The AHA Guidelines and Scientific Statements Handbook

The AHA Guidelines and Scientifi c Statements Handbook

some authorities routinely employ non-HDL-C as a
secondary target in all patients. One advantage of
non-HDL-C is that its measurement does not
require a fasting state for accuracy. Two modalities
of therapy can be employed to achieve the goals of
cholesterol-lowering therapy. These are therapeutic
lifestyle changes (TLC) and drug therapy. Lifestyle
therapies should be employed in all patients. Drug
therapy, however, is often required to achieve the

goals of therapy, particularly in persons at higher

risk.

Therapeutic lifestyle changes

ATP III [1] recommends a multifaceted lifestyle

approach to reduce risk for CHD. This approach is

designated therapeutic lifestyle changes (TLC). Its

essential features are:

Table 10.5 Drugs affecting lipoprotein metabolism

Drug class, agents
and daily doses

Lipid/lipoprotein

effects Side effects Contraindications Clinical trial results

HMG CoA reductase
inhibitors (statins)*

LDL-C ↓ 18–55%

HDL-C ↑ 5–15%

TG ↓ 7–30%

Myopathy

Increased liver enzymes

Absolute:

• Active liver disease
  Relative:


• Concomitant use of certain
  drugs‡


• Chronic liver disease (e.g.
  fatty liver, hepatitis C)

Reduced major coronary

events, CHD deaths, need

for coronary procedures,

stroke, and total mortality

Bile acid
Sequestrants†

LDL-C ↓ 15–30%

HDL-C ↑ 3–5%

TG No change or

increase

Gastrointestinal distress

Constipation

Decreased absorption

of other drugs

Absolute:

• Dysbeta-lipoproteinemia


• TG >400 mg/dL
  Relative:


• TG >200 mg/dL

Reduced major coronary

events and CHD deaths

Ezetimibe LDL-C ↓ 15–25% Few Benefi t not demonstrated
with controlled trials

Nicotinic acid¥ LDL-C ↓ 5–25%
HDL-C ↑ 15–35%
TG ↓ 20–50%

Flushing

Hyperglycemia

Hyperuricemia (or gout)

Upper GI distress

Hepatotoxicity

Absolute:

• Chronic liver disease


• Severe gout
  Relative:


• Diabetes (requires close
  monitoring)


• Hyperuricemia


• Peptic ulcer disease

Reduced major coronary

events, and possibly total

mortality

Fibric acids§ LDL-C ↓ 5–20%
(may be increased in
patients with high TG)
HDL-C ↑ 10–20%
TG ↓ 20–50%

Dyspepsia

Gallstones

Myopathy

Absolute:

• Severe renal disease


• Severe hepatic disease

Reduced major coronary

events

Suggestion of increased

non-CHD mortality

• Lovastatin (20–80 mg), pravastatin (20–40 mg), simvastatin (20–80 mg), fl uvastatin (20–80 mg), atorvastatin (10–80 mg), resuvastatin (5–40 mg).
  † Cholestyramine (4–16 g), colestipol (5–20 g), colesevelam (2.6–3.8 g) Ezetimibe (10 mg).
  ‡ Cyclosporine, gemfi brozil (or niacin), macrolide antibiotics, various anti-fungal agents and cytochrome P-450 inhibitors.
  ¥ Immediate release (crystalline) nicotinic acid (1.5–3 g), extended release nicotinic acid (Niaspan®) (1–2 g), sustained release nicotinic acid (1–2 g).
  § Gemfi brozil (600 mg BID), fenofi brate (48–200 mg), clofi brate (1000 mg BID).