The use of transgenic and gene knockout animals, gene manipulated cells, pharmacological LPA receptor agonists and antagonists have provided many insights into the biological significance of LPA and individual LPA receptors in the progression of atherosclerosis and vascular diseases.
Adjusting for vasculopathy, isolated antithrombin deficiency (HR 3.9; 95% CI: 1.4-10.9), isolated elevated lipoprotein (a) (HR 2.3; 95% CI: 1.3-4.1), and the presence of more than one prothrombotic risk factor (HR 1.9; 95% CI: 1.12-3.2) were independently associated with an increased risk of recurrence.
The purpose of this study is investigate the effects of variants in the apolipoprotein(a) gene (LPA) on vascular diseases with different atherosclerotic and thrombotic components.
The comparable strength of associations of the LPA score with coronary disease and peripheral vascular disease but not with stroke suggest that lipoprotein(a) may have effects on atherothrombotic vascular disease that are only relevant at specific sites.
Explanations for familial stroke aggregation include differential phenotypic expression of apolipoprotein (a) and apolipoprotein E, racial variations in the distribution of vascular disease, identification of the autosomal-dominant disorder cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy, specific point mutations in the mitochondrial-related disorders, and identification of the clinical significance of hereditable coagulopathies.