2026 ACC cardiology guidelines for lipid management

 a very multicenter 2026 clinical practice guideline was just released on the management of dyslipidemia from the ACC/AHA (American College of Cardiology and the American Heart Association), subsequently endorsed by the AACVPR/ABC/ ACPM/ADA/AGS/APhA/ASJPC/NLA/PCNA (see the article for interpretation of this alphabet soup):see lipid management ACC guideline2026 in dropbox, or DOI: 10.1161/CIR.0000000000001423. This is a review of a 123-page document which raises many questions. so the blog is pretty long but i think it includes lots of new and useful information

Details:

-- the basis for these guideline recommendations was from a comprehensive literature search done in late 2024

-- the focus of the search was the evaluation, management, and monitoring of individuals with dyslipidemias, including high blood cholesterol, hypertriglyceridemia, and elevated lipoprotein(a)

-- a summary of the top take-home messages, per the guideline document:

1. treat dyslipidemia earlier to reduce lifelong risk of prolonged exposure to atherogenic lipoproteins. health behavior counseling to support lifestyle optimization should start in youth, with early consideration to treat dyslipidemia earlier to reduce lifelong risk with early consideration of pharmacotherapy in youth with familial hypercholesterolemia (FH) and in young adulthood in individuals with low-density lipoprotein cholesterol (LDL-C) ≥160 mg/dL or a strong family history of premature atherosclerotic cardiovascular disease (ASCVD)
2. Use the more contemporary American Heart Association Predicting Risk of cardiovascular disease EVENTs (PREVENT) equations instead of the older Pooled Cohort Equations (PCE) for 10- and 30-year risk assessment to guide lipid-lowering therapy (LLT) in primary prevention in adults aged 30 to 79 years. Use the “CPR” Model: A) Calculate 10-year ASCVD risk; B) Personalize the estimated risk to the specific patient by considering factors not included in PREVENT-ASCVD equations; and C) possibly reclassify with selective use of coronary artery calcium (CAC) and reassess treatment recommendations.
3. Low-density lipoprotein (LDL)-lowering therapy can be considered in adults for primary prevention of ASCVD with a 10-year PREVENT-ASCVD risk estimate of 3% to <5% (borderline risk) and should be considered for those at 5% to <10% (intermediate risk) 10-year risk after a clinician–patient discussion.
4. LDL-C and non–high-density lipoprotein cholesterol (HDL-C) treatment goals are back to guide LLT. Percentage reduction in LDL-C remains a priority for all individuals as well, with goal for % reduction depending on the level of ASCVD risk.
5. Apolipoprotein B (ApoB) testing can be useful to improve risk assessment and guide therapy once LDL-C and non–HDL-C goals are met, particularly in those with elevated triglycerides (TG) (>200 mg/dL), diabetes, or low achieved LDL-C (<70 mg/dL). ApoB measurement helps identify adults with residual elevated lipoprotein-related risk that may be underestimated by the standard lipid profile
6. Lipoprotein(a) [Lp(a)] should be measured at least once to identify those individuals at higher risk of ASCVD. It is considered as a risk-enhancing factor at levels ≥125 nmol/L (50 mg/dL), which is associated with about a 1.4-fold increased ASCVD risk, and values ≥250 nmol/L (100 mg/dL) are associated with ≥2-fold higher estimated risk. The presence of elevated Lp(a) should be an indication for more intensified LDL-C lowering and management of other risk factors
7. CAC scoring in men at least 40 years of age and women at least 45 years of age can improve risk assessment and guide LDL-C and non–HDL-C goals. Both the absolute amount of CAC and the corresponding standardized percentile (currently based on age, sex, and race) have prognostic importance and help to reclassify risk in adults.
8. LDL-lowering therapy is recommended for primary prevention in adults aged 40 to 75 years with diabetes, chronic kidney disease stage 3 or 4, or human immunodeficiency virus, regardless of LDL-C level. After age 75 years, LDL-C–lowering pharmacotherapy can be considered in conjunction with lifestyle interventions to reduce ASCVD risk.
9. In secondary prevention, a goal of LDL-C <55 mg/dL (1.4 mmol/L) and non–HDL-C <85 mg/dL (2.2 mmol/L) is recommended for those at very high risk of ASCVD events. Although a smaller number of patients with ASCVD not at very high risk have an LDL-C goal of at least <70 mg/dL, the majority of those with a history of ASCVD events will likely qualify for an LDL-C goal of <55 mg/dL.
10. In patients with persistently elevated triglycerides (TG), statin therapy remains the foundation of pharmacotherapy as an adjunct to lifestyle intervention to reduce ASCVD risk. Treatment for prevention of pancreatitis may also include TG-lowering therapies, especially in individuals with TG levels ≥1000 mg/dL (11.3 mmol/L).
    
    

Commentary (my assessment of these take-home messages along with further reading of parts of their 123-page document)

1. treating dyslipidemia early
1. absolutely: Fatty streaks are evident in pretty much everyone aged 15-34; advanced atherosclerotic lesions in 2% men and 0% women aged 15-19, and in 20% of men(!) and 8% of women aged 30-34. This guideline is the first time that guidelines have emphasized the important cumulative nature of atherosclerotic disease and the need to address this early on, mostly with nonpharmacologic lifestyle changes
2. our goal in primary care is to prevent ASCVD and not to wait until there is a pretty large atherosclerotic load.
1. heart disease is still the leading cause of death in the US overall; and it still is, along with cancer, in those >70yo
1. treating before an ASCCD event (primary prevention) is especially important since 50% of those having an MI die, and the morbidity of heart or cerebrovascular events can be hugely disabling physically and psychologically
2. this is the reasoning (i assume) behind the American Pediatric Association's recommendation of universal lipid screening for children aged 9-11 and again at age 17-21, and testing those aged 2-8 and 12-16 if there is a family history of heart disease of premature dyslipidemia or unknown family history (this latter recommendation may be a tad too inclusive...)
3. and, to upstage a later issue below, we should also check lipoprotein(a) and apolipoprotein B levels, both of which confer a greater increased ASCVD risk and a clear reason to reinforce non-pharmacologic approaches and in some cases meds to lower LDL levels, especially in younger individuals to decrease long-term ASCVD events. In terms of nonpharmacologic approaches to LDL reduction, this can be a challenge. and i would argue that it typically needs to be more than a 15 minute discussion of ASCVD prevention, but re-assessment in pretty frequent follow-ups done to reinforce the long-term importance of diet, exercise, and achieving a healthy weight, best done with active patient involvement as with motivational interviewing in order to achieve effective benefit
2. using the PREVENT risk calculator
1. LDL goals based on calculated risk scores:
1. see https://professional.heart.org/en/guidelines-and-statements/prevent-calculator for the risk calculators of PREVENT, for cardiovascular disease, ASCVD, and heart failure. all three of these outcomes are based on the input from the same questionnaire and information, as noted below
2. i do have several concerns about ASCVD risk calculators in general
1. it is pretty useless to assess the 10-year risk in younger people (perhaps up to 45yo or more), given that their risk of an ASCVD event may well calculate to be low. this new clinical practice document states that the ASCVD risk assessment should be performed in those aged 30-79, which on one side misses lots of younger people with very low calculated risk but also misses many of the older ones who might well have a considerably more than 10-year life expectancy (unlike the prior risk calculator where anyone over 60yo was considered to have very high ASCVD risk, the PREVENT ones do not even include anyone over 79yo, who are without significant comorbidities, so the risk calculator may well underestimate their longer term ASCVD risk for healthy patients up to 79yo). and, as noted below, cardiovascular disease is the major cause of mortality in the elderly (along with cancer). A recent study did find that people who on average of 84.5 years old did have reduced all-cause mortality and coronary morbidity with statins for primary prevention: https://agsjournals.onlinelibrary.wiley.com/doi/10.1111/jgs.70375#xd_co_f=YTU1ZTQxNGUtYWMzZi00ZmRjLWE0OWItZDg0MGYyNzRhYmEz~ . and with our aging population, we need a risk calculator for those people in their 90's who, if healthy, have a 3.5 to 4.5 years of life expectancy. and there is reasonable argument that those with a life expectancy >1yr may well benefit (in younger people, it is pretty clear that statin benefit occurs within 6-12 months of initiating statins). we could use studies here to assess the use of LLTs in the very old in terms of morbidity as well as mortality.
2. the PREVENT risk calculators all include the same questions: sex, age, systolic blood pressure, total and HDL cholesterol levels, eGFR (presumably creatinine-based, though cystatin is a much better predictor of cardiovascular events: https://gmodestmedblogs.blogspot.com/2023/12/cystatin-c-better-predictor-of-bad.html ), diabetes (though the cardiovascular risk depends on what meds are used (GLP-1/SGLT2 helpful; insulin/sulfonylureas seem to be harmful) and the achieved level of hemoglobin A1C), current smoking within the last 30 days (though the increased ASCVD risk continues for 10-15 years after stopping smoking, and the quantity of cigarettes also matters), current use of statins (but the continued risk depends on the level of achieved LDL (total cholesterol/HDL, the non-HDL cholesterol, and the apolipoprotein B are actually better risk predictors), and antihypertensive medications (depends on blood pressure achieved and what meds are used, and in particular if the meds are chosen based on renin levels since even controlled hypertension is still associated with increased cardiovascular events if the renin levels are <1 : https://gmodestmedblogs.blogspot.com/2025/12/hyperaldosteronism-targeting-renin-level.html). This new guideline does offer three optional predictors of UACR (urine albumin/creatinine ratio), the actual A1C (again, depends on meds used), and zip code (as an estimate of social deprivation index, though this is a pretty poor one since zip code is often a much larger area than census tract, for example; and there is so much gentrification in many areas that zip code is less likely to have useful socioeconomic data and is less representative of the local population than a smaller tract)
3. and, really the glowing inadequacy of the risk calculators, including PREVENT: we do know that anything leading to chronic inflammation (ie, visceral obesity, depression, stress, air pollution, microplastics, chronic infectious diseases, chronic rheumatologic diseases, controlled HIV infections, cancers, chronic GI/pulmonary/renal diseases, immune dysfunction, Alzheimer's, migraines, other atherosclerotic disease (eg PAD), and early menopause (<45yo)) are associated with almost all of the chronic diseases we encounter. and all of these chronic diseases and psychosocial risk factors are associated with increased ASCVD risk
1. there was a really well-conducted recent study finding that racial disparities are associated with both increased mortality associated with higher inflammatory markers (they used a combo of CRP and IL-6) or racial disparities including discrimination, and that both chronic inflammation and racial disparities together were associated with an even greater all-cause mortality :https://gmodestmedblogs.blogspot.com/2026/02/racial-disparities-stress-and-mortality.html
2. lots of studies over the decades on air pollution and chronic inflammation document increased heart disease incidence, eg https://gmodestmedblogs.blogspot.com/2016/06/air-pollution-and-heart-disease.html
3. so, my bottom line is to incorporate the many psychosocial risk factors with the traditional risk factors as well as the newer ones (apoB and Lp(a)) into an overall gestalt of risk. The current guidelines suggest a goal of LDL-C <55 mg/dL (1.4 mmol/L) and non–HDL-C <85 mg/dL (2.2 mmol/L) for those at very high risk of ASCVD events. However, a metanalaysis of several secondary prevention studies documented a continuous decreased risk of recurrent cardiovascular events with an LDL <20 https://gmodestmedblogs.blogspot.com/2018/08/very-low-ldl-levels-benefit-without-harm.html. more on this below. though i should add that most of the studies in this meta-analysis of secondary prevention studies did use PCSK9s, which lower LDL levels lots but also lower Lp(a) levels.  the Fourier study, an excellent one utilizing a PCSK9 in this meta-analysis, found cardiovascular benefit down to an LDL<20 in its extended followup (see cad high risk LDL less than 20 fourier studyCirc2023, or DOI: 10.1161/CIRCULATIONAHA.122.063399), and a secondary analysis of this study found the most benefit in those having more lowering of the Lp(a) levels: see Lp(a) Fourier study PCSK9 dec events Circ2019 in dropbox, or DOI: 10.1161/CIRCULATIONAHA.118.037184)
1. there are some cardiologists who feel that there is inadequate information on the role of PCSK9 meds in some patients with high ASCVD risk including very high Lp(a) values. a brand new JAMA study found that in patients with diabetes and no known ASCVD, PCSK9 meds do lower subsequent ASCVD events: see diabetes primary ASCVD prevention with PCSK9 JAMA2026 in dropbox, or doi:10.1001/jama.2026.3277, which i will soon evaluate more fully
4. in their "top take-home messages", they do include the comment "Personalize the estimated risk to the specific patient by considering factors not included in PREVENT equations". However, there is zero definition of what those risk factors are that should be considered that are not in the PREVENT equations. This is what leads me to assess the gestalt of a composite of the medical and psychosocial risk factors in my mind and decide on what is a reasonable LDL goal, knowing that there is likely more benefit and not many increased adverse effects if i lower the LDL more if the psychosocial risk factors are present
4. they also bring up the coronary artery calcium score as a further risk quantifier; in particular, their recommendations state that if the decision regarding lipid lowering therapy (LLT) in individuals is felt to be at intermediate risk, "a CAC score should be used to further risk stratification",
1. but these CAC scores are quite inaccurate (https://gmodestmedblogs.blogspot.com/2025/10/coronary-artery-calcium-score-pretty.html) and do not pick up noncalcified coronary arteries (which are the ones that have an active lipid core with inflammation and therefore the ones that are highly susceptible to rupture causing an acute coronary syndrome; the CAC scores also do not pickup microvascular disease) and CAC assessment is clearly inferior to coronary CT angiograms (though these will also not pick up microvascular disease)
2. they further state that it is reasonable to defer LLT in those with CAC score of 0 and no higher risk conditions (diabetes, smoking, strong family history); though a CAC score >0 (even a score of 1) and intermediate risk should lead to LLT. and this applies to people with "incidentally CAC identified on noncardiac CT scans, where men >40 and women >45 who have subclinical coronary atherosclerosis but no prior ASCVD should have at least a 50% reduction in LDL and a goal of LDL<70 and non-HDL <100; if milder coronary artery calcifications found, then an LDL reduction of 30-49% and  LDL goal of <100 and non-HDL goal of <130. (I would also consider diffuse arterial calcifications at other sites as a marker of increased generaliozed atheroscleroticrisk).
3. they tiered LLT depending on the CAC score itself in men >40 or women >45 with subclinical coronary atherosclerosis (as noted in the first point, people typically have subclinical atherosclerosis at that age, ie early accumulation of coronary plaques without symptoms, right up to the point that they do have symptoms. and the first symptom can be fatal or severely disabling, ie, not much of a preventative approach...). but here are their recommendations:
1. CAC score of >1000: statin with goal to reduce LDL >50% and goal LDL<55 and non-HDL <85
2. CAC score of 300-999: statin with goal to reduce LDL at least >50% and goal LDL<70 and non-HDL <100
3. CAC score of 100-299: statin with goal LDL<70 and non-HDL <100
4. CAC score of 1-99: statin with goal to reduce LDL 30-49% and goal LDL<100 and non-HDL <130
1. the above goals preferentially prefer statins as first-line therapy, though if goal not achieved, increase statin dose or add ezetimibe or a PCSK9 or bempedoic acid
2. a systematic review found that in patients on moderate dose statins, adding ezetimibe was better than increasing the statin dose in decreasing LDL levels, decreasing adverse medication effects, and with no difference in cardiac outcomes in patients with prior ASCVD events: https://gmodestmedblogs.blogspot.com/2024/12/alternative-ldl-lowering-strategies.html
3. and, though duplicative, i will restate that there are significant weakness in the accuracy of CAC score reflecting documented coronary artery disease
5. of note, in terms of CAC found incidentally on non-cardiac CT scans supporting treating these patients, 10% were falsely considered as having CAC score >0:  https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.122.063207
6. and unexpectedly, a new paper (yesterday) at the current ACC annual meeting of the GPS-CAD study found that CAC score of 0 but a positive Coronary CT angiogram led to false positives in 7% and that the CACV score was less reliable in people of certain races and countries: https://www.medpagetoday.com/meetingcoverage/acc/120547
5. i would also add that there would be great benefit to have a 30-year risk calculator. but there really are not reliable data to base this on from 30 years ago. we did not follow several of the risk factors identified now, and there have been fundamental changes in lifestyle or diet (as an example, patients 30 years ago were informed to decrease their fat intake, leading to ingesting more carbohydrates and the subsequent epidemics of obesity and diabetes...), or meds taken, or...
3. this is just their interpretation of the results of the PREVENT-ASCVD risk calculator:
1. in primary prevention for adults aged 30-79 with LDL levewls of 70-189):
1. if low (<3%) 10-yr estimated risk for ASCVD who have LDL <160 and a 30-yr risk of <10% for those aged 30-59, counseling is recommended to reduce LDL and ASCVD risk
2. if low (<3%) 10-yr estimated risk for ASCVD who have LDL 160-189 or a 30-yr risk of >10% for those aged 30-59, a moderate-intensity statin is reasonable to reduce cumulative exposure to atherogenic lipoproteins
3. if borderline (3% to <5%) 10-yr estimated risk for ASCVD with a decision to institute statins, a moderate-intensity statin to achieve a >30% to 49% reduction in LDL to reduce ASCVD risk
4. if intermediate (5% to <10%) 10-yr estimated risk for ASCVD at least a moderate-intensity statin to achieve a >30% to 49% LDL reduction and to reduce ASSCVD risk; for those at the higher end of this risk range, a high-intensity statin to reduce LDL by >50% and reduce ASCVD risk
5. if borderline (3% to <5%) or intermediate (5% to <10%) 10-yr estimated risk for ASCVD with a decision to institute statins, it is reasonable to treat to an LDL goal <100 and non-HDL goal of <130 to reduce ASCVD risk
6. if high (>10%) 10-yr estimated risk, high-intensity statin to reduce LDL >50% to reduce ASCVD risk
7. if high (>10%) 10-yr estimated risk, high-intensity statin to a goal LDL<70 and non-HDL <100 to reduce ASCVD risk
8. if high (>10%) 10-yr estimated risk, on maximally tolerated statin, it is reasonable to add ezetimibe if a goal LDL<70 and non-HDL<100 is not achieved to reduce ASCVD risk
1. however as noted above, a systematic review found that in patients on moderate dose statins, adding ezetimibe was more effective than increasing the statin dose: https://gmodestmedblogs.blogspot.com/2024/12/alternative-ldl-lowering-strategies.html
2. and, as a cumulative comment from me, as the cumulative process that ASCVD is, and as frequently included in the ACC/AHA document, these LDL goals are likely very high to achieve the long-term primary prevention needed to ASCVD events many years later. A goal LDL<70 in some high risk individuals????
4. percent of LDL reduction is individualized to reflect the individual's need
1. though, again, there are real limitations to the risk calculators, we should try to take a more holistic assessment of the array of risk factors, and, since it seems that lower LDLs are better and without significant risk in several studies. i personally think we should err on the side of more aggressive LDL reduction
2. they comment that having LDL and non-HDL goals are "back" in the guidelines (for my commentary on the deficiencies of the major 2013 guidelines that highlighted the importance of LDL goals based on studies at that time including the TNT study of 2005, and the first change back to an LDL goal in 2017, see https://gmodestmedblogs.blogspot.com/2017/09/new-acc-guidelines-endorse-ldl-goal.html . ie, it has been abundantly clear from many studies that an LDL goal (or non-HDL, or cholesterol/HDL ratio) is really important. not sure why the 2013 guidelines were so definitive on this
5. apolipoprotein B levels are useful since they predict higher ASCVD risk over the LDL levels
1.  apoB is located on the surface of the LDL moiety in circulation. when it is high, it signifies an LDL that confers a significantly worse ASCVD outcome: a high apoB reflects the presence of small, dense LDLs that are much more easily oxidized and lead to more aggressive ASCVD): https://gmodestmedblogs.blogspot.com/2023/05/cad-presumed-mechanism-and-apob-was.html . they do comment that we should measure apoB "in those particularly with ASCVD, CKM (cardiovascular-kidney-metabolic) syndrome, type 2 diabetes and/or elevated triglycerides" and, by the way, a Mediterranean diet helps
2. i think it is important to measure apoB levels, which do respond to statins, ezetimibe and PCSK9s, in all patients, since high levels do confer higher risk of ASCVD, and, in my pretty large experience of measuring it in all of my patients, there are many, as with Lp(a), who are not in the groups they cite as the primary focus
6. Lipoprotein (a) should be measured in all people once and, if high, modify our aggressivity to treating lipids, with attempts to achieve lower LDL and non-HDL levels
1. i agree strongly that we include Lp(a) in our treatment algorithm, with confirmation in a Mendelian randomization trial: https://gmodestmedblogs.blogspot.com/2024/03/lipoprotein-a-bad-actor.html
2. a 30-year study on women's cardiovascular risk found that Lp(a) was a predictor of increased risk: https://gmodestmedblogs.blogspot.com/2024/09/30-yr-study-of-womens-cardiovasc-risk.html
3. the overall risk is that ASCVD events in men and women happen on an average of about 10 years earlier than otherwise
4. standard LLT meds (statins, ezetimibe, and they now include bempedoic acid) do not change Lp(a) levels
5. but PCSK9's do, and there are several new anti-Lp(a) drugs being tested: https://gmodestmedblogs.blogspot.com/2025/11/oral-pcsk9-improves-all-bad-lipids.html  and https://gmodestmedblogs.blogspot.com/2025/11/another-pcsk9-study-clinical-benefit.html
1. these studies with the links above really support the use of PCSK9 meds now in those with continued high ASCVD risk (primary and secondary prevention) despite maximal non-PCSK9 LDL therapy. Prior guidelines by the US and European cardiology societies recommended getting the LDL as low as possible when the Lp(a) is elevated.
2.  if/when the new direct Lp(a) meds are found to be safe and clinically effective and affordable, the newer meds in development have shown huge Lp(a) lowering, more than PCSK9s, though documenting their clinical benefit is pending.
6. and, in those with high Lp(a) levels, i think we should be testing family members who might have inherited the high Lp(a)
7. high CAC scores:
1. see above
8.  primary ASCVD prevention in adults aged 40 to 75 years with diabetes, chronic kidney disease stage 3 or 4, or human immunodeficiency virus, should lead to LLT regardless of estimated 10-year atherosclerotic risk
1. agree with the diabetes recommendation. the American Diabetes Association has been promoting this for years on all adults at age 40 for years, independent of ASCVD risk calculations or LDL levels
1. diabetes is associated with the more aggressive atherosclerotic disease given the preponderance of small, dense, more oxidizable, more atherogenic LDLs typically associated with high apolipoprotein B levels, so it may even be reasonable to start LLT at a younger age?, and with more aggressive LLT (i use an LDL goal down to 40 or less if possible, depending on other risk factors). i would go further if PCSK9 meds were prescribable (drug companies are particularly resistant...)
1. given this, it is surprising that the lipid goals in the current ACC/AHA guidelines for those without known ASCVD (though ASCVD events are more likely to happen in the future) is LDL<100 and non-HDL<130. to me, this is really asking for trouble. our goal in primary care is to minimize risk of potentially highly disabling or mortal events.... Though they do state if there are multiple risk factors, an LDL goal of <70 and non-HDL <100. again, depending on the constellation of risk factors (and continued smoking is a big one), though i think a much lower goal seems appropriate
2. this does bring up the question about women who have bad lipid panels and especially in those with diabetes (who do have a significantly higher risk of an ASCVD event). BUT we should be very careful in prescribing LLT to women who may get pregnant (lipids are needed for the embryo brain development). this guideline does state that "statins may be considered in pregnant persons at very high risk for ASCVD", citing a small retrospective study of women with a family history of familial hypercholesterolemia and put on statins, then having no different outcomes of miscarriage (8%-20%) and premature births (5%-18%); i'm pretty sure this is not really reassuring. optimal brain development in children is a good thing....
3. and, as per above, a brand new JAMA study found that in patients with diabetes and no known ASCVD, PCSK9 meds do lower subsequent ASCVD events: see diabetes primary ASCVD prevention with PCSK9 JAMA2026 in dropbox, or doi:10.1001/jama.2026.3277
2. i do find it interesting that they add HIV here as a basis for starting LLT in all HIV-positive patients, independent of LDL levels. it is clear that in those even with long-term controlled HIV, they are at increased ASCVD risk. but there are so many other problems that confer at least the higher risk that HIV does. i personally do have a lower threshold to prescribe statins to my HIV patients. but also those for with PAD and those exposed to lots of air pollution/toxic chemicals at work or home, etc as above. that being said, all of my HIV patients are on statins, with the LDL lowering goal depending on my overall gestalt...
3. kidney disease is clear. but they limit it to stage 3 and 4 CKD. this runs counter to many studies over decades finding even small elevations of creatinine or microalbinuria are associated with increased risk.  And, of note, a 2019 guideline by the same American Heart Association (https://www.ahajournals.org/doi/10.1161/ATVBAHA.119.312705#F1) stated that "the increase in atherosclerosis risk is actually observed in early CKD stages", backed by the following picture from their document:

                                       

         

9. In secondary ASCVD prevention, a goal of LDL-C <55 mg/dL (1.4 mmol/L) and non–HDL-C <85 mg/dL (2.2 mmol/L) is recommended for those at very high risk of ASCVD events. this goal of <55 is a considerable improvement over past recommendations
1. again, as above, patients with a history of heart disease who continue to have lots of risk factors (smoking, diabetes, high Lp(a) or apoB, etc) might really benefit from a much lower LDL, as per the blog mentioned above on the lower the LDL, the better and without increased risk.
2. they comment that those with ASCVD but are not at very high cardiovascular risk could have an LDL-C goal of at least <70 mg/dL (vs <55).  But, the overall data show that anyone with prior ASCVD events are in fact at a much higher absolute risk of further events. And, the lower the LDL, the lower the risk... so, i think that this stratification of recurrent ASCVD events is unwise, even though those who continue to smoke, have diabetes, etc are at an even higher ASCVD risk. ie, anyone with a prior ASCVD event should have rigorous LLT, in my opinion and practice
10. In patients with persistently elevated triglycerides (TG), statin therapy remains the foundation of pharmacotherapy
1. agree. fenofibrate does not really add much, omega-3 does help some
2. if fasting TG >1000 (with some case studies even down to the 600-800 range), it is important to decrease the TG level to prevent pancreatitis
3. not mentioned, but decreasing alcohol consumption and improving diabetes control help. i have had 2 patients over the years with very poorly controlled diabetes and triglyceride levels in the 8000+ range and LDL levels in the 3000-5000 range who subsequently had TG and LDL normalization with good diabetes control (though one of them also lost a lot of weight). diets low in sugar, refined carbohydrates, and saturated fats also help lower TGs

so, a long document with some important and some questionable recommendations to me:

-- one quite large concern with guidelines overall is that most of the suggestions are expert opinions and not evidence-based:

    -- the experts are not necessarily enmeshed in clinical medicine. many are likely researchers or heads of departments with not so much "real world" clinical practice. some organizations such as the AHA (the largest and best-funded of the medical specialty societies) in the past have promoted having consumers and a broad group of committee members on their guideline committees (dieticians, social workers, primary care, other specialties)

        -- a review of the very large numbers of people involved in this current guideline found only researchers and professors/heads of departments, along with a sizable group of industry-based individuals

        -- was there any bias here??? did the researchers and industry-based individuals have conflicts-of-interest and push disproportionately harder for their research/funding?????

    -- prior guidelines from the AHA have been very careful to note on each individual recommendation if it  was based on medical evidence along with the relevant journal citations, or based on "expert opinion"

        -- none of the recommendations in the new lipid management document note whether they were based on "expert opinion". why was there this fundamental change in guideline committee composition? and why not be explicit about the basis of the individual recommendations, or at least note on the actual quality of the evidence???

    -- a very interesting study was published in 2019 that analyzed the individual recommendations by the ACC/AHA and the ESC (European Society of Cardiology) in cardiology guidelines published from 2008 to 2018: https://gmodestmedblogs.blogspot.com/2019/04/guidelines-lacking-evidence-based.html

        -- this article found that since 2015, only 26.5% of recommendations were based on randomized controlled trials

        -- comparing studies from 2008 studies to 2018 studies: there was no meaningful change in the class 1 recommendations, defined as "there is evidence, general agreement, or both, that the treatment is useful or effective"

            -- the ACC/AHA had 9.0% of recommendations being well-supported by evidence in 2018 vs 11.7% in 2008

            -- the ESC had 17.6% of recommendations being well-supported by evidence in 2018 vs 15.1% in 2008

-- that being said, there were some important additions from the current guidelines on lipid therapy management:

    -- acknowledging the importance of measuring Lp(a) on everyone and apolipoprotein B (though they do not come out strongly to check everyone)

        -- my anecdotal experience with pretty much all of my patients is that both Lp(a) and apoB are elevated very frequently, leading to more aggressive LD control

            -- and, i do believe that perhaps our major goal in adult primary care is to identify higher risk patients early and work with them to do what is important to decrease their ASCVD risk, both through non-pharmacological and pharmacological means as needed (and really emphasizing the non-pharmacological ones are independent of their LDL, since there are so many documented non-cardiac benefits to a healthy lifestyle

            -- we should also ask our adult patients who have elevated Lp(a) to have their siblings, parents, and children tested since it runs in families

    -- providing guidance for dealing with patients where there are incidentally found coronary artery calcifications (again, overtreating the LDL may benefit them a lot, with minimal downside)

    -- they appropriately incorporate more aggressive lowering of the LDL levels in those with higher risk for ASCVD than in prior guidelines (and accepting that there should be LDL and non-HDL goals to therapy, not part of most prior guidelines)

    -- perhaps most importantly, highlighting that the atherosclerosis process consists of a long-term accretion of atherosclerotic plaques starting in asymptomatic youths, emphasizing the role of nonpharmacologic approaches in most of these younger people but also further working up those with very high LDLs for familial hypercholesterolemia, and using meds as needed if LDL>160

        -- this means that we should be assessing the full lipid profile of all adult patients we see independent of their age (in alignment with the American Pediatrics Assn approach)

        -- however, this needs the caveat of the concerns about females of reproductive potential, contouring our approach to even more aggressive nonpharmacologic means

        -- our goal for many individuals should likely be an even more aggressive LDL reduction than the <100 range they suggest as determined by the individual's constellation of risk factors.

            -- the concept here is trying to prevent the early accumulation of atherosclerotic plaques, especially since plaque volume does not decrease much with statins and PCSK9s, though there are really important effects on plaque composition by decreasing their internal inflammation. however, much of this benefit is really in those with LDL levels <20. https://pmc.ncbi.nlm.nih.gov/articles/PMC11393034/ . statins are also anti-inflammatory, decrease lipids, and increase plaque fibrosis in newly formed plaques and stabilize them.

    -- and, my own anecdotal experience over many decades of patients in the 90+ year old range (and lower) is that very few patients have had atherosclerotic events....

geoff

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