Dr. Dapo

The term "VIP patient" further perpetuates existing disparities in healthcare. Let's work to treat all of our patients like the very important people that they are. 🤝🏾👩🏻‍⚕️⚕️⚖️🩺🏥 #HealthForAll #HealthEquity #HealthIsWealth

“The higher the risk, the greater the LDL-C reduction required.” Excellent presentation by Kausik Ray at the NLA–EAS Joint Session on Primary Prevention. A key message: while the relative benefit of LDL-C lowering may attenuate as baseline risk increases, achieving meaningful absolute risk reduction requires progressively larger LDL-C reductions. 🔹 Earlier intervention 🔹 Lower LDL-C levels 🔹 Combination therapy when needed 🔹 Better implementation of guideline recommendations In lipid management, intensity should match risk. @society_eas @ProfKausikRay @nationallipid

❤️ Safe Hearts Require Safe ℹ️ 🙏🏻 Honored to share my perspective at #EAS2026 on one of the most underestimated cardiovascular risk factors of our time: misinformation. 👉Today, cardiovascular prevention is no longer limited to controlling LDL-C, blood pressure, or smoking. We must also address the growing impact of distrust, misinformation, and algorithm-driven health content on patient behavior. Key messages: 🔹 Virality is not validity 🔹 Selective truths can be as harmful as outright falsehoods 🔹 Poor information fuels fear, nocebo effects, and treatment discontinuation 🔹 Scientific societies must proactively engage in the digital space 🔹 Safe hearts require safe information ☝️The future of prevention depends not only on developing better therapies, but also on ensuring that evidence-based medicine reaches patients clearly, accurately, and effectively. @society_eas @BNordestgaard @ProfKausikRay @nationallipid @DrMarthaGulati @LondonoMd @Drlipid @DrMauinforma

👉Just published in Atherosclerosis — a true milestone for the global lipid community. 🌍🫀 ☝️The new EAS Consensus Statement on lipid clinics brings together experts from 55 countries and more than 500 lipid clinics to provide practical guidance on harmonization, organization, staffing, education, patient pathways, and funding of lipid services worldwide. 📌 Why it matters: • Establishes a global framework for lipid clinic development • Promotes equitable access to high-quality lipid care • Supports earlier diagnosis and better management of inherited and complex lipid disorders • Strengthens prevention of ASCVD on a worldwide scale • Highlights the importance of education, registries, and multidisciplinary care ☝️A fantastic initiative by the European Atherosclerosis Society Lipid Clinic Network and all contributing authors. Proud to have participated in this important international effort. ☝️A must-read for anyone involved in preventive cardiology, lipidology, cardiovascular prevention, and healthcare policy. 🔓🔗 atherosclerosis-journal.com/article/S0021-… @society_eas @ATHjournal @BNordestgaard @ProfKausikRay

New content online: Causes and consequences of discontinuation of GLP1RAs or tirzepatide dlvr.it/TSfs5G

🚨 New Commentary Published: Advancing Awareness & Testing for Lipoprotein(a) (Lp[a]) The American Heart Association’s new Lipoprotein(a) Discovery Project highlights a national effort to improve awareness, screening, and care pathways for patients with elevated Lp(a) — a genetically inherited and underrecognized cardiovascular risk factor linked to ASCVD, stroke, and aortic stenosis. With the 2026 ACC/AHA Dyslipidemia Guideline now recommending at least one lifetime Lp(a) measurement for every adult, this initiative aims to expand testing, improve clinical workflows, and strengthen patient-centered cardiovascular prevention strategies. 📖 Read the commentary here: ow.ly/reL750YZAlI #LipoproteinA #LpA #PreventiveCardiology #Cardiology #ASCVD #HeartHealth #AHA #LipidManagement #CardiovascularDisease

New research highlights the powerful role nutrition can play in early hypertension management. A higher adherence to the DASH eating pattern may help delay or reduce the need for medication initiation in adults with stage 1 hypertension. The findings reinforce what many clinicians already see in practice: lifestyle interventions aren’t just complementary—they can be foundational. The DASH diet emphasizes: 🥗 Fruits & vegetables 🌾 Whole grains 🥛 Low-fat dairy 🐟 Lean proteins 🧂 Reduced sodium intake As rates of hypertension continue to rise, evidence-based nutrition strategies could have a major impact on long-term cardiovascular health and healthcare costs. Read it here: sciencedirect.com/science/articl…

🙌 Our last manuscript is out. 👉“Safety of Very Low LDL-Cholesterol: Ten Common Concerns, Misconceptions, and Evidence-Based Clarifications” 📍Very low LDL-C levels continue to generate debate, fear, and misinformation in clinical practice. 📍In this review, we critically examined 10 of the most frequent concerns related to intensive LDL-C lowering: — Cognitive decline — Hemorrhagic stroke — Cancer — Cataracts — Hormonal dysfunction — Diabetes risk — Muscle symptoms — Older adults — Sex differences — Overall cardiovascular benefit 📍The key message is clear: RCTs, meta-analyses, and genetic evidence consistently support the safety profile of very low achieved LDL-C levels in appropriately selected high-risk patients. 📍Some adverse effects are real — particularly statin-associated dysglycemia and muscle symptoms — but their absolute risk is generally modest compared with the magnitude of ASCVD risk reduction. 📍Therapeutic inertia and misinformation remain major barriers in preventive cardiology. Evidence-based communication matters. 📍Lower LDL-C. Earlier. Longer. Safer than many still believe. ☝️Proud to collaborate with outstanding colleagues from Latin America, Europe, and beyond in this international effort. 🔗 doi.org/10.1016/j.athe… @society_eas @ATHjournal

Coronary plaque in younger women may carry a far greater prognostic signal than equivalent plaque in men. In our editorial in the Am Journal of Preventive Cardiology (doi.org/10.1016/j.ajpc…), we discuss why sex-specific interpretation of CCTA findings is essential—and why even “mild” plaque in women should prompt aggressive prevention efforts. #CardioTwitter #CCTA #WomensHeartHealth

📌Residual lipid risk in atherosclerotic cardiovascular disease #CardiovascularRisk #CardiovascularPrevention

This is my favorite study of the year. What a waste of money. But keep telling physicians to see more patients every hour. Because that is working so well….

Cardiovascular benefits of obesity therapies: an overview of obesity medicines and metabolic bariatric surgery bit.ly/3ZSLmis

Concomitant psychiatric, somatic, and social vulnerabilities in patients at greatest risk of cardiovascular disease 👇 #ESCPrev26 #EAPC_ESC

We are deeply saddened to have lost our founding chairman and the father of modern academic cardiology, Dr. Eugene Braunwald, who founded the TIMI Study Group in 1984, and with that vision profoundly shaped the practice of cardiovascular medicine across the world.

Combined oral contraceptives and hormone-replacement therapy increase the risk of venous thromboembolism, although the absolute risk is low. Transdermal estradiol and micronized progesterone carry lower risk. Learn more in the Review Article “Sex Hormone Influences on Venous Thrombotic and Cardiovascular Risk” by Leslie Skeith, MD, MHPE, and Shannon M. Bates, MDCM, from @ucalgary and @mcmasteru: nejm.org/doi/full/10.10…

Finally, I can sleep well. My decades of preaching about apoB and LDL-P concentrations have long been sustained by science, but now we find out it is the most cost-effective way to evaluate lipoprotein-mediated risk for atherogenesis. I could also finally retire, but I am not ready for that

👉 HDL and ASCVD: is high HDL-C protective, harmful, or simply misleading? 👆 HDL is biologically complex and multifunctional — lipid transport, immune modulation, endothelial signaling 👆 HDL-C reflects cholesterol content, not biological function → surrogate, not mechanism 📍 Observational epidemiology: Reports U-shaped associations between HDL-C and mortality However: Highly prone to confounding and reverse causation Driven by comorbidities (liver disease, alcohol, inflammation, frailty) → Not suitable to infer causality 📍 Causality hierarchy matters: Mendelian randomization (MR): No consistent causal protection from HDL-C Strong causal signal for ApoB-containing lipoproteins → Genetic evidence overrides observational noise 📍 Interventional trials: Raising HDL-C → no reduction in ASCVD events CETP inhibition: benefits align with ApoB lowering, not HDL-C increase 📍 Mechanistic paradigm shift: From HDL quantity → HDL function Key metric: cholesterol efflux capacity (CEC) 📍 Clinical implications: High HDL-C ≠ protective Very high HDL-C should not reassure 📍 Focus remains on: ApoB / LDL-C Lp(a) Non-HDL-C 👆 Take-home: U-shaped HDL curves are epidemiology, not biology Reverse causation ≠ protection If it’s not causal, it’s not a target HDL-C is a marker. ApoB is the mechanism. 🔓 Open Access journals.lww.com/co-lipidology/… @society_eas @JohnKastelein @CO_Lipidology

👉 We spend decades arguing about how low to push LDL-C 👆 Almost no one asks the obvious question: 🤔 How much LDL-C did our ancestors actually have? The evidence exists — five independent lines, all converging on the same uncomfortable answer. 1️⃣ The term newborn. Before any dietary or metabolic influence, a healthy neonate arrives with LDL-C of ~30–50 mg/dL. That is the LDLR operating without environmental interference. Everything that rises after birth is acquired. 2️⃣ The Tsimane (Kaplan et al., Lancet 2017) — forager-horticulturalists of the Bolivian Amazon — have a LDL-C between 70 to 90 mg/dL and the lowest prevalence of coronary atherosclerosis ever recorded in any human population. Five times less than the U.S. in adults over 75. And their LDL is rising as roads and processed food arrive. 3️⃣ PCSK9 loss-of-function variants. African American carriers of nonsense mutations (Y142X/C679X, ~2% frequency): −28% LDL-C and −88% CHD risk over 15 years (Cohen et al., NEJM 2006). Homozygous LOF carriers live with LDL-C of ~15–30 mg/dL. Perfectly healthy. Nature already ran the trial. 4️⃣ Evolutionary genetics. Recent positive selection signals exist on gain-of-function PCSK9 variants that raise LDL-C — likely adaptive in food-scarce ancestral environments. Modern hypercholesterolemia is not "normal." It is an ancestral survival advantage turned pathological by evolutionary mismatch. 5️⃣ Great apes in natural habitat: ~40–70 mg/dL LDL-C. Same genome. Different environment. 👆 Bonus — Lp(a). The KIV-2 repeat expansion that raises Lp(a) is a derived, recent variant. Low-Lp(a) alleles are ancestral. Elevated Lp(a) is a textbook antagonistic pleiotropy signal — possibly protective against bleeding early in life, atherogenic over decades 📍The convergent estimate: ancestral LDL-C was ~30–70 mg/dL. 📍An LDL-C of 130 mg/dL is not "normal." It is normal for a Western society in evolutionary mismatch. Targets of <55 mg/dL in high-risk patients — which still feel aggressive to many clinicians — are, ironically, closer to the ancestral phenotype than what we call "normal LDL" in daily practice. 🤔 The question is not "is it safe to lower LDL this much?" The question is: why did we let it rise this high? @society_eas @nationallipid

Perioperative meds matter more than we think. Continue statins and β-blockers, be cautious with aspirin, and hold SGLT2 inhibitors before surgery. Small decisions, real impact. jamanetwork.com/journals/jama/… #MedTwitter #Cardiology #Surgery #Healthcare

Beautiful. My article and thread prompted many physicians and researchers to share their own LDL-lowering regimens. This is exactly why I do it. 🙌🏼

Be PRAGMATIC Be SIMPLE From Haffner to VESALIUS: we didn’t discover anything new… we finally accepted it. 📍 1888, Haffner (NEJM) already warned us: 👉 A patient with diabetes and no MI carries a risk similar to someone who already had one. nejm.org/doi/full/10.10… 📍 2026 VESALIUS (JAMA) just removes the last excuse: 👉 Even before clinically evident atherosclerosis, the risk is already biologically active. jamanetwork.com/journals/jama/… 👆 Let’s be honest: There are NO LOW-RISK patients with diabetes There are NO INTERMEDIATE-RISK patients with diabetes 👉 There are only: HIGH RISK VERY HIGH RISK (most of them, if you actually look closely) 📌 The problem is not classification. 📌 The problem is clinical denial and therapeutic inertia. We don’t undertreat diabetes because we lack evidence. 👉 We undertreat it because we are still thinking in outdated risk categories. Atherosclerosis starts early. Diabetes accelerates it. And we… keep labeling instead of acting. @society_eas @nationallipid