
@Article{,
AUTHOR = {John T. Parissis, Stamatis Adamopoulos, Koula Venetsanou, George Kostakis, Antonios Rigas, Spilios M. Karas, Dimitrios Kremastinos},
TITLE = {Plasma proﬁles of circulating granulocyte-macrophage colony-stimulating factor and soluble cellular adhesion molecules in acute myocardial infarction. Contribution to post-infarction left ventricular dysfunction},
JOURNAL = {European Cytokine Network},
VOLUME = {15},
YEAR = {2004},
NUMBER = {2},
PAGES = {139--144},
URL = {http://www.techscience.com/ECN/v15n2/66393},
ISSN = {1952-4005},
ABSTRACT = {No in vivo data exist about the relationship of circulating granulocyte-macrophage colony
stimulating factor (GM-CSF) and soluble adhesion molecules ICAM-1 and VCAM-1 (sICAM-1 and sVCAM-1) to
the severity of acute myocardial infarction (AMI) and the pathophysiological events of post-infarction left
ventricular dysfunction. We investigated the kinetics of these inﬂammatory mediators in the plasma of patients
with AMI, and correlated the ﬁndings with the clinical severity of the disease during the ﬁrst week of
hospitalization as well as the degree of left ventricular dysfunction one month after the AMI.<br/>
Plasma levels of inﬂammatory markers were determined in 41 AMI patients (all received thrombolytic treatment)
by ELISA assays, serially during the ﬁrst week of hospitalization and one month after hospital admission. Patients
(n = 20) with uncomplicated AMI (Killip class I) were classiﬁed as group A, patients (n = 21) with AMI
complicated by heart failure manifestations (Killip classes II and III) were classiﬁed as group B, while 20 age- and
sex-matched volunteers were used as healthy controls.<br/>
A sustained increase in GM-CSF, sICAM-1 and sVCAM-1 plasma concentrations was observed only in group B
during the ﬁrst week of the study. Patients from group B exhibited signiﬁcantly higher levels of GM-CSF
(P < 0.01), sICAM-1 (P < 0.05) and sVCAM-1 (P < 0.01) than patients from group A and the healthy controls
(P < 0.001). In group B patients, signiﬁcant correlations were observed between the peak of GM-CSF levels and
the peak of serum creatine kinase-MB (r = 0.42; P < 0.05), white blood cell counts (r = 0.67; P < 0.001) and LVEF
(r = – 0.51; P < 0.01). At one month follow-up, patients (n = 17) with severe post-infarction left ventricular
dysfunction (LVEF ≤ 35%) exhibited signiﬁcantly higher levels of GM-CSF (21.8 ± 1.5 versus 11.7 ± 0.9 pg/mL,
P < 0.001), sICAM-1 (331.4 ± 18.4 versus 201.3 ± 12.1 ng/mL, P < 0.001) and sVCAM-1 (748.4 ± 34.7 versus
512.9 ± 18.8 ng/mL, P < 0.001) than did the other patients (n = 24) without this condition (LVEF > 35%).
Signiﬁcant correlations were observed between GM-CSF levels and left ventricular end-diastolic volume index
(r = 0.55; P < 0.001) or left ventricular end-systolic volume index (r = 0.49; P = 0.001).<br/>
We have found a signiﬁcant elevation of plasma GM-CSF and soluble adhesion molecules during the course of
AMI, with the highest values in patients with AMI complicated by heart failure manifestations and severe left
ventricular dysfunction. These monocyte-related inﬂammatory mediators may actively contribute to the
pathophysiology of the disease and post-infarction cardiac dysfunction.},
DOI = {}
}



