Nt. Mulvihill et al., Evidence of prolonged inflammation in unstable angina and non-Q wave myocardial infarction, J AM COL C, 36(4), 2000, pp. 1210-1216
Citations number
36
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
OBJECTIVES This study was designed to document the inflammatory response up
to one year after acute presentation with unstable angina (UA) and non-Q w
ave infarction (NQMI) as reflected by the expression of soluble cell adhesi
on molecules (CAMs).
BACKGROUND Coronary plaque inflammation is a key component in the pathogene
sis of acute coronary syndromes. Cell adhesion molecules are critical media
tors of the inflammatory process. Soluble forms of these molecules are dete
ctable in serum and are elevated acutely in patients with UA and NQMI.
METHODS Patients presenting with UA and NQMI had serum samples taken at pre
sentation and then after three, six and 12 months. A control group of simil
ar age and gender distribution was used for comparison. Levels of soluble i
nter-cellular adhesion molecule-1, vascular cell adhesion molecule-1, endot
helial-selectin and platelet-selectin were measured using an ELISA techniqu
e.
RESULTS We studied 91 patients (M/F = 73/18, mean age 62 +/- 11 years, 56 U
A and 35 NQMI) and 24 controls (M/F = 18/6, mean age 56 +/- 12 years). Leve
ls of all four soluble CAMs were significantly elevated in both UA and NQMI
patients at presentation, three and six months in comparison with controls
. Levels in UA and NQMI groups fell between six and 12 months after initial
presentation.
CONCLUSIONS The results suggest that the inflammatory stimulus triggering e
xpression of CAMs is sustained for up to six months after presentation with
either UA or NQMI and then returns toward control values over the followin
g six months. a Am Coil Cardiol 2000;36:1210-6) (C) 2000 by the American Co
llege of Cardiology.