Chlamydia pneumoniae, Herpes simplex virus and Cytomegalovirus in symptomatic and asymptomatic high-grade internal carotid artery stenosis. Does infection influence plaque stability?

Abstract

Our results do not support the hypothesis that systemic Cpn, HSV or CMV- infection or evidence of Cpn-, HSV- or CMV-DNA in carotid plaques causes plaque destabilization and cerebral thromboembolism. Plaque infection could only be observed in cases with advanced atherosclerosis.

Inflammation and Atherosclerosis

“…Similarly, a prospective study comparing serum antibody titers against C pneumoniae, herpes simplex and cytomegalovirus found no differences between patients with symptomatic and asymptomatic ICA stenosis. 76 Moreover, RT-PCR examinations of these infectious agents performed directly on carotid endarterectomy specimens found no association to plaque destabilization. In summary, these findings indicate that infectious agents might play a pathobiological role in the induction and progression of atherosclerosis, but their mere presence cannot account for acute plaque destabilization.…”

“…In search for other autoantigens as potential targets for T cells, the relation between numerous pathogens and atherosclerosis, 70,71 and more specifically plaque destabilization of the carotid artery, has been extensively studied. 60,[72][73][74][75][76] In experimental settings cytomegalovirus infection aggravated atherogenesis in apoEϪ/Ϫ mice by local and systemic immune activation. 77 In patients, elevated antibody titers against Chlamydia pneumoniae, Epstein-Barr virus and herpes simplex type-2 were associated with progression of atherosclerosis as indicated by an increase of intima-media thickness or progression of carotid artery stenosis.…”

<![CDATA[<B>Vulnerability of atherosclerotic carotid disease</B>: <B>from laboratory to operating room - part 2</B>]]>

“…A recent prospective study, analyzing the behavior of the antibodies against chlamydia, herpes virus and cytomegalovirus in 109 patients with carotid stenosis of more than 50%, did not identify differences in serum levels between groups, nor in a comparison between asymptomatic and symptomatic patients, or even comparing the US-CRP levels, making the hypothesis that infectious processes directly determine the instability of existing lesions weaker [76].…”

Bacteria and Coronary Atheroma

“…Recent evidence confirms a greater prevalence of implicated microbes in complicated or advanced lesions. 16 As such, it seems highly unlikely that bacterial infections are either necessary or sufficient to cause coronary atherosclerosis but more probably may participate or promote aspects of atherogenesis in conjunction with conventional triggers such as oxidized LDL.…”