Abstract
Lipoprotein(a) [Lp(a)] is an independent, genetically determined, and causal risk factor for cardiovascular disease. Laboratory data have suggested an interaction of Lp(a) with platelet function, potentially caused by its interaction with platelet receptors. So far, the potential association of Lp(a) with platelet activation and reactivity has not been proven in larger clinical cohorts. This study analyzed intrinsic platelet reactivity before loading with clopidogrel 600 mg and on-treatment platelet reactivity tested 24 h following loading in patients undergoing elective coronary angiography. Platelet reactivity was tested by optical aggregometry following stimulation with collagen or adenosine diphosphate as well as by flow cytometry. Lp(a) levels were directly measured in all patients from fresh samples. The present analysis included 1912 patients. Lp(a) levels ranged between 0 and 332 mg/dl. There was a significant association of rising levels of Lp(a) with a higher prevalence of a history of ischemic heart disease (p < 0.001) and more extensive coronary artery disease (p = 0.001). Results for intrinsic (p = 0.80) and on-clopidogrel platelet reactivity (p = 0.81) did not differ between quartiles of Lp(a) levels. Flow cytometry analyses of expression of different platelet surface proteins (CD41, CD62P or PAC-1) confirmed these findings. Correlation analyses of levels of Lp(a) with any of the tested platelet activation markers did not show any correlation. The present data do not support the hypothesis of an interaction of Lp(a) with platelet reactivity.
Highlights
Lipoprotein(a) [Lp(a)] is an independent and causal risk factor for premature coronary heart disease, myocardial infarction (MI), atherosclerosis, aortic valve stenosis, and stroke [1–4]
The present data do not support the hypothesis of an interaction of Lp(a) with intrinsic or on dual antiplatelet therapy platelet reactivity but confirms the importance of Lp(a) as risk factor for coronary events
These findings might be important to define the safety of evolving therapeutic options for lowering Lp(a)
Summary
Lipoprotein(a) [Lp(a)] is an independent and causal risk factor for premature coronary heart disease, myocardial infarction (MI), atherosclerosis, aortic valve stenosis, and stroke [1–4]. The association of Lp(a) with potential anti-fibrinolytic activity is well known, yet the clinical relevance of this has been recently questioned by studies showing no association of genetically determined Lp(a) levels with deep venous thromboses [9]. Several studies have indicated that there might be a potential interaction of Lp(a) with the plasma coagulation cascade and platelet function through its apo(a) component and content of oxidized phospholipids. Given the novel therapeutic options for reducing levels of Lp(a), it appears of importance to evaluate this potential interaction to define the safety of lowering Lp(a). The present study sought to investigate the potential association of Lp(a) levels with platelet activation and on-treatment platelet reactivity in a large clinical cohort
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