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High Cholesterol Message Board


High Cholesterol Board Index


[QUOTE=ARIZONA73]Of course, too high of an LDL can potentially be detrimental, but you can't just go by number values. All LDL is not the same. It is quite possible for someone with an LDL of 150 to be at less risk than someone with an LDL of 100. You need to look at other factors, such as LDL particle size and HDL levels. If your LDL is predominately Pattern B, that certainly renders the LDL more dangerous. Also, since most people are given only a calculated LDL, the amount of lipoprotein(a) is likely included in that lump-sum figure, but most of us have no idea what our Lp(a) is. But this number is important, especially since an elevated Lp(a) can carry as much as 10 times the danger of ordinary LDL. So, it really isn't fair to simply say that a person is at a higher or lower risk based on a single value if you don't take these other factors into consideration. That would be far too simplistic. You simply cannot judge a book by its cover. But that's exactly what you're doing if all you're looking at is a number.[/QUOTE]

[B]Lipoprotein (a)[/B]
Several studies274-277 report a strong association between Lp(a) levels and CHD risk. Indeed, a recent meta-analysis of reported prospective studies supports an independent predictive power for elevated Lp(a).278 In addition, concomitant elevations of Lp(a) and LDL cholesterol have been reported to have synergy in elevating risk in both men and women with hypercholesterolemia. On the basis of these studies, some authorities hold that an elevation of Lp(a) is an independent risk factor for CHD. [B]It must be noted nonetheless that several prospective studies279,280 do not confirm independent prediction.[/B] Of note, Lp(a) levels are higher in African Americans than in Caucasians, but an increased risk for CHD associated with higher Lp(a) levels in African Americans has not been documented.279 [B]Thus, the quantitative contribution of elevated Lp(a) to CHD risk beyond the major risk factors is uncertain[/B]. This uncertainty extends both to individuals and populations; in the latter, the frequency of elevated Lp(a) is not as high as for the major risk factors.

[B]Moreover, issues related to measurement of Lp(a) in clinical practice have not been fully resolved.281,282 Measurement of Lp(a) is made by immunological methods, and standardized methods are available only in a few reference laboratories[/B]. Population reference levels are available from these laboratories, but they are not widely available in clinical practice. Accurate methodology has not yet been established in most clinical chemistry laboratories; samples generally must be sent to special laboratories for measurement. As a result, extra expense in measurement is required. [B]Serum Lp(a) is relatively resistant to therapeutic lowering. Statin drugs are ineffective. Among currently available drugs, only nicotinic acid reduces Lp(a) concentrations, and only moderately.[/B]283,284 In postmenopausal women, estrogen therapy also causes some reduction in Lp(a) concentrations.285 Although these therapies typically lower elevated Lp(a) levels, they have not been widely adopted. [B]At present no clinical trial evidence supports a benefit from lowering Lp(a) levels with particular agents[/B].

Despite limitations in measurement and therapy, some authorities believe that Lp(a) measurement is a useful addition to the major risk factors for identifying persons at still higher risk than revealed by those factors. According to advocates for Lp(a), the option of measurement is best reserved for persons with a strong family history of premature CHD or those with genetic causes of hypercholesterolemia, such as familial hypercholesterolemia.281,282 An elevated Lp(a) thus presents the option to raise a person's risk to a higher level. [B]For example, if a person has a high LDL cholesterol and only one other risk factor, the finding of a high Lp(a) could count as a second risk factor to justify a lower goal for LDL cholesterol. ATP III did not find strong evidence to support this approach, but accepts it as an option for selected persons. [/B]

[B]Small LDL particles[/B]
One component of atherogenic dyslipidemia is small LDL particles. They are formed in large part, although not exclusively, as a response to elevations of triglycerides. Their presence is associated with an increased risk for CHD;125,286,287 however, [B]the extent to which they predict CHD independently of other risk factors is unresolved.288 Moreover, standard and inexpensive methodologies are not available for their measurement. For these reasons, ATP III does not recommend measurement of small LDL particles in routine practice[/B]. If the clinical decision is made to detect and measure small LDL, their presence is best used as an indicator for atherogenic dyslipidemia and the metabolic syndrome. Their elevation also supports intensified therapeutic lifestyle changes. If small LDL particles accompany elevated triglycerides or low HDL cholesterol in high-risk persons, consideration can be given to using nicotinic acid or fibric acid as components of lipid-lowering therapy. [B]Nonetheless, LDL cholesterol remains the primary target of treatment in persons with small LDL particles. [/B]





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