In honor of #CholesterolMonth, the NLA is proud to release the second installment of the Lipids Simplified Series: Lipoprotein(a) Management Simplified. Following the success of our LDL-C Management Simplified publication, we felt there was no more timely or necessary topic to tackle next than Lp(a). Authored by leading Lp(a) experts Marlys L. Koschinsky, PhD, FNLA and Christie M. Ballantyne, MD, MNLA, this article and accompanying infographic are designed to distill the complexity surrounding Lp(a) into clear, actionable guidance for clinicians. Our goal is simple: make this essential science more accessible and easier to apply in everyday practice. 🔗 Access the full article and infographic at lipid.org/resource/lipoprote…. 👉 You can find this and other NLA articles under the Articles section of our newly launched lipid.org. Stay tuned... more topics in the Lipids Simplified Series are on the way! #LipoproteinA #Lpa #ASCVD #CardiovascularPrevention @CBallantyneMD @MarlysLPA

What an all star team of preventive cardiologists! Can't wait for 9th @Heart_SCCT #PreventionSymposium ⭐️ @Bweber04 @BudoffMd @DrMichaelShapir @jplutzkymd @bwhcvls @TIMIStudyGroup

I’ve never been a fan of closing a membranous vsd with a closure device. I find they often don’t sit well and leave large residual leaks. In patients that are surgical candidates, I would advocate a surgical approach as the primary choice. #ACHD ❤️‍🩹

Wonderful to see friends, mentors, & celebrate science at #ASNC2026. Honored to be elected a Fellow of ASNC and the LDP. Grateful to the Air Force for supporting my attendance, and to my mentors for their support. @Bweber04 @cardiac_md @mdicarli @sanjaydivakaran @DorbalaSharmila

Congratulations to @almallahmo for being awarded the @MyASNC Mario Verani lecturer at #ASNC2026. He gave a very comprehensive talk on the advances in #CVNuc

Multimodality imaging of cardiac amyloidosis by @BrunoLimaMDPhD #ASNC2026 @MyASNC

💡 Key takeaways from Dr. Brittany Weber: 📏 Standardize flow measurements 🫀 Define CMD phenotypes 🔬 Run adequately powered trials 💊 Test whether improving flow improves outcomes 🌍 Expand PET access and routine flow quantification #ASNC2026 @MyASNC

Incremental value of ¹²⁴I-evuzamitide for diagnosis of cardiac amyloidosis

I am speaking at ASNC2026 31st Annual Scientific Session & Exhibition. Please check out my talk if you're attending the event! #ASNC2026 #CVNuc #THINKPET - via #Whova event app @demanddeborah #ASNC2026 @MyASNC @NJACC @AHAScience @ACCinTouch

How can CCTA help guide PCI planning? Join SCCT and SCAI TONIGHT (7-8pm ET) for a free Knowledge Lab exploring the latest expert consensus on integrating CCTA into PCI workflows — from calcified disease and bifurcations to chronic total occlusions. ow.ly/xUXY50ZGb3q

Patients with autoimmune or inflammatory disease had 22% higher odds of elevated Lp(a) vs controls. New in #JACCAdvances: jacc.org/doi/10.1016/j.jacad… #cvLipids @MWilkinsonMD

Corticosteroids in recurrent pericarditis: only in selected cases

In 65M older adults, wildfire smoke PM2.5 was assoc w/ more #CVD 🏥, peaking at concentrations of 0.26–0.32 µg/m³. The risky dose isn't the orange-sky day; it's the one that looks normal. jacc.org/doi/10.1016/j.jacc.… #JACC #AirPollution @ChenKai_yale @yuan_lu1 @hmkyale @CCHYale

In TRISCEND II, #TTVR did more than just ⬇️TR: ⬇️venous congestion, RV reverse remodeling, ⬆️forward flow & cardiac output. ⬆️effective RV function may matter more than traditional #EchoFirst preload-dependent metrics. jacc.org/doi/10.1016/j.jcmg.… #JACCIMG #vhdTR #cvVHD

Grateful to work w/ Peter Libby & team on our new @JAMACardio paper: how do we actually run CV outcomes trials in Clonal Hematopoiesis? Genetic heterogeneity, clone size, recruitment, competing risks, and statistical power all complicate trial design. 🔗jamanetwork.com/journals/jam…

ASNC has released its 2026 Guideline for Stress Testing in #SPECT & #CardiacPET MPI with updated recommendations spanning patient prep, stress protocols, safety, interpretation, reporting & lab supervision. Read it in @JNCjournal 👉shorturl.at/Ripmk

Leads cause TR by impinging on leaflets and tether by fibrosis 1 in 20 ACHD pts has a device. Currently no great solutions exist as diuretics can lead to kidney injury correct while lead revision or extraction carries risk or otherwise not practical #ACHD ❤️‍🩹

On the Lp(a)HORIZON pelacarsen results: 1. It is still prudent (and evidence-based imo) to obtain Lp(a) diagnostic testing once, ideally early in life. Knowing you are at high risk (~10% of general pop has Lp(a) > 70 mg/dL, which confers ~50% higher risk of ASCVD) should prompt TODAY what this trial called "risk-therapy optimization" in the months PRIOR to enrollment in the study. This means starting the full sweep of already approved CV risk modifying agents: statins, PCSK9i, antihypertensives, etc. This single trial result on Lp(a) perturbation does not negate the predictive value of Lp(a) dx testing 2. The HORIZON trial result definitely does NOT mean that human genetics defined targets 'don't work'. C'mon people, stop the hysteria. It just means that in a group of people with exceptionally well-controlled LDL, whose (very profound!) CV disease biology has already revealed itself as a heart attack / stroke / symptomatic PAD, lowering Lp(a) by 70-80% for a period of only 2.5-6 yrs, starting at an avg age of ~60, is not enough to significantly decrease the risk that the same biology rears its ugly head again. Many possible hypotheses remain 3. To all the investigators and pharma companies who have committed themselves to running CVOTs, applause and gratitude. These studies could potentially produce some of the most widely practice-changing and life-saving results most of us will ever see in a lifetime. Personally I remain optimistic about studies that will 'treat earlier and treat longer', especially for primary prevention. eg Lilly's lepodisiran (siRNA) trial ACCLAIM-Lp(a) includes a primary prevention arm

# CCTA Has Changed. Our Reports Must Change With It. The **2026 SCCT Expert Consensus on CCTA Interpretation and Reporting** arrives more than a decade after the 2014 document. And CCTA has changed dramatically: **Class I recommendation for CAD evaluation, CAD-RADS 2.0, multi-energy CT, Photon-Counting CT, and increasing evidence for the prognostic relevance of coronary plaque.** ## The Critical Point This is no longer only about stenosis. The document gives increasing relevance to **plaque composition, high-risk plaque features and overall plaque burden**, which can be expressed visually, by SIS, or through the **P1–P4 CAD-RADS categories**. Automated tools now also make absolute plaque quantification possible. Importantly, a CCTA should be called **normal only when there is neither plaque nor stenosis.** That is more than terminology. It reflects a change in how we define coronary disease. ## My Take CCTA reporting is progressively moving from **describing the lumen to describing atherosclerosis**. Stenosis remains important — but it is only one manifestation of the disease. The next logical step is quantitative: **Where is the stenosis? → How much atherosclerosis does this patient actually have?** ## Where PCCT Fits The consensus explicitly recognizes Photon-Counting CT and ultra-high-resolution imaging, with resolution down to approximately **0.11 mm in-plane and 0.16 mm through-plane**, reducing partial-volume and blooming artifacts and improving assessment of plaques, stents and heavily calcified stenoses. But the opportunity may go beyond better stenosis assessment. **PCCT + quantitative plaque analysis + AI could redefine the CCTA report itself:** **What disease is present? How much? What phenotype? And what should we do about it?** CCTA is no longer simply coronary angiography performed with CT. **It is becoming quantitative imaging of coronary atherosclerosis.** #CardiacCT #CCTA #SCCT #CADRADS #Atherosclerosis #CoronaryPlaque #PhotonCountingCT #PCCT #ArtificialIntelligence

Hi all, The Lp(a) HORIZON trial has released topline data and, quite shockingly, missed its primary endpoint. In other words, lowering Lp(a) in patients with prior MI, stroke or peripheral arterial disease, who were otherwise very well treated for LDL-C, blood pressure, diabetes and other risk factors, did not reduce the primary cardiovascular endpoint. We obviously need to see the full data before making firm conclusions, and I don’t want to speculate too much without the details. But this is a big enough result that it is worth summarizing what we know, what we don’t know, and what this may mean for our patients after 20+ years of trying to test the “Lp(a) hypothesis.” What we know: 1-There are hundreds if not thousands of genetic, epidemiologic and Mendelian-randomization studies showing that elevated Lp(a) is associated with MI, stroke, peripheral arterial disease and aortic stenosis. That body of evidence is very strong. 2-However, much of those data come from community-based populations, often before the era of intensive LDL-C lowering and modern secondary prevention. 3-There has been much less information about how much residual risk Lp(a) carries in someone who has already had an event and is then treated very aggressively. 4-HORIZON may have had some of the best-treated patients of any recent cardiovascular outcomes trial. Baseline LDL-C was about 65 mg/dL, a measured LDL-C contains the cholesterol carried on Lp(a), so in reality, 15-20 points lower. 5-In patients with very high Lp(a), if you correct LDL-C for Lp(a)-cholesterol, the actual LDL-C carried by LDL particles may have been closer to 45–50 mg/dL, perhaps even lower in some patients. 6-This raises a very basic question: Can you still demonstrate a major incremental benefit from lowering another apoB-containing particle when the underlying LDL burden has already been driven this low? What we don’t know: 1-What was the actual corrected LDL-C in these patients? I think it would be extremely informative to directly measure Lp(a)-C and calculate corrected LDL-C. This may tell us a lot about the biological setting in which pelacarsen was being tested. 2- What was the OxPL status? Our prior work has suggested that much of the pro-inflammatory biology associated with Lp(a) is related to its enrichment in oxidized phospholipids. Did OxPL fall? Did patients with higher OxPL derive more benefit? Was Lp(a) concentration actually identifying the patients with the most pathogenic particles? 3- Did we measure the right component of Lp(a) for trial inclusion? We generally measure molar particle concentration. But is molar concentration itself the main driver of risk, or is it partly a surrogate for what the particle carries? Cholesterol? Triglycerides? Oxidized phospholipids? Other proteins? Could two patients with the same Lp(a) concentration have very different Lp(a)-mediated risk? I think this question deserves much more attention. 3- Were the genetic data telling us exactly what we thought they were telling us? The genetic data are extremely compelling, but genetics reflect lifelong exposure. A clinical trial treats patients late in life, often after decades of arterial injury and after an event has already occurred. Those are not necessarily the same experiment. Could there also be some unrecognized biology linked to the LPA locus that we have not completely accounted for? That possibility should at least be considered. 3- Does very low LDL-C modify the Lp(a) risk relationship? Maybe Lp(a) is particularly important when LDL-C is higher, but its contribution becomes smaller once LDL-C is driven to very low levels. Again, we need the data. 4- Does aspirin or other antiplatelet therapy reduce part of the risk associated with Lp(a)? Lp(a) has potentially important prothrombotic effects. Almost everyone in a trial like HORIZON is receiving contemporary antiplatelet therapy. Could that blunt one component of the risk associated with Lp(a)? 5- Why are these patients still having events? This may be one of the most interesting questions of all. These are patients with LDL-C around 65 mg/dL, and perhaps corrected LDL-C substantially lower, yet cardiovascular events continue to occur. What is driving that residual risk? Inflammation? Thrombosis? Plaque burden that is already too advanced? Other lipoprotein characteristics? Something we are not measuring? 6- Do we need to re-examine some basic assumptions about atherosclerosis? We have spent decades focusing heavily on the quantity of circulating lipoproteins. But perhaps lipoproteins are relatively benign until they undergo biological modification in the artery wall. Oxidation may be one of those key modifications. For some patients, the answer may be to remove more particles from the circulation. For others, perhaps the better approach is to prevent their oxidation or block the downstream biological effects of oxidized lipids. The recent difficulties with anti-inflammatory approaches, including IL-6 inhibition, make these mechanistic questions even more interesting. 7- Was there something specific about pelacarsen, the degree or timing of Lp(a) lowering, advanced disease, trial duration, background therapy or patient selection that mitigated a potential benefit? We simply don’t know yet. That is why the detailed results will be so important. What does this mean for patients today? If you have already had an MI, stroke or PAD, the immediate lesson is very clear: 1- Get all of your established risk factors treated aggressively. 2- Get LDL-C/apoB very low. 3- Control blood pressure. 4- Control diabetes. 5- Don’t smoke. 6- Use appropriate antiplatelet and other guideline-directed therapies. HORIZON shows us what modern secondary prevention should look like. If you have elevated Lp(a) but have never had an event, the genetic and epidemiologic data still suggest increased lifetime risk. Until the other 4 outcome trials read out, I would continue to treat every modifiable risk factor aggressively. We should wait for those trials before drawing broad conclusions about the entire field. I think the story of Lp(a) therapy is beginning, not ending. We also need to show tremendous respect and gratitude to the patients who participated in HORIZON and to the investigators and companies that invested enormous resources to actually test the Lp(a) hypothesis, to the ultimate benefit to peole with elevated Lp(a) to best guide how to manage risk. More to come as we go forward.