| — | METHOD | smooth curve is constructed (90 = 1.0; target ≤80) Technical notesAnchor points 30/50 = 0.85 floor, 80 = 0.95, 90 = 1.0, 110 = 1.15, 160 = 1.55. No primary source. Off the 8-metric index — heart, not all-cause. |
| Ischemic cardiovascular events | B | Sniderman is 1.43 ischemic-CV, not all-cause mortality Technical notesSniderman 2011: 12 reports / 233,455: apoB RRR 1.43 vs LDL 1.25 vs non-HDL 1.34. Fatal or nonfatal ischemic events. No matching lab-ApoB → all-cause mortality dose-response meta-analysis is available. |
| Cardiovascular disease prediction | B | 0.0004 is the prediction increment (Welsh 2019) Technical notesWelsh: UK Biobank prospective cohort, 346,686 adults without baseline CVD and not taking statins. 1-SD apoB CVD 1.23 ≈ LDL 1.20; adding apoB after TC+HDL C-index 0.0004. |
| All-cause mortality (treated ApoB reduction) | A | 0.95 is treated (Khan 2019) Technical notesKhan: 29 randomized trials, 332,912 people. Per 10 mg/dL treated drop, all-cause mortality 0.95 overall, statins only 0.92; LDL-R–independent MACE 1.02. Marker, not every way of moving the number. |
| MACE | B | MR: Benefit Tracks ApoB, Not LDL-C (Ference 2017) Mendelian randomization using CETP-inhibitor and statin gene scores: a CETP score alone (concordant LDL-C and apoB drop) carried MACE OR 0.946 (0.921–0.972), but combining it with an HMGCR (statin) score — same LDL-C drop, blunted apoB drop — gave MACE OR 0.985 (0.955–1.015), not significant. The cardiovascular benefit tracked the apoB change, not the LDL-C change. MACE, not all-cause mortality. |
| CHD | B | Multivariable MR Favors ApoB Over LDL-C (Richardson 2020) Technical notesMultivariable Mendelian randomization (UK Biobank plus CARDIoGRAMplusC4D, 60,801 CHD cases / 123,504 controls): apoB alone carried CHD OR 1.73 (1.56–1.91) per 1-SD. Modeled together with LDL-C and triglycerides, only apoB retained a robust effect (OR 1.92, 95% CI 1.31–2.81); triglycerides weakened to OR 1.12 (1.02–1.23); LDL-C’s association reversed to OR 0.85 (0.57–1.27). CHD, not all-cause mortality. |
| New-onset ASCVD | B | Other Lipids Vanish Once ApoB Is In the Model (Sniderman 2024) Technical notesUK Biobank cohort of 293,876 adults free of CVD, 19,982 new-onset ASCVD events over median 11 years: residual apoB risk after accounting for LDL-C and HDL-C carried HR 1.06 (1.04–1.07), while the residual associations of LDL-C, non-HDL-C, and triglycerides disappeared once apoB was in the model. New-onset ASCVD, not all-cause mortality. |
| All-cause mortality | C | High ApoB, Low LDL Still Raises Death (Johannesen 2021) Technical notesCopenhagen cohort of 13,015 statin-treated adults, median 8 years: those with discordantly high apoB and low LDL-C carried all-cause mortality HR 1.21 (1.07–1.36) and MI HR 1.49 (1.15–1.92), while high LDL-C with low apoB did not raise all-cause mortality. Treated residual risk, not the untreated apoB value this calculator’s slider represents. |
| MACE and CAD | B | Discordance Tracks ApoB Over LDL Particle Count (Epstein 2025) Technical notesUK Biobank cohort of 41,099 adults (9,663 MACE, 1,754 CAD events): when apoB and LDL particle number (LDL-P) disagreed, risk tracked apoB. At 2% apoB-above-LDL-P, MACE and CAD carried HR 1.1; at 30% apoB-above-LDL-P, MACE rose to HR 1.4 and CAD to HR 2.5. MACE and CAD, not all-cause mortality. |