Lipid and Atherosclerosis Meds

HMG-CoA reductase inhibitors

Statins

1st line choice always for lipid management

Proto: Atorvastatin

MOA: inhibit HMG-CoA reductase → ↓ cholesterol synthesis in liver → ↑ LDL receptors → ↑ LDL removal from blood → ↓ LDL

↓ Risk of MI (myocardial infarction) & stroke and stabilize arterial plaques

ADRs: Muscle pain/weakness, GI upset, ↑ liver enzymes; rhabdomyolysis, teratogenic

Severe muscle pain/weakness + dark urine → report immediately

Note: high intensity statin = more hepatotoxic

Cholesterol absorption inhibitors

Proto: ezetimibe

MOA: ↓ cholesterol absorption in small intestine → ↑ hepatic LDL receptors → ↓ LDL

Used in combo w/ statins, never alone

ADR: Diarrhea, abdominal pain, fatigue; may ↑ liver enzymes; rare myopathy

PCSK9 Inhibitors

Proto: Alirocumab

MOA: Block PCSK9 → prevent LDL receptor destruction → ↑ LDL removal from blood → ↓↓ LDL

Powerful and fast LDL decrease

ADR: Injection-site reactions, flu-like symptoms, nasopharyngitis

subQ

Bile acid sequestrants

other lipid lowering therapy

MOA: bind to bile acids in sm int → dec LDL

ADRs: constipation, may inc TG

inc fluid and fiber intake

separate from other meds

Niacin (vit b3)

MOA: dec TGs and LDL

ADRs: flushing, inc BS, hepatotoxic

rarely used

Prescription omega-3 fatty acids

MOA: dec TG production → dec blood TGs

ARDs: GI upset, inc bleeding risk, a-fib

used for extreme hyperTG (>500 mg/dL)

Fibrates

Primary TG lowering drug

Ex: Fenofibrate (prototype), gemfibrozil

MOA: Activate PPAR-α → ↑ breakdown/removal of triglycerides → ↓↓ TG (dec risk of pancreatitis and hypertriglyceridemia)

ADR: GI upset, ↑ liver enzymes, gallstones; myopathy/rhabdomyolysis

Fenofibrate is generally preferred over gemfibrozil with a statin bc gemfibrozil has a greater risk of statin-associated muscle toxicity