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Lp(a) may affect post-MI fibrinolysis without predicting thrombolysis response; leaves open its role as a modifiable target pending prospective trials.
New data on the interactions between lipoprotein (a) [Lp(a)] and the coagulation-fibrinolytic system, which emphasize the importance of the activity of lysine-binding sites on apolipoprotein (a) [apo(a)], provide an increasingly strong basis for the role of Lp(a) in thrombosis. Further insights into the genetic control of Lp(a) levels show that inherited factors other than the size of the apo(a) gene are important. The clinical relationship between Lp(a) and coronary heart disease has been more firmly established by two further large prospective cohort studies. The consensus that the concentration of Lp(a) does not predict the outcome of thrombolytic therapy still holds, although Lp(a) does affect endogenous fibrinolysis after myocardial infarction. The effect of Lp(a) on mortality should soon be known.
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Seed et al. (1995) studied this question.
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