This lecture was conducted during the Nephrology Unit Grand Ground by Nephrology Registrar under Nephrology Division, Department of Medicine in King Saud University. Nephrology Division is not responsible for the content of the presentation for it is intended for learning and /or education purpose only.

Eman Saad Algadi 427200141

presented on Wed 23-11-2011

Definition• Elevation of measured serum lipid components:• Total cholesterol.• LDL cholesterol • Friedewald formula is LDL = total cholesterol - HDL -

(triglycerides/5). • Triglycerides (TGs)

• Or low HDL.

• Accelerate development of atherosclerosis.• A modifiable major risk of CAD.

Why? (causes)

When to screen?

✽All men older than 35 & all women older than 45. (level A evidence by USPSTF)

✽Men age 20-35 & women age 20-45 in the presence of risk factors:• Type 2 diabetes• FHx early CAD• Possibility of familial hyperlipidemia• Any combination of cardiac risk factors: smoking, obesity, hypertension, or sedentary lifestyle.

Routine screening of TC and HDL every 5 years is recommended by National Institutes of Health (NIH) &

the American Heart Association (AHA)

Steps to Approach hyperlipidemiarecommended by The Adult Treatment Panel III (ATP III) of the National Cholesterol Education Program

Complete lipid profile after 9- 12 hour fast

Determine CHD risk

category

1- Identify CHD/ CHD risk equivalent (high risk)

If the patient have•Clinical CHD•Symptomatic carotid artery disease•Peripheral arterial disease •Abdominal aortic aneurysm.

•Diabetes is regarded as a CHD risk equivalent

2- Identify major risk factors (other than LDL-C)

• Cigarette smoking

• Hypertension (BP >140/90 mmHg or on antihypertensive medication)

• Low HDL cholesterol (<40 mg/dL)• HDL cholesterol >60 mg/dL is a “negative” risk

factor; it removes one risk factor from the total count

• Family history of premature CHD• CHD in male first degree relative <55 years.

• CHD in female first degree relative <65 years.

• Age (men >45 years; women >55 years)

If 2+ risk factors (other than LDL) present without CHD/CHD risk equivalent: assess 10-year Framingham risk score•>20% — CHD risk equivalent • 10-20% •<10%

Risk categories

Risk Category LDL Goal

LDL Level at Which

to Initiate Therapeutic

lifestyle changes

LDL Level at Which to

Consider Drug Therapy

HIGH RISK:CHD or CHD Risk Equivalents(10-year risk >20%)

<100 mg/dL

≥100 mg/dL ≥130 mg/dL(100-129 mg/dL: drug optional)

MODERATLY HIGH RISK:≥ two risk factors(10-year risk 20-10 %)

<130 mg/dL

≥130 mg/d ≥130 mg/dL

MODERATE RISK:≥ two risk factors(10-year risk < 10 %)

≥160 mg/dL

LOW RISK:One or no risk factors

<160 mg/dL

≥160 mg/dL ≥190 mg/dL(160-189 mg/dL: LDL-lowering drug optional)

Therapeutic lifestyle changes• lipid-lowering diet: • Reduce Saturated fat <7% of calories.• Reducing cholesterol <200 mg/day.• Consider increased soluble fiber (10-25 g/day)

•Weight management• Increased physical activity•Smoking cessation (increases HDL by 4 mg/dL and reduces total mortality in patients with CAD).

• Statins reduce overall mortality in primary and secondary prevention of CAD. (level A evedince)

StatinsHMG-CoA reductase inhibitors.

LDL ↓18-55%HDL ↑5-15%TG ↓7-30%

• Myopathies (<1% # fibrates)

• Rhabdomyolysis (< 0.2%)

• Abnormal Liver function test (< 2%)

Contraindicated in active liver disease and pregnancy

Drug therapy

•

Bile acid sequestrants(Cholestyramine)

LDL ↓15-30%HDL ↑3-5%TG No change or increase

• GI distress

• Constipation

• Decreased absorption of other drugs

Contraindicated in hyperTG

Drug therapy

•

Nicotinic acid

LDL ↓5-25%HDL ↑15-35%TG ↓20-50%

• Flushing• Hyperglyce

mia• Hyperurice

mia (or gout)

• Upper GI distress

• Hepatotoxicit

Contraidicated in:•Chronic liver disease•Severe gout•Diabetes•Hyperuricemia•Peptic ulcer disease

Drug therapy

Fibrates (Gemfibrozil)

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

• Dyspepsia

• Gallstones

• Myopathy

Contraindicated in:•Severe renal disease•Severe hepatic disease

Drug therapy

• Lacks clinical outcome data (monotherapy or combined with a statin)

Ezetimibe LDL ↓18%

Contraindicated in active liver disease when combined with a statin

Drug therapy

• Omega-3 fatty acids do not clearly demonstrate reductions in mortality (level A evidence)

Omega-3 fatty acids

• Dyspepsia.• Burping.• Fishy taste

Drug therapy

• If TGs are greater than 500 mg/dL, they become the primary target of therapy due to the risk of acute pancreatitis.

• Niacin, fibrates, or omega-3 fatty acids should be used until the TG level is less than 500 mg/dL.

• If the LDL goal has been achieved and the TC level is greater than 200 mg/dL: non-HDL (TC - HDL) becomes the secondary goal of treatment.

• Niacin, fibrates, and omega-3 fatty acids along with diet and exercise to achieve this goal.

Complementary/Alternative Therapy •Garlic.• Red yeast rice.• Artichoke.

• may modestly reduce cholesterol, but patient-oriented evidence is lacking.

• Vitamin E does not reduce mortality, recurrent events, or nonfatal stroke after an acute myocardial infarction

References: • Third Report of The National Cholesterol Education Program

(NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA. 2001;285:2486-97.

• Pignone MP,, et al. Screening for lipid disorders. Systematic Evidence Review No. 4 Rockville, Md.: Agency for Healthcare Research and Quality, 2001.

• Maeda K, Noguchi Y, Fukui T. The effects of cessation from cigarette smoking on the lipid and lipoprotein profiles: a meta-analysis. Prev Med.2003;37:283-90.

• Hooper L, Thompson RL, Harrison RA, et al. Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: systematic review. BMJ.2006;332:752-60.

• hekelle PG, Morton SC, Jungvig LK, et al. Effect of supplemental vitamin E for the prevention and treatment of cardiovascular disease. J Gen Intern Med.2004;19:380-9.

THANK YOU!