Increased release of the soluble form of the adhesion molecules L-selectinand ICAM-1 but not E-selectin during attacks of angina pectoris

Myocardial ischemia leads to the activation of neutrophils as well as endot helial cells. The interaction between these cells is dependent on certain a dhesion glycoproteins which are expressed on their surface. Adhesion of neu trophils to endothelium, mediated by adhesion molecules, has been shown to result in coronary capillary plugging and impairment of coronary blood flow . In certain conditions, upon cell activation, adhesion proteins may be rel eased in soluble form into the circulating blood. The purpose of our study was to verify whether myocardial ischemia occurring during angina episodes results in the release of the soluble adhesion molecules, L-selectin, E-sel ectin, and intracellular adhesion molecule-1 (ICAM-1), into the circulation . Plasma samples were collected by venepuncture from 15 patients admitted t o the emergency room with chest pain caused by attacks of angina pectoris a nd 15 patients with noncardiac chest pain. To confirm the diagnosis, all pa tients underwent an exercise stress test and, if not conclusive, Tc-99m MIB I SPECT or coronary arteriography. Another set of plasma samples were taken from each patient in the absence of chest pain. In addition, blood for ana lysis was obtained from 15 sex- and age-matched healthy subjects. Soluble a dhesion molecules plasma levels were measured by standard enzyme-linked imm unosorbent assay. In patients with angina pectoris, plasma levels of solubl e L-selectin estimated during chest pain were significantly higher than in the control group and decreased in the absence of chest pain. Similarly, th e mean concentration of soluble ICAM-1 at the time of angina onset was sign ificantly elevated in the patients in comparison with the control group and remained higher, although not significantly, in the absence of chest pain. In patients with noncardiac chest pain, plasma levels of soluble L-selecti n did not differ significantly from those observed in control subjects. In this group of patients, the plasma levels of soluble ICAM-1 estimated durin g pain onset and in the absence of this symptom were not significantly elev ated. On the contrary, the mean values of soluble E-selectin in the patient s with ischemic cardiac pain during chest pain and in the absence of this s ymptom, as well as those in the patients with noncardiac chest pain during or without symptoms, remained unchanged in comparison with the control grou p. During attacks of angina pectoris an increase in the plasma levels of th e soluble adhesion molecules, ICAM-1 and L-selectin, was noted, possibly re flecting activation of neutrophils and endothelial cells during myocardial ischemia. However, E-selectin plasma levels remained unchanged in response to myocardial ischemia.