IM2.18 | Dyslipidemia Management in IHD — Summary & Reflection

KEY TAKEAWAYS

Dyslipidaemia classification:
- Fredrickson types I–V; clinically: isolated elevated LDL (FH, secondary), mixed (elevated LDL + TG), isolated hypertriglyceridaemia (Type IV/V), low HDL
- Clinical signs: tendinous xanthomata (FH), xanthelasma, corneal arcus, eruptive xanthomata (severe TG), lipaemia retinalis
- Secondary causes to exclude: hypothyroidism (TSH), nephrotic syndrome, obstructive liver disease, diabetes, drugs (glucocorticoids, thiazides, beta-blockers)

Lipid targets (ESC/EAS 2019):
- Very high risk (post-ACS, established CVD, FH, CKD 3–5): LDL-C <55 mg/dL (1.4 mmol/L)
- High risk (ASCVD 5–10%, DM without complications): LDL-C <70 mg/dL (1.8 mmol/L)
- Moderate risk: LDL-C <100 mg/dL; Low risk: <116 mg/dL

Drug therapy:
- Statins: first-line; high-intensity (atorvastatin 40–80 mg or rosuvastatin 20–40 mg) for high/very high risk; side effects: SAMS (CK <4× ULN → continue; CK >4× ULN → reduce/switch; CK >40× ULN + AKI = rhabdomyolysis → stop + IV fluids); new-onset DM (~10% relative risk increase); LFT monitoring only if symptoms
- Ezetimibe: NPC1L1 inhibitor; additional 18–24% LDL reduction added to statin; first add-on if LDL target not met; IMPROVE-IT evidence
- PCSK9 inhibitors: monoclonal antibodies; 50–60% additional LDL reduction; for very high risk patients not at target on statin + ezetimibe; FOURIER + ODYSSEY evidence
- Fibrates: PPARα agonists; TG reduction 30–50%; for severe TG (>500 mg/dL — pancreatitis prevention); avoid gemfibrozil + statin (myopathy)
- Omega-3 (icosapentaenoic acid 4 g/day): REDUCE-IT — 25% MACE reduction in statin-treated patients with TG >150 mg/dL

Monitoring: lipid profile 4–12 weeks after any change; annual once stable; CK only if symptoms; LFTs at baseline

REFLECT

Return to Ramesh and Priya from the opening hook. For Ramesh — an asymptomatic 48-year-old with an LDL-C still above target and new-onset muscle aching on atorvastatin 40 mg — the statin side effect you are dealing with is the most common reason patients discontinue life-saving therapy. How would you explain to Ramesh, in plain language, why the muscle aching is not a reason to stop the statin permanently, and what practical steps you are taking to find a regimen that is both effective and tolerable? For Priya — a 35-year-old with LDL 325 mg/dL and tendinous xanthomata — the diagnosis has implications that extend beyond her. Her father almost certainly had FH and died of MI at 42; her siblings and children are at 50% risk of inheriting the same mutation. What is your responsibility as a clinician beyond prescribing her statin — and how would you initiate the cascade screening conversation with her family in a way that is informative without being alarming?