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Case-control data do not support Lp(a) for CHD severity assessment; leaves open causal independence and mechanistic pathways.
These results indicate that elevated plasma Lp(a) levels may be an independent risk factor for CHD but unrelated to the severity and extension of CHD. Furthermore, there is no good evidence that the presumed link between Lp(a) and CHD is mediated by increased levels of markers of inflammation, or interference with markers of fibrinolysis or coagulation.
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Imhof et al. (2003) studied this question.
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