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Lp(a) lacks sound prospective evidence as a vascular risk factor; leaves open its causal role in atherothrombosis pending in vivo studies.
Lipoprotein (a) [Lp(a)] has been recognized for nearly 30 years, and increasingly, associated with the processes of atherogenesis and thrombogenesis. Despite this, the physiological and pathological function (and factors that influence levels) of Lp(a) remain largely unknown. Most experimental evidence supporting the mechanisms of vascular disease, thrombogenesis and atherogenesis have been generated in vitro, and to date, no in vivo confirmation exists. There is also a lack of sound evidence for Lp(a) as a risk factor in prospective as opposed to case-controlled studies. A fuller understanding of Lp(a) is still required in the molecular biology of atherogenesis and thrombogenesis.
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Lip et al. (1995) studied this question.
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