Dyslipedemia: Statin txs; HMG CoA reductase inhibitors

1. AE

1.1. well tolerated

1.2. monitor LFTs (elevated hepatic transaminases), Gi upset, myopathy w/ elevated creatinine kinase

1.3. BB warning: slight increase in blood glucose and DM risk

1.4. Drug interactions

1.4.1. various CP450 inhibitors

1.4.2. caution w/fibrates an nicotinic acid (increased myopathy risk

2. Contraindications:

2.1. pregnancy and nursing mothers

2.2. myopathy risk enhanced in

2.2.1. high dose statin

2.2.2. renal insufficiency

2.2.3. >70yo

3. low intensity

3.1. LDL reduction<30%

4. Statin FU

4.1. baseline: lipid panel, liver enzymes, creatinine kinase, renal fxn

4.2. RTO6 weeks for fasting lipid panel

4.3. annual LFT and fasting lipids when goal is met

4.4. risk for myopathy in pts on combo therapy->assess frequently for sxs

5. MOA: inhibit hepatic enzymes HMG CoA reductase

5.1. rate limiting step in cholesterol biosynthesis

5.1.1. less cholesterol

5.1.1.1. increased LDL receptors to increase LDL removal from circulation

6. pravastatin, simvastatin, fluvastatin, pivastatin

6.1. Usually in high dose: rosuvastatin, atorvastatin

6.2. ONLY pivastatin is minimally metabolized by liver thru CP450

7. used in

7.1. primary and secondary prevention of atherosclerosis

7.2. firstline

7.2.1. to reduce CV risk

7.2.2. LDL lowering therapy

7.3. LDL reduced by 18-55%, HDL increased by 5-15%, TG reduced 7-30%

7.4. nighttime dosing; cinical trials show decreased MI, revascularization procedures, CVA, and PAD

8. high intesity

8.1. to lower LDL by at least 50% from baseline

9. moderate intensity

9.1. secondary prevention >75

9.2. primary prevention: high risk adults and diabetic adults

9.3. lower LDL by 30-49%