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CHAPTER 3 Pre-Exercise Evaluations 49
powerful risk factor for CVD and that lowering of LDL cholesterol results in a striking
reduction in the incidence of CVD. Table 3.2 summarizes the ATP III classifications
of LDL, total, and high-density lipoprotein (HDL) cholesterol and triglycerides.
According to ATP III, a low HDL cholesterol level is strongly and inversely
associated with the risk for CVD. Clinical trials provide suggestive evidence that
raising HDL cholesterol levels reduces the risk for CVD. However, it now known
that the serum HDL cholesterol level does not assess HDL’s functional properties
and it remains uncertain whether raising HDL cholesterol levels per se, independent
of other changes in lipid and/or nonlipid risk factors, always reduces the
risk for CVD. In view of this, ATP III does not identify a specific HDL cholesterol
goal level to reach with therapy. Rather, nondrug and drug therapies that raise
HDL cholesterol that also are part of the management of other lipid and nonlipid
risk factors are encouraged by ATP III.
There is growing evidence for a strong association between elevated triglyceride
levels and CVD risk. Recent studies suggest that some species of triglyceride-rich
lipoproteins, notably, cholesterol-enriched remnant lipoproteins, promote atherosclerosis
and predispose to CVD. Because these remnant lipoproteins appear to
have atherogenic potential similar to that of LDL cholesterol, ATP III recommends
that they be added to LDL cholesterol to become a secondary target of therapy for
persons with elevated triglycerides. To accomplish this, non-HDL cholesterol is
calculated by subtracting HDL cholesterol from the total cholesterol level.
The metabolic syndrome is characterized by a constellation of metabolic risk
factors in one individual. Abdominal obesity, atherogenic dyslipidemia (i.e., elevated
triglycerides, small LDL cholesterol particles, and reduced HDL cholesterol),
elevated blood pressure, insulin resistance, prothrombotic state, and
proinflammatory state generally are accepted as being characteristic of the metabolic
syndrome. The root causes of the metabolic syndrome are overweight and
obesity, physical inactivity, and genetic factors. Because the metabolic syndrome
has emerged as an important contributor to CVD, ATP III places emphasis on the
metabolic syndrome as a risk enhancer.
ATP III designates hypertension, cigarette smoking, diabetes, overweight and
obesity, physical inactivity, and an atherogenic diet as modifiable nonlipid risk factors,
whereas age, male sex, and family history of premature CVD are nonmodifiable
nonlipid risk factors for CVD. Triglycerides, lipoprotein remnants, lipoprotein (a),
small LDL particles, HDL subspecies, apolipoproteins B and A-1, and total cholesterol-to-HDL
cholesterol ratio are designated by ATP III as emerging lipid risk factors.
Thrombogenic and hemostatic factors, inflammatory markers (e.g., high-sensitivity
C-reactive protein), impaired fasting glucose, and homocysteine are designated
by ATP III as emerging nonlipid risk factors. Regarding the latter, recent studies suggest
that homocysteine-lowering therapy does not result in a reduction in CVD risk.
The guiding principle of ATP III and subsequent updates by the National
Heart, Lung, and Blood Institute, American Heart Association, and American College
of Cardiology is that the intensity of LDL-lowering therapy should be
adjusted to the individual’s absolute risk for CVD (8,10,15). The ATP III treatment
guidelines and subsequent updates by the National Heart, Lung, and Blood Institute,
American Heart Association, and American College of Cardiology are summarized
in the ACSM Resource Manual.