Chlamydia pneumoniae aggravates vein graft intimal hyperplasia in a rat model

Cpn 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/μm2 was 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.In conclusion, in a well defined animal model we present here for the first time evidence for a role of Chlamydia pneumoniae in the process of venous graft failure.Besides internal mammary arteries, autologus saphenous vein grafts are commonly used for coronary artery bypass grafting (CABG) in angina pectoris patients, resistant to aggressive medical therapy or patients with advanced coronary artery stenosis not suitable for percutaneous transluminal coronary angioplasty (PTCA). Although the initial results of venous grafts are excellent, the symptoms tend to recur due to vein graft degeneration and stenosis greatly limiting the long term success of bypass surgery. Early failure occurs within the first 1 to 2 months probably from primary thrombosis often due to technical failure or poor runoff in severely stenotic distal coronary arteries [1]. Late failure occurs from several months to years after bypass surgery and is caused by neointimal hyperplasia (NIH) with subsequent atherosclerosis in the saphenous vein graft [2]. NIH, defined as the accumulation of phenotypically altered medial smooth muscle cells (SMC) and extracellular matrix in the intimal component of the vein, is most prominent in the venous graft within the first year. Several factors interact to influence the development of NIH mostly initiated by ischemia of the venous wall, mechanical trauma and hemodynamic