T. Siminiak et al., Increased release of the soluble form of the adhesion molecules L-selectinand ICAM-1 but not E-selectin during attacks of angina pectoris, HEART VESS, 13(4), 1998, pp. 189-194
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.