Study Points

Hyperlipidemias and Atherosclerotic Cardiovascular Disease

Course #90843 - $40 • 10 Hours/Credits

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  1. Atherosclerotic cardiovascular disease (ASCVD) accounts for approximately what percentage of deaths in the United States?

    INTRODUCTION AND EPIDEMIOLOGY OF ATHEROSCLEROTIC CARDIOVASCULAR DISEASES

    Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of death in developing countries and accounts for 25.7% of all deaths in the United States and 47% of deaths in Europe [1,2]. It has been estimated that by 2030 ASCVD will account for approximately 23 million annual deaths worldwide, an increase of more than 5 million from current estimates [3].

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  2. Approximately what percentage of Americans 20 years of age or older have total blood cholesterol levels in excess of 240 mg/dL?

    INTRODUCTION AND EPIDEMIOLOGY OF ATHEROSCLEROTIC CARDIOVASCULAR DISEASES

    Data published in the National Health and Nutrition Examination Survey revealed that an estimated 12.1% of Americans 20 years of age and older have total blood cholesterol concentrations of 240 mg/dL (6.2 mmol/L) or greater, which are associated with high risk of cardiovascular morbidity and mortality [15].

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  3. Which of these statements regarding atherosclerosis is TRUE?

    ETIOLOGY OF ATHEROSCLEROSIS

    Atherosclerosis is a chronic inflammatory process that targets medium- and large-sized arteries. This process is initiated during childhood and progresses slowly with age. However, the condition is rapidly accelerated by a variety of genetic and environmental factors, and hyperlipidemia is a major risk factor in the pathogenesis and progression of atherosclerosis [12,14,26,27].

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  4. All of the following are progressive stages of atherosclerosis, EXCEPT:

    ETIOLOGY OF ATHEROSCLEROSIS

    The pathologic processes underlying atherosclerosis can be categorized into three progressive stages: fatty streak formation, plaque formation, and plaque disruption [12,27,28,29,30,31].

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  5. Which of the following is NOT considered a biomarker for ASCVD?

    RISK FACTORS FOR HYPERLIPIDEMIA

    As discussed, hyperlipidemia has been established as a main risk factor in the development of atherosclerosis and ASCVD. Together with obesity, hypertension, diabetes, smoking, and physical inactivity, hyperlipidemia is a known modifiable risk factor of ASCVD. Additionally, several biomarkers, including C-reactive protein (CRP), hyperhomocysteinemia, and lipoprotein(a), are also considered modifiable risk factors of ASCVD. Modifiable risk factors play a major role in the pathogenesis of ASCVD because they activate the endothelium and stimulate the release of proinflammatory mediators and cell surface adhesion molecules. Because modifiable risk factors account for up to 90% of population-attributable cardiac risk, regulation of these factors has a beneficial effect on the primary and secondary prevention of ASCVD [11,12].

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  6. The role of lipoprotein(a) in atherogenesis relates to a variety of mechanisms, EXCEPT:

    RISK FACTORS FOR HYPERLIPIDEMIA

    Numerous clinical studies have also revealed that high levels of lipoprotein(a) are associated with significant increases in ASCVD [12,27,31,46,47,48]. Lipoprotein(a) is a subtype of LDL that includes apoprotein A (Apo A) in its structure. The role of lipoprotein(a) in atherogenesis relates to a variety of mechanisms including inhibition of fibrinolysis by preventing the transformation of plasminogen to plasmin, enhanced capacity to traverse the arterial endothelium, and low affinity for the LDL-receptor mediated clearance from circulation [47]. High lipoprotein(a) concentrations (greater than 30 mg/dL) in patients with an elevated total cholesterol:HDL ratio (greater than 5.5) or other major risk factors indicates the need for a more aggressive therapy to further lower LDL [23,49].

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  7. Dietary lipids account for what percentage of calories in western diets?

    AN OVERVIEW OF LIPIDS

    Dietary lipids provide 30% to 40% of calories in Western diets. With the exception of the essential fatty acids (e.g., linoleic, linolenic), most lipids can also be synthesized by humans. Triglycerides, specifically, account for more than 95% of dietary lipid intake. Cholesterol from animal sources and small amounts of plant sterols comprise the majority of dietary lipid intake. Free fatty acids, phospholipids, and fat-soluble vitamins account for the remaining lipids from dietary sources [46,50,53].

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  8. What is the main site of lipid transformation and absorption?

    AN OVERVIEW OF LIPIDS

    Dietary fat is digested by enzymes produced in the mouth, stomach, and pancreas. The small intestine is the main site of lipid transformation and absorption. In the small intestine, triglycerides are hydrolyzed by gastric and pancreatic lipases, phospholipids are transformed by phospholipase A2 into lysophospholipids and fatty acids, and cholesterol is hydrolyzed by bile salts and pancreatic hydrolase (also known as cholesterol esterase).

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  9. Which of the following statements regarding chylomicrons is FALSE?

    AN OVERVIEW OF LIPOPROTEINS

    Chylomicrons are large lipoproteins 75–1,200 nm in diameter that are very rich in lipids (98% content), mainly triglycerides (83%) and cholesterol (8%), and have the lowest protein content (2%) of all lipoproteins. Chylomicrons are only synthesized in the intestine and are produced in large amounts during fat ingestion [53]. In normolipidemic individuals they are present in the plasma for 3 to 6 hours after fat ingestion and are absent after 10 to 12 hours fasting [14].

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  10. Increased LDL levels can result from

    AN OVERVIEW OF LIPOPROTEINS

    Genetic mutations of either the LDL receptor or Apo B-100 alter the effectiveness of the binding and increase the plasma concentration of LDL. Familial hypercholesterolemia and familial defective Apo B-100 are examples of clinical conditions that result from these genetic mutations [82,83]. Homozygotes for familial hypercholesterolemia inherit two mutant LDL receptor genes and present with a 6- to 10-fold elevation in plasma LDL from birth. These patients suffer from advanced CHD starting in early childhood [72,84].

    The expression of LDL receptors in the liver is also regulated by the intracellular enzyme HMG-CoA reductase. Inhibition of HMG-CoA reductase, for example by the administration of statins, not only results in direct inhibition of the intracellular synthesis of cholesterol but indirectly increases the expression of LDL receptors and therefore promotes the LDL-receptor-mediated removal of circulating cholesterol.

    The LDL receptor is also relevant from a clinical perspective because both thyroid hormones and estrogens stimulate its expression in the liver [80,85]. Consequently, deficiencies of these hormones decrease the availability of LDL receptors and result in increased concentrations of circulating LDL and increased risk of ASCVD [14,80].

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  11. Which of the following statements regarding HDLs is TRUE?

    AN OVERVIEW OF LIPOPROTEINS

    HDLs are the smallest (5–12 nm in diameter) but the densest lipoproteins (33% protein content). HDL removes cholesterol from the periphery and transports it to the liver [53]. HDLs are a heterogeneous population classified based on size, density, and apoprotein content. The two most important subclasses of HDL express either Apo A-I alone or both Apo A-I and A-II, but the clinical relevance of the various subtypes is unknown [88].

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  12. Research has shown that moderate-to-high HDL levels may help to prevent ASCVD. The main goal for patients with hyperlipidemias should be to

    AN OVERVIEW OF LIPOPROTEINS

    In vitro and in vivo studies have revealed that HDL has anti-inflammatory and antioxidant properties and inhibits atherogenesis. It has been suggested that high levels of HDL have a protective effect on the development of atherosclerosis and ASCVD [88,92].

    However, authors of a systematic review of clinical studies concluded that "simply increasing the amount of circulating HDL does not necessarily confer cardiovascular benefits" and that reduction of LDL should remain "the primary goal for lipid-modifying interventions" [93]. Other researchers concluded that raising endogenous HDL levels in humans to reduce the development of atherosclerosis "has yet to be established conclusively" [88]. Together, these studies further support the recommendation that lowering LDL should remain the target goal for patients with hyperlipidemia and/or at risk for ASCVD-related conditions [22,24].

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  13. As primary hyperlipidemia progresses, the following signs and symptoms develop, EXCEPT:

    CLASSIFICATION OF HYPERLIPIDEMIAS

    At the early stages, primary hyperlipidemias are asymptomatic. However, as the disease progresses, a constellation of signs and symptoms develop, such as eruptive xanthomas (located on the trunk, back, buttocks, elbows, knees, hands, and feet), severe hypertriglyceridemia (greater than 2,000 mg/dL), lipemic plasma (i.e., plasma develops a creamy supernatant when incubated overnight), and lipemia retinalis (i.e., creamy white-colored blood vessels in the fundus) often associated with premature CHD or peripheral vascular disease [46,100,103].

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  14. With an incidence greater than 25% in the United States, the most common form of hyperlipidemia is

    CLASSIFICATION OF HYPERLIPIDEMIAS

    Polygenic hypercholesterolemia, also known as nonfamilial hypercholesterolemia, is the most common form of hyperlipidemia, with a prevalence of more than 25% in the American population [106]. Polygenic hypercholesterolemia is a typical example of the combination of multiple genetic deficiencies that result in decreased activity of the LDL receptor and reduction of LDL clearance. This underlying genetic susceptibility, not yet completely understood, becomes apparent with dietary intake of saturated fats, obesity, and sedentary lifestyle. Twenty percent of polygenic hypercholesterolemia patients have a family history of CHD. Patients present with mild-to-high increases in total cholesterol (250–350 mg/dL or 6.5–9.0 mmol/L) and LDL (130–250 mg/dL or 3.33–6.45 mmol/L). A combination of lifestyle changes (e.g., reduction in saturated fat) and lipid-lowering drugs (e.g., statins, bile acid sequestrants, ezetimibe, niacin) effectively control the condition [31,107].

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  15. Secondary hyperlipidemias can be precipitated by the use of certain medication treatments. These treatments include estrogen therapy, atypical antipsychotics, corticosteroids, and

    CLASSIFICATION OF HYPERLIPIDEMIAS

    Secondary hyperlipidemias can also be associated with a number of drug-induced conditions such as estrogen therapy (increased triglycerides and increased total cholesterol), atypical antipsychotics (increased triglycerides), corticosteroids (increased total cholesterol), selective α-blockers without intrinsic sympathetic activity or α-antagonism (increased total cholesterol and decreased HDL), and thiazides (modest increase in total cholesterol and LDL) [67,114].

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  16. Secondary hyperlipidemia with elevated cholesterol is the main dyslipidemia in patients with

    CLASSIFICATION OF HYPERLIPIDEMIAS

    In summary, secondary hyperlipidemias with elevated triglycerides are the primary lipid abnormality in patients with obesity, diabetes, alcohol abuse, hormone replacement therapy, and atypical antipsychotic therapy. Secondary hyperlipidemias with elevated cholesterol are the main dyslipidemia in patients with chronic renal failure, hypothyroidism, and typical β-blocker use (e.g., propranolol, atenolol).

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  17. The primary goal of lipid therapy in high-risk patients is to reduce LDL cholesterol by

    APPROACHES TO CLINICAL MANAGEMENT OF HYPERLIPIDEMIAS

    Management of existing hyperlipidemia is a cornerstone in the prevention and management of ASCVD. In large randomized controlled trials, LDL lowering has been consistently shown to reduce the risk of ASCVD. However, in clinical practice, absolute responses in LDL levels to statin therapy depend on baseline LDL levels and the intensity of lipid-lowering therapy. A given dose of statins produces a similar percentage reduction in LDL levels across a broad range of baseline levels; therefore, percentage reduction is a more reliable indicator of statin efficacy. The 2018 AHA/ACC guideline uses percentage reduction to estimate the efficacy of statin therapy, with the primary goal being a ≥50% reduction in LDL levels [24].

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  18. Which of the following statements regarding lipid management through lifestyle change is TRUE?

    LIFESTYLE MODIFICATION

    It is important to adapt the dietary pattern to the patient's calorie requirements, personal and cultural food preferences, and nutrition therapy for other medical conditions, including diabetes. A successful dietary approach to lipid lowering requires instruction by a dietitian or other knowledgeable healthcare professional.

    Instructions to patients should not be presented as a list of "foods to avoid" but rather should provide dietary alternatives and teach the patients how to make appropriate dietary choices and control portions. A balanced diet, particularly in the modality known as the Mediterranean diet, is associated with a significant reduction in cardiovascular events and mortality [116,117,118]. The Mediterranean diet is characterized by meals predominately consisting of vegetables/fruits, lean protein, and healthy fats (e.g., olive oil) and the moderate consumption of wine. Plans such as those offered by the USDA's Dietary Guidelines for Americans, the AHA Diet and Lifestyle Recommendations, and the DASH Eating Plan can also help the patient achieve recommended lifestyle changes [119,120,121].

    Physical activity stimulates the activity of lipoprotein lipase in adults as well as in children, lowers triglycerides and VLDL, and promotes cardiovascular fitness and weight loss [31,122]. As such, patients should be encouraged to engage in moderate-intensity physical activity on most days of the week unless contraindicated.

    Although dietary changes should always be included in the treatment of hyperlipidemias, the length of time given to lifestyle changes prior to initiation of pharmacotherapy remains controversial. In patients with low cardiovascular risk, it has been proposed that the efficacy of dietary and other lifestyle changes can be assessed in two to three visits over a two- to three-month period. Drug therapy is recommended only in select patients with moderately-high LDL (≥160 mg/dL) or patients with very-high LDL (190 mg/dL). High-intensity or maximal statin therapy plus ezetimibe and/or a PCKS9 inhibitor is recommended for the patient at very-high risk (i.e., history of multiple major ASCVD events) [24].

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  19. Bile acids are the source of what percentage of cholesterol in the intestine?

    LIPID-LOWERING MEDICATIONS

    Bile acid-binding resins, also known as bile acid sequestrants, are cationic polymers that bind to the negatively charged bile acids in the lumen of the intestine. The bile-acid complex cannot be absorbed by the intestinal mucosa and is subsequently eliminated in the feces [129]. Bile acids are the source of 75% of cholesterol in the intestine, and inhibition of their reabsorption effectively disrupts chylomicron formation and decreases the availability of cholesterol and triglycerides in the liver.

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  20. The cholesterol absorption inhibitor ezetimibe can increase the efficacy of what other treatment by 25%?

    LIPID-LOWERING MEDICATIONS

    Ezetimibe selectively targets and inhibits the transporter NPC1L1, preventing the uptake of cholesterol and phytosterol across the intestinal lumen. Ezetimibe is indicated as adjunctive therapy to diet for the reduction of total cholesterol, LDL, and Apo B in patients with primary (heterozygous familial and nonfamilial) hyperlipidemia [109,133]. It lowers LDL by 15% to 20% and causes minimal increases in HDL, but its beneficial effect on prevention of CHD remains unclear. This agent is synergistic with statins and, if taken in conjunction, can lower LDL by up to 25% in addition to the results obtained by statins alone [109,134]. Ezetimibe is available in a combination formulation with the statin simvastatin under the brand name Vytorin. A second combination formulation combining ezetimibe with the statin atorvastatin, brand name Liptruzet, received U.S. Food and Drug Administration (FDA) approval in 2013. However, Liptruzet was recalled in 2014 for packaging issues and discontinued in 2016 [109,133,135,136].

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  21. Of the following, which statin is among the most effective in its class?

    LIPID-LOWERING MEDICATIONS

    The first statin to be tested and approved for clinical use, lovastatin, was isolated from the mold Aspergillus terreus, and pravastatin and simvastatin are chemically modified derivatives of the original molecule. Atorvastatin, fluvastatin, and rosuvastatin are synthetic compounds with distinct molecular structures. Lovastatin, pravastatin, and simvastatin are inactive prodrugs that require hydroxylation in the liver into their active forms. Although all statins are clinically very effective, rosuvastatin, atorvastatin, and simvastatin have the highest drug efficacy in this class (Table 5).

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  22. In addition to lowering lipid levels, statins are thought to have all of the following pleiotropic effects, EXCEPT:

    LIPID-LOWERING MEDICATIONS

    In addition to the lipid-lowering actions of statins, studies suggest that the drugs are also implicated in a number of additional actions known as pleiotropic effects. This includes modulation of endothelial function, decrease in vascular inflammation, neuroprotection, and immunomodulation by inhibition of major histocompatibility complex II expression, which is upregulated in patients with myocarditis, multiple sclerosis, and rheumatoid arthritis [143,144,145]. Statins have been linked to a reduction in the risk of developing Alzheimer disease independent of the drugs' lipophilicity [145,146].

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  23. To achieve optimum lipid control in patients with dyslipidemia, the initial dosage of any statin should be based on which factor?

    LIPID-LOWERING MEDICATIONS

    As stated, the percentage reduction in LDL levels is used to estimate the efficacy of statin therapy, with the primary goal being a ≥50% reduction [24]. In clinical practice, absolute responses in LDL levels to statin therapy depend on baseline levels and the intensity (i.e., low, moderate, or high) of lipid-lowering therapy [24].

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  24. Compared to statin monotherapy, bile acid- binding resin/statin combinations decrease LDL levels by what percentage?

    LIPID-LOWERING MEDICATIONS

    The combination of statins with other lipid-lowering drugs further improves the lipid-lowering outcome. The combination of simvastatin with ezetimibe lowers LDL by an additional 18% to 20% compared with simvastatin alone [147]. Administration of a statin with a bile acid-binding resin (e.g., cholestyramine, colestipol) produces 20% to 30% greater reductions in LDL than statins alone [148,149].

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  25. Niacin, or nicotinic acid, is also known as what vitamin?

    LIPID-LOWERING MEDICATIONS

    Niacin, also known as nicotinic acid or vitamin B3, is a water-soluble vitamin that at physiologic levels is a substrate for nicotinamide adenine dinucleotide (NAD) and NAD phosphate (NADP), important cofactors in intermediary metabolism. Niacin is available in normal- or extended-release formulation as well as in conjunction with lovastatin (as Advicor).

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  26. Which of the following statements regarding niacin is TRUE?

    LIPID-LOWERING MEDICATIONS

    Niacin has low cost, a long history of clinical trials, and extensive use as a safe lipid-lowering drug, supported by evidence that it is effective in the prevention of ASCVD [31]. However, it is no longer recommended, except in specific clinical situations, such as a patient with triglyceride levels >500 mg/dL, a patient who is not able to achieve desired response, or a patient with intolerance to other therapies [109]. Although niacin has a mild LDL-lowering action, randomized controlled trials do not support its use as an add-on to statin therapy, and it is not listed as an LDL-lowering drug option in the 2018 AHA/ACC guideline [24]. Niacin has not been shown to reduce ASCVD outcomes beyond that achieved with statin use, and it may be associated with harm [167,168,169].

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  27. Omega-3 fatty acids are abundant in what dietary sources?

    LIPID-LOWERING MEDICATIONS

    Omega-3 polyunsaturated fatty acids are considered essential fatty acids because humans, as well as other mammals, are unable to synthesize these compounds efficiently. Eicosapentaenoic (EPA) and docosahexaenoic acids (DHA) are omega-3 polyunsaturated fatty acids derived from alpha-linolenic acid (ALA). Although humans are able to transform negligible amounts of ALA into EPA and DHA (<1%), dietary supplementation is the only physiologically relevant source [173]. Omega-3 fatty acids EPA and DHA are abundant in fatty fish, such as salmon, mackerel, sardines, trout, and herring, and other seafood sources, as well as in walnuts and canola, flaxseed, and linseed oils. Vegetable oils such as soybean, corn, sunflower, safflower, and cotton seed oils are good dietary sources of omega-6 fatty acids, which will be discussed in detail later in this course [57,174,175,176].

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  28. Because they can be synthesized in the body, which of these fatty acids are considered non-essential?

    LIPID-LOWERING MEDICATIONS

    Omega-6 polyunsaturated fatty acids such as gamma-linoleic acid (GLA) are derived from linoleic acid. Omega-9 polyunsaturated fatty acids, unlike omega-3 and omega-6, are non-essential because they can be synthesized in humans. The most relevant omega-9 fatty acid is oleic acid, which is present in olive oil, and supplementation is not required.

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  29. According to the AHA/ACC, for patients 75 years of age or younger with clinical ASCVD on high-intensity therapy, the target percentage LDL reduction should be

    CLINICAL GUIDELINES FOR THE TREATMENT OF HYPERLIPIDEMIAS

    AHA/ACC RECOMMENDATIONS FOR STATIN THERAPY

    AgePatient FactorsRecommendationTarget % LDL
    Patients With ASCVD
    ≤75 yearsClinical ASCVDHigh-intensity statin (initiate or continue)≥50%
    Clinical ASCVD and contraindication to high-intensity statinModerate-intensity statin (initiate or continue)30% to 49%
    Clinical ASCVD, at very high risk, being considered for PCKS9 inhibitor therapyMaximally-tolerated LDL-lowering therapy (with maximally tolerated statin and ezetimibe)
    Clinical ASCVD, at very high risk, on maximally tolerated LDL-lowering therapy, with LDL ≥70 mg/dL or non-HDL ≥100 mg/dLIt is reasonable to add PCSKP-I following clinician-patient discussion
    Clinical ASCVD, on maximally tolerated statin therapy, at very high risk, with LDL ≥70 mg/dLIt is reasonable to add ezetimibe
    ≥75 yearsClinical ASCVD and evaluated for ASCVD risk reduction, statin adverse effects, drug-drug interactions, patient frailty and preferencesIt is reasonable to initiate moderate- or high-intensity statin30% to 49%
    Currently tolerating high-intensity statin therapy and evaluated for ASCVD risk reduction, statin adverse effects, drug-drug interactions, patient frailty and preferencesIt is reasonable to continue high-intensity statin
    Clinical ASCVD, currently receiving maximally tolerated statin therapy but LDL level remains ≥70 mg/dLIt may be reasonable to add ezetimibe
    Heart failure and reduced ejection fraction attributable to ischemic heart disease and reasonable life expectancy (3 to 5 years), not on statin therapy due to ASCVDMay consider initiation or moderate-intensity statin therapy
    Clinical ASCVD, on maximally tolerated statin therapy, at very high risk, with LDL ≥70 mg/dLIt is reasonable to add ezetimibe
    Patients With Severe Hypercholesterolemia
    20 to 75 yearsLDL ≥190 mg/dLMaximally-tolerated statin therapy≥50%
    LDL ≥190 mg/dL, achieves <50% reduction in LDL while receiving maximally tolerated statin and/or have LDL ≥100 mg/dLEzetimibe therapy is reasonable
    Baseline LDL ≥190 mg/dL, achieves <50% reduction in LDL levels and has fasting triglycerides ≤300 mg/dL while taking maximally tolerated statin and ezetimibe therapyConsider adding a bile acid sequestrant
    30 to 75 yearsHeterozygous FH with LDL ≥100 mg/dL while taking maximally tolerated statin and ezetimibe therapyConsider adding a PCSK9 inhibitor≥50%
    40 to 75 yearsBaseline LDL ≥220 mg/dL, achieves on-treatment LDL ≥130 mg/dL while receiving maximally tolerated statin and ezetimibe therapyConsider adding a PCSK9 inhibitor≥50%
    Patients With Diabetes
    40 to 75 yearsDiabetesModerate-intensity statin, regardless of estimated 10-year ASCVD risk
    Diabetes and LDL 70-189 mg/dLReasonable to assess 10-year risk of first ASCVD event using race-, sex-specific pooled cohort equations
    Diabetes with multiple ASCVD risk factorsReasonable to prescribe high-intensity statin≥50%
    ≥75 yearsDiabetes and on statin therapyReasonable to continue statin therapy 
    Diabetes and 10-year ASCVD risk ≥20%May be reasonable to add ezetimibe to maximally tolerated statin≥50%
    >75 yearsDiabetesMay be reasonable to initiate statin therapy after clinician-patient risk discussion
    20 to 39 yearsDiabetes with specific risk enhancersaMay be reasonable to initiate statin therapy
    Patients With No Diabetes But Other Risk Factors
    40 to 75 yearsLDL ≥70 mg/dL and 10-year ASCVD risk ≥7.5%Moderate-intensity statin, if favored by clinician-patient risk discussion
    aDiabetes of long durations (≥10 years type 2, ≥20 years type 1), albuminuria, eGFR <60 mL/min/1.73 m2, retinopathy, neuropathy, ankle-brachial index <0.9
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  30. The 2018 AHA/ACC guideline recommendations for a heart-healthy dietary pattern include all of the following, EXCEPT:

    LIFESTYLE MODIFICATION

    The 2018 AHA/ACC guideline supports the recommendations for lifestyle changes outlined in the previous guideline on lifestyle management [24,115]. Adults who would benefit from LDL lowering are advised to follow a dietary pattern that [115]:

    • Emphasizes the intake of fruits, vegetables, and whole grains

    • Includes low-fat dairy products, poultry, fish, legumes, nontropical vegetable oils, and nuts

    • Limits the intake of sweets, sugar-sweetened beverages, and red meats

    • Allows for no more than 5% to 6% of calories from saturated fat

    • Reduces calories from trans fat

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  • Back to Course Home
  • Participation Instructions
    • Review the course material online or in print.
    • Complete the course evaluation.
    • Review your Transcript to view and print your Certificate of Completion. Your date of completion will be the date (Pacific Time) the course was electronically submitted for credit, with no exceptions. Partial credit is not available.