Sir,—Considerable research energy is being directed towards cell adhesion molecules, and the recent review by Hillis and Flapan1 provides a useful introduction. As they allude to, blockade of the interaction between leucocytes and the endothelium by agents that mimic or inhibit these adhesion molecules may become a new class of therapeutic agent.2 ,3 However, Hillis and Flapan only briefly draw our attention to the presence of soluble forms of these adhesion molecules in plasma.

The importance of these soluble forms is probably underestimated, as they may interfere with, or frustrate, attempts to reduce leucocyte–endothelial interactions in vivo, as has already been shown in vitro.4 ,5 In addition, soluble adhesion molecules may be useful in dissecting the various pathophysiological events in cardiovascular disease, as it may be presumed that changes in concentrations may relate to activation or damage to various cells, such as the platelet and endothelium, which are pertinent to cardiovascular pathophysiology.

For example, the selectin family of adhesion molecules has three members, and corresponding soluble concentrations are measurable in the plasma. Soluble P selectin is believed to be the product of activated platelets, despite the endothelium having a membrane bound form.6 ,7 Increased concentrations have been found in a number of conditions: thrombotic disorders, diabetes, and ischaemic heart disease. Importantly, raised concentrations in the last group of patients is predictive of adverse events.8-10 Although increased concentrations of soluble E selectin are the result of cytokine activation of endothelial cells in vitro,11raised plasma concentrations have been reported in variant angina,12 …