Hypercholesterolemia, characterized by elevated cholesterol levels in the blood, is a type of hyperlipidemia, which involves increased blood lipids, including total cholesterol, LDL (low-density lipoprotein), and triglycerides. A diagnosis is typically made when total cholesterol levels exceed 5.2 mmol/L. This condition falls under the broader category of lipid disorders, which affect the body's metabolism and are associated with a heightened risk of cardiovascular diseases.

Cholesterol serves critical functions in the body, including being a fundamental component of cell membranes, and acting as a precursor for steroid hormones and bile acids. However, because cholesterol cannot dissolve in water, it must be transported through the bloodstream within lipoproteins, which are categorized by their density into VLDL (very-low-density lipoprotein), IDL (intermediate-density lipoprotein), LDL, and HDL (high-density lipoprotein).

The causes of hypercholesterolemia can be either congenital or acquired. Congenital forms are less common and include conditions like:

Type I Hyperchylomicronemia + Type IIa Familial Hypercholesterolemia + Type III Familial Dysbetalipoproteinemia + Type IV Familial Hypertriglyceridemia

• Type I Hyperchylomicronemia: An autosomal recessive condition that leads to high triglyceride levels but is not associated with an increased risk of atherosclerosis. Symptoms can include eruptive xanthomas, pancreatitis, and hepatosplenomegaly.

• Type IIa Familial Hypercholesterolemia: An autosomal dominant condition resulting from mutations in the LDL receptor, leading to elevated LDL levels and an early onset of atherosclerotic cardiovascular disease.

• Type III Familial Dysbetalipoproteinemia: An autosomal recessive condition caused by defective ApoE, leading to elevated cholesterol and triglycerides and an increased risk of cardiovascular disease.

• Type IV Familial Hypertriglyceridemia: An autosomal dominant condition that significantly increases the risk of acute pancreatitis.

Acquired causes are more prevalent and include factors like obesity, diabetes mellitus, physical inactivity, alcoholism, hypothyroidism, nephrotic syndrome, cholestatic liver disease, Cushing's disease, and certain medications such as oral contraceptive pills, high-dose diuretics, and metoprolol.

Managing hypercholesterolemia often involves addressing these underlying causes, whether they are lifestyle-related or associated with other health conditions, alongside direct treatments aimed at lowering lipid levels.

Dyslipidemia classification according to Frederickson

The Frederickson classification, also known as the Fredrickson-Levy-Lees classification, organizes dyslipidemias into types based on the pattern of lipoproteins elevated in the plasma. This system helps in understanding the genetic basis of lipid disorders and their clinical implications, especially regarding the risk of atherosclerosis and pancreatitis. Here's a summary of the classification:

Type 1 – Familial Hyperchylomicronemia (Autosomal Recessive)

• Clinical Manifestations: Eruptive xanthomas, hepatosplenomegaly, recurrent episodes of acute pancreatitis and/or abdominal pain, lipemia retinalis, bile duct stenosis.

• Lipoprotein Defect: Chylomicrons.

• Total Cholesterol: Normal to mildly increased.

• Total Triglycerides: Very increased.

• Overnight Plasma: Creamy top layer.

• Risk for Atherosclerosis: None.

Type 2a – Familial Hypercholesterolemia (Autosomal Dominant)

• Clinical Manifestations: Premature atherosclerosis, arcus lipoides, tuberous/tendon xanthomas.

• Lipoprotein Defect: LDL.

• Total Cholesterol: Very increased.

• Total Triglycerides: Normal.

• Overnight Plasma: Clear.

Type 2b – Familial Combined Hyperlipidemia (Autosomal Dominant)

• Clinical Manifestations: Premature atherosclerosis, arcus lipoides, xanthelasma.

• Lipoprotein Defect: LDL and VLDL.

• Total Cholesterol: Very increased.

• Total Triglycerides: Increased.

• Overnight Plasma: Clear.

Type 3 – Familial Dysbetalipoproteinemia (Autosomal Recessive)

• Clinical Manifestations: Premature atherosclerosis, palmar and tuberoeruptive xanthomas.

• Lipoprotein Defect: Remnants of VLDL and chylomicrons.

• Total Cholesterol: Increased.

• Total Triglycerides: Increased.

• Overnight Plasma: Turbid.

Type 4 – Familial Hypertriglyceridemia (Autosomal Dominant)

• Clinical Manifestations: Premature atherosclerosis, tuberoeruptive xanthomas, acute pancreatitis, features of hyperglycemia.

• Lipoprotein Defect: VLDL.

• Total Cholesterol: Normal to mildly increased.

• Total Triglycerides: Very increased.

• Overnight Plasma: Turbid.

This classification emphasizes the genetic predisposition to dyslipidemias and their associated risks, helping clinicians tailor prevention and treatment strategies for cardiovascular diseases.

Pathophysiology

The pathophysiology of dyslipidemias, particularly hypercholesterolemia, involves complex interactions that lead to an increased risk of cardiovascular diseases. Elevated levels of low-density lipoprotein (LDL) and reduced levels of high-density lipoprotein (HDL) are central to the development of atherosclerosis, a condition characterized by the buildup of fatty deposits within arterial walls. This buildup can eventually lead to the narrowing and hardening of arteries, significantly increasing the risk of cardiovascular events such as coronary heart disease, myocardial infarction, stroke, and peripheral arterial disease.

Clinical Features

Though hypercholesterolemia might not present symptoms initially, chronic elevation of serum cholesterol levels can manifest in several ways:

Skin Manifestations + Eye Manifestations + Other Manifestations 

Skin Manifestations

• Xanthomas: These are nodular lipid deposits in the skin and tendons, resulting from the extravasation of plasma lipoproteins into tissues due to extremely high levels of triglycerides and/or LDL.

Eruptive Xanthomas + Tendinous Xanthomas + Palmar Xanthomas + Xanthelasmas

• Eruptive Xanthomas: Yellow papules with an erythematous border, found on the buttocks, back, and extensor surfaces of the extremities, associated with hypertriglyceridemia or lipoprotein lipase deficiency.

• Tendinous Xanthomas: Firm nodules in tendons, often in the extensor tendons of hands and Achilles tendon, seen in severe hypercholesterolemia with elevated LDL levels.

• Palmar Xanthomas: Yellow plaques on the palms, associated with type III hyperlipoproteinemia and increased VLDL.

• Xanthelasmas: Nodular lipid deposits around the eyelids, typically bilateral yellow flat plaques on the upper eyelids (nasal side). They are often idiopathic but can occur with hypercholesterolemia, hyperapobetalipoproteinemia, and elevated LDL levels. Xanthelasmas have an increased incidence in individuals with diabetes mellitus, elevated plasma lipoproteins, and are more frequently found in postmenopausal women.

Eye Manifestations

Lipemia Retinalis: + Arcus Lipoides Corneae

• Lipemia Retinalis: A condition where retinal vessels appear opaque and white, visible during a fundoscopic exam.

• Arcus Lipoides Corneae: A lipid deposit in the cornea, often appearing as a white or gray ring around the corneal edge, more common in older individuals but can indicate high cholesterol levels when seen in younger people.

Other Manifestations

Fatty Liver (Hepatic Steatosis) + Pancreatitis

• Fatty Liver (Hepatic Steatosis): Excess fat accumulation in the liver cells, often associated with obesity, insulin resistance, and high triglyceride levels.

• Pancreatitis: Severe hypertriglyceridemia, typically with levels greater than 11.3 mmol/L, can lead to acute pancreatitis due to the toxic effects of high triglyceride levels on the pancreatic tissue.

Atherosclerosis and Secondary Diseases

The progression of atherosclerosis can lead to several severe cardiovascular diseases:

Coronary Heart Disease + Myocardial Infarction + Stroke + Peripheral Arterial Disease + Carotid Artery Stenosis + Cholesterol Embolization Syndrome

• Coronary Heart Disease: Narrowing of the coronary arteries that supply blood to the heart, leading to angina and risk of myocardial infarction.

• Myocardial Infarction: Commonly known as a heart attack, it occurs when blood flow to a part of the heart is blocked for a long enough time that part of the heart muscle is damaged or dies.

• Stroke: Occurs when the blood supply to part of the brain is interrupted, leading to brain damage.

• Peripheral Arterial Disease: Atherosclerosis affecting the legs, causing pain and difficulty walking.

• Carotid Artery Stenosis: Narrowing of the carotid arteries, which can lead to reduced blood flow to the brain and stroke.

• Cholesterol Embolization Syndrome: Small pieces of cholesterol plaques break off and block small blood vessels, leading to tissue damage.

Managing dyslipidemia involves a combination of lifestyle changes, such as diet and 

exercise, and medications aimed at lowering lipid levels to reduce the risk of these complications.

Atherosclerosis progression can lead to severe cardiovascular diseases, including coronary heart disease, myocardial infarction, stroke, peripheral arterial disease, carotid artery stenosis, and cholesterol embolization syndrome. Managing dyslipidemia involves lifestyle changes and medications to reduce the risk of complications.

Diagnostics

Diagnostics for lipid disorders, including hypercholesterolemia and other forms of dyslipidemia, are an essential part of cardiovascular risk assessment and management. The approach involves initial screening followed by more detailed investigations to confirm the diagnosis and identify any underlying causes or associated risks. Here’s a structured overview of the diagnostic process:

Initial Screening

Routine Laboratory Testing

• Routine Laboratory Testing: Lipid disorders are often detected during routine health examinations or cardiovascular risk assessments. The key to initial screening is a blood lipid profile that includes measurements of total cholesterol, LDL (low-density lipoprotein), HDL (high-density lipoprotein), and triglycerides.

Confirmatory Testing

Fasting Lipid Profile

• Fasting Lipid Profile: For accurate diagnosis, a fasting lipid profile is recommended. This test measures total cholesterol, HDL, and triglycerides, with LDL levels either directly measured or estimated using the Friedewald formula:

LDL=total cholesterol−HDL−(0.2×fasting triglycerides).

• Diagnostic Criteria: A diagnosis of dyslipidemia is considered when LDL levels are greater than 3.4 mmol/L and/or HDL levels are less than 1 mmol/L. Confirmation requires pathological values on two separate occasions.

Identifying Underlying Causes

• Additional tests to identify possible causes or contributing factors include:

Fasting Blood Glucose or HbA1c + TSH Level + Liver Function Tests + Urine Analysis

• Fasting Blood Glucose or HbA1c: To screen for diabetes mellitus.

• TSH Level: To check for hypothyroidism, which can affect lipid levels.

• Liver Function Tests: Since liver disorders can influence lipid metabolism.

• Urine Analysis: For general health assessment and to check for kidney disorders.

Lipid Parameters for Assessment

Total Cholesterol + LDL Cholesterol + HDL Cholesterol

• Total Cholesterol:

  • <5.2 mM: Optimal

  • 5.2-6.2 mM: Borderline

  • 6.2 mM: High

• LDL Cholesterol:

  • <2.6 mM: Optimal

  • 2.6-3.3 mM: Near optimal

  • 3.4-4.1 mM: Borderline high

  • 4.1-4.9 mM: High

  • 4.9 mM: Very high

• HDL Cholesterol:

  • <1 mM: Low

  • 1.55 mM: Optimal

Further Workup for Confirmed Dyslipidemia

Patients with confirmed dyslipidemia should undergo further evaluation to assess for cardiovascular disease (CVD) and other major risk factors. This includes screening for:

CVD and Risk Equivalents + Major CVD Risk Factors

• CVD and Risk Equivalents: Myocardial infarction, stroke, symptomatic carotid artery stenosis, peripheral artery disease, abdominal aortic aneurysm, diabetes mellitus, and chronic kidney disease.

• Major CVD Risk Factors: Smoking, hypertension, elevated total cholesterol/LDL/low HDL, family history of CHD in a first-degree relative (male <55 years; female <65 years), and age (male ≥45 years; female ≥55 years).
  

This comprehensive diagnostic approach allows clinicians to not only confirm the presence of dyslipidemia but also to understand its potential impact on the patient's cardiovascular health and guide the appropriate management strategy.

Treatment

The treatment of lipid disorders aims to lower serum lipid levels, particularly LDL cholesterol, and increase HDL cholesterol to reduce the risk of cardiovascular disease (CVD). This is achieved through a combination of lifestyle modifications and medical therapy. Here’s an overview of the current strategies for managing lipid disorders:

Lifestyle Modifications

Dietary Changes + Weight Management + Physical Activity

• Dietary Changes: Emphasize a diet low in saturated fats and cholesterol. Increase intake of fruits, vegetables, whole grains, and lean protein sources.

• Weight Management: Achieve and maintain a healthy weight to help lower lipid levels and reduce CVD risk.

• Physical Activity: Regular physical exercise helps improve lipid profiles and overall cardiovascular health.

Medical Therapy

• Statins: The primary choice for lowering LDL cholesterol due to their proven efficacy in reducing the risk of CVD events. Statins work by inhibiting the enzyme HMG-CoA reductase, which is crucial for cholesterol synthesis in the liver.

• Second-Line Lipid-Lowering Agents: Include medications such as ezetimibe (which reduces intestinal cholesterol absorption), fibrates (primarily used to lower triglyceride levels), and PCSK9 inhibitors (for patients with genetic dyslipidemias or those who do not achieve target LDL levels with statins).

• Treatment of Xanthomas and Xanthelasmas: Generally, not required unless for cosmetic reasons. Surgical removal can be considered, but there is a risk of recurrence.

Management of Congenital Disorders

Lifestyle Modifications and Lipid-Lowering Agents: + LDL Apheresis

• Lifestyle Modifications and Lipid-Lowering Agents: High-dose statin therapy combined with ezetimibe is recommended for managing hypercholesterolemia. Fibrates are used for hypertriglyceridemia.

• LDL Apheresis: May be necessary in severe cases, especially in familial hypercholesterolemia, to mechanically remove LDL particles from the bloodstream.

ACC/AHA Guidelines for Statin Therapy

The American College of Cardiology/American Heart Association (ACC/AHA) guidelines recommend initiating moderate- to high-intensity statin therapy based on the patient’s risk profile:

Clinical atherosclerotic cardiovascular disease (ASCVD)+ LDL ≥ 4.9 mM + Diabetes Patients Aged 40–75 Years + Individuals Aged 40–75 Years with a 10-Year ASCVD Risk > 7.5%

• Clinical atherosclerotic cardiovascular disease (ASCVD): High-intensity statin therapy is recommended, with moderate-intensity therapy for individuals over 75 years.

• LDL ≥ 4.9 mM: High-intensity statin therapy.

• Diabetes Patients Aged 40–75 Years: Statin therapy based on risk assessments.

• Individuals Aged 40–75 Years with a 10-Year ASCVD Risk > 7.5%: Statin therapy is indicated.

Prevention and Screening

Screening Recommendations

• Screening Recommendations: Based on overall CVD risk. High-risk individuals, such as those with other CVD risk factors, should begin screening earlier (men > 20–25 years; women > 30–35 years). Low-risk individuals should start screening at older ages (men > 35 years; women > 45 years).

The goal is to individualize treatment based on the patient’s risk factors, genetic predispositions, and potential for benefit from therapy. Regular monitoring of lipid levels, along with adjustments in therapy and lifestyle interventions, is crucial for managing lipid disorders effectively.

Mind Map: Hypercholesterolemia

Central Idea: Hypercholesterolemia

• Characterized by elevated cholesterol levels in the blood

Main Branches:

1. Hyperlipidemia

   • Involves increased blood lipids

     • Total cholesterol

     • LDL (low-density lipoprotein)

     • Triglycerides

2. Diagnosis

   • Total cholesterol levels exceed 5.2 mmol/L

3. Lipid Disorders

   • Affect body's metabolism

   • Associated with heightened risk of cardiovascular diseases

Sub-branches:

• Cholesterol Functions

  • Component of cell membranes

  • Precursor for steroid hormones and bile acids

• Cholesterol Transport

  • Transported through bloodstream within lipoproteins

    • VLDL (very-low-density lipoprotein)

    • IDL (intermediate-density lipoprotein)

    • LDL

    • HDL (high-density lipoprotein)

Causes of Hypercholesterolemia

Congenital Causes

• Type I Hyperchylomicronemia

  • Autosomal recessive

  • High triglyceride levels

  • Symptoms: eruptive xanthomas, pancreatitis, hepatosplenomegaly

• Type IIa Familial Hypercholesterolemia

  • Autosomal dominant

  • Mutations in LDL receptor

  • Elevated LDL levels

  • Early onset of atherosclerotic cardiovascular disease

• Type III Familial Dysbetalipoproteinemia

  • Autosomal recessive

  • Defective ApoE

  • Elevated cholesterol and triglycerides

  • Increased risk of cardiovascular disease

• Type IV Familial Hypertriglyceridemia

  • Autosomal dominant

  • Increased risk of acute pancreatitis

Acquired Causes

• Obesity

• Diabetes mellitus

• Physical inactivity

• Alcoholism

• Hypothyroidism

• Nephrotic syndrome

• Cholestatic liver disease

• Cushing's disease

• Certain medications

  • Oral contraceptive pills

  • High-dose diuretics

  • Metoprolol

• The Frederickson Classification (Fredrickson-Levy-Lees)

  • Type 1 – Familial Hyperchylomicronemia (Autosomal Recessive)

    • Clinical Manifestations:

      • Eruptive xanthomas

      • Hepatosplenomegaly

      • Recurrent episodes of acute pancreatitis

      • Lipemia retinalis

      • Bile duct stenosis

    • Lipoprotein Defect: Chylomicrons

    • Total Cholesterol: Normal to mildly increased

    • Total Triglycerides: Very increased

    • Overnight Plasma: Creamy top layer

    • Risk for Atherosclerosis: None

  • Type 2a – Familial Hypercholesterolemia (Autosomal Dominant)

    • Clinical Manifestations:

      • Premature atherosclerosis

      • Arcus lipoides

      • Tuberous/tendon xanthomas

    • Lipoprotein Defect: LDL

    • Total Cholesterol: Very increased

    • Total Triglycerides: Normal

    • Overnight Plasma: Clear

  • Type 2b – Familial Combined Hyperlipidemia (Autosomal Dominant)

    • Clinical Manifestations:

      • Premature atherosclerosis

      • Arcus lipoides

      • Xanthelasma

    • Lipoprotein Defect: LDL and VLDL

    • Total Cholesterol: Very increased

    • Total Triglycerides: Increased

    • Overnight Plasma: Clear

  • Type 3 – Familial Dysbetalipoproteinemia (Autosomal Recessive)

    • Clinical Manifestations:

      • Premature atherosclerosis

      • Palmar and tuberoeruptive xanthomas

    • Lipoprotein Defect: Remnants of VLDL and chylomicrons

    • Total Cholesterol: Increased

    • Total Triglycerides: Increased

    • Overnight Plasma: Turbid

  • Type 4 – Familial Hypertriglyceridemia (Autosomal Dominant)

    • Clinical Manifestations:

      • Premature atherosclerosis

      • Tuberoeruptive xanthomas

      • Acute pancreatitis

Mind Map: Pathophysiology of Dyslipidemias

Central Idea: Dyslipidemias, like hypercholesterolemia, contribute to cardiovascular diseases.

Main Branches:

• Dyslipidemias

• Hypercholesterolemia

Sub-Branches:

1. Pathophysiology

   • Complex Interactions

   • Increased Cardiovascular Risk

2. Key Lipoproteins

   • Low-Density Lipoprotein (LDL)

   • High-Density Lipoprotein (HDL)

3. Atherosclerosis

   • Fatty Deposits in Arterial Walls

   • Arterial Narrowing and Hardening

4. Cardiovascular Events

   • Coronary Heart Disease

   • Myocardial Infarction

   • Stroke

   • Peripheral Arterial Disease

Mind Map: Clinical Features of Hypercholesterolemia

Skin Manifestations

• Xanthomas

  • Eruptive Xanthomas

  • Tendinous Xanthomas

  • Palmar Xanthomas

  • Xanthelasmas

Eruptive Xanthomas

• Yellow papules with an erythematous border

• Found on buttocks, back, and extensor surfaces of extremities

• Associated with hypertriglyceridemia or lipoprotein lipase deficiency

Tendinous Xanthomas

• Firm nodules in tendons

• Often in extensor tendons of hands and Achilles tendon

• Seen in severe hypercholesterolemia with elevated LDL levels

Palmar Xanthomas

• Yellow plaques on palms

• Associated with type III hyperlipoproteinemia and increased VLDL

Xanthelasmas

• Nodular lipid deposits around eyelids

• Bilateral yellow flat plaques on upper eyelids (nasal side)

• Associated with hypercholesterolemia, hyperapobetalipoproteinemia, and elevated LDL levels

• Increased incidence in individuals with diabetes mellitus and elevated plasma lipoproteins, more common in postmenopausal women

Mind Map: Eye Manifestations

Lipemia Retinalis

• A condition where retinal vessels appear opaque and white, visible during a fundoscopic exam.

  • Arcus Lipoides Corneae

    • A lipid deposit in the cornea, often appearing as a white or gray ring around the corneal edge.

    • More common in older individuals.

    • Can indicate high cholesterol levels in younger people.

Other Manifestations

• Fatty Liver (Hepatic Steatosis)

  • Excess fat accumulation in liver cells.

  • Associated with obesity, insulin resistance, and high triglyceride levels.

• Pancreatitis

  • Severe hypertriglyceridemia can lead to acute pancreatitis.

  • Toxic effects of high triglyceride levels on pancreatic tissue.

Mind Map: Atherosclerosis and Secondary Diseases

Central Idea: Atherosclerosis Progression and Associated Diseases

• Coronary Heart Disease

  • Angina

  • Risk of Myocardial Infarction

• Myocardial Infarction

  • Heart attack

  • Heart muscle damage

• Stroke

  • Brain damage

  • Interrupted blood supply

• Peripheral Arterial Disease

  • Leg pain

  • Difficulty walking

• Carotid Artery Stenosis

  • Reduced brain blood flow

  • Stroke risk

• Cholesterol Embolization Syndrome

  • Cholesterol plaque blockage

  • Tissue damage

Management of Dyslipidemia

• Lifestyle Changes

  • Diet

  • Exercise

• Medications

  • Lowering lipid levels

Mind Map: Diagnostics for Lipid Disorders

Central Idea: Diagnostics for lipid disorders are crucial for cardiovascular risk assessment and management.

Main Branches:

1. Initial Screening

   • Routine Laboratory Testing

2. Confirmatory Testing

   • Fasting Lipid Profile

Sub-branches:

• Routine Laboratory Testing

  • Blood lipid profile

    • Total cholesterol

    • LDL

    • HDL

    • Triglycerides

• Fasting Lipid Profile

  • Total cholesterol

  • HDL

  • Triglycerides

  • LDL calculation

    • LDL = total cholesterol - HDL - (0.2 x fasting triglycerides)

• Diagnostic Criteria

  • Dyslipidemia diagnosis

    • LDL > 3.4 mmol/L

    • HDL < 1 mmol/L

  • Confirmation

    • Pathological values on two separate occasions

Identifying Underlying Causes

• Additional Tests

  • Fasting Blood Glucose or HbA1c

  • TSH Level

  • Liver Function Tests

  • Urine Analysis

• Fasting Blood Glucose or HbA1c

  • Screen for diabetes mellitus

• TSH Level

  • Check for hypothyroidism affecting lipid levels

• Liver Function Tests

  • Influence on lipid metabolism

• Urine Analysis

  • General health assessment

  • Check for kidney disorders

• Lipid Parameters for Assessment

  • Total Cholesterol

  • LDL Cholesterol

  • HDL Cholesterol

• Total Cholesterol

  • <5.2 mM: Optimal

  • 5.2-6.2 mM: Borderline

  • >6.2 mM: High

• LDL Cholesterol

  • <2.6 mM: Optimal

  • 2.6-3.3 mM: Near optimal

  • 3.4-4.1 mM: Borderline high

  • 4.1-4.9 mM: High

  • >4.9 mM: Very high

• HDL Cholesterol

  • <1 mM: Low

  • >1.55 mM: Optimal

• Further Workup for Confirmed Dyslipidemia

  • Patients with Dyslipidemia

    • Evaluation for Cardiovascular Disease (CVD)

      • CVD and Risk Equivalents

        • Myocardial infarction

        • Stroke

        • Symptomatic carotid artery stenosis

        • Peripheral artery disease

        • Abdominal aortic aneurysm

        • Diabetes mellitus

        • Chronic kidney disease

      • Major CVD Risk Factors

        • Smoking

        • Hypertension

        • Elevated total cholesterol/LDL/low HDL

        • Family history of CHD in a first-degree relative (male <55 years; female <65 years)

        • Age (male ≥45 years; female ≥55 years)

Treatment of Lipid Disorders

Lifestyle Modifications

• Dietary Changes

  • Emphasize a diet low in saturated fats and cholesterol.

  • Increase intake of fruits, vegetables, whole grains, and lean protein sources.

• Weight Management

  • Achieve and maintain a healthy weight.

• Physical Activity

  • Engage in regular physical exercise.

Medical Therapy

• Statins

  • Inhibit cholesterol production in the liver.

• Fibrates

  • Lower triglyceride levels and increase HDL cholesterol.

• Bile Acid Sequestrants

  • Bind bile acids in the intestine to lower cholesterol levels.

• PCSK9 Inhibitors

  • Lower LDL cholesterol levels by increasing the liver's ability to remove LDL from the blood.

Mind Map: Medical Therapy

Central Idea: Medical interventions for various conditions

Statins

• Primary choice for lowering LDL cholesterol

• Inhibit HMG-CoA reductase enzyme

Second-Line Lipid-Lowering Agents

• Ezetimibe

• Fibrates

• PCSK9 inhibitors

Treatment of Xanthomas and Xanthelasmas

• Not usually required

• Surgical removal as an option

Management of Congenital Disorders

• Specific interventions for genetic conditions

Lifestyle Modifications and Lipid-Lowering Agents

• High-dose statin therapy with ezetimibe

• Fibrates for hypertriglyceridemia

LDL Apheresis

• Used in severe cases

• Removes LDL particles from the bloodstream

ACC/AHA Guidelines for Statin Therapy

• Initiating Statin Therapy

  • Clinical ASCVD

  • LDL ≥ 4.9 mM

  • Diabetes Patients Aged 40–75 Years

  • Individuals Aged 40–75 Years with a 10-Year ASCVD Risk > 7.5%

• Clinical ASCVD

  • High-intensity statin therapy

  • Moderate-intensity therapy for individuals over 75 years

• LDL ≥ 4.9 mM

  • High-intensity statin therapy

• Diabetes Patients Aged 40–75 Years

  • Statin therapy based on risk assessments

• Individuals Aged 40–75 Years with a 10-Year ASCVD Risk > 7.5%

  • Statin therapy indicated

• Prevention and Screening

  • Screening Recommendations

    • Based on overall CVD risk

    • High-risk individuals start screening earlier

      • Men > 20–25 years

      • Women > 30–35 years

    • Low-risk individuals start screening at older ages

      • Men > 35 years

      • Women > 45 years