Ruptured Syphilitic Aneurysm: A Cause of Sudden Death in a Man with Human Immunodeficiency Coinfection.

Syphilis, a sexually transmitted infection caused by the bacterium Treponema palladium, is experiencing a worldwide resurgence. The risk of syphilis infection is particularly high in men who have sex with men (MSM), especially those who are human immunodeficiency virus (HIV)-positive. Untreated syphilis can lead to rare but severe late-stage complications, including syphilitic aortitis. Herein, we present an autopsy case of a ruptured thoracic aneurysm that resulted from an undetected case of syphilitic aortitis in an HIV-positive Japanese MSM with undiagnosed syphilis. Although no syphilitic skin lesions were observed on the body, anatomical changes consistent with a syphilitic etiology were present at the site of the rupture, including medial aortic scarring with "tree-bark"-like atherosclerotic plaque. In addition, heart blood was positive for T. palladium in a latex agglutination test. This case highlights for forensic pathologists the importance of recognizing syphilis as a possible underlying cause of sudden death among HIV-positive MSM.

CCL19-CCR7-dependent reverse transendothelial migration of myeloid cells clears Chlamydia muridarum from the arterial intima.

Regions of the normal arterial intima predisposed to atherosclerosis are sites of ongoing monocyte trafficking and also contain resident myeloid cells with features of dendritic cells. However, the pathophysiological roles of these cells are poorly understood. Here we found that intimal myeloid cells underwent reverse transendothelial migration (RTM) into the arterial circulation after systemic stimulation of pattern-recognition receptors (PRRs). This process was dependent on expression of the chemokine receptor CCR7 and its ligand CCL19 by intimal myeloid cells. In mice infected with the intracellular pathogen Chlamydia muridarum, blood monocytes disseminated infection to the intima. Subsequent CCL19-CCR7-dependent RTM was critical for the clearance of intimal C. muridarum. This process was inhibited by hypercholesterolemia. Thus, RTM protects the normal arterial intima, and compromised RTM during atherogenesis might contribute to the intracellular retention of pathogens in atherosclerotic lesions.

Proliferation of smooth muscle cells stimulated by Porphyromonas gingivalis is inhibited by apple polyphenol.

BACKGROUND: Porphyromonas gingivalis (Pg) is thought to be involved in the progression of occlusive arterial lesions, whereas vascular smooth muscle cell (SMC) proliferation is considered to be involved in occlusive arterial disease. We previously showed that bacteremia caused by Pg infection induced proliferation of mouse aortic SMCs. Furthermore, human SMCs stimulated with human plasma incubated with Pg showed a marked transformation from the contractile to proliferative phenotype. In the present study, we examine the involvement of Pg gingipains and fimbriae in induction of the SMC transformation and proliferation, and effective inhibitors. METHODS: Pg strains including gingipain- and fimbria-null mutants were incubated in human plasma, after which the bacteria were removed and the supernatants were added to cultured SMCs. To evaluate the effects of inhibitors, Pg organisms were incubated in plasma in the presence of apple polyphenol (AP), epigallocatechin gallate, KYT-1 (Arg-gingipain inhibitor), and KYT-36 (Lys-gingipain inhibitor). RESULTS: Plasma supernatants from wild-type and fimbria-mutant cultures markedly stimulated cellular proliferation, whereas those containing gingipain-null mutants showed negligible effects. SMC proliferation was also induced by plasma treated with trypsin. Furthermore, plasma supernatants cultured in the presence of KYT-1/KYT-36 and AP showed significant inhibitory effects on SMC proliferation, whereas cultures with epigallocatechin gallate did not. CONCLUSION: Our results suggest that Pg gingipains are involved in the induction of SMC transformation and proliferation, whereas this was inhibited by AP.

Quantification and location of Chlamydia pneumoniae-specific antigen in the walls of abdominal aortic aneurysms.

BACKGROUND: To evaluate the prevalence and quantity of Chlamydia pneumoniae-specific antigen in the three layers (intima, media, and adventitia) of abdominal aortic aneurysms (AAAs), so as to further investigate the pathogenesis of AAAs. METHODS: Aortic walls were collected from 20 patients with AAA and 11 healthy organ donors. Immunohistochemistry was used to identify the C pneumoniae-specific antigen, and image analysis system was used to quantify and locate it. RESULTS: The positive rate of C pneumoniae-specific antigen was higher in the AAA group than in the control group (100% vs. 54.54%, p = 0.003), positive intensity decreased from the tunica intima to the adventitia in the AAA group (16.32% ± 2.13%, 14.84% ± 1.80%, and 14.25% ± 1.67%, respectively, p = 0.003). In the control group, positive cells were mainly found in focal lesion areas. CONCLUSION: We have demonstrated the presence and differentiation of C pneumoniae-specific antigen in the three layers of AAAs, which are in accordance with pathology, thus suggesting a pathogenic role of the antigen.

[The implication of Chlamydia pneumoniae in damage to human aortic endotheliocytes in atherosclerosis].

A cytological technique was used to study the impressions of the aortic intima of dead patients. Endothelial cell Chlamydia pneumoniae (CP) was detected in 26 (56.5%) of 46 dead patients; the bacterium was found in the unaffected intact intimal areas in 9 (19.6%) cases. Three morphological forms of CP--inclusions, spots, and aggregates were described. The whole life cycle of CP and the specific features of disintegration of the host cell--the endothelium were observed. CP leads to extensive infection and aponecrotic death of all types of endothelial cells above the fatty streaks and plaques. Focal chlamydial destruction of an endothelial layer results in intimal surface erosion and thrombogenesis. An inflammatory response to damaged endothelial cells may be responsible for the initiation and progression of atherosclerosis and plaque destabilization.

Molecular analysis of aortic intimal hyperplasia caused by Porphyromonas gingivalis infection in mice with endothelial damage.

BACKGROUND AND OBJECTIVE: Porphyromonas gingivalis infection is thought to be a significant etiological factor in the development of cardiovascular diseases. However, scant definitive evidence has been presented concerning the pathological molecular mechanisms of these disorders. In the present study, we performed a molecular analysis of the developmental mechanisms of aortic intimal hyperplasia induced by P. gingivalis. MATERIAL AND METHODS: The effects of P. gingivalis-induced bacteremia on intimal hyperplasia were evaluated using a mouse model of aortic hyperplasia created by photochemical-induced endothelial cell injury. Alterations of gene expression profiles in injured blood vessels of the mice were extensively analyzed using DNA microarray assays to identify the key molecules involved in P. gingivalis-induced hyperplasia. In addition, human aneurismal specimens from patients with or without P. gingivalis infection were analyzed histochemically. RESULTS: Intravenous administration of P. gingivalis dramatically induced intimal hyperplasia in the mouse model. Concomitantly, S100 calcium-binding protein A9 (S100A9) and embryonic isoform of myosin heavy chain (SMemb), a proliferative phenotypic marker of smooth muscle cells, were significantly overexpressed on the surfaces of smooth muscle cells present in the injured blood vessels. Similarly, increased expressions of S100A9 and SMemb proteins were observed in aneurismal specimens obtained from P. gingivalis-infected patients. CONCLUSION: We found that bacteremia induced by P. gingivalis leads to intimal hyperplasia associated with overexpressions of S100A9 and SMemb. Our results strongly suggest that oral-hematogenous spreading of P. gingivalis is a causative event in the development of aortic hyperplasia in periodontitis patients.

Upregulation of S100 calcium-binding protein A9 is required for induction of smooth muscle cell proliferation by a periodontal pathogen.

We investigated the effect of a periodontal pathogen, Porphyromonas gingivalis, on human aortic smooth muscle cell (hAOSMC) proliferation as mechanisms of atherosclerosis. Cultured hAOSMCs exposed to the supernatant of plasma incubated with P. gingivalis showed a marked transformation from a contractile to proliferative phenotype, resulting in enhancement of cell growth. DNA microarray analysis revealed a P. gingivalis-dependent upregulation of S100A9 in hAOSMCs. Small interference-RNA for S100A9 dramatically attenuated the effect of P. gingivalis on transformation and proliferation of hAOSMCs. Our data suggested that upregulation of S100A9 mediated by P. gingivalis is an important event in the development of aortic intimal hyperplasia.

Porphyromonas gingivalis infection accelerates intimal thickening in iliac arteries in a balloon-injured rabbit model.

BACKGROUND: Current epidemiologic data suggest that a localized infection (periodontitis) can disseminate into the distant tissues, and subgingival bacteria can migrate in the bloodstream, thereby contributing to independent systemic disease processes. To test this hypothesis, we investigated the effect of repeated systemic inoculations with Porphyromonas gingivalis (Pg) on intimal hyperplasia in iliac arteries in a rabbit model of balloon injury. METHODS: One week after single balloon injury to the iliac artery, 30 male New Zealand rabbits were randomly assigned to intravenous inoculation with 100 microl live Pg (10(7) colony-forming units; n = 15) or vehicle (n = 15) once weekly for 4, 8, or 12 consecutive weeks. Arteries were fixed by perfusion and removed for analysis of neointimal lesion formation. We measured intimal and medial lesion areas in iliac artery cross-sections as well as the intimal/medial ratio (I/M). We also analyzed Pg 16S ribosomal DNA amplification with polymerase chain reaction, systemic proinflammatory mediators with enzyme-linked immunosorbent assay, and immunolocalization of macrophages in the balloon-injured arteries. RESULTS: At 12 weeks, iliac intimal hyperplasia was accelerated, and I/M was significantly increased in Pg-inoculated animals (I/M 3.961 +/- 0.536 in the Pg group versus 3.585 +/- 0.353 in the control animals; P <0.01). Pg-inoculated animals also had significant increases in macrophage infiltration at 12 weeks, C-reactive protein levels at all time points, and interleukin-6 levels at 12 weeks. Moreover, Pg ribosomal DNA was found in the injured arteries of Pg-inoculated animals, but only after 12 weeks. CONCLUSION: Long-term systemic challenge with Pg, an oral pathogen, may accelerate intimal hyperplasia in balloon-injured iliac arteries.

Morphometrical quantification of Chlamydia pneumoniae and Mycoplasma pneumoniae in human atherosclerotic abdominal aortic aneurysms.

OBJECTIVE: Atherosclerotic inflammation with a possible role of infectious agents can contribute to the pathogenesis of abdominal aortic aneurysms (AAA). The finding of Chlamydia pneumoniae (CP) in these lesions in previous non-quantifying studies ranged from 0-100%. The objective is to quantify the presence of CP and Mycoplasma pneumoniae (MP) in AAA. METHODS: The thickness, and the number of cells positive for CP detected by the immunohistochemistry (immunoperoxidase, which is a type of immunohistochemical stain used in molecular biology, medical research, and clinical diagnostics), and the percentage of the area occupied by the Mycoplasma pneumoniae detected by in situ hybridization in three layers of the aorta were measured using an image-analysis system in 10 necropsies of abdominal aneurysmatic aortas. Three groups were used as controls: 1) samples of the same aortas, outside the aneurysms, except if the dilatation took the whole sub-renal portion of the artery (n=7); 2) aortas with severe atherosclerosis but without aneurysms (n=10); 3) aortas without or with mild atherosclerosis (n=10). All specimens were obtained at necropsies. Wald's test was used to compare groups; significance level was established at 5%. RESULTS: The tunica intima was thinner and the tunica media was thicker in the normal cases than in the other groups (p<0.01). Positive cells for CP were found in all groups, more frequently at the adventitia; no significant difference was detected between the groups (p>0.05). MP was also detected in all groups. This agent predominated in the group of patients with atherosclerosis, but without aneurysms at both tunica intima and adventitia; nevertheless, there were no significant differences between the groups (p>0.05). CONCLUSIONS: Our data suggested that the bacteria we focused to, does not play an important role in the pathogenesis of AAA.

Inflammation, heat shock proteins and periodontal pathogens in atherosclerosis: an immunohistologic study.

BACKGROUND: Inflammation is a significant component of atherosclerosis lesions. Bacteria, including periodontopathogens, have been demonstrated in atherosclerotic plaques and cross-reactivity of the immune response to bacterial GroEL with human heat shock protein 60 has been suggested as a link between infections and atherosclerosis. METHODS: In this study, the nature of the inflammatory infiltrate and the presence of human heat shock protein 60 and GroEL were examined in 31 carotid endarterectomy specimens. Additionally, monoclonal antibodies were used to detect the presence of six bacteria, including those implicated in periodontal disease. RESULTS: The inflammatory cell infiltrate of the lesions was dominated by CD14(+) macrophages and CD4(+) T cells. Most cells of the infiltrate as well as the endothelium were HLA-DR(+), indicating activation; however, there was an absence of CD25 expression, demonstrating that the activated T cells were not proliferating. Few CD1a(+) and CD83(+) cells were noted. Human heat shock protein 60 expression was evident on endothelial cells and cells with the appearance of smooth muscle cells and lymphocytes. GroEL and bacteria were detected within intimal cells. Chlamydia pneumoniae, Porphyromonas gingivalis, Fusobacterium nucleatum, Tannerella forsythia, Prevotella intermedia, and Actinobacillus actinomycetemcomitans were found in 21%, 52%, 34%, 34%, 41%, and 17% of arteries, respectively. CONCLUSION: These results give evidence for a specific immune response associated with atherosclerosis. Whether bacteria initiate the observed inflammation in atherosclerotic lesions is not clear; however, the present study shows that maintenance of inflammation may be enhanced by the presence of periodontopathic bacteria.

The effect of bacterial contamination on neointimal hyperplasia in vascular grafts.

Neointimal hyperplasia (NH) is the most significant contributing factor to long-term vascular graft failure. Inflammation is known to be important in its development; however, the role of bacterial infection is unclear. We examined the effect of contamination with common organisms on the development of NH in expanded polytetrafluoroethylene grafts. Thirty adult pigs were randomized into one of four groups: no infection, contamination with Staphylococcus aureus, mucin-producing Staphylococcus epidermidis, or Pseudomonas aeruginosa. An expanded polytetrafluoroethylene graft (6 mm x 3 cm) was placed as a common iliac artery interposition graft and was inoculated with 1-2 x 10(8) of the selected organism before closure. Grafts were explanted 6 weeks postoperatively. Microbiologic, histological, and morphometric evaluations were performed. All grafts were patent at the time of euthanasia. The mean areas of NH were 5.45 mm(2) in sterile grafts, 8.36 mm(2) in S. aureus, 7.63 mm(2) in S. epidermidis, and 11.52 mm(2) in P. aeruginosa grafts. Comparison of means via analysis of variance showed that P. aeruginosa grafts had significantly higher formation of NH than sterile grafts (P = 0.025). NH production in infected grafts appears to be organism specific and is significantly higher with P. aeruginosa than common Gram-positive organisms. Increased NH from subclinical infection may be a significant factor contributing to late graft failures.

Pathogen burden, inflammation, proliferation and apoptosis in human in-stent restenosis. Tissue characteristics compared to primary atherosclerosis.

Pathogenic events leading to in-stent restenosis (ISR) are still incompletely understood. Among others, inflammation, immune reactions, deregulated cell death and growth have been suggested. Therefore, atherectomy probes from 21 patients with symptomatic ISR were analyzed by immunohistochemistry for pathogen burden and compared to primary target lesions from 20 stable angina patients. While cytomegalovirus, herpes simplex virus, Epstein-Barr virus and Helicobacter pylori were not found in ISR, acute and/or persistent chlamydial infection were present in 6/21 of these lesions (29%). Expression of human heat shock protein 60 was found in 8/21 of probes (38%). Indicated by distinct signals of CD68, CD40 and CRP, inflammation was present in 5/21 (24%), 3/21 (14%) and 2/21 (10%) of ISR cases. Cell density of ISR was significantly higher than that of primary lesions (977 +/- 315 vs. 431 +/- 148 cells/mm(2); p < 0.001). There was no replicating cell as shown by Ki67 or PCNA. TUNEL(+) cells indicating apoptosis were seen in 6/21 of ISR specimens (29%). Quantitative analysis revealed lower expression levels for each intimal determinant in ISR compared to primary atheroma (all p < 0.05). In summary, human ISR at the time of clinical presentation is characterized by low frequency of pathogen burden and inflammation, but pronounced hypercellularity, low apoptosis and absence of proliferation.

Detection of Chlamydophila pneumoniae in dendritic cells in atherosclerotic lesions.

Dendritic cells (DCs) populate atherosclerotic lesions and might be involved in the regulation of immune reactions in atherosclerosis. The present work was undertaken to examine a possible association of DCs with Chlamydophila pneumoniae in human atherosclerotic plaques obtained by endarterectomy. C. pneumoniae was identified in 17 of 60 (28%) atherosclerotic plaques by a combination of immunohistochemistry and polymerase chain reaction (PCR). Double immunohistochemistry identified the presence of C. pneumoniae within S100(+) DCs that were localised predominantly in the deep layer of the intima under the necrotic core. Quantitative analysis showed that there were no differences in the numbers of DCs between C. pneumoniae(+) and C. pneumoniae(-) groups of atherosclerotic specimens. There were also no differences in the expression of Lag-antigen and HLA-DR by DCs between the groups of specimens. Markers of DC activation CD80 and CD86 were absent from both groups of specimens. Flow cytometry analysis of the effects of C. pneumoniae infection on immature monocyte-derived DCs in vitro showed no changes in the expression of CD1a, MHC class II, CD80 and CD86. The results of this study demonstrate that C. pneumoniae might infect DCs within the atherosclerotic intima but whether the presence of C. pneumoniae in DCs affects the intensity of immune reactions in atherosclerosis needs further clarification.

[Prevalence of intimal pathogen burden in acute coronary syndromes]. / Prävalenz von intimalem Pathogen burden bei akutem Koronarsyndrom.

Increasing evidence supports a link between serological evidence of prior exposure to infectious pathogens, pathogen burden, and the risk for future myocardial infarction and death in patients with coronary artery disease. Based on this concept, we evaluated the intimal presence of four pathogens in human coronary atheroma, clinically associated with acute coronary syndromes (ACS) and stable angina (SA), and the effect of pathogen burden on the expression of human heatshock protein 60 (hHSP60), a key protein in (auto-)immune pathogenesis of atherosclerosis. Coronary atherectomy specimens retrieved from 53 primary target lesions of patients with ACS (n=33) or SA (n=20) were assessed immunohistochemically for the presence of Chlamydia pneumoniae (C. pn.), Helicobacter pylori (H.p.), Cytomegalovirus (CMV) and Epstein-Barr Virus (EBV), and for the expression of hHSP60. Chlamydia pneumoniae was present in 74%, Helicobacter pylori in 32%, CMV in 13% and EBV in 42%. Exclusively C.pn. revealed a prevalence in ACS (91%) vs SA (45%; p<0.001). Immunohistochemical analysis revealed 6 lesions without, 21 lesions with 1, 17 lesions with 2, 6 lesions with 3 and 3 lesions with 4 infectious agents. As an important finding, the mean value in ACS lesions was significantly increased compared to those in SA (1.9 vs 1.1; p<0.01). ACS-subgroup analysis revealed the highest mean value in patients with pain at rest within the last two days (Braunwald class III). In addition, expression of hHSP60 was significantly higher in ACS (8.7%) compared to SA (1.3%; p<0.001). Pathogen burden correlated highly significant (p<0.01) with the expression of hHSP60 (r=0.44).Our data demonstrate the impact of intimal pathogen burden in plaque instability, and suggest the presence of (auto-)immunoreactions against upregulated hHSP60 as an important pathomechanism that may contribute to acute coronary syndromes.

High prevalence of Chlamydia pneumoniae antibodies in white-coat hypertensives.

Previous studies have linked essential sustained hypertension with Chlamydia pneumoniae (C. pneumoniae) and changes in intima-media thickness (IMT) of carotid arteries. The aim of this study was to examine if similar associations exist in subjects with white-coat hypertension. C. pneumoniae IgA and IgG antibody titers were measured in 125 patients with white-coat hypertension and 54 normotensives. All participants underwent a 24 h ambulatory blood pressure (BP) monitoring, clinic BP readings and common-internal carotid artery IMT measurements. Seventy subjects of the white-coat group (56%) and 15 of the control group (27.8%) had IgG titers >/=80 (crosstabs; P<0.001). IgA titers were elevated in 75 subjects of the white-coat group (60%) and 10 (18.5%) of the control group (crosstabs; P<0.001). The IMT of the carotid arteries in the white-coat group was significantly higher than that of the normotensive group (t-test; P<0.001 and P<0.001, respectively). In contrast, carotid IMT did not differ between C. pneumoniae-seropositive and C. pneumoniae-seronegative groups concerning both IgG and IgA antibody titers. Our findings suggest that both C. pneumoniae antibody titers and carotid IMT were increased in subjects with white-coat hypertension. The preceding associations strengthen prior evidence in favor of the opinion that white-coat hypertension is not an innocent phenomenon.

Early atherosclerosis and Chlamydia pneumoniae infection in the coronary arteries.

In non-atheromatous segments of coronary arteries a sequence of preatherosclerotic changes was identified which consisted of medial thickening followed by intimal thickening. More recently, Chlamydia pneumoniae seropositivity was associated with enhanced intima-media thickness of arteries. In the present study the intimal and medial thickness of coronary artery of young adults were measured, and were correlated with the presence of Chlamydia pneumoniae antigens. Proximal and distal segments of the left anterior descending coronaries (LAD) obtained at autopsy from young adults (15-34 years) were studied. The thickness and cellular density of the intima and of the media without clear-cut atherosclerotic changes were measured by image analysis. The hypertrophy index was calculated as the ratio of cell density and the thickness of the respective layer. Atherosclerotic lesions occurring elsewhere in the same coronary were noted and graded by severity. The presence of Chlamydia pneumoniae verified by immunohistochemistry was correlated with the severity of lesions and with the hypertrophy index. In the proximal segments, atherosclerosis of LAD was associated with the widening of both the intima and the media of lesion free-sites. In the distal coronary segments the proportion of the intimal thickening had a significant association with atherosclerosis. Compared to non-infected arteries, Chlamydia pneumoniae infection was associated with higher hypertrophy index in the intima as well as in the media. The rate of Chlamydia pneumoniae positivity increased with the severity of lesions. As a conclusion: in the LAD coronary, the intimal thickening is the main preatherosclerotic change. Chlamydia pneumoniae may favour arterial wall hypertrophy and plays a role in lesion progression.

The adventitia of atherosclerotic coronary arteries frequently contains Chlamydia pneumoniae.

The presence of Chlamydia pneumoniae in the human arterial system has mainly been determined in atherosclerotic plaque, whereas the adventitia has remained relatively unexplored. We assessed the presence of C. pneumoniae in all three vessel wall layers of coronary (n=72) and brachial (n=48) arteries in relation to local atherosclerosis. Immunohistochemical staining of C. pneumoniae was observed in plaque and adventitia. Cells stained for C. pneumoniae were detected in the same areas as cells stained for macrophages in adjacent sections. C. pneumoniae staining in the adventitia was associated with the extent and severity of atherosclerosis. Coronary sections with C. pneumoniae staining in both adventitia and plaque more often contained advanced atherosclerosis than sections with staining only in the adventitia. Staining was observed more often in the coronary artery than in the brachial artery (24/72 vs. 5/48 and 51/72 vs. 8/48 for plaque and adventitia, respectively, P=0.004 and P<0.001). PCR confirmed the presence of C. pneumoniae DNA in the adventitia. In summary, the adventitia of atherosclerotic coronary arteries frequently contains C. pneumoniae that seems to be located within macrophages. These results might indicate a possible route for infected circulating macrophages to home into atherosclerotic lesions in the artery via vasa vasorum.

Chlamydia pneumoniae seropositivity is associated with carotid artery intima-media thickness.

BACKGROUND AND PURPOSE: Infection may both augment the atherosclerotic process and contribute to later manifestations of overt clinical disease. Chlamydia pneumoniae elementary bodies have been detected in atherosclerotic lesions. The aim of the present study was to investigate whether elevated titers of antibodies and circulating immune complexes to C pneumoniae were associated with ultrasound findings indicating presence of atherosclerosis in the carotid artery. METHODS: Serum titers of antibodies to C pneumoniae (IgM, IgA, IgG, and circulating immune complex) were related to intima-media thickness (IMT) and plaque status measured by B-mode ultrasound in the carotid artery in 113 men with treated hypertension and at least 1 of the following risk factors: hypercholesterolemia, smoking, or diabetes. RESULTS: Any of the titers was elevated in 56 (50%) men, and common carotid artery IMT was thicker in this group compared with the 57 men without any elevated titers (1.00 versus 0.92 mm, P<0.05). There were no accompanying differences in blood pressure, lipid levels, blood glucose, or smoking. Elevation of separate antibody types and circulation immune complex were also associated with increased IMT. In the latter group, systolic blood pressure was higher among seropositive patients compared with those who had no circulating immune complex. Seropositivity was not related to plaque status. CONCLUSIONS: Seropositivity for C pneumoniae was associated with an increased intima-media thickness in the common carotid artery but not plaque status in hypertensive men at high risk for cardiovascular disease.

Does focal destruction of the thoracic aorta wall by Staphylococcus aureus lead to the development of infected aneurysms? An experimental study.

OBJECTIVE: The infrequency of infected aneurysms suggests that either infection of segments of the aortic wall is uncommon, or that infections do not always lead top infected aneurysm formation. The purpose of the study was to determine whether focal Staphylococcus aureus infection of aortic wall segments leads consistently to the development of infected aneurysms and to evaluate the segments in which infection did not lead to the infected aneurysm formation. METHODS: Twenty pigs were inoculated with 0.1 ml of a Staphylococcus aureus inoculum in three segments of the thoracic aorta wall (study group). In another 10 pigs, 0.1 ml of saline solution was injected in three segments of the thoracic aorta wall (control group). STUDY GROUP: histological abnormalities and bacterial culture of the inoculation sites were evaluated at 10 days (n = 5 pigs), 30 days (n = 5 pigs), and 90 days (n = 10 pigs). CONTROL GROUP: histological abnormalities were evaluated at 10 days (n = 5 pigs) and 90 days (n = 5 pigs). STUDY GROUP: infected aneurysms developed in only two animals killed at 30 days. At 90 days, destruction of the elastic tissue, scar tissue and neointima formation were found in all the aortic segments studied. CONTROL GROUP: no significant changes were found in any of the segments evaluated. CONCLUSION: In our experimental model, acute local infection by S. aureus caused the development of infected aortic aneurysm in only 10% of the animals. In the remaining 90%, healing of the site of infection followed resolution of the infection.