Hperlipidemia:- Treatment and Management Presented by:- Dr. Tewari.

Hperlipidemia:- Treatment Hperlipidemia:- Treatment and Managementand Management

Presented by:-Presented by:-

Dr. TewariDr. Tewari

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Hyperlipidemia is a risk factor for accelerated vascular disease.

It is a major modifiable risk factor for coronary artery disease,

cerebrovascular disease, and peripheral vascular disease.

The most aggressive treatment of elevated lipids should be reserved

for those patients at highest risk for vascular disease:

Patients with a documented history of coronary artery disease,

cerebrovascular disease, or peripheral vascular disease.

Patients with a history of diabetes or hypertension.

Patients with an LDL-C level above 160 mg/dL.

Patients with elevated triglycerides, low levels of HDL cholesterol,

and those who smoke.

Screening recommendations for the general population are:

Every 5 years for males age 35-65

Every 5 years for females age 45-65.

Screening for adults under age 35 and over age 65 should

generally be limited to those with risk factors for

vascular disease which include:

Family history

of premature vascular disease<50 male, <60 female)

Smoking

Hypertension

Diabetes

Documented vascular disease

Elevated cholesterol levels are generally classified as:

Desirable: TC<200 mg/dL, HDL>35 mg/dL, LDL<130

Borderline: TC 200-239, HDL>35 mg/dL, LDL 131-160,

and fewer than 2 risk factors and without vascular disease

High: presence of vascular disease and LDL>160 or

TC>240 mg/dL or HDL <35 mg/dL, or 2 or more risk factors.

An additional factor to consider is the

total cholesterol/HDL ratio. The goal is to keep the ratio

below 5:1; the optimum ratio is 3.5:1.

Treatment

Step 1: Provide information on dietary modification,

physical activity, and risk factor reduction.

Diet should generally consist of =<30% fat,

<8-10% saturated fat, <300 mg/d cholesterol.

Step 2: Provide information on dietary modification,

physical activity, and risk factor reduction.

Diet should generally consist of =<30% fat,

<7% saturated fat, <200 mg/d cholesterol.

Patients who fail maximal diet therapy may be candidates for

drug therapy

Risk Category

Without CHD and with fewer than two risk factors

Goal LDL

< 160 mg/dL

Without CHD and with two or more risk factors < 130 mg/dL

With CHD <_100 mg/dL

TABLE 1Determining Patient-Specific LDL Goals Through Risk Factors

Risk-factor score*

† Age: men > 45 years; women >55 years or

postmenopausal without ERTCurrent smokerHypertensionDiabetesCHD in first-degree relative (male relative <55 years;

female relative <65 years)HDL <35 mg per dL (0.9 mmol per L);

subtract 1 risk factor if HDL >60 mg per dL

LDL goal, by risk-factor score†

0 to 1 point: <160 mg per dL (<4.15 mmol per L)2 or more points: <130 mg per dL (<3.35 mmol per L)Patients with history of CHD: <100 mg per dL (<2.60 mmol per L)

Medication Selection

The drugs of first choice for elevated LDL cholesterol are

the bile acid sequestrants (cholestyramine, colestipol)

and nicotinic acid (niacin). These medications are effective

and have no serious side effects. They can have troublesome

side effects requiring member education to improve

compliance. Niacin is preferred in the presence of elevated

triglycerides (exceeding 250 mg/dL). Bile acid sequestrants

should not be used as a single agent in the presence of

elevated triglycerides.

HMG CoA reductase inhibitors (lovastatin, pravastatin,

fluvastatin, and simvastatin) are very effective for lowering LDL levels

in patients who do not tolerate or respond to the first line agents

of choice.

Fibrates (Gemfibrazil and clofibrate) have moderate effects on

LDL levels but are more effective in lowering elevated triglycerides.

Combination therapy may be used on high risk patients who fail

to respond to diet and single agent medication regimens. Combining a

bile acid sequestrant with either nicotinic acid or an

HMG CoA reductase inhibitor can markedly lower LDL levels

As a group, statins decrease total and LDL cholesterol levels

All statins have a minimal effect in raising HDL levels

Atorvastatin is the most effective in reducing LDL

However, unlike the more extensively studied agents

(e.g., pravastatin, simvastatin), atorvastatin has not been proved to

reduce total morbidity and mortality.

The most common adverse effects of the statins are

gastrointestinal disturbances, headache, myalgias and rash.

STATINS

Monitoring

The patient should take the statin for at least four weeks before

repeating lipid level tests. Recheck lipid levels in three months

Muscle aches are the statins' most feared adverse effect

Niacin (Nicotinic Acid)

Niacin is the oldest lipid-lowering agent that has been proved to

decrease cardiovascular morbidity and total mortality

It reduces serum triglyceride, total cholesterol and

LDL cholesterol values

It also has the beneficial effect of raising HDL levels.

An extended-release form of niacin (Niaspan) has the same

beneficial lipid-altering effects as standard niacinAlthough less effective than the statins in decreasing LDL levels,

ER niacin can increase HDL values by 20 percent, decrease triglyceride

levels by 25 percent

Adverse Effects

Flushing is the most common side effect

Abdominal pain, nausea and vomiting (all less than 8 percent

Avoid concomitant ingestion of alcohol or hot beverages

Patients who take extended-release niacin tend to have

fewer adverse effects than those who use standard

niacin preparations

Monitoring

Periodic liver function tests are mandatory

Every 12 weeks for the first year and then every six months

May promote glucose intolerance

Can also increase uric acid levels

TABLE 7National Cholesterol Education Program (NCEP) Guidelines:

Serum Triglyceride Action Limits

Triglyceride value Intervention

<200 mg per dL Normal value.

Some recommend a lower

normal value of 150 mg per dL

200 to 400 mg per L Primary treatment

is lifestyle modification:

weight control, low-fat, low-cholesterol diet, regular exercise,

smoking cessation and (in selected patients) alcohol restriction.

Medication may be considered in patients with established CHD,

family history of premature CHD, concomitant total

total cholesterol level of >=240 mg per dL and HDL

value of <35 mg per dL, genetic form of hypertriglyceridemia

(e.g., dysbetalipoproteinemia or familial combined hyperlipidemia)

or multiple risk factors.

400 to 1,000 mg per dL Treatment as in previous category

but with an emphasis on controlling

causes of secondary

hypertriglyceridemia. Medication is

recommended by some authorities and

certainly should be used if the patient has

a history of acute pancreatitis.

>1,000 mg per dL Vigorous triglyceride-lowering efforts

are required because of increased risk for

pancreatitis. Treat causes of secondary

hypertriglyceridemia (e.g., diabetes mellitus).

Institute very-low-fat diet, curtail alcohol;

if triglyceride level of <1,000 mg per dL is not

achieved, use medications.

Fibrates are used to treat hypertriglyceridemia.

This class of drugs includes clofibrate (Atromid-S), gemfibrozil (Lopid)

and fenofibrate (Tricor)

Fibric Acid Derivatives (Fibrates

Medication is generally not used to treat hypertriglyceridemia unless

fasting serum triglyceride levels are greater than 400 mg per dL

Fibrates decrease triglyceride values by 20 to 45 percent and increase

HDL levels by 7 to 15 percent.

Adverse Effects

Gastrointestinal intolerance (abdominal pain, nausea, vomiting,

diarrhea, constipation, dyspepsia) is the most common adverse effect

associated with fibrate therapy

Neuromuscular (headache, dizziness, vertigo, arthralgias) and

dermatologic reactions

Incidence of myalgias and rhabdomyolysis increases with

concomitant use of a statin

Gemfibrozil has been associated with cholelithiasis in 1 percent

of the patients

Fibrates increase gallbladder and hepatic cholesterol concentrations

Bile Acid Sequestrants

Cholestyramine (LoCholest) and colestipol (Colestid) are the two

bile acid sequestrants currently available

These agents lower LDL (20 percent) and raise HDL (5 percent).

Maximal therapeutic effect is evident after one month of therapy.

Adverse Effects

Gastrointestinal disturbances

Interfere with intestinal absorption of various vitamins and minerals

Decrease the absorption of numerous medications, including

levothyroxine, penicillin, propranolol, thiazide diuretics and digoxin

Combination regimens should be considered for use in patients

who fail to meet target values and are compliant with their current therapy

Myopathy and rhabdomyolysis are serious concerns when statins

are combined with fibrates or niacin

Compliance with bile acid sequestrants is a problem

The statins have the best compliance or maintenance rates, followed by

niacin, gemfibrozil and bile acid sequestrants

Combination therapy increases the likelihood of reaching target values,

but poor compliance is a variable that can foil even the most aggressive

therapeutic interventions.

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