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Lipoprotein (a): Molecular and Epidemiologic basis about its role in cardiovascular diseases

Abstract:

In 1963, Kare Berg at the University of Oslo discovered Lp(a) as a new human plasmatic antigen set. The interest in Lp(a) increased in 1974 when Berg's team reported an association between high plasma levels of Lp(a) and coronary heart diseases. A number of case-control studies have confirmed their observation and suggested that Lp(a) may be an independent risk factor for premature cardiovascular disease. Several prospective and case-control studies have shown that Lp(a) is an independent risk factor for coronary artery disease, stroke, peripheral vascular disease, accelerated post-transplant atherosclerosis and post-angioplasty reestenosis. Lp(a) is now identified as a genetic trait autosomally transmitted, coded by one of the most polymorphic genes known in humans. Variations in this gene are a major determinant of Lp(a) plasma levels, which differ considerably between individuals and also across populations. The liver is the main organ responsible for its synthesis and catabolism. However, the key receptor that mediates this process has not been found yet, nor any of the enzymes involved. Even though some pharmacologic approaches using niacin, fibric acid derivatives, alcohol-extracted soy protein, growth hormone, and IGF-1 have been tested in order to diminish Lp(a) concentration in high risk patients, none is a therapeutic option to successfully decrease Lp(a) levels.