🔥🫀 Inflammation is no longer a hypothesis—it’s a therapeutic target The 2025 ACC Scientific Statement on Inflammation and Cardiovascular Disease marks a turning point: inflammation is now recognized as a causal, measurable, and actionable driver of cardiovascular risk, not just a bystander . 🧠 Key paradigm shift Even in statin-treated patients with optimal LDL-C, residual inflammatory risk—best captured by high-sensitivity C-reactive protein (hsCRP)—strongly predicts recurrent events and cardiovascular death. In fact, post-statin hsCRP is often more prognostic than LDL-C itself. 📏 Measure what you want to treat The statement makes a bold recommendation: 👉 Near-universal hsCRP screening in both primary and secondary prevention. hsCRP <1 mg/L → low risk 1–3 mg/L → intermediate risk 3 mg/L → high inflammatory risk Persistently elevated hsCRP (>2 mg/L) identifies patients who remain vulnerable despite guideline-directed therapy. 💊 Anti-inflammatory therapies: what works (and what doesn’t) ❌ Broad immunosuppression failed (e.g. methotrexate in CIRT). ✅ Targeted inflammation inhibition works: Canakinumab (CANTOS) proved the inflammation hypothesis—reducing events without lowering LDL-C. Low-dose colchicine (0.5 mg/day) reduced recurrent CV events by ~25% and is now FDA-approved for secondary prevention. 🚧 New frontiers: IL-6 inhibition (ziltivekimab, clazakizumab) in CKD, HFpEF, ACS—results expected soon. 🧘‍♂️ Lifestyle is anti-inflammatory medicine Mediterranean/DASH diets 🥗, omega-3 intake 🐟, exercise 🏃‍♀️, weight control, and smoking cessation are explicitly framed as anti-inflammatory interventions, not just “healthy habits.” 🖼️ Imaging: promising, not ready Advanced imaging of vascular inflammation (e.g. perivascular fat attenuation index) is exciting—but not yet for routine clinical use. 🔮 Bottom line Atherosclerosis is an inflammatory disease with lipid involvement. The time has come to treat cholesterol and inflammation—with biomarkers, lifestyle, and targeted therapies—moving cardiovascular prevention into a new era 🚀

🚀 Calcium Score & CCTA: Key Highlights from the 2025 AHA Scientific Statement (DOI: 10.1161/CIR.0000000000001394) Non-obstructive CAD in Chest Pain Patients 🧊 1. CAC = Atherosclerotic Burden, Not Just a Number CAC is one of the strongest predictors of future ASCVD risk—better than biomarkers or stenosis alone. 📉 CAC = 0 → high NPV for obstructive CAD (but not zero risk: ~10% still have non-calcified plaque, especially if young or high-risk). 🔥 CAC ≥1000 = extreme risk → annual CV mortality similar to 2ndry prevention populations. 📊 CAC → intensity of preventive therapy: from lifestyle (CAC 0) → to statins (CAC ≥100) → to high-intensity LLT + aspirin (CAC ≥300). 🧮 2. CAC for Risk Upgrading & Therapy Decisions CAC ≥100 or ≥75th percentile supports starting statins even in borderline/intermediate-risk patients. - hidden high-risk phenotypes (eg, DM or preDM patients with CAC ≥100). 🌈 CAC from non-gated PET/SPECT CT is increasingly used and correlates well with dedicated CAC scans. 🫀 3. CCTA: The New Backbone of Chest Pain Evaluation The 2021 Chest Pain Guidelines expanded CCTA → leading to a surge in detecting nonobstructive CAD (NOCA). CCTA is essential because: - plaque beyond the lumen (including noncalcified plaque). - vessels down to ~2 mm (even smaller with photon-counting CT). - high-risk plaque features (LAP, positive remodeling, spotty calcification). 👁️ CCTA reveals that up to 50% of symptomatic patients have NOCA. 🧨 4. High-Risk Plaque on CCTA = High Future Event Risk High-risk markers include: 📦 High total plaque volume 🟣 Low-attenuation plaque (>4%) ➕ ≥2 high-risk features (per CAD-RADS 2.0) 🔥 Pericoronary adipose tissue (PCAT) inflammation These features predict MI better than stenosis, shifting the paradigm from stenosis-centric to plaque-centric care. 📈 5. CCTA-Based Risk Staging (CAD-RADS 2.0 + Plaque Volume) Stage 0 → no plaque Stage 1–2 → increasing plaque burden Stage 3 → high-risk NOCA 🎯 Treatment intensity escalates with plaque volume, not stenosis alone. 🔄 6. CAC + CCTA = The Most Powerful Combination CAC quantifies calcified burden → great for long-term risk and therapy escalation. CCTA quantifies total plaque (calcified + noncalcified) → great for short-term event risk. 💡 7. Why This Matters Most ACS events originate from nonobstructive lesions. 📢 The statement pushes clinicians to: Detect early plaque (especially noncalcified). Classify risk by plaque burden + inflammation. Intensify therapy before stenosis develops. #PCCT #Atherosclerosis #PhotonCountingCT #CCT #yesCCT