Dyslipidemia
Adult-Gerontology Acute Care Practice Guidelines
Definition
A.Hyperlipidemia: Elevation of total cholesterol (TC), phospholipids, or triglycerides (TG).
B.Hyperlipidemia can be inherited or caused by secondary diagnoses.
C.It increases the risk of atherosclerosis, leading to stroke and heart disease.
D.Dyslipidemia: Elevation of plasma cholesterol, TGs, or both, or a decreased high-density lipoprotein level (HDL) that augments atherosclerosis.
Incidence
A.Framingham Heart Study noted an epidemiological link between elevated cholesterol and atherosclerotic cardiovascular disease (ASCVD).
B.Current statistics also show that elevated cholesterol is responsible for an estimated 2.6 million deaths per year worldwide.
C.An estimated 31% of U.S. adults have elevated TG (>150 mg/dL).
Pathogenesis
A.Disease process starts in gastrointestinal tract with hydroxymethylglutaryl-coenzyme A (HMG-CoA).
B.HMG-CoA is a precursor that undergoes complex biochemical reactions to produce cholesterol.
C.Once synthesized, cholesterol travels through the plasma.
D.The liver also plays a role, converting very low-density lipoprotein (VLDL) to low-density lipoprotein (LDL), which moves through the plasma.
E.Also, dietary cholesterol that moves from the small intestines to the liver through the serum with LDLs must be considered.
F.Cholesterol is an important organic molecule for cell membrane integrity and serves as precursor to steroid hormones, vitamin D, and bile acid. However, with increased levels of cholesterol, concern is for atherosclerosis.
G.Atherosclerosis is an inflammatory process where various cells and mediators undergo a cascade of reactions to form plaques in the vasculature.
1.Various factors trigger inflammation, such as elevated glucose, tobacco by-products, elevated blood pressure (BP), and oxidized LDLs.
2.With increased inflammation, there is increased permeability and injury to vessel walls. The result is increased accumulation of LDLs within the tunica intima layer of the vasculature.
3.The inflammation causes increased activation of inflammatory mediators (i.e., monocytes and macrophages).
4.Inflammatory mediators uptake the oxidized LDLs, leading to transformation of macrophages into foam cells, also known as fatty streaks within the vasculature.
5.Foam cells eventually result in plaque formation with fibrous caps; when the thin top layer of these caps dislodges, exposing highly thrombotic necrotic contents, platelet aggregation and cardiac ischemia can result.
Predisposing Factors
A.Hereditary: Genetic component for the metabolism of LDL.
1.Familial hypercholesterolemia (FH): A type of hyperlipidemia (HLD) caused by genetic mutation (chromosome 19) where those affected have TC greater than 300 mg/dL and LDL greater than 200 mg/dL (other variations exist with TC >1,000 mg/dL).
B.Diet: Foods high in saturated fat and cholesterol.
C.Lifestyle: Physical inactivity, which can lead to increased cholesterol levels.
D.Comorbidities.
1.Secondary causes of hyperlipidemia: Hypothyroidism, diabetes mellitus (DM), nephrotic syndrome, Cushing disease, chronic kidney disease (CKD), and medications (oral contraceptives, diuretics).
2.Secondary causes of elevated TGs: Obesity, DM, alcohol use, CKD, and medications (estrogen).
3.Concern for metabolic syndrome: Large waist circumference, elevated TGs, low HDL level, elevated BP, elevated glucose levels.
Subjective Data
A.Common complaints/symptoms.
1.Rarely any complaints from hyperlipidemia alone.
2.Concern exists from its sequelae, such as cardiovascular disease, peripheral vascular disease (PVD) secondary to claudication, and neurological diseases (i.e., transient ischemic attack [TIA] and cerebrovascular accident [CVA]).
B.Common history of present illness (HPI).
1.Determine the duration of a patient’s hyperlipidemia diagnosis and how the diagnosis occurred (i.e., detected during routine screening versus after an acute event such as an myocardial infarction [MI] or CVA/TIA).
2.Assess a patient’s routine monitoring of his or her cholesterol—when levels were last checked and how they have evolved over time.
3.Assess a patient’s past medical history for associated comorbidities such as hypertension (HTN), MI, peripheral artery disease (PAD)/PVD, coronary artery disease (CAD), carotid artery stenosis, or DM II. It is also important to assess for any underlying liver disease, which is a contraindication to statin use.
4.If a patient is utilizing lipid-lowering medication, assess for side effects, such as myopathies that are commonly appreciated in statin use. If a patient is utilizing nonpharmacological interventions, such as diet and exercise, those interventions should also be reviewed.
5.Determine if a patient is experiencing any cardiovascular or neurological complaints as a result of the hyperlipidemia.
C.Family and social history.
1.Assess for family history of hyperlipidemia, dyslipidemia, CAD, DM type 2, PVD, PAD, and neurological complications (CVA, TIA).
2.Understand dietary routine, exercise/activity levels, and use of tobacco and alcohol consumption.
D.Review of systems.
1.Evidence of weight gain.
2.Skin changes: Yellow deposits (xanthomas).
3.Cardiac symptoms: Chest pain, palpitations, decreased exercise tolerance, shortness of breath, and dyspnea on exertion.
4.Peripheral vascular status: Claudication.
5.Neurological (if concern for CVA or TIA): Changes in mental status, vision, speech, sensation, and strength.
Physical Examination
A.Vital signs: Determine body mass index (BMI) and consider comorbid HTN.
B.Skin: Check for xanthomas.
C.Ophthalmologic: Perform funduscopic examination and check for possible corneal arcus.
D.Neck: Auscultate carotid arteries and evaluate for carotid bruits.
E.Cardiovascular: Inspect for lifts/heaves/visible pulsations, assess point of maximum impulse (PMI), palpate for thrills, and auscultate using diaphragm and bell for murmurs and extra heart
sounds.
F.If concern for CVA/TIA—consider complete neurological examination.
Diagnostic Tests
A.For the evaluation of dyslipidemia, the U.S. Preventive Services Task Force (USPSTF) strongly recommends (level A evidence) the routine screening of males 35 years old and older and females 45 years old and older for lipid disorders.
B.Evaluation should consist of fasting (9–12 hours fast) lipid panel for TC, LDL, and HDL (see Table 3.3).
C.For secondary causes of dyslipidemia, workup should include a complete blood count, complete metabolic panel, fasting glucose, thyroid-stimulating hormone (TSH), and urinary protein.
D.Lipid measurement should be accompanied by evaluation for other cardiovascular risk factors, including an ECG, stress testing, and echocardiogram.
Differential Diagnosis
A.The focus of the differential diagnosis in dyslipidemia is on primary versus secondary causes.
1.Primary causes—inherited disorder.
2.Secondary causes.
a.Hypothyroidism.
b.Corticosteroids.
c.Alcoholism.
d.Smoking.
e.Obstructive liver disease.
TABLE 3.3 Diagnostic Interpretation of Lipid Panel
HDL, high-density lipoprotein; LDL, low-density lipoprotein; TC, total cholesterol.
f.Renal failure.
g.Uncontrolled diabetes.
h.Nephrotic syndrome.
Evaluation and Management Plan
A.General plan.
1.The National Cholesterol Education Program (NCEP) and Adult Treatment Panel (ATP) III have created a process for the management of elevated cholesterol.
2.Determine LDL, TC, and HDL levels.
3.Identify any comorbidities, including cardiovascular disease or its equivalents (DM, PAD, abdominal aortic aneurysm).
4.Identify modifiable and unmodifiable risk factors: Low HDL, tobacco use, HTN, age (males >45 years and females >55 years), and family history of CAD.
5.Assess overall cardiovascular risk and determine goal LDL.
6.Initiate therapeutic lifestyle changes (TLC) plan if LDL is higher than goal: Consists of increased physical activity, weight management, and low trans fat and low cholesterol diet.
7.Utilize medications if LDL remains above goal.
8.Assess for metabolic syndrome and evaluate TGs.
9.Treat elevated HDL and TGs if required.
B.Patient/family teaching points.
1.Emphasize medication compliance, use of TLC plan, and elimination of modifiable risk factors (i.e., tobacco cessation).
2.Stress importance of compliance with clinician appointments.
C.Pharmacotherapy.
1.Lipid management.
a.Statins (HMG-CoA reductase inhibitor).
i.Important considerations regarding side effects of statins.
ii.Elevation in liver enzymes (usually alanine aminotransferase [ALT]).
iii.Myalgias: Occurs in approximately 10% of patients, can be dose dependent; switching to different statin can help relieve symptoms.
iv.Rhabdomyolysis: Myalgias plus creatine kinase (CK) levels greater than 10,000 U/L can result in renal failure.
v.Myositis: Myalgias with CK less than 10,000 U/L.
b.Bile acid sequestrants.
c.Cholesterol absorption inhibitors.
d.Injectable medications (monoclonal antibodies); works by allowing liver to absorb increased level of cholesterol, thus decreasing circulating plasma cholesterol).
2.Medications for high TG.
a.Fibrates.
b.Niacin.
c.Omega-3 fatty acids supplements.
Follow-Up
A.Check lipid levels per American College of Cardiology (ACC) and American Heart Association (AHA) recommendations, which stipulate checking levels at 4 to 12 weeks after initiating (or changing) statin therapy and then every 3 to 12 months thereafter.
B.Obtain baseline liver and CK levels before initiating statin therapy (routine monitoring not required).
Consultation/Referral
A.Consult with lipidologist in the following situations.
1.Suspicion for primary genetic disorder.
2.Unsuccessful treatment plans despite optimal therapy and patient compliance.
3.Comorbid liver disease if limiting therapeutic options.
4.Young adults in whom long-term therapy and monitoring is a consideration.
Special/Geriatric Considerations
A.Patients with statin intolerance. Use the following.
1.Lower intensity statin or nondaily moderate intensity statin.
2.Low-dose statin with selective cholesterol-absorption therapy (ezetimibe), bile acid sequestrants, or niacin.
3.Nonstatin monotherapy with goal of 30% reduction in LDL levels.
B.Geriatric considerations.
1.Patients at least 65 to younger than 80 years of age with ASCVD or DM: Consider moderate or high intensity statin (once risks/benefits assessed by provider and patient).
2.For secondary cardiovascular prevention in patients 80 years of age or older: Consider moderate intensity statin once risks/benefits assessed by provider and patient.
Bibliography
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