness that necessitates lifestyle and nutritional adjustments, as well as the use of additional lipid-lowering drugs.
Patients with premature coronary artery disease (CAD), defined as CAD occurring in males before the age of 55 to 60 years and females before the age of 65 years, had the greatest level of hyperlipidemia. Under the previously mentioned circumstances, the incidence of hyperlipidemia is around 75-85 percent, compared to approximately 40 to 48 percent in a comparable age control population without the presence of early coronary artery disease.
Over 50% of American people have higher LDL levels, and it is estimated that only 35% of those individuals properly control their high LDL levels, indicating an undertreated condition. When compared to rates in Europe and the United States, it appears that nations with lower overall rates of obesity and saturated fat intake had a lower prevalence of hyperlipidemia and eventual coronary artery disease.
If a child is underweight or obese at the age of two, he or she may develop secondary (non-genetic) pediatric hyperlipidemia.
Causes of hyperlipidemia
Hyperlipidemia is classified into two types: primary (inherited) hyperlipidemia and secondary (acquired) hyperlipidemia. Primary hyperlipidemia is caused by a variety of genetic disorders that a patient may inherit at birth, whereas secondary hyperlipidemia is caused by a different underlying etiology, such as an unhealthy diet, medications (amiodarone, glucocorticoids), hypothyroidism, uncontrolled diabetes, and/or a poor lifestyle regimen.
Lipoprotein metabolism disorders are frequently hereditary, making a patient's family history even more significant. In one research, for example, around 54% of individuals with a history of early coronary artery disease had an underlying genetic illness. Most individuals have a polygenic inheritance pattern for hyperlipidemia, and the disorder's symptoms are mostly determined by secondary variables such as (central) obesity, saturated fat consumption, and the cholesterol content of a person's diet.
Cholesterol is the most prevalent circulating fatty material implicated in the atherogenic process. It has two origins: Exogenous sources range from 300 to 700 mg per day, resulting from an excessive consumption of dietary lipids, particularly those of animal origin; endogenous sources range from 800 to 1200 mg per day, resulting from the action of the liver.
Diabetes, chronic renal failure, nephrotic syndrome, hypothyroidism, aging, and sedentary lifestyle are all common causes of hypercholesterolemia and/or rise in triglycerides, in addition to high animal fat consumption. Other iatrogenic reasons include the use of certain medications, such as thiazide diuretics, beta-blockers, estrogen-progestin contraceptives, and antiretrovirals.
Genetic dyslipidaemias, which are more uncommon, are the cause of alterations in the blood lipid rate of around 60% and are frequently responsible for cardiovascular disease at a young age.
Hyperlipidemia, namely high LDL (hypercholesterolemia), is one of the most common risk factors for the progression of atherosclerosis and subsequent vascular disease. It is simply described as increased lipid or fat concentrations in the blood. Endothelial damage, hyperlipidemia, inflammatory and immunologic variables, plaque erosion or rupture, hypertension, and smoking are all factors that contribute to the formation of atherosclerosis.
Atherosclerosis is typically asymptomatic until plaque stenosis reaches 70% to 80% of the vessel's width. Atherosclerosis develops as a result of underlying endothelial damage, which appears to be caused by nitric oxide depletion inside the endothelium. This procedure causes increased inflammation right surrounding the site of malfunction, allowing lipids to accumulate inside the endothelium wall's innermost layer.
The lipids are then consumed by macrophages, resulting in the formation of "foam cells." The accumulation of cholesterol within the "foam cells" leads to mitochondrial malfunction, apoptosis, and, eventually, necrosis of the underlying tissues. Smooth muscle cells encase the pack of "foam cells" or debris, resulting in the formation of a fibrotic plaque that prevents the underlying lipids (debris) from being eliminated.
Tissue factor, in conjunction with enhanced platelet activity, is regarded as a main activator of coagulation, increasing the risk of plaque rupture and thrombosis. Atherosclerotic plaques develop by two separate mechanisms: a gradual, chronic plaque build-up that leads to luminal stenosis over time, vs an abrupt beginning of fast luminal blockage due to plaque rupture and thrombosis. Both methods are capable of creating clinically serious illness, which should be handled as soon as feasible by a clinician.
Most patients' hyperlipidemia is polygenic in nature, and the disorder's presentation is heavily impacted by factors such as (central) obesity, saturated fat consumption, and the cholesterol content of a person's diet. Another process includes high amounts of "apo B-100" lipoproteins in the blood, which can contribute to atherosclerotic disease even if the patient has no other risk factors. A person's risk of developing hyperlipidemia and cardiovascular disease is frequently influenced by a mix of hereditary and environmental variables.
Many systemic disorders can produce dyslipidemia and atherosclerosis issues by activating an inflammatory sub-layer with clinical or sub-clinical values. Here are several examples:
- Crohn disease
- Inflammatory bowel disease
- Chronic obstructive pulmonary disease
- Chronic pain
- Pediatric alopecia areata
- Chronic kidney disease
Patients with underlying hyperlipidemia are frequently asymptomatic, thus collecting a detailed and complete history is critical. It is critical to obtain a thorough understanding of each patient's family history of cardiovascular disease, hyperlipidemia, and/or familial hypercholesterolemia; their diet and exercise habits; tobacco, alcohol, or drug use; the presence of coronary artery disease; risk factors or a history of CAD; and/or symptoms of peripheral arterial disease or angina.
A focused physical exam, in addition to acquiring a complete history, is quite crucial. Accurate blood pressure readings, observing the patient's skin for xanthomas, listening for carotid and femoral bruits for evidence of stenosis, listening for an S4 heart sound, and palpating for intact peripheral pulses in all four extremities are quick and simple physical exam findings that can help you diagnose hyperlipidemia.
In hypercholesterolemic individuals, palpate all pulses and listen for carotid and femoral bruits. Also, if the patient is under 50 years old, closely inspect the tendon xanthoma (Achilles tendon and extensor tendons on the dorsum of the hand), xanthelasma, and arcus senilis. A detailed assessment of the heart for supra-valvar aortic stenosis owing to atheroma deposition is recommended in individuals with probable familial hypercholesterolemia.
Diagnosis of hyperlipidemia
Several experts have created lipid screening standards, which include the "lipid profile" to test cholesterol and triglyceride levels. Guidelines range in terms of when primary care physicians should begin screening for hyperlipidemia and how frequently they should do so. In general, regular lipid screening should begin when a male reaches the age of 35 (assuming no other cardiovascular risk factors exist) or when a female reaches the age of 25. (if the patient has other cardiovascular risk factors).
Lipid screening every five years is suitable for low-risk patients, and more regular screening is indicated as the patient's cardiovascular risk increases.
As previously indicated, the most significant laboratory test to get is a fasting lipid profile, which includes LDL, HDL, triglycerides, and total cholesterol. For a more thorough test, v-LDL, total cholesterol: HDL, and LDL: HDL ratios can be added. It is important to refrain from eating or drinking anything other than water for 9 to 12 hours in order to avoid skewing the lipid panel results (mainly the triglyceride levels).
Before beginning a statin for high LDL levels, it is critical to conduct liver function testing to check that there is no prior liver damage, as statins might worsen this problem. A Hgb A1c level is required to screen for diabetes mellitus for risk stratification reasons, and blood pressure levels should always be examined to verify the patient does not have underlying hypertension.
A TSH test should also be conducted to rule out any underlying thyroid issues, and a simple urine should be performed to check for albuminuria. These tests are essential for risk-stratification of your patient in order to appropriately estimate the possible dangers vs advantages of starting medicinal therapy in a hyperlipidemic patient.
Treatment for hyperlipidemia
The choice to treat increased LDL cholesterol levels is based on the patient's main physician's assessment of total cardiovascular risk, which should be thoroughly addressed with the patient. In general, the absolute risk reduction associated with lipid-lowering medication for hyperlipidemia is smaller than in individuals with established underlying cardiovascular disease.
Only therapies for increased LDL cholesterol have been shown to be clinically beneficial in people without a known diagnosis of cardiovascular disease. There is no clinical evidence that treating hypertriglyceridemia or low HDL cholesterol levels is beneficial.
Diet and lifestyle changes are the primary therapy approaches, with the addition of lipid-lowering medicines as needed. Patients with mild hyperlipidemia and low ASCVD risk (less than 7.5 percent 10-year risk) should follow a low fat, low carbohydrate diet and engage in moderate to vigorous physical exercise (recommended 30 minutes per day, 5 to 6 days per week).
The AHA recommends reducing saturated fat consumption to roughly 5% of daily calories and minimizing total trans-saturated fat consumption as much as feasible. Quitting smoking, reducing blood pressure, and losing weight have all been shown to reduce the risk of vascular disease. Patients with moderate to high ASCVD risk (above 7.5 percent 10-year risk) should be given lipid-lowering "statin" drugs.
The most comprehensive meta-analysis of primary prevention studies in hyperlipidemia patients revealed an all-cause mortality benefit and that lowering LDL cholesterol is beneficial in lowering cardiovascular events, particularly myocardial infarction risk.
For the great majority of patients, from low risk to high risk, there is a clear and demonstrated benefit to statin medication, and if side effects and budgetary restraints did not exist, virtually all patients would be recommended statin therapy. As a result, the adverse effects and expenses of these medications should be balanced against the particular patient's possible benefit from taking the prescription.
In most clinical studies, if the physician and patient agree to begin medical therapy with statins, the total risk reduction in cardiovascular events is often about 20 to 30 percent. The often referred to studies on which the majority of guidelines are based included pravastatin 40 mg, lovastatin 20 to 40 mg, atorvastatin 10 mg, and rosuvastatin 10 mg, therefore typical recommendations are to take one of these statins.
Close follow-up with patients who begin lipid-lowering statin treatment is always recommended. The great majority of the advantages of statin medication are derived from the moderate dosage, with the addition of high-intensity therapy providing a significantly smaller benefit. The advantage of high-intensity treatment, on the other hand, remains clinically considerable and should be considered for all high-risk patients.
If a patient develops an allergy or intolerance to a statin medicine, it is recommended that the dose be reduced or that the patient switch to a different lipid-lowering medication entirely. Evolocumab (PCSK9 inhibitor) lowered LDL cholesterol levels considerably more than ezetimibe in individuals who had experienced muscle-related statin intolerances. However, both of these drugs are viable secondary therapy alternatives.
When screening a patient for hyperlipidemia, diagnostic doctors must compile a complete list of differentials. Primary diseases, such as familial hypercholesterolemia, familial mixed hyperlipidemia, dysbetalipoproteinemia, should always be considered.
When identifying a patient with hyperlipidemia, the following secondary disease processes must also be considered: obstructive liver disease or biliary blockage, hypothyroidism, nephrotic syndrome, chronic renal insufficiency, anorexia, obesity, metabolic syndrome, and diabetes. To limit the differential and determine the accurate diagnosis, a detailed history and physical with extensive labs should be acquired.
Diet for hyperlipidemia
Modification of nutritional components, intake of particular foods, use of food additives and supplements, and main dietary approaches are all dietary variables that impact lipid levels. Red yeast rice supplements have comparable effects to statin drugs and are tolerated better in certain people.
Regular aerobic exercise has been shown to lower cholesterol levels, especially when undertaken for at least 120 minutes per week. Because brief physician counseling has little effect on unselected patients, efforts should be focused on patients who are motivated and ready to make lifestyle changes.
Hyperlipidemia is frequently a life-long illness process, however it is usually relatively controllable. If hyperlipidemia is not treated, the condition progresses and can lead to severe underlying vascular disease processes, which can be deadly. Continuous, long-term exposure to elevated blood lipid levels in early adulthood raises the person's later risk of coronary heart disease in a dose-dependent manner.
Adults who are continuously exposed to moderate or severe elevations in non-HDL cholesterol levels have an increased risk of developing coronary heart disease and would benefit from aggressive medical treatment modalities such as high-intensity statin therapy in addition to dietary and lifestyle changes.
Over a 20-year period, individuals who got statin medication for five years had increased survival rates and a clinically meaningful reduction in cardiovascular disease. This evidence backs up the findings of multiple previous research and trials that show a considerable reduction in cardiovascular risk when statin medicine is used effectively and a proactive treatment approach is used.
Complications of untreated or undertreated hyperlipidemia include all sorts of vascular disease, which can be deadly. Coronary artery disease, peripheral artery disease, cerebrovascular accidents, aneurysms, type II diabetes, excessive blood pressure, and even mortality are examples.
Myopathy, renal damage, arthralgia, extremities aches, nausea, myalgia, increased liver enzymes/hepatotoxicity, diarrhea, and rhabdomyolysis are some of the statin drug risks. up to 5% to 20% of people using a statin medicine have muscular intolerance. A lower dose of the statin should be tried, as should a switch to another lipid-lowering medicine such as ezetimibe or evolocumab.
Hyperlipidemia is defined as unusually high amounts of lipids (fats, cholesterol, or triglycerides) or lipoproteins in the blood. The word hyperlipidemia refers to the laboratory finding as well as an umbrella term for any of the different acquired or inherited illnesses that originate in that finding. Hyperlipidemia is a subset of dyslipidemia as well as a subset of hypercholesterolemia. Hyperlipidemia is generally a chronic condition that necessitates continual therapy to keep blood lipid levels under control.
Treatment of hyperlipidemia is evolving as we better understand the underlying pathophysiology and improve on previous medicinal interventions. This page will provide an overview of hyperlipidemia's history, diagnosis, and most recent treatment guidelines.
Aerobic exercise has been shown to increase the levels of the HDL-cholesterol protein, which has an anti-atherogenic action: the HDL transports cholesterol from the artery walls and peripheral tissues to the liver, and the same HDL has an antioxidant and anti-inflammatory capacity that induces the release of nitric oxide (vasodilator compound). According to estimates, adding 10 minutes of physical activity to daily exercise improves HDL concentration by 1.4 mg/dl, and an adequate training program can boost cholesterol HDL by 4.6 percent on average.
All hyperlipidemic patients must grasp how the condition affects their organs and the health dangers it may cause. A healthy diet, smoking cessation, and lifestyle changes should always be considered. If pharmaceutical therapy is required, the risks and advantages of each medicine should be discussed before beginning. Both the primary care physician and the pharmacist have a responsibility to educate the patient about drug adherence, side effects, interactions, and the overall risks vs benefits of the medications given.