Plasma sGPVI, Platelet Function, Bleeding, and Ischemic Events in Patients Undergoing PCI

Why did you (and your colleagues) write this paper? What was its main purpose?

Platelet Glycoprotein VI shedding, as a mechanism to reduce thrombotic risk associated with activated platelets, leads to increased levels of soluble glycoprotein VI (sGPVI) in circulation. Limited data are available in patients with chronic coronary syndromes (CCSs) treated with percutaneous coronary intervention (PCI) with respect to factors that influence plasma sGPVI levels, association of sGPVI with platelet reactivity in patients on antiplatelet therapy, and the ability of sGPVI to predict ischemic and bleeding events after PCI. Thus, the main purpose of the study was to assess the potential value of sGPVI as a predictor of ischemic and bleeding risk in patients with CCS undergoing PCI.

What are the main conclusions?

The main conclusions are that in patients with CCS undergoing PCI, plasma levels of sGPVI did not correlate with ADP- and collagen-induced platelet aggregation and that patients with higher baseline plasma levels of sGPVI may carry an increased risk of bleeding at 30 days after PCI but no excess risk of ischemic events.

What are the paper's implications?- to the public? -to medical professionals?

Our findings suggest that sGPVI may be used as a marker of bleeding risk in patients with CCSs after PCI. This may be particularly important considering that patients with CCSs are poorly characterized in terms of bleeding risk and that all existing clinical bleeding risk scores poorly discriminate patients in terms of the risk for bleeding or ischemic events.

Are the findings clinically significant? Should the findings change practice?

We believe that the findings of the current study are clinically relevant in that they suggest that sGPVI may be a specific marker candidate for bleeding in patients with CAD. In this regard, the study helps to better characterize patients with CAD after PCI in terms of the risk for bleeding events, known to be strongly associated with subsequent prognosis. However, in the light of limitations, such as the study being a subgroup analysis of a phase 2 randomized trial, which was underpowered to assess prognostic value of plasma sGPVI, limited prognostic value of high-sensitivity cardiac troponin threshold used to detect myocardial injury and the inclusion of all Bleeding Academic Research Consortium (BARC) classes in the co-primary endpoint of the study, it is too early to conclude whether these findings may change the practice. Thus, more studies are needed to define the role of sGPVI as a marker of bleeding and ischemic risk in patients with CAD.