Lp(a) resembles LDL particle, structurally, with Apo B100 and, in addition, with  Apo A, as main apoprotein constituents. This similarity could explain the positive correlation observed between higher LDL and Lp(a) levels in atherosclerosis development, so elevation of LDL levels, and commonly hyperlipidaemia, is usually considered a general feature, as well as one of the main risk factors.

Lp(a) usually is not measured by normal laboratories, moreover the traditional Friedewald formula included the Lp(a)-cholesteol into LDLc !! Few laboratories are able to evaluate Lp(a) isoforms. The structure of apo(a) is very specify,and apo(a) is NOT present in normal LDL particles. The metabolic pathway of Lp(a) and LDL are quite different. Actually, Lp(a) is an atherogenic particle with thrombogenic effects, so very dangerous, particularly if some isoforms are present. Their role in atherogenesis and in myocardial infarction is underestimate by clinicians !! In my opinion the measurement of Lp(a) plasma concentration must be included in routine evaluation of lipid profile and values higher than 30 mg/dL may be regarded as "increasing CHD risk" while values > 60-70 mg/dL are very very dangerous (patients with hyperlp(a)emia do not respond to statin therapy and frequently shows early onset CHD). If lp(a) is > 100 mg/dL, the prognosis might be unfavorable also in young people ! Lp(a) apheresis might be a solution for more severe patients. In my opinion, on the basis of unpublished data, also very LOW lp(a) values (< 2 mg/dL) can be regarded as dangerous, particularly in females (....omissis....)

I totally agree with Antonio Vittorino. Besides the intrinsic risk involving high Lp(a) levels, fact which can facilitate by itself, for instance, endothelial dysfunction or foam cell formation, it is noteworthy the high thrombogenic properties of this type of lipoproteins.

WELL ! Thank you Dr Sànchez. We have the same opinion and we strongly suggest the Lp(a) measurement for ATS/CHD ("""risk""") estimate or, better, for hyperlp(a)emia  diagnosis. 

Small size, and higher concentration of plasma Lp(a) particles over 30 mg/dL increase the risk of CVD. Several polipeptide components in apo(a) named "Kringles" have similar  prothrombogenic  effect  as plasminogen. Of course, Friedewald formula for calculate LDL-Cholesterol includes LP(a), another fact against this formula.Lp(a) must be measured in  human dyslipemia studies.

I agree with most of the reviews: We measure Lp (a) in all cases of intermediate risk or high risk. Also with Regina in his commentary on the failure of the Friedewald formula to estimate LDL cholesterol when Lp (a) is high, but it is in my opinion the Friedewld formula underestimates the risk attributable to LDL on these occasions.

Moreover, we can find strong elevations of Lp (a) in patients in whom cardiovascular risk calculated, is not high. In my opinion, and considering that 20% of the population (by definition, since the cutoff is consensus on population 80th percentile), the quantification of Lp (a) should be part of all studies of cardiovascular risk .

Another issue is what to do when the Lp (a) is high or very high. IN my opinion, when it is high should be more aggressive about other risk factors, and when it is very high, I agree with Antonio Vittorino Gaddi: why not use LDLaféresis ?.

In the past, we use LDL apheresis (with specific selective columns and, in some case, with non selective columns for cost reasons) and we made some studies, with Sergei Pokrowsky, G Ghiselli and other, on Lp(a) apheresis. Actually, Prof.ssa Claudia Stefanutti, in Rome is a big expert in this filed. In my opinion the main concerns about Lp(a) apheresis are a) the column selectivity and b) the clinical outcomes and c) the length of inter-apheretic period, taking into account that  the between-pateint variability of rate of Lp(a) reappearance in plasma is very high (see the paper of Ghiselli&Gaddi in Chem Phys Lipids. 1994 Jan;67-68:305-11). The problem is complex both from technical, methodological and clinical point of view. HOWEVER, in very severe iperLp(a) patients with overt clinical picture (premature atherosclerosis, myocardial infarction and so on) the apheresis may be considered.

Lp(a) has been proven as a causative factor for atherosclerotic disease, but is not recommended for screening in primary prevention. It appears that Lp(a) measurement can be of some value in some patients with cardiovascular disease (secondary prevention) especially those with family history of premature atherosclerotic disease (levels and structure of Lp(a) is strongly genetically idetermined). Such narrow recommendations are probably due to lack of drugs effectively reducing Lp(a). The only exception is nicotinic acid in rather high doses and therefore it is difficult to avoid unpleasant side effects. However finding high Lp(a) level in an individual patient may incline a clinician to intensify therapy of easier modifiable risk factors.