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VAP Explained
The best way to explain the VAP test is line-by-line using your VAP results as a guide.
Direct Measured Lipid Profile
- Total Cholesterol (NCEP guidelines <200mg/dL) is defined as the sum of HDL+LDL+VLDL. The TC is only a number and cannot be used in any way to diagnosis a person’s risk for heart disease, MI, or stroke.
- HDL Cholesterol (NCEP guidelines >40mg/dL) is the sum of all the sub fractions that make up the HDL total, which are HDL2 and HDL3.
- LDL Cholesterol (NCEP guidelines <130mg/dL) is defined as the sum of LDL-R + Lp(a) + IDL. LDL Cholesterol is a sum of three different subfractions.
- Triglycerides (NCEP guidelines <150mg/dL) are based on the concentration of the triglyceride rich molecules IDL and VLDL.
The rest of the test describes the risk to the patient because it dissects the above values
so that the physician can treat the cholesterol sub fraction that is of risk potential.
Additional lipid subclass information such as direct LDL, LDL pattern density, Lipoprotein (a)
and HDL2 will increase detection rates to 90% of all patients who will have heart disease, up from
40% with the traditional lipid panel.
For Informed Clinical Judgment Use
This section of the test is where the decisions for treatment should arise.
HDL Cholesterol Panel
- HDL2 turns out to be the protective sub-fraction of HDL, so that
total HDL measurements (if mostly HDL3) may under-estimate the real atherogenic risk to patients.
Low HDL2 is a risk for CAD even in patients with normal cholesterol. It is also an independent
risk factor for diabetics with peripheral vascular disease. Campos H, Arterioscler Thromb Vas Biol.
1995 Aug 15(8) 213-9
- HDL3 though important, it does not play as large a role in protection
against CAD as HDL2. Therefore, emphasis should remain on the HDL2 subfraction when evaluating
a patients HDL cholesterol status. Larnarche B, Arterioscler Thromb Vas Biol. 1997 Jun; 17(6): 1098-105
This is critical because it is not total HDL that protects but rather HDL2.
LDL Cholesterol Panel
- LDL-R is the patient’s real LDL value. This value is derived from the total LDL cholesterol
value minus the Lp(a) and the IDL cholesterol values. This directly measured LDL-R is what is responsible
for the largest of majority of atherosclerosis cases and this is what most physicians treat. This fraction
is typically, though not always, attributed to diet.
- Lp(a) is also known as the “widow maker” or “heart attack” cholesterol. When elevated Lp(a)
is associated with the atherogenic lipoprotein profile (low HDL2, elevated dense LDL, IDL, dense VLDL and VLDL)
the increase risk is 25. If two or more non-lipid risk factors are also present (hypertension, diabetes,
cigarette smoking, or high total Homocysteine) the increased risk is 122. Lp(a) is entirely genetic or metabolic
in origin and therefore, lifestyle or diet does not modify this subfraction. The only way to reduce this
subfraction is drug intervention. Sandkamp M, Clin Chem. 1990 Jan;36(1):20-3 and Williams RR, Arterioscler
Thromb Vasc Biol. 1997 Nov;17(11):2783-92
- IDL, also known as intermediate density lipoprotein, is an independent risk factor for CAD.
IDL is under very strong genetic or metabolic control and usually requires drug interaction to regulate if
values are abnormal or patient is at risk. Zambon A, et al. Curr Opin Lipidol. 1998 Aug;9(4):329-36
- LDL Pattern (desirable result is pattern A) refers to the density of the LDL cholesterol.
It is important to realize that this describes the density of the LDL-R and has nothing to do with the value
of the LDL. There is a 50/50 chance of pattern being a hereditary problem or lifestyle/diet problem. In
either case this is a serious condition.
One point that must be understood before one goes any further is that all LDL-R cholesterol over 100mg/dL is considered a risk.
Now with this in mind there are forms of LDL that are “safer” than others. LDL pattern A is the safest and
biologically preferred form. The large buoyant LDL is remove by the receptor dependant pathway, hence HDL
receptor dependant pathway. It requires a max time (found on the lower right hand portion of the VAP test)
of 118.0 sec or higher. LDL pattern A/B is a mixture of pattern A and pattern B and requires a max time of
117.99 sec-115.01 sec. LDL pattern B (also called dense LDL) is any time below 115.00 sec max time. Pattern
B LDL carries the highest threat because it is much more susceptible to oxidation (one of the main causes for
atherosclerosis) and remains in the blood stream 40% longer than LDL pattern. Also, it being smaller and more
dense, it can infiltrate the endothelial lining of the arties much easier. Once in the lining the particle
deposits its cholesterol burden initiating the process of atherosclerosis by cell mediated removal of cholesterol.
So, a person with an LDL-R 125mg/dL is considered mildly elevated but in conjunction with LDL pattern B the
risk are elevated tremendously. Treatment for LDL pattern B and elevated LDL cholesterol are different so both
must be known. Superko HR. Am J Cardiol. 1998 Nov 5;82(9A):34Q-46Q
Again, with either pattern A or B, all LDL-R cholesterol over 100mg/dL is considered a risk.
Triglyceride-rich Lipids Panel
- VLDL, VLDL3 as well IDL are all triglyceride-rich lipids. It has
been shown that elevated levels of VLDL3 are an independent risk factor for CAD. But how much is
too much? There is some controversy over this issue but some consensus has been observed. If the
VLDL3 is greater than 10mg/dL then treatment consideration should be observed.
Rubenfire M., Prog Cardiovasc Dis. 1998 Sep-Oct; 41(2):95-116
Homocysteine
hsCRP
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