Executive Summary
Modern cholesterol treatment is not a contest to find the single “best” drug. The central objective is to reduce cumulative exposure to atherogenic ApoB-containing particles enough to match the patient’s absolute cardiovascular risk. Statins remain the foundation because they combine large LDL-C reductions, decades of randomized outcomes evidence, low cost and broad availability. The 2026 ACC/AHA dyslipidemia guideline continues to place statin therapy at the center of LDL-lowering treatment while allowing earlier use of evidence-based nonstatins when the LDL-C reduction required is too large for one drug, when treatment goals are not reached or when statins are not tolerated. [1]
The nonstatin era is now mature. Ezetimibe has randomized event-reduction evidence from IMPROVE-IT and usually adds a further 15–20% LDL-C reduction to statin therapy. Bempedoic acid lowers LDL-C by roughly 18–25% and reduced cardiovascular events in statin-intolerant high-risk patients in CLEAR Outcomes. PCSK9 monoclonal antibodies produce approximately 50–60% additional LDL-C lowering and reduced events in FOURIER and ODYSSEY OUTCOMES. These therapies are not merely “backup drugs”; in very-high-risk patients or in those starting far above goal, combination therapy may be the most rational way to reach an evidence-based target quickly. [3-6]
Two newer PCSK9-directed approaches require a more precise interpretation. Inclisiran produces durable LDL-C lowering of about 50% with infrequent dosing, but its dedicated cardiovascular outcomes trials had not reported definitive event results by August 2026. Enlicitide (Lipfendra), approved by the U.S. FDA in July 2026, is the first oral PCSK9 inhibitor and lowers LDL-C by roughly 55–60% in phase 3 lipid trials. Its approval is for LDL-C lowering, not because a completed outcomes trial has yet shown fewer myocardial infarctions or strokes. The distinction between biomarker efficacy and outcomes evidence must remain explicit. [7-10]
A separate category includes drugs that reduce cardiovascular risk without functioning primarily as LDL-lowering therapies. GLP-1 receptor agonists and SGLT2 inhibitors are highly important in selected patients with obesity, diabetes, heart failure or chronic kidney disease, but they do not replace treatment of elevated LDL-C or ApoB. Likewise, severe inherited disorders such as homozygous familial hypercholesterolemia may require specialist therapies including evinacumab or lipoprotein apheresis. [13-15]
The practical question is therefore not “Which cholesterol drug is strongest?” It is “How much LDL-C/ApoB reduction is needed, how quickly is it needed, what outcome evidence applies to this patient, what can the patient tolerate and adhere to, and which combination reaches the goal with the least unnecessary burden?”
Statins remain the default foundation. Ezetimibe, bempedoic acid and PCSK9 monoclonal antibodies have cardiovascular outcomes evidence. Inclisiran has powerful LDL-C lowering with outcomes trials still ongoing. Enlicitide adds an oral PCSK9 option approved for LDL-C lowering in July 2026, with dedicated cardiovascular outcomes evidence still pending.
Figure 1. A modern LDL-lowering treatment ladder. Therapy can be combined earlier when baseline risk is high or the required LDL-C reduction is large.
Related guides: statin therapy guide • ezetimibe • PCSK9 inhibitor guide • bempedoic acid and CLEAR Outcomes
1. Start with the treatment goal, not the drug name
The most common medication mistake is to begin with a favored drug and work backward. The evidence-based order is the opposite. First define the patient’s risk category, current LDL-C and non-HDL-C, the desired percentage reduction, and whether atherosclerosis is already established. In secondary prevention, the 2026 ACC/AHA guideline recommends an LDL-C goal below 55 mg/dL for most very-high-risk patients and below 70 mg/dL for the smaller group with ASCVD who do not meet very-high-risk criteria. In primary prevention, treatment intensity depends on PREVENT-ASCVD risk, diabetes, chronic kidney disease, HIV, severe hypercholesterolemia, family history, CAC and other risk enhancers. [1]
Once the required LDL-C reduction is known, drug choice becomes much more rational. Someone who needs a 15% additional reduction may reach goal with ezetimibe. Someone who is 80 mg/dL above a secondary-prevention target may require a high-intensity statin plus a PCSK9-directed therapy rather than six months of slow sequential escalation. The 2026 framework allows clinicians to choose among nonstatins according to the magnitude of LDL-C lowering needed, patient characteristics, tolerability, access and evidence, rather than following one rigid sequence for every patient. [1,2]
| Therapy class | Typical LDL-C effect | Hard outcomes evidence | Route / cadence | Best mental model |
|---|---|---|---|---|
| High-intensity statin | ≥50% reduction | Strong, broad primary and secondary prevention evidence | Daily oral | Default foundation when indicated |
| Ezetimibe | ~15–25%; usually ~15–20% additional on statin | Yes, IMPROVE-IT | Daily oral | Simple low-burden add-on |
| Bempedoic acid | ~18–25% | Yes, CLEAR Outcomes in statin-intolerant high-risk patients | Daily oral | Evidence-based oral option when statins are limited |
| PCSK9 monoclonal antibody | ~50–60% additional | Yes, FOURIER / ODYSSEY OUTCOMES | Injection every 2–4 weeks | Large LDL reduction with proven event benefit |
| Inclisiran | ~50% | Dedicated outcomes trials ongoing as of Aug 2026 | Injection initially, 3 months, then every 6 months | Adherence-friendly LDL lowering; outcome benefit not yet directly proven |
| Enlicitide (Lipfendra) | ~55–60% in phase 3 lipid trials | Dedicated outcomes evidence pending | Daily oral | First oral PCSK9 inhibitor; major LDL effect without injections |
2. Statins: still the foundation
Statins inhibit HMG-CoA reductase, reducing hepatic cholesterol synthesis and increasing LDL-receptor activity. High-intensity atorvastatin or rosuvastatin typically lowers LDL-C by at least 50%, while moderate-intensity regimens generally lower it by 30–49%. The clinical importance is not merely the laboratory effect. Large randomized trial programs and meta-analyses show that reducing LDL-C with statins lowers myocardial infarction, ischemic stroke, coronary revascularization and other major vascular events in proportion to the absolute LDL-C reduction and baseline risk. [2]
Statins also change plaque biology. Intensive LDL lowering reduces lipid-rich and noncalcified plaque and promotes a more stable phenotype. Calcification may increase or become denser during therapy, which can look alarming on serial CAC or CCTA but does not mean the treatment is accelerating clinical risk. The correct outcome target is fewer events and lower ApoB exposure, not a cosmetically “better” calcium score.
The main reasons statins fail in real-world care are not lack of efficacy but undertreatment, side-effect attribution, fear generated by misinformation, and poor long-term adherence. The 2026 guideline emphasizes that muscle symptoms should be evaluated systematically rather than automatically labeled as complete statin intolerance. Secondary causes, drug interactions, exercise-related injury and other muscle disorders should be considered. Most patients can ultimately tolerate some statin dose, sometimes using a different statin, lower dose or less-than-daily regimen combined with a nonstatin. [1,11]
This hub summarizes the role of statins. Detailed plaque effects, inflammation, safety and the full statin-intolerance algorithm belong in the dedicated owner pages “Statins: What They Really Do to LDL, Inflammation and Coronary Plaque” and “Statin Intolerance and Muscle Symptoms.”
3. Ezetimibe: the low-friction add-on
Ezetimibe blocks intestinal NPC1L1-mediated cholesterol absorption. It is generic, once daily, has few systemic adverse effects and combines cleanly with statins because the mechanisms are complementary. In practice, adding ezetimibe often lowers LDL-C by another 15–20% beyond the statin effect; monotherapy commonly produces a 15–25% reduction.
IMPROVE-IT was decisive because it showed that LDL lowering through a nonstatin mechanism could reduce cardiovascular events. More than 18,000 patients after acute coronary syndrome were randomized to simvastatin plus ezetimibe or simvastatin alone. The combination achieved lower LDL-C and a modest but statistically significant reduction in long-term cardiovascular events. The lesson was larger than ezetimibe itself: event reduction follows sufficient lowering of causal atherogenic lipoproteins, not loyalty to one drug class. [3]
Ezetimibe is particularly useful when a small-to-moderate additional LDL-C reduction will reach goal, when minimizing statin dose improves tolerability, when cost matters, or as one component of a combination regimen. Its weakness is simply magnitude: if a patient needs another 50–60% LDL-C reduction, ezetimibe alone is unlikely to solve the problem.
4. Bempedoic acid: an outcomes-proven oral option for statin limitation
Bempedoic acid inhibits ATP-citrate lyase upstream of HMG-CoA reductase. The drug is activated primarily in the liver rather than skeletal muscle, which is one reason it became attractive for patients who report statin-associated muscle symptoms. LDL-C lowering is usually in the range of 18–25%, with larger reductions when combined with ezetimibe.
CLEAR Outcomes randomized 13,970 statin-intolerant patients with established cardiovascular disease or high cardiovascular risk. Bempedoic acid reduced the primary four-component major adverse cardiovascular endpoint from 13.3% to 11.7% (hazard ratio 0.87) while lowering LDL-C and hsCRP. The trial established bempedoic acid as more than a laboratory alternative: it has direct randomized cardiovascular outcomes evidence in the population for whom it is most clinically relevant. [6]
The safety profile requires the same honesty. Hyperuricemia and gout were more common, and cholelithiasis also occurred more often. Bempedoic acid should not be marketed as a side-effect-free “statin replacement.” For patients who can tolerate effective statin therapy, the much larger statin evidence base remains relevant. For true or partial statin intolerance, however, bempedoic acid is now an evidence-based tool rather than a compromise of convenience.
5. PCSK9 monoclonal antibodies: large LDL reduction with proven event benefit
Evolocumab and alirocumab are injectable monoclonal antibodies that bind circulating PCSK9, preventing it from degrading hepatic LDL receptors. The result is a large increase in LDL clearance, usually producing approximately 50–60% additional LDL-C lowering on top of background therapy.
FOURIER demonstrated that evolocumab added to statin therapy reduced cardiovascular events in patients with established ASCVD. ODYSSEY OUTCOMES showed that alirocumab reduced major ischemic events after acute coronary syndrome. These trials established PCSK9 inhibition as a proven event-reduction strategy, not simply a way to create striking lipid panels. [4-5]
PCSK9 monoclonal antibodies are most compelling when the required LDL-C reduction is large, when established ASCVD or familial hypercholesterolemia places the patient at high risk, or when oral therapy cannot achieve the target. Their disadvantages are practical rather than mechanistic: injections, insurance authorization, cost and persistence. Modern treatment should therefore consider access and adherence as part of efficacy. A drug that lowers LDL-C by 60% only on paper is less useful than a slightly less potent regimen the patient can maintain for years.
6. Inclisiran: durable LDL lowering, but do not borrow outcomes evidence
Inclisiran is a small interfering RNA that suppresses hepatic PCSK9 production. After the initial and three-month doses, maintenance dosing is twice yearly. Phase 3 lipid trials produced approximately 50% LDL-C lowering, making inclisiran especially attractive when adherence to frequent self-injection or daily oral therapy is a major concern. [7]
The evidence boundary is important. The 2026 ACC/AHA guideline explicitly notes that dedicated trials are still evaluating whether inclisiran’s LDL-C reduction translates into fewer cardiovascular events. VICTORION-2P remained active, not recruiting, with no results posted in June 2026. Therefore, the correct statement is not “inclisiran has no reason to work”; LDL and ApoB causality make benefit biologically plausible. The correct statement is that direct randomized event-reduction evidence for this specific agent was still pending at the evidence cutoff. [1,8]
Evolocumab and alirocumab have completed cardiovascular outcomes trials. Inclisiran targets the same PCSK9 pathway but has a different modality and dosing pattern. Its LDL-lowering efficacy is established; its dedicated cardiovascular outcomes evidence must be reported on its own timeline.
7. Enlicitide (Lipfendra): the oral PCSK9 era
Enlicitide is a macrocyclic oral PCSK9 inhibitor. In the CORALreef Lipids phase 3 trial, once-daily enlicitide produced roughly 56% placebo-adjusted LDL-C lowering at 24 weeks and sustained major lipid effects through one year. The U.S. FDA approved Lipfendra on 17 July 2026 as an adjunct to diet and exercise to reduce LDL-C in adults with hypercholesterolemia, including heterozygous familial hypercholesterolemia. It is the first oral PCSK9 inhibitor approved in the United States. [9-10]
This is a meaningful treatment advance because route of administration is a real barrier. A daily tablet may appeal to people who would otherwise avoid or discontinue injections. It also creates a new practical comparison: daily oral adherence versus infrequent injections. That is a patient-level decision rather than a universal hierarchy.
The evidence boundary is again essential. FDA approval is based on LDL-C lowering, not on a completed cardiovascular outcomes trial demonstrating fewer myocardial infarctions or strokes with enlicitide itself. It is reasonable to expect large ApoB lowering to be clinically relevant, but “expected from causal biology” and “demonstrated in this drug’s outcomes trial” are not identical claims. Until the dedicated outcomes program reports, the site should keep those sentences separate. [9-10]
8. Severe inherited disease: when the standard ladder is not enough
Homozygous familial hypercholesterolemia and other extreme inherited lipid disorders are qualitatively different from ordinary primary-prevention hypercholesterolemia. LDL-receptor function may be severely impaired, LDL-C can be extraordinarily high from childhood and cumulative arterial exposure can be extreme before adulthood. These patients require specialist care and often need multiple mechanisms simultaneously.
Evinacumab targets ANGPTL3 and can lower LDL-C even when LDL-receptor activity is profoundly limited, which makes it especially important in homozygous familial hypercholesterolemia. Lipoprotein apheresis physically removes ApoB-containing lipoproteins from the circulation and remains a resource-intensive but important option in selected patients with severe familial disease or progressive ASCVD despite maximal therapy. These are not population-level alternatives to ordinary statin-based care; they are specialist tools for a fundamentally different risk problem. [14-15]
9. Statin intolerance: preserve treatment, not the label
The phrase “statin intolerant” covers a spectrum. Some patients cannot tolerate one specific statin or dose; others tolerate a lower dose; a much smaller group cannot tolerate any meaningful statin exposure despite careful rechallenge. The clinical goal should be to preserve as much proven LDL-lowering therapy as is reasonably tolerated rather than turning the diagnostic label into an all-or-nothing identity.
The 2026 guideline recommends evaluating secondary causes and drug interactions, acknowledging symptoms rather than dismissing them, and informing patients about the cardiovascular risk of treatment discontinuation. In patients with ASCVD who cannot reach goals on the tolerated statin dose, bempedoic acid, ezetimibe or a PCSK9 monoclonal antibody, alone or in combination, are recommended evidence-based options. [1]
This is also where combination therapy becomes elegant. A small tolerated statin dose plus ezetimibe, for example, may produce far more LDL-C lowering than repeated attempts to force a high statin dose that the patient will eventually abandon. Similarly, a PCSK9-directed therapy can provide a large reduction while preserving whatever oral therapy is tolerable.
10. GLP-1 and SGLT2 drugs: cardiovascular medicines, not LDL substitutes
Cardiovascular prevention has expanded beyond lipid pharmacology. GLP-1 receptor agonists reduce cardiovascular events in selected patients with type 2 diabetes and, in the SELECT trial, semaglutide reduced major cardiovascular events in people with overweight or obesity and established cardiovascular disease even without diabetes. SGLT2 inhibitors have major cardiovascular and renal benefits in diabetes, heart failure and chronic kidney disease. [12-13]
These drugs belong in the Medications hub because real patients do not experience risk in isolated silos. A patient may simultaneously need LDL lowering, blood-pressure treatment, a GLP-1 drug for obesity or diabetes, and an SGLT2 inhibitor for heart failure or kidney protection. But they should not be sold as interchangeable with statins or PCSK9 therapy. A GLP-1 drug does not neutralize a high ApoB burden, and an excellent LDL-C does not eliminate heart-failure or kidney risk.
Lipid-lowering drugs primarily reduce risk by lowering atherogenic particle exposure. GLP-1 and SGLT2 therapies reduce cardiovascular risk through metabolic, hemodynamic, renal and other pathways. High-risk patients may appropriately need both categories.
11. Special situations change the treatment equation
Pregnancy, conception and breastfeeding
Most lipid-lowering drugs are deferred during conception, pregnancy and lactation because long-term safety data are limited and short-term interruption is acceptable for most lower-risk patients. The FDA removed the blanket contraindication to statin use in pregnancy in 2021, allowing individualized consideration in unusually high-risk situations, but most pregnant patients should still stop statins. Bile-acid sequestrants and, in severe familial disease, lipoprotein apheresis may be considered under specialist care. The dedicated pregnancy article owns the drug-by-drug details.
Adults older than 75 years
Age alone is not a reason to automatically stop LDL-lowering therapy. After age 75, the 2026 guideline supports individualized pharmacotherapy together with lifestyle, weighing existing ASCVD, frailty, life expectancy, polypharmacy, adverse effects and patient goals. The potential absolute benefit can remain large in robust older adults with high baseline risk.
Young adults
The opposite error is waiting too long in younger people with severe LDL elevation. The 2026 guideline emphasizes earlier treatment across the life course and supports consideration of pharmacotherapy in young adults with LDL-C at least 160 mg/dL or a strong family history of premature ASCVD. Years of avoidable ApoB exposure matter even when 10-year risk looks low.
12. Choosing a regimen: use the amount of LDL reduction needed
| Clinical situation | What the problem is | Reasonable medication logic | Common error |
|---|---|---|---|
| Mildly above goal on tolerated statin | Need ~10–20% more LDL reduction | Add ezetimibe | Doubling the statin dose repeatedly for a small incremental effect |
| True partial statin intolerance | Need meaningful LDL lowering with limited statin dose | Keep tolerated statin + ezetimibe and/or bempedoic acid; consider PCSK9 mAb if risk or gap is large | Abandoning all therapy because one statin caused symptoms |
| Very-high-risk ASCVD far above <55 mg/dL goal | Need a large and rapid LDL reduction | Early combination therapy, often statin + ezetimibe + PCSK9-directed therapy | Slow serial escalation that leaves the patient above goal for months |
| Adherence problem with frequent dosing | Potent therapy is needed but persistence is the weak link | Consider route and cadence: twice-yearly inclisiran vs PCSK9 mAb vs daily oral enlicitide | Choosing by potency alone while ignoring adherence |
| HoFH / extreme inherited LDL | Standard LDL-receptor strategy may be insufficient | Specialist multidrug therapy, evinacumab and/or apheresis as appropriate | Treating severe genetic disease like routine mild hypercholesterolemia |
| Obesity / diabetes / CKD plus elevated LDL | Multiple causal pathways are active | Treat LDL/ApoB and use indicated GLP-1 or SGLT2 therapy for metabolic/cardiorenal risk | Assuming one drug class substitutes for the other |
14. Practical treatment framework
Define the risk category and whether clinical ASCVD, diabetes, CKD, HIV, familial hypercholesterolemia or significant CAC/plaque is present.
Measure the baseline LDL-C and non-HDL-C and decide how much absolute and percentage reduction is required. Use ApoB selectively when standard markers may underestimate particle burden.
Use the maximally tolerated statin when indicated, unless a genuine contraindication or carefully evaluated intolerance changes the plan.
If the required reduction exceeds what the statin can deliver, add combination therapy based on magnitude needed, outcome evidence, cost, route and adherence.
Use ezetimibe when a modest additional reduction is enough or when simplicity and cost are priorities.
Use bempedoic acid when an evidence-based oral nonstatin is needed, especially in statin-intolerant patients, while monitoring gout/hyperuricemia risk.
Use PCSK9 monoclonal antibodies when a large LDL reduction and proven cardiovascular event benefit are required.
Consider inclisiran when infrequent dosing meaningfully improves adherence, while stating that dedicated outcomes evidence remains pending.
Consider enlicitide as an oral high-potency PCSK9 option where approved and appropriate, without overstating uncompleted outcomes evidence.
Escalate severe inherited disease to a lipid specialist rather than stretching the standard algorithm beyond its evidence.
Treat metabolic, renal and heart-failure risk with indicated GLP-1 or SGLT2 therapies in parallel rather than assuming LDL lowering solves every risk pathway.
Recheck lipids after treatment changes at an interval appropriate for the drug and clinical setting, then reassess adherence, response and side effects before adding complexity.
“How much additional LDL-C/ApoB reduction does this patient need, and which evidence-based combination can deliver it reliably for years?” That question is usually more useful than “Which cholesterol drug is strongest?”
16. Frequently asked questions
Do I have to try every drug in order?
No. The regimen should match cardiovascular risk, baseline LDL-C, the size of the reduction required, tolerability, cost and access. The 2026 framework allows more flexible selection and earlier combination therapy in high-risk patients.
Is ezetimibe weaker than a statin?
It usually lowers LDL-C less, but it has randomized outcomes evidence and is highly useful as an add-on. “Weaker” is the wrong question when a 15–20% additional reduction is exactly what is needed.
Is bempedoic acid only for people who cannot take statins?
Its strongest completed outcomes evidence comes from statin-intolerant high-risk patients. That does not make it useless elsewhere, but CLEAR Outcomes should not be generalized beyond the population it actually studied.
Are PCSK9 injections proven to prevent heart attacks?
Yes. Evolocumab and alirocumab reduced cardiovascular events in major randomized outcomes trials.
Does inclisiran prevent cardiovascular events?
Its LDL-C lowering is established, but dedicated cardiovascular outcomes trials were still ongoing at the August 2026 evidence cutoff.
Is enlicitide the same as an injectable PCSK9 inhibitor?
It targets circulating PCSK9 through an oral macrocyclic peptide rather than an injected monoclonal antibody. LDL lowering is in a similar high-potency range, but completed outcomes evidence for enlicitide itself is still pending.
If I take semaglutide, do I still need LDL treatment?
Possibly yes. GLP-1 therapy can reduce cardiovascular risk in the right population, but it does not replace treatment of elevated LDL-C or ApoB when lipid-lowering therapy is indicated.
What if my LDL is already very low?
The answer depends on why it is low, the patient’s risk category, current therapy, side effects and other residual risk factors. Very low LDL-C achieved in modern trials has generally been reassuring in appropriately selected high-risk patients, but medication should be individualized rather than escalated for competition.
References
1. Blumenthal RS, Morris PB, Gaudino M, et al. 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia. Circulation. 2026;153(17):e1154-e1276. doi:10.1161/CIR.0000000000001423.
2. Cholesterol Treatment Trialists' Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010;376(9753):1670-1681. doi:10.1016/S0140-6736(10)61350-5.
3. Cannon CP, Blazing MA, Giugliano RP, et al. Ezetimibe Added to Statin Therapy after Acute Coronary Syndromes. N Engl J Med. 2015;372:2387-2397. doi:10.1056/NEJMoa1410489.
4. Sabatine MS, Giugliano RP, Keech AC, et al. Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease. N Engl J Med. 2017;376:1713-1722. doi:10.1056/NEJMoa1615664.
5. Schwartz GG, Steg PG, Szarek M, et al. Alirocumab and Cardiovascular Outcomes after Acute Coronary Syndrome. N Engl J Med. 2018;379:2097-2107. doi:10.1056/NEJMoa1801174.
6. Nissen SE, Lincoff AM, Brennan D, et al. Bempedoic Acid and Cardiovascular Outcomes in Statin-Intolerant Patients. N Engl J Med. 2023;388:1353-1364. doi:10.1056/NEJMoa2215024.
7. Ray KK, Wright RS, Kallend D, et al. Two Phase 3 Trials of Inclisiran in Patients with Elevated LDL Cholesterol. N Engl J Med. 2020;382:1507-1519. doi:10.1056/NEJMoa1912387.
8. ClinicalTrials.gov. NCT05030428. VICTORION-2P: Study of Inclisiran to Prevent Cardiovascular Events in Participants With Established Cardiovascular Disease. Record updated June 11, 2026; active, not recruiting; no results posted at evidence cutoff.
9. U.S. Food and Drug Administration. FDA Approves First Oral PCSK9 Inhibitor to Lower LDL Cholesterol in Adults with High Cholesterol. July 17, 2026.
10. Navar AM, Mikhailova E, Catapano AL, et al. A Placebo-Controlled Trial of the Oral PCSK9 Inhibitor Enlicitide. N Engl J Med. 2026;394:529-539. doi:10.1056/NEJMoa2511002.
11. Cholesterol Treatment Trialists' Collaboration. Effect of statin therapy on muscle symptoms: an individual participant data meta-analysis of large-scale, randomised, double-blind trials. Lancet. 2022;400(10355):832-845. doi:10.1016/S0140-6736(22)01545-8.
12. Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes. N Engl J Med. 2023;389:2221-2232. doi:10.1056/NEJMoa2307563.
13. Zinman B, Wanner C, Lachin JM, et al. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes. N Engl J Med. 2015;373:2117-2128. doi:10.1056/NEJMoa1504720.
14. Raal FJ, Rosenson RS, Reeskamp LF, et al. Evinacumab for Homozygous Familial Hypercholesterolemia. N Engl J Med. 2020;383:711-720. doi:10.1056/NEJMoa2004215.
15. Thompson GR. LDL apheresis. Atherosclerosis. 2003;167(1):1-13. doi:10.1016/S0021-9150(02)00251-4.