Rapid Review·Cardiovascular

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Cardiovascular Pharmacology

T1Must know

Lipid-Lowering Therapy

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Key takeaways

lowering low-density lipoprotein (LDL) prevents events in proportion to the fall.
statins have the outcome data, the non-statin LDL drugs add on top, and triglyceride drugs mainly prevent pancreatitis.
on Hyperlipidemia; this page is the drugs.
competitive inhibition of HMG-CoA reductase, with pleiotropic plaque stabilization and antioxidant effects (the reason for early high-dose statins in acute coronary syndrome).
  • LDL and triglycerides fall, high-density lipoprotein (HDL) rises.
myalgia, statin-associated myopathy, myositis and rhabdomyolysis (dark urine, kidney injury), raised liver enzymes and hepatotoxicity (stop only if over 3 times normal), a small rise in new-onset diabetes.
CYP3A4 inhibitors (azoles, macrolides, protease inhibitors, amiodarone, diltiazem, grapefruit) raise simvastatin, lovastatin and atorvastatin levels.
  • Pravastatin and rosuvastatin are not CYP3A4-dependent.
pregnancy and breastfeeding, and active liver disease.
hold, check creatine kinase and thyroid function, then rechallenge at a lower dose or with a different statin.
step up in order.
  • A maximally tolerated high-intensity statin: recheck at 4 to 12 weeks.
  • Add ezetimibe: if LDL is still above goal (70, or 55 at very high risk).
  • Add a PCSK9 inhibitor: if still above goal.
address secondary causes, then a fibrate or omega-3 (pancreatitis prevention).
stop statins and ezetimibe; a bile acid sequestrant if needed.
a lipid panel 4 to 12 weeks after any change, then every 3 to 12 months; baseline liver enzymes; creatine kinase only for muscle symptoms; uric acid with niacin.

How it's tested

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High-yield images1
The lipid pathway with each drug at its point of action. Liver: statins block HMG-CoA reductase converting HMG-CoA to mevalonate; niacin reduces VLDL output; PCSK9 inhibitors block PCSK9-mediated LDL receptor degradation so more receptors recycle to the surface. Blood: lipoprotein lipase liberates free fatty acids from chylomicrons and VLDL, and fibrates upregulate it through PPAR-alpha. Adipose: niacin inhibits lipolysis. Intestine: ezetimibe blocks cholesterol absorption at the brush border and bile acid resins block bile acid reabsorption.

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