An interactive visual tool for patients and practitioners built on the 2026 ACC/AHA Dyslipidemia Guidelines. Real-time plaque modeling, particle biology, CKM pathways, and live therapy simulation.
Not all lipoproteins are equal. Size, density, apolipoprotein cargo, and oxidation potential determine whether they traffic cholesterol safely — or embed it into vessel walls over decades.
22–25 nm · ApoB-100 · PRIMARY ATHEROGENIC AGENT
8–12 nm · ApoA-I · REVERSE CHOLESTEROL TRANSPORT
20–70 nm · ApoB-100 + Apo(a) · CLASS 1 TEST ONCE
30–80 nm · ApoB-100 + ApoC-III · NEW 2026 FOCUS
ApoB-100 binds proteoglycans in intimal matrix. Penetration size-dependent.
Retained LDL oxidized by ROS → oxLDL triggers immune cascade.
Macrophages engulf oxLDL via scavenger receptors → fatty streak formation.
SMC proliferation forms fibrous cap over necrotic lipid core → vulnerable plaque.
Cap ruptures, thrombus forms → acute coronary syndrome or stroke.
Cross-sectional views at increasing cumulative LDL-C exposure. Stenosis % reflects combined particle burden, not a single time point.
Adjust risk parameters and watch the coronary artery respond in real time — both in longitudinal cross-section and transverse view. Up to 80 years of cumulative exposure modeled.
Estradiol, progesterone, testosterone, and thyroid hormone (T3) each have measurable, directional effects on lipid metabolism. Toggle your patient's profile to see adjusted risk and lipid outputs. Note: These effects represent physiologic mechanisms supported by evidence — not yet incorporated into 2026 ACC/AHA guidelines.
Not all plaque is equal. Soft (lipid-rich, vulnerable) plaque carries dramatically higher rupture risk than calcified (hard) plaque. The Cleery CTA platform revolutionizes our ability to distinguish them non-invasively.
High risk of rupture · Thin fibrous cap · Active inflammation
Lower rupture risk · Dense fibrous cap · Healed/scarred lesion
Coronary CT Angiography with AI-enhanced plaque analysis can non-invasively characterize plaque composition, identify vulnerable lesions, and guide treatment intensity — capabilities that standard CAC scoring alone cannot provide.
Distinguishes low-attenuation (lipid-rich), fibrous, and calcified plaque components using Hounsfield unit analysis. Soft plaque HU <30 signals highest vulnerability.
Identifies positive remodeling index >1.1, pericoronary fat attenuation, napkin-ring sign, and spotty calcification — each independently predicts ACS events.
Computational fluid dynamics applied to CTA data estimates fractional flow reserve non-invasively — identifies hemodynamically significant lesions without catheterization.
Quantifies total atherosclerotic burden (TAB) — non-calcified, mixed, and calcified segments. Serial imaging tracks regression with aggressive LLT. ORION-3/FOURIER extension data.
Fat attenuation index (FAI) quantifies perivascular inflammation — elevated FAI predicts cardiac events independent of traditional risk factors and plaque burden.
Serial CCTA demonstrates statin-induced plaque stabilization: cap thickening, lipid core reduction, calcification progression. PCSK9 inhibitor data shows plaque regression at LDL <55 mg/dL.
Clinical Implication: A patient with CAC score of 0 may still harbor non-calcified soft plaque detectable only on CCTA. Conversely, high CAC (≥400) indicates substantial calcified burden with lower acute rupture risk than equivalent soft plaque — but significant stenosis risk. The 2026 guidelines selectively recommend CAC for risk reclassification; CCTA provides the full picture when CAC results are borderline or discordant with clinical risk.
Plaque component identification on coronary CTA is based on tissue attenuation (HU). Understanding this spectrum is essential for interpreting Cleery and CCTA reports.
Toggle therapies and adjust doses to see cumulative LDL-C reduction, non-HDL impact, and residual ASCVD risk. Based on 2026 ACC/AHA guideline pharmacotherapy evidence.
Foundation of all LLT
Generic, well-tolerated
Statin-intolerant option
Very-high-risk / residual LDL
When TG ≥150 mg/dL
Each agent in the simulator acts on a specific step of hepatic lipoprotein handling. This figure maps the full pathway: LDL receptor uptake and recycling, the PCSK9 degradation axis (where PCSK9 inhibitors act), de novo synthesis (suppressed by statins), and the VLDL to IDL to LDL cascade with HDL reverse transport. Sex hormone effects are included to show how estradiol and testosterone shift the lipid picture across systems.
Hormone effects vary by route and dose; transdermal estradiol is triglyceride-neutral, and the testosterone HDL effect is greater with oral or supraphysiologic dosing. Sources: Walsh et al., NEJM 1991; hormone-lipid literature; physiologic-dose data.
Cardiovascular-Kidney-Metabolic syndrome is one interconnected biological system. See how early lifestyle intervention redirects the risk curve — from age 5 to age 80.
Hover nodes to reveal bidirectional biological pathways. Particles flow continuously along active edges.
Primordial prevention window. Screen lipids 9–11.
Insulin resistance, VLDL overproduction begins.
T2D, CKD 3–4, HTN — no CVD event yet.
CAC positive, subclinical atherosclerosis on imaging.
MI, stroke, HFpEF with CKM drivers ongoing.
Toggle intervention pathways to see how risk curves diverge. Earlier interventions create the greatest lifetime benefit through compounding protection.
Visceral fat drives VLDL overproduction. Every 10 lb excess ≈ +5 mg/dL TG, −2 mg/dL HDL. Directly worsens plaque in Module 2 calculator.
GFR decline impairs TG clearance, raises Lp(a), creates dysfunctional HDL. Standard LDL-C underestimates CKD vascular risk — ApoB needed.
T2D shifts LDL particle profile to small-dense — more oxidizable, more atherogenic per particle, poorly captured by LDL-C alone.
IL-6, TNF-α from adipose tissue increase hepatic VLDL synthesis, reduce HDL function, and directly destabilize fibrous plaque caps.
Gut dysbiosis produces TMAO — an atherogenic metabolite amplified by red meat intake. Mediterranean diet directly reduces TMAO production.
Poor sleep (Life's Essential 8) disrupts cortisol/insulin rhythms, elevates TG and CRP. Sleep deprivation accelerates all CKM pathways.