An injectable antibody that switches off a liver protein, producing one of the largest, most reliable drops in harmful cholesterol available. Added to standard treatment it lowers heart attacks, strokes, and artery-opening procedures and can shrink existing plaque. Safety looks clean, mostly minor injection-site effects. Its life-extending promise stays unproven; high cost limits access. (Full Review)
| Marker | Target | Why |
|---|---|---|
| LDL cholesterol | < 55 mg/dL (often < 30 achieved) | Primary target and main driver of plaque |
| ApoB | < 60–80 mg/dL | Counts actual atherogenic particle number |
| Lp(a) | < 75 nmol/L (≈ < 30 mg/dL) | Independent, inherited risk particle |
| hs-CRP | < 1.0 mg/L | Gauges residual vascular inflammation |
| Fasting glucose / HbA1c | 70–85 mg/dL; HbA1c < 5.4% | Surveillance for the theoretical metabolic concern |
| ALT / AST | ALT < 25 (women) / < 30 (men) U/L | Safety check driven mainly by concurrent statin |
Cadence: Baseline, then lipid/ApoB panel at 4–12 weeks after starting, then every 6–12 months; metabolic markers at least annually