In its severest forms, decompression sickness (DCS) may extend systemically and/or induce severe neurological deficits, including paralysis or even death. It seems that the sterile and ischemic inflammatory phenomena are consecutive to the reaction of the bubbles with the organism and that the blood platelet activation plays a determinant role in the development of DCS. According to the hypotheses commonly put forward, the bubbles could either activate the platelets by direct contact or be the cause of abrasion of the vascular epithelium, which would expose the basal plate glycogen and then prompt the platelets to activate. The purpose of this study is to confirm anti-platelet drugs specific to GPIIb/IIIa integrin could prevent DCS, using a rat model. There is a significant difference concerning the incidence of the drug on the clinical status of the rats (p = 0.016), with a better clinical outcome for rats treated with tirofiban (TIR) compared with the control rats (p = 0.027), even if the three anti-GPIIb/IIIa agents used have limited respiratory distress. TIR limited the decrease in platelet counts following the hyperbaric exposure. TIR help to prevent from DCS. TIR is specific to GPIIb/IIIa whereas eptifibatide and abciximab could inhibit αVβ3 and αMβ2 involved in communication with the immune system. While inhibiting GPIIb/IIIa could highlight a platelet-dependent inflammatory pathway that improves DCS outcomes, we wonder whether inhibiting the αVβ3 and αMβ2 communications is not a wrong approach for limiting mortality in DCS.

No information is available on the clinical use of abciximab during breastfeeding. Because abciximab is a large protein molecule with a molecular weight of 47,615, the amount in milk is likely to be very low and absorption is unlikely because it is probably destroyed in the infant's gastrointestinal tract. Until more data become available, abciximab should be used with caution during breastfeeding, especially while nursing a newborn or preterm infant.

The risk and benefit ratio of glycoprotein IIb/IIIa inhibitors with dual oral antiplatelet therapy after failed thrombolysis and rescue percutaneous coronary intervention (PCI) is unclear. Using a randomized placebo-controlled, double-blind design, we compared intravenous (IV) and intracoronary (IC) abciximab delivery in 74 patients referred for rescue transradial PCI. The primary angiographic end points were the final thrombolysis in myocardial infarction flow and myocardial blush grades. Secondary end points included acute and 6-month outcomes using angiographic parameters, platelet aggregation parameters, cardiac biomarkers, cardiac magnetic resonance measurements (CMR) and clinical end points. After rescue PCI, normal thrombolysis in myocardial infarction 3 flows were obtained in 70% in the IC group, 48% in the IV group, and 71% in the placebo group, respectively (p = 0.056). Final myocardial blush grades 2 and 3 were obtained in 43% and 39% in the IC group, 48% and 26% in the IV group, and 46% and 42% in the placebo group (p = 0.67), respectively. Acutely, peak release of cardiac biomarkers, necrosis size, myocardial perfusion and no-reflow as assessed by CMR, and clinical end points were similar between the groups and did not suggest a benefit for IC or IV abciximab compared with placebo. There was no increase in bleeding or access site-related complications with abciximab compared with placebo. Clinical, angiographic, and CMR outcomes at 6 months remained comparable between the groups. In patients with ST-elevation myocardial infarction presenting with failed thrombolysis undergoing transradial rescue PCI, IC or IV abciximab had no significant clinical impact.