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ARTICLE

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

John T. Parissis, Stamatis Adamopoulos¹, Koula Venetsanou, George Kostakis, Antonios Rigas, Spilios M. Karas, Dimitrios Kremastinos¹

First Department of Cardiology, Amalia Fleming Hospital, Athens Greece
1 Second Department of Cardiovascular Medicine, Onassis Cardiac Surgery Center, Athens, Greece

* Corresponding Author: John T. Parissis,

European Cytokine Network 2004, 15(2), 139-144.

Accepted 13 February 2004;

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.
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.
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).
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.

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