Introduction

Since their discovery in 1842, platelets have commanded an increasingly prominent position in the pathophysiology of thrombosis, although this has been almost exclusively in arterial disease. However, Virchow was most likely the first to link changes in the blood (that we would today interpret as rheology, vascular function, and the soluble and cellular constituents of the blood) with venous thrombosis.

There are three major lines of approach that we can take in order to test the hypothesis that platelets are intimately involved in the development of DVT and PE. The pharmacological approach considers clinical trials of antiplatelet drugs (such as aspirin) in well-defined groups of high-risk patients that demonstrate a reduction in the rate and/or risk of thrombosis. The laboratory approach can be used to demonstrate changes in platelet function ex vivo or in levels of platelet-specific markers (such as beta thromboglobulin) in the plasma of those at risk of, with, or having suffered, a thrombotic event. More recently, radionucleotide and other imaging with labelled platelets, antibodies, probes or other agents provide additional evidence of the role of platelets in DVT and PE. Whilst there are considerable animal data on the subject of venous thromboembolism, this overview will be confined to human studies.

Clinical trials

The most commonly used and most successful antiplatelet drug is aspirin, which is well established as secondary prevention in vascular (arterial) disease.