Chlamydia pneumoniae aggravates vein graft intimal hyperplasia in a rat model

<p>Abstract</p> <p>Background</p> <p>Along with angioplasty, autologus vein grafts are commonly used for artery bypass grafting in patients with advanced arterial stenosis and drug-resistant angina pectoris. Although initially a successful procedure, long-term functionality is limited due to proliferation and migration of smooth muscle cells. Like in atherosclerosis, common chronic infections caused by viruses and bacteria may contribute to this process of vein graft failure. Here we investigated the possible role of <it>Chlamydia pneumoniae </it>(<it>Cpn</it>) in the pathogenesis of venous graft failure in an experimental animal model. In 2 groups (n = 10 rats/group), an epigastric vein-to-common femoral artery interposition graft was placed. Immediately thereafter, rats were infected with <it>Cpn </it>(5*10⁸IFU) or injected with control solutions. Rats were sacrificed three weeks after surgery and the grafts were harvested for morphometrical and immunohistochemical analysis.</p> <p>Results</p> <p><it>Cpn </it>administration immediately after vein grafting resulted in a significant increase in medial cross-sectional area, wall thickness and total wall area. There were no significant differences in T-cell or macrophage influx. Likewise, although positive immunostaining for both HSP60 and CRP could be detected, no differences were found between groups. Based on the observation that the number of cells/μm²was also not altered, we conclude that Cpn infection stimulates smooth muscle cell proliferation by hereunto unknown molecular mechanisms, resulting in a significant increase in intimal hyperplasia.</p> <p>Conclusion</p> <p>In conclusion, in a well defined animal model we present here for the first time evidence for a role of <it>Chlamydia pneumoniae </it>in the process of venous graft failure.</p

Endograft-preserving therapy of a patient with Coxiella burnetii-infected abdominal aortic aneurysm: a case report

<p>Abstract</p> <p>Introduction</p> <p><it>Coxiella burnetii</it>, the causative agent of Q fever, may cause endocarditis and vascular infections that result in severe morbidity and mortality. We report a case of a <it>C. burnetii</it>-infected abdominal aorta and its management in a patient with a previous endovascular aortic aneurysm repair.</p> <p>Case presentation</p> <p>A 62-year-old Caucasian man was admitted to our hospital three months after endovascular aortic aneurysm repair with a bifurcated stent graft. He had increasing abdominal complaints and general malaise. A computed tomography scan of his abdomen revealed several para-aneurysmal abscesses. Surgery was performed via midline laparotomy. The entire abdominal wall of his aneurysmal sac, including the abscesses, was removed. The vascular endoprosthesis showed no macroscopic signs of infection. The decision was made to leave the endograft in place because of the severe cardiopulmonary comorbidities, thereby avoiding suprarenal clamping and explantation of this device with venous reconstruction. The proximal and distal parts of the endograft were secured to the aortic wall and common iliac artery walls, respectively, to avoid future migration. Polymerase chain reaction for <it>C. burnetii </it>was positive in all specimens of aortic tissue. Specific antibiotic therapy was initiated. Our patient was discharged in good clinical condition after six days.</p> <p>Conclusions</p> <p>In our patient, the infection was limited to the abdominal aneurysm wall, which was removed, leaving the endograft in place. Vascular surgeons should be familiar with this bailout procedure in high-risk patients.</p

Effect of Cpn administration on total wall (A) cross-sectional area, medial cross-sectional area (B) and wall thickness (C) three weeks after vein grafting

<p><b>Copyright information:</b></p><p>Taken from "aggravates vein graft intimal hyperplasia in a rat model"</p><p>http://www.biomedcentral.com/1471-2180/7/111</p><p>BMC Microbiology 2007;7():111-111.</p><p>Published online 6 Dec 2007</p><p>PMCID:PMC2222630.</p><p></p> * P < 0.05 (values compared with control)

Photomicrographs showing subsequent immunolabeling of a venous bypass graft 3 weeks after surgery (A: CRP, C:HSP60) as well as their representative negative controls (B, D)

<p><b>Copyright information:</b></p><p>Taken from "aggravates vein graft intimal hyperplasia in a rat model"</p><p>http://www.biomedcentral.com/1471-2180/7/111</p><p>BMC Microbiology 2007;7():111-111.</p><p>Published online 6 Dec 2007</p><p>PMCID:PMC2222630.</p><p></p