The effect of elevated lipoprotein(a) on autologous platelets function: a retrospective analysis

Platelet labeling is used to study platelets in vivo in terms of diagnosing intravascular thrombosis, as well as studying their role and biological activity in atherosclerosis. A low labeling efficiency (LE) can negatively impair testing results. Labeling efficiency depends on various factors, including low-density-lipoprotein (LDL)-cholesterol levels in the blood. Lipoprotein(a) (Lp(a)) is a lipoprotein subclass that when elevated, is frequently associated with the premature development of cardiovascular disease through activation of different signaling pathways and cell surface receptors.

We retrospectively studied 51 patients with isolated elevated Lp(a) (>50 mg/dL, ranging up to 440 mg/dL) compared to patients with normal lipid profiles who underwent autologous radioactive platelet labeling during the time period of January 2001-September 2013 at the Vienna General Hospital. Platelets were radiolabeled according to ISORBE consensus.

LE was decreased in patients with elevated Lp(a). Cross-incubation of hyper-Lp(a) patients with normal Lp(a) plasma and vice versa demonstrated that platelets themselves and not the plasmatic environment are accountable for the decline in LE. Furthermore, LE positively correlated with an increase in platelet incubation time, the highest LE being seen after 30 minutes.

This study determined that extremely elevated Lp(a) profiles, especially values greater than 150 mg/dL, may significantly impair platelets function such as labeling results. Platelets are responsible for the decrease in LE in hyper-Lp(a) patients. Non-HDL-Lp is the most informative parameter of impaired LE. We thus recommend to include Lp(a) in the list of parameters that need to be taken into consideration in studying autologous radiolabeled platelets.