stage 4, clinical CVD.<\/li>\n<\/ul>\nHealio spoke with Bailey about what primary care physicians need to know about CKM, new guidelines, therapies and more.<\/p>\n
Healio: How has the concept of <\/b>CKM c<\/b>hanged the way PCPs should risk-stratify patients vs. traditional siloed approaches?<\/b> <\/p>\n
Bailey:<\/b> The CKM approach is exciting because, in the past, a patient really had to be stage 4 before they ever got to see me in cardiology, which put them in the highest risk category. We already knew they were at the highest risk because they\u2019d had an ischemic event like heart attack or stroke or they were diagnosed with heart failure. Now, with these CKM categories, there\u2019s the recognition that we should start addressing risk with the first abnormality \u2014 excess or dysfunctional adiposity. I think we do good in medicine when we have numbers and recommendations. So, I think this guide really gives people something to aim for.<\/p>\n
Healio: <\/b>With the emergence of <\/b>sodium-glucose cotransporter 2 (<\/b>SGLT-2<\/b>)<\/b> inhibitors, GLP-1 receptor agonists, <\/b>m<\/b>ineralocorticoid <\/b>r<\/b>eceptor <\/b>a<\/b>ntagonists<\/b> (MRAs) <\/b>and <\/b>a<\/b>ngiotensin <\/b>r<\/b>eceptor-<\/b>n<\/b>eprilysin <\/b>i<\/b>nhibitor<\/b>s (<\/b>ARNIs<\/b>)<\/b>, how can PCPs sequence these therapies in patients newly diagnosed with heart failure?<\/b> <\/p>\n
Bailey<\/b>:<\/b> It\u2019s important for PCPs, or anybody on the front lines taking care of patients, to know that heart failure is really a clinical diagnosis. If you think a patient has heart failure based on their symptoms \u2014 inability to exercise without breathlessness, can\u2019t sleep at night because they\u2019re short of breath, lower extremity edema, increased abdominal girth \u2014 that is a clinical diagnosis, and you really should investigate. That\u2019s the first step.<\/p>\n
The ejection fraction on echocardiogram can be normal in patients who have heart failure \u2014 I think that\u2019s also important to recognize. With HFpEF, the ejection fraction is normal, and those patients can have filling pressures that are normal at rest. So again, if the patient has symptoms that sound like heart failure, even if they have an echocardiogram that looks overall pretty benign or normal, you should still go down that heart failure pathway. This may include additional testing like serum BNP or referral to cardiology.<\/p>\n
Once you have someone who has a diagnosis of heart failure, if you\u2019re in the heart failure with reduced ejection fraction (HFrEF) category (EF <40%), we have four pillars of care that all patients should be on at optimal doses.<\/p>\n
If you\u2019re in the mildly reduced heart failure category (EF 41%-49%), SGLT-2 inhibitors are still an across-the-board recommendation. For this category, I would say there are more individual patient factors that determine what medications they should be on. In general, beta-blockers, ARNIs and MRAs are recommended as well. <\/p>\n
When we\u2019re talking about HFpEF above 50%, everyone should also be on an SGLT-2 inhibitor. MRAs should be used across the board \u2014 either steroidal (spironolactone and eplerenone) or nonsteroidal (finerenone; Kerendia, Bayer). Nonsteroidals have the most compelling clinical data in 2026. Blood pressure should be controlled. They should be on an [angiotensin receptor blocker (ARB)] or an ARNI to get blood pressure down. And then if they have dysfunctional adiposity, which most of these patients do, and a BMI of over 30, we really should be considering a GLP-1 receptor agonist (semaglutide; Ozempic\/Wegovy, Novo Nordisk) or a GLP-1\/GIP combo drug (tirzepatide; Mounjaro, Eli Lilly) with cardiovascular outcomes.<\/p>\n
Healio: <\/b>What other updates in heart failure should PCPs know about?<\/b> <\/p>\n
Bailey:<\/b> There\u2019s a lot going on with heart failure. I think we\u2019re getting better at separating people into categories of heart failure. To me, that\u2019s the most exciting part, because we\u2019ve long recognized clinically that patients with HFpEF behave differently, but we haven\u2019t been good at further classifying those patients into discrete treatment groups.<\/p>\n
I now think of my patients with HFpEF as having either the obesity\/cardiometabolic phenotype or something else. And if it\u2019s something else, then I\u2019m going to go through the algorithms to try to figure out what that something else is. That could be an infiltrative cardiomyopathy like amyloid, which is among the most common, but there are others. It could be something like hypertrophic cardiomyopathy, which also will sometimes present down this pathway. But that first branch point is whether it is the obesity, diabetes or hypertension phenotype, or something else. <\/p>\n
Healio: What are a few notable updates in atherosclerotic cardiovascular disease?<\/b> <\/p>\n
Bailey:<\/b> The new dyslipidemia guideline is really exciting. I recommend everyone become familiar with it, because the key message is recognition of lipid abnormalities, earlier treatment to lower levels for longer, and more aggressive treatment for the people who are at the highest risk. Even with our prior guidelines, we haven\u2019t done a good job with any of those things.<\/p>\n
We have multiple ways to lower LDL in 2026. We have statins, which is our mainstay. We have ezetimibe, which has long been available as an oral medicine. We also now have another oral medicine that has a cardiovascular outcomes trial, bempedoic acid (Nexletol, Esperion). And we have PCSK9 inhibitor monoclonal antibodies (evolocumab; Repatha, Amgen; and alirocumab; Praluent, Sanofi\/Regeneron) as well as sPCSK9 inhibitor small interfering RNAs (inclisiran; Leqvio, Novartis). So, we have lots of pathways we can hit. There is now evidence in a high-risk primary prevention group with diabetes or atherosclerosis that PCSK9 inhibitor monoclonal antibody therapy translates to a significant reduction in clinical events. That\u2019s the first time we\u2019ve seen that.<\/p>\n
Then we have new pathways in lipids that we\u2019re thinking about: lipoprotein(a), which is a genetically mediated lipoprotein. It is independent of diet, it is independent of exercise, and it doesn\u2019t change over the lifetime much. And so, our lipid guidelines for the first time recommend a once-in-a-lifetime check for everybody for lipoprotein(a), because about 20% of the population has an elevated level. We know that elevated Lp(a) levels are associated with an elevated lifetime risk of ASCVD. And now we\u2019re exploring therapies that actually target lipoprotein(a) to see if that translates into a reduction in clinical events. There are at least three large trials going on, but none of these have reported results yet.<\/p>\n
There is an algorithm for refining risk assessment in the new guidelines using CPR (calculate, personalize and reclassify\/reassess). You can use things like nontraditional risk factors or a calcium score to either move people up or down in risk. So, you really get this approach in which you treat more people to lower targets over a longer period, but there\u2019s a lot of personalization that\u2019s allowed within that.<\/p>\n
Healio: You stated that timing to referral matters now more than ever. Can you elaborate on why this is?<\/b> <\/p>\n
Bailey:<\/b> In the world of cardiology, we are looking at earlier interventions for patients. An earlier diagnosis would lead us to treat the patient differently. Amyloid is a good example of that. Historically, with HFpEF, I really didn\u2019t think about amyloid very much. But in 2026, I think about it in every patient with HFpEF. It really changes the treatment paradigm drastically if I diagnose a patient with amyloid. Same thing with valvular heart disease. A lot of times, we don\u2019t meet these patients until they\u2019re in the moderate or severe category. But really, there are probably things we could do earlier that may potentially alter that care trajectory. Even if it\u2019s a one-time meeting to say \u201ceverything\u2019s fine.\u201d That\u2019s OK. But we get to meet people earlier vs. very advanced late stage. The same is true in chronic coronary disease and prevention.<\/p>\n
\n<\/video-js>\nAlison L. Bailey, MD, FACC, FASPC, discusses the take-home messages of her talk on updates in cardiology. Healio: What is the take-home message of your talk for primary care physicians?<\/b> <\/p>\n
Bailey:<\/b> The most important takeaways from my talk were recognizing that cardiovascular risk is a spectrum. We should recognize it as early in life as possible. And that includes things like blood pressure, weight, physical activity, lipids and glucose status. And then we should manage that risk aggressively from birth to death.<\/p>\n
Medicine is a team sport, and cardiovascular disorders are so common in the United States. It really takes more than just the cardiologist or just the primary care physician. We really want to be team-based and manage these patients together, because they have cardiovascular, kidney and cardiometabolic dysfunction, and these disorders have the same risk factors for development and progression and contribute to increased cardiovascular and CKM risk.<\/p>\n
For more information: <\/h2>\n Alison L. Bailey, MD, FACC, FASPC<\/b>, <\/b>can be reached at dr.alison.bailey@icloud.com as well as X, @a_l_bailey.<\/p>\n\n
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Sources\/Disclosures<\/h3>\n Source: <\/h2>\n Bailey AL. Update in cardiology. Presented at: ACP Internal Medicine Meeting; April 16-18, 2026; San Francisco.<\/p>\n
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