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In a study of 546 Brazilian men, when those with CAC score 75th percentile were compared with those in the < 75th percentile, only slight differences in TC and LDL were found [13]. The association between racial differences, lipoprotein and lipoprotein particle size, and CAC score was examined as part of the HEART SCORE study. To quote the authors, “we found no significant association between lipoprotein or lipoprotein particle size and the extent of sub-clinical atherosclerosis as measured by CAC, whether in whites or blacks” [14]. A large study determined CAC scores for over 22,000 men and 8000 women. Hypercholesterolemia

was

defined

the

ranges

as TC > 200 mg/dL or the use of lipid lowering agents. of 0, 1.0-9.9, 10-99.9, 100-399.9, and 400.

The CAC scores For men the

were stratified into percentage with

hypercholesterolemia was essentially constant (40-42%) for the three upper CAC ranges and women the percentages for these three score groups were 49-52%. Thus there was essentially

for no

association between elevated TC and CAC scores over a huge these results were not stratified by statin use [15]. In a study published in 2005, over 4900 asymptomatic persons

range from 10 to > 400. Unfortunately,

aged 50-70 were scanned for coronary

calcium. It and in fact

was found that CAC scores predicted CAD events independent of more accurately than the standard risk factors or C-reactive protein

the standard risk factors levels. This study found

no correlation deviation, not

between CAC scores and range) and TC was 224 ±

LDL levels. In this cohort, LDL levels were 33 mg/dL. Thus the range of levels, which

143 ±33 (standard is greater than the

standard deviations, were large enough to cholesterol levels and CAC scores [16]. Hecht et al [17] examined the correlation

provide

a meaningful

test

of the

association between

between

serum lipids

and

CAC

scores in over 1000

TC/HDL

the

and

LDL, HDL burden.

consecutive ratio did not

asymptomatic individuals referred for EBT. They found that TC, correlate with either the prematurity or extent of calcified plaque

In a large multi-ethnic between LDL and HDL

study, Kronmal and the change

et al [18] found only a very weak to insignificant associations in CAC scores over time, i.e. the progression of atherosclerosis.

Thus 10 studies mostly fail to find a significant or clinically meaningful correlation between an established measure of the extent or progression of atherosclerosis and circulating TC or in some cases LDL. In fact, other risk factors such as smoking and hypertension did indeed correlate in many studies, but cholesterol never made the grade. Thus the electron-beam tomography studies are consistent with the autopsy studies, which is gratifying since, if we ignore small differences between visually and EBT identified plaques, both approaches are looking at more or less similar pathology.

CORONARY ANGIOGRAPHY Coronary angiography involves inserting a catheter into the femoral artery in the groin and pushing it up through the aorta until it reaches the coronary vessels. A contrast medium is then injected to allow imaging of the individual coronary arteries and these images can reveal blockage attributed to atherosclerosis. Thus studies can examine the correlation between serum cholesterol and angiographically identified deposits and narrowing in the coronary arteries. But coronary angiography is not without its morbidity and mortality and is generally performed only on individuals with at very high risk or with severe symptoms of heart disease who are young or middle-aged. Thus these studies are not representative of the asymptomatic public. In addition there will be some patients who have familial hypercholesterolemia. This would introduce a bias since, as will be discussed below, it is not at all clear that the atherosclerosis that accompanies this syndrome can be compared to that found in individuals who do not have the mutation. Any study heavily weighted with individuals having very high cholesterol levels will be confounded by the potential presence of subjects with this syndrome. Also, in many studies, cholesterol lowering drugs were being used, further confusing the question.

Thus if the issue is the Cholesterol Hypothesis, angiographic results do not appear to be a very good way to study its validity. On the other hand, both the autopsy and calcium score approaches allow the examination of asymptomatic individuals which is much more to the point and less subject to confounding and bias. Nevertheless, as Ravnskov [8] discusses at length, angiographic studies that examined the relationship between

cholesterol

levels,

their

changes,

and

the

presence

and

progression

of

atherosclerosis

frequently

found

inconsistent results where progression levels. In his words, “to prove that high

occurred in cholesterol

the presence of both is the villain—not just

increasing and decreasing cholesterol an innocent bystander—demands that

a change in the atherosclerosis in

cholesterol concentration the same direction. But in

for each all studies

individual is followed by a change these changes occurred haphazardly.”

in the

degree of

Also,

most of the

International Health News

November 2007

Page 13

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