I guess, with the exception of Denmark we have no clear epidemiological evidence in other European Countries to respond to this question. Less uncertaintes can be ascribed to values above the suggested threshold, in particular if associated to coronary or non coronary ischemic events. We deserve epidemiological studies everywhere in Europe and outside E. Warm regards.

I think that all of us (humans) have similar chromosoms patterns, which create the basis of principal similarity of general methabolic pathway include Lp(a) synthesis and catabolism. I am strong beliver that we can't found too much differenses on the country base. But of course we have to pay attention to the second level of culture truditionof like diet etc,. Friendly speaking nobody till today do not know  what could be the "normal" range of the Lp(a) concentration in the human blood?!

Two provocative questions:

1. Lp(a) - this is good or bad player in our body?

2. In case of "bad" could it be possible that the normal range - 0 mg/dl?

BR

I can not imagine any scenario in which Lp (a) can play a positive role, except (very hypothetically) that can help, through the collection of cholesterol, in wound repair or favoring coagulation in specific points . But yes I can imagine a lot of negative effects: procoagulant effect, blocking the LDL respect to its receptors, LDL prooxidant effect of extending its half-life, among others.

What is certain is the relatively high prevalence of Lp (a) high or very high in SCA in young people or of increased CVD (epidemiological studies) associated with elevated Lp (a) (http://76.227.214.59 / assets/1/7/LP (a). pdf).

From here, my question is whether the effect is continuous or if genetic determiant that make the concentration of Lp (a) high (and therefore, when we consider that is raised?) are also those that generate the risk high cardiovascular related ,and if elevations have the same meaning in different populations.

In fact, in population studies as DRECE (unpublished data), the distribution of the concentrations of Lp (a) is strongly skewed to the left, with a high prevalence of almost undetectable and the appearance of the existence of several overlapping populations as these values rise.

Hi Juan. I would agree with Claudia in saying that the importance of Lp(a) as a risk factor can only be shown by epidemiological studies. Your 80th percentile cutoff of 30 mg/dL for a Spanish population compared to 50 mg/dL in a Danish population simply represents the Lp(a) concentration distribution in those populations. There are obviously some aspects that influence the Lp(a) in each BUT whether there is a difference in the atherogenic impact in each population is a different question? It may just mean that your Spanish population has a lower risk of CVD caused by Lp(a) than the Danish population ( but I don't know the data for this).

Thank you Dale, of course particular high risk clinical conditions connected to Lp(a) as Isolated HyperLp(a)lipoproteinemia or severe Combined form of HYLp(a) associated / not associated to progressive coronary artery disease are to be treated to reach the lowest concentration of Lp(a), possibly, in any country. The point is that population studies (along with genetic studies) deserve to better investigate not only the risk threshold, through the percentile distribution, but also the other determinants enhancing the individual risk as suggested by Sergei. This will offer, at least theoretically, the possibility of better profiling the subjects at high and very high risk starting an effective treatment as early as possible exactly as it is generally accepted for Familial Hypercholesterolemia. Thank you.

Concentration of Lp(a) 45 mg /dl would have the same value as a risk factor not only in Spain and Denmark, but possibly in all European region. The importance of Lp(a) as a risk factor can only be known through a better epidemiological data obtained in a large number of population in a particular region. Such epidemiological information has been widely generated in Denmark and Finland as compared to other countries in Europe and hence their observations pertaining to risk factor would be more acceptable atleast for Caucassion population.                 Thanking You

As long as we don´t know why Lp(a) increases the risk we must rely on epidemiological data and thresholds like the 80th percentile. If I remember the original paper from the Danish group right they wrote that the risk increases continuously.