he most important cause of acute myocardial infarction (AMI) is plaque rupture in the coronary arteries with subsequent thrombosis. The risk of plaque rupture appears to be related to the composition of the atherosclerotic plaque. The same population of bloodderived monocytes/macrophages that transforms the atherosclerotic lesions into foam cells interacts with T lymphocytes and smooth muscle cells via growth factors and cytokines. 1 At the site of plaque rupture or erosion, inflammation processes play a role in destabilizing the fibrous cap tissue, thus enhancing the risk of coronary thrombosis. 2 However, the precise mechanisms causing plaque rupture are not fully understood. A large body of evidence points to the involvement of an inflammatory response in the pathophysiology of myocardial ischemia-reperfusion injury. 3 Leukocyte accumulation in the myocardium may amplify tissue damage by activating cardiomyocytes and by releasing deleterious substances such as inflammatory cytokines, 4,5 thromboxane A2, 6 oxygen-free radicals 7 and platelet activating factor (PAF). 8 Leukocytes and endothelium express adhesion molecules when stimulated, for example by cytokines, and their expression is considered to play a pivotal role in the localization and development of an inflammatory reaction. E-selectin as a selectin-type adhesion molecule, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) are immunoglobulin-type adhesion molecules, which are located on the surface of activated endothelial cells and bind leukocytes. Previous animal studies have clearly demonstrated that PAF antagonists, 9 and inhibition of ICAM-1 10,11 and selectin-type adhesion molecules 12 using monoclonal antibodies, significantly reduce the degree of myocardial injury that results from coronary artery occlusion and reperfusion. The aim of this study was to characterize these soluble adhesion molecules, PAF and interleukin-6 as inflammatory cytokines in patients with AMI in order to examine the possible role of these factors in the pathophysiology of AMI.
Methods
Study PatientsThe blood PAF levels were measured in 8 consecutive patients with AMI who were admitted within 12 h of the onset of symptoms and in 98 normal volunteers (Control). The study patients with AMI consisted of 6 men and 2 women, ranging in age from 47 to 79 years, with a mean age of 62.2±10.4 (mean ± SD) years (Study 1). We also measured the plasma levels of interleukin-6, soluble Eselectin (sE-selectin), soluble ICAM-1 (sICAM-1) and soluble VCAM-1 (sVCAM-1) in 30 patients with AMI who were admitted within 12 h of the onset of symptoms and in 15 patients with stable effort angina (SEA). The patients with AMI consisted of 26 men and 4 women, ranging in age from 30 to 80 years, with a mean age of Jpn Circ J 1999; 63: 362 -366 (Received August 31, 1998; revised manuscript received January 29, 1999; accepted February 5, 1999 Although acute myocardial infarction (AMI) may involve both plaque rupture and ischemia-reperfusion injury, the pathogenes...