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June 18/25, 2019 Circulation. 2019;139:e1082–e1143. DOI: 10.1161/CIR.0000000000000625 e1108

CLINICAL STATEMENTS AND GUIDELINES myalgias)S4.4.4.1-9 and distinctive risks may also develop because of the broader age context (eg, multimorbidity, polypharmacy, sarcopenia, falls, frailty, and cognitive decline),S4.4.4.1-15 potentially confounding effective statin therapy. Aggregate risks increase with age and may become disproportionate to the extent that risks outweigh potential for meaningful benefit. Deprescribing statins becomes an important option to be considered.S4.4.4.1-18 Related studies are evolving, particularly in the palliative care domain. One randomized trialS4.4.4.1-9 and several nonrandomized studies (albeit of relatively lower quality) show feasibility and utility of deprescribing in older adults with significant management complexity.S4.4.4.1-16,S4.4.4.1-17 Nonetheless, these studies also show that decisions about statins are not intuitive because many frailer or more complex patients may prefer to stay on statins precisely because they are at greatest cardiovascular risk.S4.4.4.1-16 Therefore, it is warranted that decisions about statin therapy be individualized and derived from clinician–patient discussions. Moreover, given the predictable fluctuations of health dynamics, such shared decisions should be reconsidered regularly. 3.	 Multiple studies indicate the utility of CAC measurement in identifying the absence of atherosclerotic pathophysiology in older adultsS4.4.4.1-10,S4.4.4.1-11 Moreover, with reduced costs, the long-term consequences of using low-dose computed tomography for CAC screening are much less concerning for older patients. If CAC score is zero, the patient may be reclassified to a lower-risk status to avoid statin therapy.S4.4.4.1-11The BioImage study also indicated that scanning for carotid plaque did not down-classify as many individuals as did a CAC score of zero but still improved specificity of statin assignment.S4.4.4.1-11 Limiting statin therapy to those with CAC scores greater than zero, combined with clinical judgment and patient preference, could provide a valuable awareness with which to inform shared decision-making.

4.4.4.2. Young Adults (20 to 39 Years of Age) Much of atherosclerosis begins in young adulthood.S4.4.4.2-1 Progression of atherosclerosis thereafter becomes clinically manifest as ASCVD in middle age or later years. Thus, prevention of clinical ASCVD optimally begins early in life. In children or adolescents, atherosclerosis may begin to appear in those with hypercholesterolemia; in this age range, more aggressive cholesterollowering may be indicated. Development of atherosclerosis in young adults most commonly is multifactorial and occurs most rapidly in individuals with multiple risk factors (eg, hypercholesterolemia, hypertension, cigarette smoking, diabetes mellitus, and obesity).S4.4.4.2-2 As discussed in these guidelines (Section 4.2.) FH often goes undiagnosed. Young adults with primary elevations of LDL-C ≥190 mg/dl have a long-term ASCVD burden,S4.4.4.2-3 and statin therapy is recommended. In adults with hypercholesterolemia, cascade screening often identifies other family members with elevated LDL-C (Section 4.2.).

However even moderate hypercholesterolemia can accelerate development of atherosclerosis.S4.4.4.2-4 Secondary causes of elevated cholesterol—hypothyroidism (TSH), obstructive liver disease (liver panel), renal disease and nephrosis (creatinine and urine analysis) as well as dietary and medication history—should be addressed appropriately.S4.4.4.2-5 Elevations of LDL-C persisting after excluding secondary causes suggests genetic forms of hypercholesterolemia. Young adults who experience prolonged exposure to hyperlipidemia prior to age 55 are shown to have significantly increased risk of coronary heart disease.S4.4.4.2-6 Intensive lifestyle change has the potential to reduce the hyperlipidemia and associated ASCVD risk factor burden. A smaller group, but even at higher risk, are young adults with persistent, moderate hypercholesterolemia (LDL-C 160-189 mg/dL), especially when risk-enhancing factors, such as a family history of premature AS- CVD, are present. Since there is increased probability of genetic FH in this LDL-C range, clinical judgment would suggest that these high risk young adults will benefit from long-term statin therapyS4.4.4.2-7 (Section 4.2.). Indeed, it has been shown that those with higher LDL-C can gain as much or more benefit from cholesterol reduction as do those with lower pretreatment LDL-C but at higher risk.S4.4.4.2-8,S4.4.4.2-9 In young adults without phenotypically severe hypercholesterolemia, risk assessment should begin by estimation of lifetime risk.S4.4.4.2-10 The pooled cohort equations (PCE) can be used to estimate lifetime risk starting at age 21 years (see Section 4.4.2.). This information can inform a focused risk discussion designed to improve high-risk lifestyle behaviors including tobacco use, sedentary lifestyle and/or poor diet.S4.4.4.2-11,S4.4.4.2-12 When young adults with hypercholesterolemia or multiple risk factors are identified, lifestyle intervention is indicated. To date, no longterm RCTs with cholesterol-lowering drugs have been carried out in those 20 to 39 years age. However, a primary prevention RCT in those younger individuals at low to moderate short-term risk, but at high lifetime risk has been proposed.S4.4.4.2-13 One approach to identifying young adults who could benefit from statins or drug combination would be to detect significant coronary atherosclerosis with coronary artery calcium (CAC) scores. Its use for this purpose has been suggested.S4.4.4.2-14 But again, absence of RCT data precludes guideline recommendations at this time.

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