[Relation between local CMV infection and inflammatory cytokine expressionon in pts sheduled for CABG].

Introduction: Cytomegalovirus (CMV) infection has been suggested to play a role in the development of cardiovascular diseases. It has not yet been established yet whether the possible adverse vascular effect is associated with chronic inflammation process caused by CMV. The aim of our study was to evaluate a possible role of CMV infection in local inflammatory activation in pts with coronary artery disease (CAD).

Material And Methods: We enrolled 55 patients (mean age 62 years, 42 males, 13 females) with angiographically proven CAD scheduled for CABG surgery. Vessel specimens retrieved from ascending aorta (as a part of routine proximal venous graft development procedure) and peripheral blood mononuclear cells (PBMC) were evaluated for the transcriptional activity of IL-6 and TNF-alpha (the key cytokines involved in atherosclerosis) and for CMV DNA presence. Polymerase chain reaction reaction was performed in order to detect DNA of CMV as well as IL-6 and TNF-alpha transcriptional activity.

Results: CMV was present in 67.3% of aortic and in 60% of blood specimens accordingly; median level in aorta tissues: 114.63 +/- 116.54, PBMC: 107.89 +/- 132.39; non statistically significant (NS). An inflammatory response expressed as IL-6 and TNF-alpha transcriptional activity equaled in aorta 159.93 +/- 120.15, 299.55 +/- 154.89 and in PBMC: 190.85 +/- 122.08, 249.64 +/- 32.4; (NS). CMV DNA in PBMC was associated with CMV DNA in aortal tissue p = 0.0049. The analysis revealed positive correlation between IL-6 transcriptional activity and CMV DNA titer in aortic samples R = 0.35, p = 0.036. There were no statistically significant correlations between TNF-alpha transcriptional levels and CMV DNA concentration. Statistical analysis was made by use of Statistica 8.0; StatSoft program. We used arithmetical mean value, standard deviation, Spearmann correlation, X2 and U Mann-Whitney test.

Conclusions: A local inflammatory response expressed against CMV could be a marker of longstanding inflammatory response that eventually would cause advanced clinical atherosclerosis. Our findings support the infectious theory and an association between CMV infection and atherosclerosis.