Translating AHA/ACC cholesterol guidelines into meaningful risk reduction
The new recommendations detail refined, personalized lipid management and emphasize multiple levels of evidence. The result? Care is more complex but patients might benefit more.
PRACTICE RECOMMENDATIONS
› Reduce the low-density lipoprotein cholesterol (LDL-C) level in patients with clinical atherosclerotic cardiovascular disease (ASCVD) using high-intensity statin therapy or maximally tolerated statin therapy. A
› Use an LDL-C threshold of 70 mg/dL to prompt consideration of adding nonstatin therapy in patients who have very high-risk ASCVD. A
› Start high-intensity statin therapy in patients who have primary hypercholesterolemia (LDL-C level ≥ 190 mg/dL) without calculating the 10-year ASCVD risk. A
› Begin moderate-intensity statin therapy in patients 40 to 75 years of age who have diabetes mellitus and an LDL-C level ≥ 70 mg/dL without calculating 10-year ASCVD risk. A
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Medical therapy. The decision to start lipid-lowering therapy should be made after a physician–patient discussion that considers costs of therapy as well as patient preferences and values in the context of shared decision-making. Discussion should include a review of major risk factors (eg, cigarette smoking, elevated blood pressure, and the LDL-C level), the PCE risk score, the presence of risk-enhancing factors (TABLE 21), potential benefits of lifestyle changes and statin therapy, and the potential for adverse drug effects and drug–drug interactions.1
If the estimated ASCVD risk is 7.5%-19.9%, starting moderate-intensity statin therapy is recommended. Risk-enhancing factors favor initiation of statin therapy, even in patients at borderline risk (5%-7.5%). If risk is uncertain, the CAC score can be used to facilitate shared decision-making.1 The use of CAC is in agreement with the USPSTF statement that CAC can moderately improve discrimination and reclassification, but has an unclear effect on downstream health care utilization.15 Importantly, CAC should not be measured routinely in patients already taking a statin because its primary role is to facilitate shared decision-making regarding initiation of statin therapy.16
If the 10-year ASCVD risk is ≥ 20%, high-intensity statin therapy is advised, without need to obtain the CAC score. If high-intensity statin therapy is advisable but not acceptable to, or tolerated by, the patient, it might be reasonable to add a nonstatin drug (ezetimibe or a bile-acid sequestrant) to moderate-intensity statin therapy.1
Risk-enhancing factors (TABLE 21) apply to intermediate- and borderline-risk patients. Importantly, these factors include membership in specific ethnic groups, conditions specific to females, and male–female distinctions in risk. Risk-enhancing factors also incorporate biomarkers that are often measured by lipid specialists, such as lipoprotein(a) (Lp[a]) and apolipoprotein B (ApoB).1
Lp(a) is an atherogenic particle, akin to an LDL particle, that consists of a molecule of apolipoprotein (a) (a nonfunctional mimic of a portion of plasminogen) covalently bound to ApoB, like the one found on the LDL particle. Lp(a) is proportionally associated with an increased risk for ASCVD and aortic stenosis at a level > 50 mg/dL.17 A family history of premature ASCVD is a relative indication for measuring Lp(a).1
Continue to: When and why to measure CAC
