Elevated levels of adhesion molecules in septic patients with pre-existing coronary artery disease

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Introduction

Sepsis, as well as coronary artery disease (CAD), is associated with high levels of circulating adhesion molecules[1,2]. Elevated plasma levels of these molecules may have clinical significance as markers of endothelial injury [2]. The purpose of the study was to investigate whether CAD influences the liberation of plasma adhesion molecules, cytokines and markers of the NO-system in septic patients and if these parameters may serve for identification of patients at greater risk for cardiovascular complications in sepsis.

Methods

After approval by the local ethical committee and obtaining informed consent from relatives, 44 septic patients were included in this study, of whom 24 patients met the criteria of CAD [3]. Measurements were performed within 12 h (early sepsis) of onset of sepsis and after 72 h (late sepsis). Soluble adhesion molecules sE-selectin, and soluble intercellular adhesion molecule (sICAM)-1 were analyzed by commercially available ELISA. NO-markers were measured by the Griess reaction and cyclic guanosine monophosphate (cGMP) by competitive radioimmunoassay.

Results

Basic patient characteristics did not differ between groups. CAD patients showed significantly increased sICAM-1 levels in early and late sepsis (Table 1) but this failed to be predictive for cardiovascular complications. ICAM-1 and cGMP correlated positively in both groups with the intravenously administered norepinephrine dosage in early and late sepsis. Cardiac index, oxygen delivery and mixed venous oxygen saturation were significantly decreased in CAD patients in early and late sepsis (P<0.05), whereas VO₂ did not differ significantly between both groups. Mortality was increased in tendency in CAD patients (75% vs 50% in non-CAD).

Conclusion

Plasma levels of sICAM-1, sE-selectin and cGMP were elevated in CAD but may not serve as markers for cardiovascular complications in sepsis. The tendency in increased mortality rate could be due to an impaired endothelial reserve in CAD patients.

Table 1 Table 1