Surgery for acquired cardiovascular disease: antiseptic treatment of contaminated vein grafts.

AIM: Saphenous vein grafts harvested for use as bypass conduits can be contaminated intraoperatively, e.g. by being inadvertently dropped to the floor of the operating room (OR). This study was performed to investigate microorganisms most likely contaminating vein grafts and to assess the possible efficacy of measures to treat potentially contaminated vein grafts antiseptically for further use. METHODS: In a first step we determined the microbiological flora of the OR using surface cultures and cultures from intentionally dropped vein grafts. Several antiseptic agents (PVP-iodine 10%, octenidinhydrochloride 0.1%, polyhexanide 1%) were evaluated for their in vitro efficacy to disinfect artificially contaminated vein segments. The most promising antiseptic regimen was tested on veins contaminated in a real OR setting. Finally, we tested for possible alterations in mechanical properties of the veins caused by antiseptic treatment. RESULTS: Coagulase-negative staphylococci where the predominant bacteria recovered from the OR with 59.9%. Antiseptic treatment with a combination of octenidine and PVP-iodine resulted in a higher rate of negative cultures than any single agent. Treatment of 50 saphenous vein grafts contaminated in the OR with the combination regimen resulted in only 3 positive cultural results within 7 days. Mechanical tear-stress testing comparing antiseptically treated vein grafts with controls showed no difference in their resistance to tear stress. CONCLUSION: Antiseptic treatment of contaminated vein grafts was shown to be effective in a high percentage of cases without altering mechanical properties of grafts and may be an option for the surgeon in case of a contamination.

Harvest surgical site infection following coronary artery bypass grafting: risk factors, microbiology, and outcomes.

BACKGROUND: Our goals were to evaluate the risk factors predisposing to saphenous vein harvest surgical site infection (HSSI), the microbiology implicated, associated outcomes including 30-day mortality, and identify opportunities for prevention of infection. METHODS: All patients undergoing coronary artery bypass grafting (CABG) procedures from January 2000 through September 2004 were included. Data were collected on preoperative, intraoperative, and postoperative factors, in addition to microbiology and outcomes. RESULTS: Eighty-six of 3578 (2.4%) patients developed HSSI; 28 (32.6%) of them were classified as deep. The median time to detection was 17 (range, 4-51) days. An organism was identified in 64 (74.4%) cases; of them, a single pathogen was implicated in 50 (78%) cases. Staphylococcus aureus was the most frequently isolated pathogen: 19 (38% [methicillin-susceptible S aureus (MSSA) = 12, methicillin-resistant S aureus (MRSA) = 7]). Gram-negative organisms were recovered in 50% of cases, with Pseudomonas aeruginosa predominating in 11 (22%) because of a single pathogen. Multiple pathogens were identified in 14 (22%) cases. The 30-day mortality was not significantly different in patients with or without HSSI. Multivariate analysis showed age, diabetes mellitus, obesity, congestive heart failure, renal insufficiency, and duration of surgery to be associated with increased risk. CONCLUSION: Diabetes mellitus, obesity, congestive heart failure, renal insufficiency, and duration of surgery were associated with increased risk for HSSI. S aureus was the most frequently isolated pathogen.

Increased infiltration of Chlamydophila pneumoniae in the vessel wall of human veins after perfusion.

BACKGROUND: Several studies have suggested an association between Chlamydophila pneumoniae (Cp) infection and atherosclerosis. A recent study detected Cp DNA in the saphenous vein of 12% of all patients before bypass grafting and in 38% of failed grafts. We used a system in which human veins were perfused with autologous blood under arterial pressure. MATERIALS AND METHODS: Veins were surplus segments of saphenous veins of coronary artery bypass grafting (CABG) patients. Vein grafts were perfused with the blood of the same patient after CABG procedures. Veins were analysed for Cp-specific membrane protein using immunohistochemical and PCR analysis. Veins were analysed before and after perfusion (up to 4 h). The number of Cp positive cells was then quantified in the vein layers. RESULTS: Cp protein was detected within macrophages only. In non-perfused veins, Cp was present in the adventitia in 91% of all patients, in the circular (64%) and longitudinal (23%) layer of the media. No positivity was found in the intima. Perfusion subsequently resulted in a significant increase of Cp positive cells within the circular layer of the media that, however, differed strongly between different patients. Cp DNA was not detected by PCR in those specimens. CONCLUSION: Cp protein was present in 91% of veins, but the number of positive cells differed remarkably between patients. Perfusion of veins resulted in increased infiltration of Cp into the circular layer. These results may point to a putative discriminating role of Cp with respect to graft failure between different patients.

Prevalence of periodontal pathogens in subgingival lesions, atherosclerotic plaques and healthy blood vessels: a preliminary study.

BACKGROUND AND OBJECTIVE: Previous studies have reported different periodontal bacteria in atherosclerotic lesions, but their involvement in plaque formation remains unclear. The aim of the present study was to investigate the presence of 20 periodontal bacteria in atherosclerotic samples and healthy blood vessels (used as controls) and to clarify their relationship in regard to clinical and bacteriological periodontal status. MATERIAL AND METHODS: The day before vascular surgery the patients had a thorough periodontal examination and bacteriological samples were taken from periodontally diseased sites. Atheromatous plaques, internal mammary arteries and saphenous veins were harvested during surgery. A DNA-DNA hybridization procedure was used to screen periodontal and vascular samples for the 20 selected bacterial species. RESULTS: Periodontal samples from the severe periodontitis group were found to have a higher prevalence and biomass of bacterial species than the moderate periodontitis group. In vessel samples, the prevalence of the same 20 bacterial species analyzed together was similar in the two groups, except for saphenous veins. CONCLUSION: The presence of periodontal pathogens in atherosclerotic plaques and in apparently healthy vessels appeared to reflect a higher level of bacteremia rather than infection of endothelial cells.

No evidence for a direct role of Helicobacter pylori and Mycoplasma pneumoniae in carotid artery atherosclerosis.

BACKGROUND: That infections with certain pathogens, by initiating an inflammatory response, may contribute to the development of atherosclerosis is suggested by clinical and experimental evidence. AIM: To analyse atherosclerotic plaques of the carotid artery, samples of apparently healthy greater saphenous veins and circulating leucocytes from the same individual patients for the presence of Helicobacter pylori and Mycoplasma pneumoniae. METHODS: Samples from 36 patients undergoing carotid endarterectomy for symptomatic carotid artery stenosis were analysed by polymerase chain reaction for the presence of DNA specific for H. pylori and M. pneumoniae. IgG antibody titres against H. pylori and M pneumoniae and plasma levels of soluble E-selectin, soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 were determined. RESULTS: M. pneumoniae-specific DNA was detected in the atherosclerotic plaques of 13 of 36 (36.1%) patients, in the saphenous veins of 9 of 36 (25%) patients and in the leucocytes of 27 of 36 (75%) patients. No salient association was observed between the presence of M. pneumoniae-specific DNA in leucocytes and atherosclerotic plaques or veins. A marked correlation between the presence of M. pneumoniae in the respective specimens and the studied inflammatory markers or the presence of anti-M. pneumoniae antibodies was not observed. H. pylori-specific DNA could not be detected in the specimens tested. CONCLUSIONS: The absence of H. pylori and the random distribution of M. pneumoniae in tissue samples obtained from patients with symptomatic carotid artery stenosis do not support a role for these pathogens in the development of atherosclerosis due to a direct interaction of the bacteria with the vasculature.

Rupture of a saphenous vein coronary artery bypass graft due to Aspergillus necrotizing vasculitis.

We present the first, unusual case of a lethal mediastinal hemorrhage caused by rupture of a saphenous vein aortic coronary bypass graft due to Aspergillus species necrotizing vasculitis in an immunocompetent patient 18 days after redo coronary artery bypass surgery. The patient had neither signs for mediastinitis nor for another source of Aspergillus infection.

Liposomal entrapment of cefoxitin to improve cellular viability and function in human saphenous veins.

Liposomal cefoxitin was prepared and applied to the pretreatment of human saphenous vein (HSV) for implantation. The possible use of liposomal cefoxitin to improve cellular viability and function and to maintain its potential sterilization effect was investigated. Entrapment efficiency and size distribution of liposomal cefoxitin were 75.7% and 652 +/- 75.7 nm, respectively. The weight ratio between cefoxitin and liposome was calculated at 1 : 40.6. When cefoxitin was entrapped with liposome, the released amount of cefoxitin was not affected by temperature conditions (37 degrees C, 25 degrees C, and 4 degrees C). The amount of free cefoxitin present in HSV reached 59% at 0.5 h and gradually decreased with time, while liposomal cefoxitin showed a maximum amount (63%) at 1.5 h, indicating that liposomal cefoxitin seemed to control the initial amount of cefoxitin present in HSV. Liposomal cefoxitin showed better viabilities of whole cells and endothelial cells dissociated from HSV than free cefoxitin and remarkably superior function of endothelial cells, as determined by Griffonia simplicifolia agglutinins-fluorescein isothiocyanate/propidium iodide double-staining methods combined with flow cytometry and endothelial nitric oxide synthase assay, respectively. In terms of sterilization effect, there was no significant difference between liposomal cefoxitin and free cefoxitin. These results suggest that liposomal entrapment of cefoxitin could improve cellular viability and functions and maintain the original sterilization effect.

Chlamydia pneumoniae in carotid artery atherosclerosis: a comparison of its presence in atherosclerotic plaque, healthy vessels, and circulating leukocytes from the same individuals.

BACKGROUND AND PURPOSE: There is growing clinical and experimental evidence that infections with Chlamydia pneumoniae might contribute to the development and progression of atherosclerosis. However, studies detecting the pathogen in atherosclerotic lesions examined either only atherosclerotic vessels or control vessels without atherosclerosis obtained from a different group of individuals. We analyzed atherosclerotic plaques of the carotid artery, samples of apparently healthy greater saphenous veins, and circulating leukocytes from the same individual patients for the presence of C pneumoniae. METHODS: From each of 46 patients undergoing carotid endarterectomy for symptomatic carotid artery stenosis, these samples were analyzed by nested polymerase chain reaction for C pneumoniae-specific DNA. Furthermore, we determined IgA and IgG titers specific for the pathogen and plasma levels of C-reactive protein in these patients. RESULTS: C pneumoniae DNA was detected in 86.9% of the leukocytes and in 82.6% of the atherosclerotic plaques but in only 6.5% of the saphenous veins. In 85% of patients who also had leukocytes positive for C pneumoniae, the atherosclerotic plaques were positive and the saphenous veins were negative. The presence of C pneumoniae-specific DNA in leukocytes significantly coincided with the presence of the respective DNA in the plaques of the carotid arteries (P=0.0002). No association between the presence of C pneumoniae and specific IgA or IgG levels was seen. C-reactive protein levels were significantly higher in patients with chlamydia-positive atherosclerotic plaques and with positive leukocytes than in patients with negative plaques of the carotid arteries or negative leukocytes, respectively (P<0.01, P<0.05). CONCLUSIONS: Our observation of >80% incidence of C pneumoniae in atherosclerotic plaques of the carotid artery does not prove causality between an infection with the pathogen and the development of atherosclerosis. It must be emphasized, however, that >90% of apparently healthy saphenous veins were negative for C pneumoniae. Given the structural and functional differences between veins and arteries, careful interpretation of our results regarding a possible causative role of C pneumoniae seems warranted.

Chlamydia pneumoniae in infrequently examined blood vessels.

AIM: To determine the prevalence of Chlamydia pneumoniae DNA in infrequently examined blood vessels. METHODS: Vessels obtained from 15 men and six women at coronary artery bypass surgery were tested by a nested polymerase chain reaction (PCR) assay for C pneumoniae DNA. RESULTS: Chlamydia pneumoniae DNA was detected in four of six atheromatous ascending aorta specimens but in none of eight non-atheromatous aorta specimens, in six of 11 atheromatous internal mammary artery specimens but in none of seven non-atheromatous internal mammary artery specimens, in five of seven long saphenous vein specimens showing evidence of disease but in none of 12 specimens without evidence of disease, and in two of three previously grafted veins. Overall, C pneumoniae occurred significantly more often in diseased than in normal vessels (p = < 0.00001). CONCLUSIONS: Chlamydia pneumoniae is often present in diseased areas of arteries, including the internal mammary arteries, and even in diseased areas of veins. It is not present in apparently healthy areas of either type of vessel.

Detection of Chlamydia pneumoniae but not cytomegalovirus in occluded saphenous vein coronary artery bypass grafts.

BACKGROUND: A causal relation between atherosclerosis and chronic infection with Chlamydia pneumoniae and/or cytomegalovirus (CMV) has been suggested. Whether the unresolved problem of venous coronary artery bypass graft occlusion is related to infection with C pneumoniae and/or CMV has not been addressed. METHODS AND RESULTS: Thirty-eight occluded coronary artery vein grafts and 20 native saphenous veins were examined. Detection of C pneumoniae DNA was performed by use of nested polymerase chain reaction (PCR). Homogenisates from the specimen were cultured for identification of viable C pneumoniae. Both conventional PCR and quantitative PCR for detection of CMV DNA were applied. Differential pathological changes (degree of inflammation, smooth muscle cell proliferation [MIB-1]) were determined and correlated to the detection of both microorganisms. C pneumoniae DNA could be detected in 25% of occluded vein grafts. Viable C pneumoniae was recovered from 16% of occluded vein grafts. Except for 1 native saphenous vein, all control vessels were negative for both C pneumoniae detection and culture. All pathological and control specimens were negative for CMV DNA detection. Pathological changes did not correlate with C pneumoniae detection. CONCLUSIONS: Occluded aorto-coronary venous grafts harbor C pneumoniae but not CMV. The detection of C pneumoniae in occluded vein grafts warrants further investigation.