he testing opportunity is nonfasting, only the values for total choles-terol and HDL cholesterol will be usable. In such a case, if total cholesterol is $200 mg/dL or HDL is ,40 mg/dL,
a follow-up lipoprotein profile is needed for appropriate management based on LDL
CHD risk: The latter carry a risk for major coronary events equal to that of established
CHD, ie,.20% per 10 years equivalents comprise:
• Other clinical forms of atherosclerotic disease (peripheral arterial disease, abdominal aortic aneurysm, and symptomatic carotid artery disease)
• Multiple risk factors that confer a 10-year risk for CHD >20%.
The second category consists of persons with multiple (2+) risk factors in whom 10-year risk for CHD is <20%. The third category consists of persons having 0-1 risk factor; with few exceptions,
persons in this category have a 10-year risk ,<10%.
First, the number of risk factors is counted (Table 3). Second, for persons with multiple (2+) risk factors, 10-year risk assessment is carried out with Framingham scoring (see Appendix) to identify individuals whose short-term risk warrants consideration of intensive treatment. Risk factors used in Framingham scoring include age, total cholesterol, HDL cholesterol, blood pressure, and cigarette smoking.
Among these are life-habit risk factors and emerging risk factors. The former include obesity,
physical inactivity, and atherogenic diet; the latter consist of lipoprotein(a), homocysteine, prothrombotic and proinflammatory factors, impaired fasting fasting glucose, and evidence of subclinical atherosclerotic disease. The lifehabit risk factors are direct targets for clinical intervention but are not used to set a lower LDL cholesterol goal of therapy.
Factors characteristic of the metabolic syndrome are abdominal obesity, atherogenic dyslipidemia (elevated triglyceride, small LDL particles, low HDL cholesterol), raised
blood pressure, insulin resistance (with or without glucose intolerance), and
prothrombotic and proinflammatory states Primary Prevention. The risk factors of the metabolic syndromeare highly concordant; in aggregate they enhance risk for CHD at any
given LDL cholesterol level. For purposes of ATP III, the diagnosis of the metabolic syndrome is made when 3 or more of the risk determinants shown in TABLE 8 are present. These determinants include a combination of categorical and borderline risk factors that
can be readily measured in clinical practice
The clinical approach to primary prevention is founded on the public health approach that calls for lifestyle changes, including (1) reduced intakes of saturated fat and cholesterol, (2) increased physical activity, and (3) weight control, to lower population cholesterol levels and reduce CHD risk, One aim of primary prevention is to reduce longterm risk (.10 years) as well as shortterm risk (#10 years).
Before star LDL lowering treatmentit should rule out, Causes of secondary dyslipidemia include:
• Obstructive liver disease
• Chronic renal failure
• Drugs that increase LDL cholesterol and decrease HDL cholesterol (progestins, anabolic steroids, and corticosteroids).
ATP III specifies an LDL cholesterol level of ,100 mg/dL as the goal of therapy in secondary prevention.
If baseline LDL cholesterol is ³130 mg/ dL, intensive lifestyle therapy and maximal control of other risk factors should be started.
If LDL cholesterol levels are 100-129 mg/dL, • Initiate or intensify lifestyle and/or drug therapies specifically to lower LDL.
• Emphasize weight reduction and increased physical activity in persons with the metabolic syndrome.
• Delay use or intensification of LDL lowering therapies and institute treatment of other lipid or non lipid risk factors; consider use of other lipid modifying drugs (eg, nicotinic acid or fibric acid
+2àin 10-20% - If LDL remains>130 mg/dL after 3 months of TLC, consideration can be given to starting an LDL-lowering drug to achieve the LDL goal of <130 mg/dL. In general, persons hospitalized for a coronary event or procedure should be discharged on drug therapy if the LDL
cholesterol is $130 mg/dL. If the LDL is 100-129 mg/dL, clinical judgment should be used
Thefinding that elevated triglycerides are an independentCHDrisk factor suggests
thatsometriglyceride-rich lipoproteins are atherogenic. The latter are partially degraded VLDL,commonlycalled remnant lipoproteins. Inclinical practice, LDL cholesterol is the most readily available measure of atherogenic remnant lipoproteins. Thus, VLDL cholesterol
can be a target of cholesterol-lowering therapy. The goal for non- HDLcholesterol in persons with high serumtriglycerides can be set at 30 mg/dL higher than that for LDL cholesterol
(TABLE 9) on the premise that a VLDL cholesterol level#30 mg/dL is normal
ATP III identifies the sum of LDL+VLDL cholesterol (termed non- HDLcholesterol [total cholesterol−HDL cholesterol]) as a secondary target of therapy in persons with high triglycerides ($200 mg/dL). The goal for non- HDLcholesterol in persons with high serumtriglycerides can be set at 30 mg/dL higher than that for LDL cholesterol
Thereare2approachestodrug therapy. First, thenon-HDLcholesterol goal can be achieved by intensifying therapy withanLDL-loweringdrug; second, nicotinic acid or fibrate can be added, if used with appropriate caution, to achieve thenon-HDLcholesterol goal by further lowering VLDL cholesterol When a low HDL cholesterol is associated with high triglycerides (200-499 mg/dL), secondary priority goes to achieving the non-HDL cholesterol goal, as outlined earlier. Also, if triglycerides are ,200 mg/dL (isolated low HDL cholesterol), drugs forHDL raising (fibrates or nicotinic acid) can be considered
Executive Summary of the 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) - PDF