Antihyperlipidemics Flashcards
Types of lipids
Low density lipoproteins (LDL)
Very low density lipoproteins (VLDL)
Triglycerides (TG)
High density lipoproteins (HDL)
emerging data on additional lipoproteins
LDL and lipid lowering therapy
“bad” cholesterol & primary target of lipid lowering Tx
CV risk and LDL
CV risk increases w/increasing LDL
Origin and role of VLDL
secreted by liver, some are converted to LDL
Export TGs to peripheral tissues
tend to see w/ingestion of excessive calories
TGs: what is hypertriglyceridemia associated with?
pancreatitis
pancreatitis typically at very high levels, e.g., >500mg/dL
Why is a fasting lipid panel recommended?
TGs increase after food–
new evidence shows may not change >10%, so not so important
Drugs that may induce hypertriglyceridemia
TPN, propofol, cleviprex (clevidipine), protease inhibitors, alcohol
HDL and lipid therapy
“good” cholesterol & secondary target for dyslipidemia
HDL and CV risk
declines w/higher HDL
Secondary causes of elevated LDL and TG
Diet, medications, comorbid conditions, disordered/altered metabolism
altered metabolism is most common
ATP III Guidelines: Total cholesterol (mg/dL)
Optimal/desirable, near optimal, borderline high, high
- Optimal/desirable: <200
- borderline high: 200-239
- high: > 240
ATP III Guidelines: LDL cholesterol (mg/dL)
Optimal/desirable, near optimal, borderline high, high
- Optimal/desirable: <100
- near optimal: <100-129
- borderline high: 130-159
- high: 160-189
- very high: _>_190
ATP III Guidelines: TGs (mg/dL)
Optimal/desirable, borderline high, high
- Optimal/desirable: <150
- near optimal
- borderline high: 150-199
- high: >/=200
ATP III Guidelines: HDL Cholesterol (mg/dL)
Optimal/desirable, near optimal
- Optimal/desirable: >/=60
- near optimal: >40 men, >50 women
ATP III Guidelines
Former guidelines based on risk factors
Niacin + statin
previously what we did but no added benefit so no longer rec’d to combine
2013 ACC/AHA Guidelines
- Replaced ATP III
- no longer to Tx LDL chol targets
- Non statin therpay discouraged in most cases
- Lifestyle modification rec’d for all pts
- 10yr ASCVD risk calculator - risk category determines what level of statin therapy
Statins: when risk may outweigh benefit / C/Is / avoid in…
- Risk > benefit: NYHA class II-IV HF; Maintenance hemodialysis; LDL-C <70mg/dL
- **Avoid in: **severe hepatic impairment
- **C/I: **pregnancy & lactation
Initial evaluation: labs
- Fasting lipid panel: to assess adherence and predicted response
- ALT
- CK
- HbA1c
- Hx of prior or current muscle Sx
Evaluation: lipid panel
- LDL-D >190mg/dL should assess for secondary cause or screen family for familial hyperlipidemia
- TG: >500mg/dL should be treated
- Repeat 4-12 w, then q3-12mths when response established
Evaluation: significance of ALT
result >3x ULN is C/I to statin therapy
Pharmacologic therapy for dyslipidemia
- HMG-CoA reductase inhibitors (statins)
- fibrates
- bile acid sequestrants
- sterol absorption inhibitor
- nicotinic acid
- omega3 ethyl esters
- plant sterols/stanols
- red yeast chinese rice
Statins: Agents
Lovastatin/Mevacor
Pravastatin/Pravachol
Simvastatin/Zocor
Fluvastatin/Lescol XL
*Atorvastatin/Liptor
*Rosuvastatin/ Crestor
*can be dosed High intensity
Statins: MOA
Inhibits HMG-CoA reductase from converting HMG-CoA to cholesterol,
thereby reducing cholesterol synthesis.
Up-regulates LDL receptors on hepatocytes.
Statins: Adverse Effects
rare confusional state or memory impairment, hepatic dysfunction, myopathy, rhabdomyolysis, DM, hemorrhagic stroke
Statins: timing of dose
some agents more effective when given in evening when most chol synthesis occurs
Who is at highest risk for AEs from statins?
multiple comorbidities including renal or hepatic impairment; Hx statin intolerance or muscle d/os; unexplained ALT >3x ULN; Age >75y; genetic polymorphisms or concomitant drugs that decrease statin metabolism/clearance