Hyperbaric oxygenation (HBO) for correction of platelet haemostasis disorders in coronary heart disease (CHD) is reasonable due to the associated hypocoagulation. However, in practice, the baseline state of platelet activity is not considered when prescribing HBO therapy. Available publications lack information on structural changes in the platelet membrane associated with the of phospholipase A2 (PLA2) activity, and on the HBO effect on the various steps of hemostasis.

OBJECTIVE

To study changes in serum PLA2 concentration and its relation to platelet aggregation activity during HBO in patients with stable CHD.

MATERIAL AND METHODS

We examined 42 patients with stable angina FC II—III, 27 received antiplatelet therapy (Cardiomagnyl 75 mg: acetylsalicylic acid + magnesium hydroxide), and 15 patients did not. All patients received a 10-day course of HBO at 1.2 atmosphere mode for 40 min. Platelet hemostasis and serum PLA2 concentration were evaluated. Platelet aggregation was tested using Biola LA-230-2 aggregation analyzer (Biola Scientific, Russia). The platelets count and mean platelet volume (MPV) were determined on a Mindray BS-3200 hematology analyzer (Mindray, China). PLA2 levels were determined by enzyme immunoassay using Model 680 microplate reader (Bio-Rad, USA). Residual platelet reactivity was evaluated by 5.0 ADP-induced aggregation.

RESULTS

Assessment of the HBO effect on the functional state of platelets depending on their aggregation activity and the therapy taken showed a significant increase in spontaneous aggregation and ADP-induced aggregation at inducer concentration of 1.0 μM (p=0.049) in patients with baseline hyperaggregation taking Cardiomagnyl after HBO. No significant changes in PLA2 concentration were observed. At the same time, patients with baseline hyperaggregation who did not take antiplatelet agents had no changes in platelet aggregation activity and a decreased serum PLA2. In patients with baseline normal aggregation receiving an antiplatelet drug, a course of HBO had no effect on platelet aggregation activity and PLA2 level. In patients with baseline normal aggregation who did not take antiplatelet agents, a course of HBO resulted in significant decrease in PLA2 levels and no changes in platelet aggregation activity. In patients with low aggregation activity (hypoaggregation) who took antiplatelet agents, a significant increase in spontaneous aggregation and no change of serum PLA2 after an HBO course was observed.

CONCLUSION

The study showed a divergent response to the hyperbaric oxygen, depending on the antiplatelet therapy and the background aggregation.