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Published on: May 7, 2012
Cytomegalovirus and proliferative signals in the vascular wall of CABG patients
M Westphal1, I Lautenschlager, C Backhaus
1Department of Cardiac Surgery, University of Rostock, Rostock, Germany.
Insights
Human cytomegalovirus (CMV) infection in aortic smooth muscle cells promotes atherosclerosis by increasing growth factors and endothelial activation. Traditional risk factors enhance CMV manifestation, suggesting CMV’s role in atherosclerosis progression.
Area of Science:
- Cardiovascular Research
- Infectious Diseases
- Pathology
Background:
- Atherosclerosis is a complex disease influenced by various factors.
- The role of human cytomegalovirus (CMV) in promoting atherosclerosis requires further elucidation.
- Understanding CMV's impact on vascular inflammation is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the mechanism by which CMV may promote atherosclerosis.
- To examine the expression of inflammatory and proliferative signals in the aortic wall of CMV-positive and CMV-negative patients undergoing coronary artery bypass grafting (CABG).
Main Methods:
- Aortic biopsies and blood samples from 68 CABG patients were analyzed for CMV-DNA using PCR and in situ hybridization.
- Immunohistochemistry was employed to assess the expression of pp65 antigen, adhesion molecules (ICAM-1, VCAM-1, E-selectin), growth factors (PDGF-AA, TGF-beta), and Ki-67.
- Logistic regression analysis correlated CMV presence with vascular inflammation and traditional atherosclerosis risk factors.
Main Results:
- CMV-DNA was detected in the aortic tissue of 76% of patients, primarily within vascular smooth muscle cells.
- CMV-positive patients exhibited increased expression of adhesion molecules and growth factors in the aortic endothelium compared to CMV-negative patients.
- Elevated C-reactive protein (CRP), adhesion molecules, and growth factors correlated positively with CMV presence. Female gender, smoking, and hyperlipidemia were identified as risk factors for CMV positivity.
Conclusions:
- CMV-DNA in smooth muscle cells stimulates local growth factor production and endothelial activation, contributing to atherosclerosis progression.
- Traditional atherogenic risk factors increase the likelihood of aortic CMV manifestation.
- CMV plays a significant role in mediating the progression of atherosclerosis.
Objective:
To further elucidate the mechanism by which cytomegalovirus (CMV) may promote atherosclerosis, we studied the expression pattern of cellular inflammatory and proliferative signals in the aortic wall of CMV(+) and CMV(-) patients undergoing coronary artery bypass grafting (CABG).
Methods:
Aortic biopsies and blood samples of 68 CABG patients were investigated for CMV-DNA by PCR and IN SITU hybridisation. Expression of pp65 antigen, adhesion molecules (ICAM-1, VCAM-1, E-selectin), growth factors (PDGF-AA, TGF-beta), and the cellular proliferation factor Ki-67 was studied by immunohistochemistry. Logistic regression was used to test the correlation between the presence of CMV, vascular inflammation, and traditional noninflammatory risk factors for atherosclerosis.
Results:
CMV-DNA was detected in the aortic tissue of 52 (76%) patients, and was localised predominantly in vascular smooth muscle cells. In CMV(+) patients, the expression of adhesion molecules and growth factors in the aortic endothelium was increased compared with CMV(-) patients. A positive correlation of elevated CRP, the induction of adhesion molecules and growth factors and CMV(+) was found. Female gender, smoking, and hyperlipidaemia were identified as risk factors for CMV(+).
Conclusions:
CMV-DNA in smooth muscle cells induces local growth factor expression as well as endothelial activation, both of which can promote the progression of atherosclerosis. Since traditional atherogenic risk factors increase the likelihood of aortic CMV manifestation, we suggest that CMV plays a crucial role in mediating the progression of atherosclerosis.
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