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1.  Detection of Chlamydia pneumoniae and Helicobacter pylori DNA in Human Atherosclerotic Plaques by PCR 
Journal of Clinical Microbiology  2000;38(12):4408-4411.
Chlamydia pneumoniae and Helicobacter pylori can cause persistent infections of the respiratory and gastrointestinal tract, respectively. It has been suggested that persistent infection of arteries with these bacteria can contribute to the development of atherosclerosis. The aims of this study were to determine the presence of C. pneumoniae and H. pylori DNA in atherosclerotic plaque samples by PCR and to evaluate the correlation between clinical status and DNA positivity of these bacteria. Eighty-five consecutive patients (mean age, 59 ± 10; 75 male, 10 female) undergoing coronary artery bypass grafting, carotid endarterectomy, and surgery of the abdominal aorta for atherosclerotic obstructive lesions were included in the study. Forty-six endarterectomy specimens from the atherosclerotic lesions and 39 specimens from healthy regions of the ascending aorta, which were accepted as the control group, were excised. The presence of microorganism DNA in endarterectomy specimens was assessed by PCR. C. pneumoniae DNA was found in 12 (26%) of 46 endarterectomy specimens and none of the healthy vascular-wall specimens (P < 0.001), while H. pylori DNA was found in 17 (37%) of 46 endarterectomy specimens and none of the controls (P < 0.001). Either C. pneumoniae or H. pylori DNA was positive in 23 (50%) of 46 patients and none of the controls (P < 0.001). Six of the atherosclerotic lesions showed coexistence of both of the microorganism DNAs. The presence of C. pneumoniae and H. pylori DNA in a considerable number of atherosclerotic plaques but their absence in healthy vascular wall supports the idea that they may have a role in the development of atherosclerosis, especially in countries where infection is prevalent and where conventional risk factors fail to explain the high prevalence of atherosclerotic vascular disease.
PMCID: PMC87613  PMID: 11101572
2.  No detection of Helicobacter pylori in atherosclerotic plaques in end stage renal disease patients undergoing kidney transplantation 
Indian Journal of Nephrology  2013;23(4):259-263.
Chronic infection known to be a predisposing factor for the development of atherosclerosis. Several studies have found a possible role of Helicobacter pylori in the pathogenesis of atherosclerosis. The aim of this study was to investigate the presence of H. pylori in atherosclerotic plaques in iliac arteries in 25 end stage renal disease (ESRD) patients undergoing kidney transplantation. Esophagogastroduodenoscopy was performed in all patients before transplantation. Biopsy specimens obtained from gastric antrum were sent for pathologic evaluation. Gastric H. pylori infection was confirmed by microscopic assessment and rapid urease test. Arterial specimens were obtained from iliac arteries during kidney transplantation. Presence of H. pylori DNA in atherosclerotic plaques and healthy vessel samples was evaluated by the polymerase chain reaction (PCR). The mean age of patients was 44.1 ± 22.6 years. Risk factors in patients with atherosclerosis were hypertension (68%), diabetes mellitus (20%), hyperlipidemia (20%), positive family history (16%). Atherosclerotic plaques were found in 21 (84%) patients. PCR analysis did not detect H. pylori in any case. There was a significant relationship of atherosclerosis with hypertension (P = 0.006) but not with diabetes mellitus and hyperlipidemia (P = 0.5). There was no significant relationship between atherosclerosis and gastric H. pylori infection (P = 0.6). This study revealed no association between the presence of H. pylori as a pathogen of vessel walls and atherosclerosis in ESRD.
PMCID: PMC3741968  PMID: 23960340
Atherosclerosis; end stage renal disease; helicobacter pylori; kidney transplantation
3.  Detection of Chlamydia pneumoniae but not Helicobacter pylori in atherosclerotic plaques of aortic aneurysms. 
Journal of Clinical Microbiology  1996;34(11):2766-2769.
Recent reports suggest an association between Chlamydia pneumoniae and Helicobacter pylori bacteria and atherosclerosis. We studied 51 patients (mean age, 68.3 years) who underwent abdominal aortic aneurysm surgery. For each patient we performed a microimmunofluorescence test for immunoglobulin G (IgG), IgA, and IgM antibodies to C. pneumoniae specific antigen (TW-183). Anti-H. pylori antibodies were determined by means of an EIA-G test. Each aortic aneurysm surgical specimen was sampled into multiple sections of 0.3 cm2 each and frozen at -20 degrees C. Two samples of each aneurysm were used for a nested PCR with two sets of C. pneumoniae and two sets of H. pylori specific primers. Specimens were treated with a solution containing 20 mM Tris-HCl, Tween 20-Nonidet P-40 (0.5% [vol/vol] each), and 100 micrograms of proteinase K per ml and incubated at 60 degrees C for 1 h and at 98 degrees C for 10 min. DNA was extracted twice with phenol-chloroform-isoamylic alcohol and precipitated with sodium acetate-ethanol by standard methods. Forty-one patients were seropositive for C. pneumoniae with past-infection patterns in 32 patients (16 < or = IgG < 512; 32 < or = IgA < 256) and high antibody titers in 9 patients (IgG > or = 512). In 26 of 51 patients, C. pneumoniae DNA was detected in aortic aneurysm plaque specimens. Of these patients, 23 had a serologic past-infection pattern, 2 had an acute reinfection pattern, and 1 was seronegative. Forty-seven of 51 patients were seropositive for H. pylori. In all cases PCR showed no evidence of H. pylori presence in plaque specimens. This study provides data on a possible C. pneumoniae involvement in the pathogenesis of aortic aneurysm and additional evidence for an association between this agent and atherosclerosis. Conversely, notwithstanding a high H. pylori seroprevalence observed, our results tend to rule out the possibility of a direct involvement of H. pylori in atherosclerosis.
PMCID: PMC229401  PMID: 8897180
4.  Non-detection of Chlamydia species in carotid atheroma using generic primers by nested PCR in a population with a high prevalence of Chlamydia pneumoniae antibody 
The association of Chlamydia pneumoniae with atherosclerosis is controversial. We investigated the presence of C. pneumoniae and other Chlamydia spp. in atheromatous carotid artery tissue.
Forty elective carotid endarterectomy patients were recruited (27 males, mean age 65 and 13 females mean age 68), 4 had bilateral carotid endarterectomies (n= 44 endarterectomy specimens). Control specimens were taken from macroscopically normal carotid artery adjacent to the atheromatous lesions (internal controls), except in 8 cases where normal carotid arteries from post mortem (external controls) were used. Three case-control pairs were excluded when the HLA DRB gene failed to amplify from the DNA. Genus specific primers to the major outer membrane protein (MOMP) gene were used in a nested polymerase chain reaction (nPCR) in 41 atheromatous carotid specimens and paired controls. PCR inhibition was monitored by spiking with target C. trachomatis. Atheroma severity was graded histologically. Plasma samples were tested by microimmunofluorescence (MIF) for antibodies to C. pneumoniae, C. trachomatis and C. psittaci and the corresponding white cells were tested for Chlamydia spp. by nPCR.
C. pneumoniae was not detected in any carotid specimen. Twenty-five of 38 (66%) plasma specimens were positive for C. pneumoniae IgG, 2/38 (5%) for C. trachomatis IgG and 1/38 (3%) for C. psittaci IgG.
We were unable to show an association between the presence of Chlamydia spp. and atheroma in carotid arteries in the presence of a high seroprevalence of C. pneumoniae antibodies in Northern Ireland.
PMCID: PMC55344  PMID: 11553320
5.  Cytomegalovirus Infection and Atherosclerosis in Candidate of Coronary Artery Bypass Graft 
Although there is enough evidence that infectious agents such as Chlamydia pneumonia and Helicobacter pylori may play a pathogenic role in atherosclerosis, this role for cytomegalovirus (CMV) is yet controversial.
The aim of the present study was to detect CMV-DNA in atherosclerotic plaques in patients who underwent coronary artery bypass graft (CABG).
Patients and Methods:
In this case-control study, candidates for CABG (cases) and patients with valvular or congenital malformation but without atherosclerotic plaques (controls) were studied from 2012 to 2013 at Golestan hospital, Ahvaz, IR Iran. Demographic and laboratory data were collected. Atherosclerotic and histological samples were obtained from visible plaques and from aorta by the surgeon. All the samples were examined for the presence of CMV-DNA by polymerase chain reaction (PCR) method using a commercial kit (SinaClon, Tehran, IR Iran).
The mean ages in case and control groups were 60.8 ± 6.8 and 57.5 ± 11.5 years, respectively, with no significant difference (P = 0.09). Thirty patients (54.5%) in case and 32 (58.2%) in control groups were male with no significant difference (P = 0.7). CMV-DNA was present in 8 (14.5%) of the cases and 2 (4%) of the controls. CMV-DNA was associated with higher risk of atherosclerosis (OR: 7.7, 95% CI = 1.1-51.4, P = 0.03). Of the total normal aortic samples (55 in cases and 55 in controls), there was no individual with simultaneous positive CMV-DNA among aortic atherosclerotic and normal tissue samples.
The presence of CMV-DNA in aortic plaques is associated with increased risk of atherosclerosis. CMV infection may be considered as an independent risk factor for this event.
PMCID: PMC4377172  PMID: 25834719
Arteriosclerosis; Coronary Vessels; Cytomegalovirus; DNA
6.  Association of Carotid Plaque Lp-PLA2 with Macrophages and Chlamydia pneumoniae Infection among Patients at Risk for Stroke 
PLoS ONE  2010;5(6):e11026.
We previously showed that the burden of Chlamydia pneumoniae in carotid plaques was significantly associated with plaque interleukin (IL)-6, and serum IL-6 and C-reactive protein (CRP), suggesting that infected plaques contribute to systemic inflammatory markers in patients with stroke risk. Since lipoprotein-associated phospholipase A2 (Lp-PLA2) mediates inflammation in atherosclerosis, we hypothesized that serum Lp-PLA2 mass and activity levels and plaque Lp-PLA2 may be influenced by plaque C. pneumoniae infection.
Methodology/Principal Findings
Forty-two patients underwent elective carotid endarterectomy. Tissue obtained at surgery was stained by immunohistochemistry for Lp-PLA2 grade, macrophages, IL-6, C. pneumoniae and CD4+ and CD8+ cells. Serum Lp-PLA2 activity and mass were measured using the colorimetric activity method (CAM™) and ELISA, respectively. Serum homocysteine levels were measured by HPLC. Eleven (26.2%) patients were symptomatic with transient ischemic attacks. There was no correlation between patient risk factors (smoking, coronary artery disease, elevated cholesterol, diabetes, obesity, hypertension and family history of genetic disorders) for atherosclerosis and serum levels or plaque grade for Lp-PLA2. Plaque Lp-PLA2 correlated with serum homocysteine levels (p = 0.013), plaque macrophages (p<0.01), and plaque C. pneumoniae (p<0.001), which predominantly infected macrophages, co-localizing with Lp-PLA2.
The significant association of plaque Lp-PLA2 with plaque macrophages and C. pneumoniae suggests an interactive role in accelerating inflammation in atherosclerosis. A possible mechanism for C. pneumoniae in the atherogenic process may involve infection of macrophages that induce Lp-PLA2 production leading to upregulation of inflammatory mediators in plaque tissue. Additional in vitro and in vivo research will be needed to advance our understanding of specific C. pneumoniae and Lp-PLA2 interactions in atherosclerosis.
PMCID: PMC2882946  PMID: 20543948
7.  Carriage of Mycoplasma pneumoniae in the Upper Respiratory Tract of Symptomatic and Asymptomatic Children: An Observational Study 
PLoS Medicine  2013;10(5):e1001444.
In order to determine the possible asymptomatic carriage of Mycoplasma pneumoniae in the upper respiratory tracts of children, Emiel Spuesens and colleagues investigate the prevalence of M. pneumoniae in symptomatic and asymptomatic children at a hospital in The Netherlands.
Please see later in the article for the Editors' Summary
Mycoplasma pneumoniae is thought to be a common cause of respiratory tract infections (RTIs) in children. The diagnosis of M. pneumoniae RTIs currently relies on serological methods and/or the detection of bacterial DNA in the upper respiratory tract (URT). It is conceivable, however, that these diagnostic methods also yield positive results if M. pneumoniae is carried asymptomatically in the URT. Positive results from these tests may therefore not always be indicative of a symptomatic infection. The existence of asymptomatic carriage of M. pneumoniae has not been established. We hypothesized that asymptomatic carriage in children exists and investigated whether colonization and symptomatic infection could be differentiated by current diagnostic methods.
Methods and Findings
This study was conducted at the Erasmus MC–Sophia Children's Hospital and the after-hours General Practitioners Cooperative in Rotterdam, The Netherlands. Asymptomatic children (n = 405) and children with RTI symptoms (n = 321) aged 3 mo to 16 y were enrolled in a cross-sectional study from July 1, 2008, to November 30, 2011. Clinical data, pharyngeal and nasopharyngeal specimens, and serum samples were collected. The primary objective was to differentiate between colonization and symptomatic infection with M. pneumoniae by current diagnostic methods, especially real-time PCR. M. pneumoniae DNA was detected in 21.2% (95% CI 17.2%–25.2%) of the asymptomatic children and in 16.2% (95% CI 12.2%–20.2%) of the symptomatic children (p = 0.11). Neither serology nor quantitative PCR nor culture differentiated asymptomatic carriage from infection. A total of 202 children were tested for the presence of other bacterial and viral pathogens. Two or more pathogens were found in 56% (63/112) of the asymptomatic children and in 55.5% (50/90) of the symptomatic children. Finally, longitudinal sampling showed persistence of M. pneumoniae in the URT for up to 4 mo. Fifteen of the 21 asymptomatic children with M. pneumoniae and 19 of the 22 symptomatic children with M. pneumoniae in this longitudinal follow-up tested negative after 1 mo.
Although our study has limitations, such as a single study site and limited sample size, our data indicate that the presence of M. pneumoniae in the URT is common in asymptomatic children. The current diagnostic tests for M. pneumoniae are unable to differentiate between asymptomatic carriage and symptomatic infection.
Please see later in the article for the Editors' Summary
Editors' Summary
Pneumonia (a form of acute respiratory infection) is the single largest cause of death in children worldwide, killing an estimated 1.2 million children aged five and under every year, particularly in South Asia and sub-Saharan Africa. In these settings, bacterial infections with Streptococcus pneumoniae and Haemophilus influenzae are the most common causes of bacterial pneumonia. However, in high-income settings, bacterial infection with Mycoplasma pneumoniae is a major cause of upper and lower respiratory tract infections in children: over one-third of childhood cases of community-acquired pneumonia that require admission to a hospital are caused by M. pneumoniae. Currently, diagnosis of M. pneumoniae infections relies on the detection of antibodies against M. pneumoniae in the blood or detection of bacterial DNA in samples from the upper respiratory tract through polymerase chain reaction (PCR) tests.
Why Was This Study Done?
Other bacteria, such as Streptococcus pneumoniae, are commonly present in children without causing infection, a situation known as asymptomatic carriage. However, to date, it is unknown whether M. pneumoniae is also commonly carried in the upper respiratory tract of children without causing symptoms or leading to infection. The possibility of asymptomatic carriage of M. pneumoniae could have major implications for the interpretation of the results of diagnostic tests and also for clinical management. So in this study conducted in The Netherlands, the researchers investigated whether asymptomatic carriage of M. pneumoniae exists and also whether symptomatic infection could be differentiated from asymptomatic carriage by current diagnostic methods.
What Did the Researchers Do and Find?
Between 2008 and 2011, the researchers recruited children aged between three months and 16 years attending a hospital in Rotterdam for an elective surgical procedure (asymptomatic group) or admitted with a respiratory tract infection (symptomatic group). All children had blood tests and respiratory samples (nasopharyngeal swab) taken on admission and were tested for other pathogens. The researchers invited children who tested positive for M. pneumoniae by PCR to attend for further follow-up and tested them monthly for the presence of M. pneumoniae DNA in the upper respiratory tract until the test was negative on two occasions. Using these methods, the researchers recruited 726 children over the study period—405 in the asymptomatic group and 321 in the symptomatic group. The researchers found that the prevalence of M. pneumoniae did not differ between the asymptomatic group and the symptomatic group, with prevalences of 21.2% and 16.2%, respectively (the prevalence of M. pneumoniae also did not differ significantly between those with lower versus upper respiratory infection). There were also no differences in prevalence in the asymptomatic and symptomatic groups when diagnosed using blood tests. The researchers found a high rate of multiple, coexisting bacterial and viral pathogens in both asymptomatic and symptomatic children: two or more pathogens were found in 56% (63/112) of the asymptomatic children and in 55.5% (50/90) of the symptomatic children. Furthermore, season and the year of enrollment affected the prevalence of M. pneumoniae in the asymptomatic group, ranging from 3% during the spring of 2009 to 58% during the summer of 2010. Finally, of the 21 children from the asymptomatic group who participated in the follow-up study, 15 (71%) tested negative within one month, and in the symptomatic group, 19 of 22 children (86%) tested negative after the first visit.
What Do These Findings Mean?
These findings show that M. pneumoniae is carried at high rates in the upper respiratory tracts of healthy children, and that this asymptomatic carriage cannot be differentiated from symptomatic respiratory tract infection by diagnostic tests (serology or PCR). As the prevalence of M. pneumoniae varied between year and season, carriage of M. pneumoniae may follow a cyclic epidemic pattern. This study is from a single study site in one city in The Netherlands, with a relatively small number of children, and so these findings may not be generalizable to other populations. However, as this study suggests that current diagnostic tests do not discriminate between carriage and infection, clinicians may need to reconsider the clinical significance of a positive test result. Future studies are needed to address this diagnostic challenge and also to investigate possible factors that may affect the progression of asymptomatic carriage of M. pneumoniae to symptomatic infection.
Additional Information
Please access these websites via the online version of this summary at
MicrobeWiki has more information on M. pneumoniae
Lab Tests Online explains current tests for M. pneumoniae
PMCID: PMC3653782  PMID: 23690754
8.  The Probable Role of Cytomegalovirus in Acute Myocardial Infarction 
Coronary artery disease (CAD) is the most common cause of death worldwide and many studies have been performed on reduction of its prevalence.
This case control study was designed to investigate the presence of Cytomegaloviruses, Chlamydia pneumoniae and Helicobacter pylori in atherosclerotic plaques of cadaveric coronary endothelium of patients with and without acute myocardial infarction.
Patients and Methods:
Sixty cadavers in two equal groups were analyzed. Acute myocardial infarction group included cadavers with acute myocardial infarction and atherosclerotic plaque. The non- acute myocardial infarction group included those with innocent atherosclerotic plaques in autopsy, expired due to other causes. Specimens from coronary vessels’ atherosclerotic plaque were taken and studied by polymerase chain reaction for Cytomegaloviruses, C. pneumoniae and H. pylori.
Cadavers of 26 males and 34 females underwent autopsy procedures. Their mean age at the time of death was 48.17 ± 18.74 years. Unknown causes (20%), hanging (20%), head trauma (16.7%) and multiple traumas (13.3%) were the most common causes of death in the non- acute myocardial infarction group. PCR test results were negative for C. pneumoniae and H. pylori in all cadavers of both groups. Nine cadavers from the acute myocardial infarction group and one from the non- acute myocardial infarction group showed positive PCR results for Cytomegaloviruses (30% and 3.33%, respectively). There was a significant difference between the two groups regarding Cytomegaloviruses positivity in coronary artery plaques (P < 0.01, odd ratio: 12.42, 95% CI: 10.46 to 15.73).
A significant proportion of coronary atherosclerotic plaques in cadavers with confirmed acute myocardial infarction were detected to be infected with Cytomegaloviruses while no infections of C. pneumoniae and H. pylori were detected.Coronary artery disease (CAD) is the most common cause of death worldwide and many studies have been performed on reduction of its prevalence.
PMCID: PMC4138660  PMID: 25147687
Atherosclerosis; Cadaver; Chlamydia pneumonia; Coronary Artery Disease; Cytomegalovirus; Helicobacter pylori
9.  Overexpression of YKL-40 Predicts Plaque Instability in Carotid Atherosclerosis with CagA-Positive Helicobacter Pylori Infection 
PLoS ONE  2013;8(4):e59996.
YKL-40 has been demonstrated to be related to atherosclerosis, but its role in predicting plaque status and the outcome of carotid atherosclerosis (CAS) caused by CagA-positive helicobacter pylori remains unclear. This study was aimed to investigate the role of YKL-40 in predicting the outcome of carotid atherosclerosis with CagA-positive Helicobacter pylori infection.
The serum concentrations of YKL-40, C-reaction protein in 310 patients undergoing color Duplex assessment of carotid atherosclerosis were recorded and divided into 3 groups according to the infectious statuses of helicobacter pylori. We also examined serum YKL-40, C-reaction protein and the plaque morphology in animal model of carotid atherosclerosis with different types of helicobacter pylori infection.
Overexpression of YKL-40 was only found in carotid atherosclerosis group with CagA-positive helicobacter pylori infection; C-reaction protein failed to distinguish different infectious statuses of helicobacter pylori infection. In patients with CagA-positive helicobacter pylori infection, elevated YKL-40 expression was accompanied by more severe clinical symptoms. We also confirmed similar findings in rabbit model of carotid atherosclerosis with CagA-positive helicobacter pylori infection. We found that in 7 rabbits treated with anti-helicobacter pylori therapy, the serum YKL-40 level decreased and the plaque became more stable.
Our findings suggested that increased serum YKL-40 level indicates plaque instability and more severe clinical symptoms of carotid atherosclerosis with CagA-positive helicobacter pylori infection. Compared with C-reaction protein, YKL-40 seems to be a more specific predictor of plaque status and outcome of carotid atherosclerosis with CagA-positive helicobacter pylori infection.
PMCID: PMC3616092  PMID: 23573226
10.  Detection of Helicobacter pylori DNA in Aortic and Left Internal Mammary Artery Biopsies 
Texas Heart Institute Journal  2008;35(2):130-135.
We investigated the relationship between acute coronary ischemia and the presence of Helicobacter pylori DNA in aortic regions that were absent macroscopic atheromatous plaques.
The study group (Group 1) consisted of 42 patients who underwent coronary artery bypass grafting. Biopsy samples were obtained from 2 different locations: from regions of the aorta that were free (macroscopically) of atheromatous plaque (Group 1A), and from the internal mammary artery (Group 1B). The control group (Group 2) of 10 patients who had no atherosclerotic vascular disease provided aortic tissue samples for comparison. The real-time polymerase chain reaction method was used to detect H. pylori DNA in all biopsy samples.
Eleven of 42 aortic tissue samples (26%) in Group 1A were positive for H. pylori DNA. Neither biopsies from the left internal mammary arteries of those patients nor biopsies from the aortas of the control group (Group 2) were positive for H. pylori DNA. There was a statistically significant difference between 1A and 1B in terms of H. pylori positivity (P=0.001). In Group 1 as a whole, acute coronary ischemia was more prevalent in the H. pylori-positive patients than in the H. pylori-negative patients (P=0.001).
To our knowledge, this is the 1st study to investigate the detection of H. pylori DNA in aortic biopsy samples that are macroscopically free of atheromatous plaque. Such detection in patients who have atherosclerotic coronary artery disease could be an important indication of the role of microorganisms in the pathogenesis of atherosclerosis.
PMCID: PMC2435450  PMID: 18612444
Aorta; arteriosclerosis/etiology; Helicobacter infections/complications; Helicobacter pylori/pathogenicity; polymerase chain reaction; prospective studies; real-time PCR; mammary arteries; muscle, smooth, vascular
11.  The assessment of carotid intima media thickness and serum Paraoxonase-1 activity in Helicobacter pylori positive subjects 
The role of inflammation in the pathogenesis and progression of atherosclerosis has been increasingly discussed. Although the seroepidemiological studies have suggested a relationship between Helicobacter pylori (H. pylori) infection and atherosclerosis; the issue is still controversial. It is well known that abnormal lipid profil is related to atherosclerosis and the measurement of carotid-intima media thickness (CIMT) is one of the surrogate marker of atherosclerosis. The serum concentration of high-density lipoprotein (HDL-C) has been known to have an inverse correlation with the development of atherosclerosis. Paraoxonase-1 (PON1) is a major anti-atherosclerotic component of HDL-C. PON1 activity is related to lipid peroxidation and prospective cardiovascular risk. The aim of this study was to investigate CIMT and serum PON1 activities along with lipid parameters in H. pylori positive and negative subjects.
Thirty H. pylori positive subjects and thirty-one negative subjects were enrolled. H. pylori infection was diagnosed by the presence of positivity of stool H. pylori antigen test or Carbon 14 labeled urea breath test. Serum PON1 activity was measured spectrophotometrically. Traditional cardiovascular risk factors were investigated and laboratory analysis included measurement of serum triglycerides (TG), total cholesterol (TC), high-density lipoprotein (HDL-C) and low-density lipoprotein cholesterol (LDL-C). We assessed CIMT by high-resolution ultrasound of both common carotid arteries.
We found that the mean and maximum values of right and overall CIMT in H. pylori positive subjects were significantly thicker than those of H. pylori negative subjects. There was no significant differences in serum HDL-C, LDL-C, TC levels and TC/HDL-C ratios between two groups. Serum TG levels of H. pylori positive subjects were significantly higher than those of H. pylori negative subjects (p = 0.014). We found that PON1 activities were significantly lower in H. pylori positive subjects compared with negative subjects. No significantly correlation was observed between PON1 and CIMT values.
There is an increase in CIMT values in patients with H. pylori positive compared to H. pylori negative subjects. PON1 activity decrease significantly in H. pylori positive subjects. However, an association between PON1 and CIMT was not found. These data indicated that H. pylori may have a role in atherosclerotic processes, however, further studies are needed to evaluate the exact mechanisms.
PMCID: PMC2936361  PMID: 20804546
12.  Chlamydia pneumoniae antigens, rather than viable bacteria, persist in atherosclerotic lesions 
Journal of Clinical Pathology  2000;53(12):911-916.
Aims—To evaluate the nature of the presence of Chlamydia pneumoniae or of other members of the order Chlamydiales in atherosclerotic lesions.
Methods—Consecutive sections of 13 carotid artery specimens obtained at necropsy and of C pneumoniae infected HEp2 cells were analysed using: (1) immunocytochemistry (ICC) to detect C pneumoniae membrane protein; (2) in situ hybridisation (ISH) using a polymerase chain reaction (PCR) fragment of the omp1 gene to detect C pneumoniae specific DNA; (3) ISH using an oligonucleotide probe to detect Chlamydiales specific 16S rRNA; (4) PCR to detect C pneumoniae 16S rDNA; and (5) in situ DNA nick end labelling (TUNEL) to detect fragmented DNA.
Results—Staining by ICC and ISH of infected HEp2 cells showed characteristic inclusions. Chlamydia pneumoniae membrane protein was demonstrated in macrophages in advanced atherosclerotic lesions (six of six), but not in fatty streaks (none of two), or normal arteries (none of five). ISH assays using both probes and PCR were all negative, indicating the absence of both specific C pneumoniae DNA and Chlamydiales specific 16S rRNA. Only after treatment with DNAse I were uniformly sized dots demonstrated by the TUNEL assay in inclusions of infected HEp2 cells. The TUNEL assay showed a similar staining pattern in macrophages in five carotid artery specimens, of which four were also positive for C pneumoniae membrane protein. Both macrophage populations were morphologically similar and were similarly distributed.
Conclusions—No evidence was obtained for the involvement of other members of the order Chlamydiales in atherosclerosis. The presence of C pneumoniae antigen in the absence of DNA and 16S rRNA suggests that antigens, rather than viable bacteria, persist in atherosclerotic lesions.
Key Words: Chlamydia pneumoniae • Chlamydiales • immunocytochemistry • in situ hybridisation • polymerase chain reaction • DNA fragmentation • atherosclerosis
PMCID: PMC1731134  PMID: 11265175
13.  Histological composition and progression of carotid plaque 
Thrombosis Journal  2007;5:4.
To analyse histological composition and progression of carotid plaque.
Thirty-one patients (22 males, mean age 68.03 ± 7.3 years) admitted for carotid endarterectomy for extracranial high-grade internal carotid artery stenosis (≥ 70% luminal narrowing) were enrolled. The patients were divided into 2 groups according to symptomatology (group I, 17 symptomatic patients; and group II, 14 asymptomatic patients). A histological analysis and inflammatory cell quantification of each excised carotid plaque was made. Nine carotid arteries were removed from human cadavers that were not preselected for carotid artery disease. These specimens were used as a control tissue without any macroscopic signs of atherosclerotic plaques.
Fifty eight percent of all carotid plaques were classified as complex plaque with possible surface defect, hemorrhage or thrombus. The inflammatory cells concentration did not differ between the two groups. All specimens from human cadavers were classified as preatheroma with extracellular lipid pools.
Asymptomatic and symptomatic patients could have the same histological components on their carotid plaques. Fibrotic and calcific plaques could become vulnerable as complex plaques with surface defect, hemorrhage and thrombus could remain silent. Asymptomatic carotid stenosis should be followed close with no invasive diagnostic methods and clinical evaluation.
PMCID: PMC1808443  PMID: 17324272
14.  Predictors of the Extent of Carotid Atherosclerosis in Patients Treated with Radiotherapy for Nasopharyngeal Carcinoma 
PLoS ONE  2014;9(12):e116284.
To determine the predictors of the extent of carotid atherosclerosis in patients treated with radiotherapy (RT) for nasopharyngeal carcinoma (NPC).
The present study investigated 129 post-RT NPC patients. Carotid atherosclerotic parameters, such as carotid intima-media thickness, carotid arterial stiffness and carotid plaque burden (plaque score, the presence of plaque and ≥50% stenosis) were assessed using ultrasonography. The association between carotid atherosclerotic parameters and nine potential predictors, including age, gender, post-RT duration, radiation dose, chemotherapy, diabetes mellitus, hypertension, hypercholesterolemia, and smoking, were determined using multiple regression. The cutoff values of age, post-RT duration and number of cardiovascular risk factors for the presence of carotid plaque or ≥50% carotid stenosis were analyzed using receiver operating characteristic (ROC) curve analysis. Multiple testing was corrected using Benjamini-Hochberg false discovery rate.
Age, post-RT duration and number of cardiovascular risk factors were significantly associated with carotid plaque burden (corrected P value, Pcor<0.05). Age of 44.5 years (sensitivity = 99.2% and specificity = 50%, Pcor<0.01) and post-RT duration of 8.5 years (sensitivity = 75.7% and specificity = 64.3%, Pcor<0.001) were the cutoff values for detecting carotid plaque, while post-RT duration of 13.5 years (sensitivity = 66.7% and specificity = 71.6%, Pcor<0.001) and 1.5 cardiovascular risk factors (sensitivity = 40.7% and specificity = 84.3%, Pcor<0.05) were the cutoff values for screening ≥50% carotid stenosis.
Age, post-RT duration and number of cardiovascular risk factors are significant predictors of carotid atherosclerosis in post-RT NPC patients. Post-RT NPC patients, who are at least 45 years old, with post-RT duration of 9 years or above, and/or have ≥2 cardiovascular risk factors, are more susceptible to carotid atherosclerosis.
PMCID: PMC4281159  PMID: 25551559
15.  Experiences with carotid endarterectomy at Sree Chitra Tirunal Institute 
Atherosclerotic carotid artery disease poses a grave threat to cerebral circulation, leading to a stroke with its devastating sequelae, if left untreated. Carotid endarterectomy has a proven track record with compelling evidence in stroke prevention.
a) To confirm that carotid endarterectomy (CEA) is safe and effective in preventing stroke at both short and long term. b) to demonstrate long term patency of internal carotid artery when arteriotomy repair is performed using autologous saphenous vein patch.
Materials and Methods:
During ten years, from September 1997 to February 2008, thirty nine patients who underwent consecutive carotid endarterectomy at our institute, form the basis of this report. Their age ranged from thirty to seventy eight years, with a mean age of 56. There were four women in this cohort. Thirty seven patients were symptomatic with >70% stenosis and two were asymptomatic with >80% stenosis, incidentally detected. Imaging included Duplex scan and MRA for carotid territory and brain, and non-invasive cardiac assessment. Co-morbidities included smoking, hypertension, diabetes, and coronary artery disease. Carotid Endarterectomy was performed under general anaesthesia, using carotid shunt and vein patch arteriotomy repair.
All the patients made satisfactory recovery, without major adverse cerebral events in this series. Morbidities included Transient Ischemic Attack (TIA) in two, needing only medications in one, and carotid stenting in the other. Minor morbidities included neck hematoma in two and transient hypoglossal paresis in three patients. Yearly follow-up included duplex scan assessment for all the patients. Two patients died of contralateral stroke, two of myocardial events and two were lost to follow up. Thirty three patients are well and free of the disease during the follow up of three to 120 months.
Carotid endarterectomy provided near total freedom from adverse cerebral events and its catastrophic sequelae, leading to excellent outcome, both short as well as long term.
PMCID: PMC2771972  PMID: 19893664
Carotid artery; stenosis; stroke; carotid endarterectomy
16.  Fractalkine Is Expressed in Early and Advanced Atherosclerotic Lesions and Supports Monocyte Recruitment via CX3CR1 
PLoS ONE  2012;7(8):e43572.
Fractalkine (CX3CL1, FKN) is expressed in the inflamed vascular wall and absence of FKN reduces atherogenesis. Whether FKN is expressed throughout all stages of atherosclerotic disease and whether it directly contributes to monocyte recruitment to atherosclerotic lesions is not known. We collected human atherosclerotic plaque material and blood samples from patients with carotid artery disease undergoing endarterectomy. Plaques were analyzed by immunohistochemistry and qPCR. We found that FKN is expressed at all stages of atherosclerotic lesion formation, and that the number of FKN-expressing cells positively correlates with the number of CX3CR1-positive cells in human carotid artery plaques. In the circulation, soluble FKN levels are significantly elevated in the presence of high-grade (sub-occlusive) stenosis. To determine the role of the FKN-CX3CR1 axis for monocyte adhesion in vivo we then performed intravital videofluorescence microscopy of the carotid artery in ApoE−/− mice. Notably, FKN-CX3CR1 interactions are critical for recruitment of circulating monocytes to the injured atherosclerotic vascular wall. Thus, this chemokine dyad could represent an attractive target for anti-atherosclerotic strategies.
PMCID: PMC3423360  PMID: 22916279
17.  Biomarker Discovery in Serum from Patients with Carotid Atherosclerosis 
Cerebrovascular Diseases Extra  2011;1(1):115-129.
Blood-based biomarkers of atherosclerosis have been used to identify patients at high risk for developing stroke. We hypothesized that patients with carotid artery disease would have a distinctive proteomic signature in blood as compared to a healthy control population without carotid artery disease. In order to discover protein biomarkers associated with increased atherosclerotic risk, we used two different strategies to identify biomarkers from patients with clinically defined atherosclerosis who were undergoing endarterectomy for atherosclerotic carotid artery disease. These patients were compared with healthy matched controls.
Serum was obtained from patients undergoing endarterectomy (EA; n = 38) and compared to a group of age-matched healthy controls (n = 40). Serum was fractionated using anion exchange chromatography and three different surface-enhanced laser desorption/ionization (SELDI) chip surfaces and then evaluated with mass spectrometry (MS) and two-dimensional difference gel electrophoresis (2D-DIGE).
A random forest (RF) analysis of the SELDI-MS protein peak data distinguished these two groups with 69.2% sensitivity and 73.2% specificity. Four unique SELDI peaks (4.2, 4.4, 16.7 and 28 kDa, all p< 0.01) showed the greatest influence in the RF model. The EA patients with a history of prior clinical atherosclerotic plaque rupture manifested as either stroke or transient ischemic attack (symptomatic; n = 16) were compared to patients with carotid atherosclerosis but no clinical evidence of plaque rupture (asymptomatic; n = 22). Analysis of the SELDI spectra did not separate these two patient subgroups. A subgroup analysis using 2D-DIGE images obtained from albumin-depleted serum comparing symptomatic (n = 10) to asymptomatic EA patients (n = 10) found 4 proteins that were differentially expressed (p < 0.01) in the symptomatic patients. These proteins were identified as α1-antitrypsin, haptoglobin and vitamin D binding protein that were downregulated and α2-glycoprotein precursor that was upregulated in the symptomatic EA group.
SELDI-MS data analysis of fractionated serum suggests that a distinct protein signature exists in patients with carotid atherosclerosis compared to age-matched healthy controls. Identification of 4 proteins in a subset of patients with symptomatic and asymptomatic carotid atherosclerosis suggests that these and other protein biomarkers may assist in identifying high-risk patients with carotid atherosclerosis.
PMCID: PMC3343755  PMID: 22566989
Asymptomatic patients; Atherosclerosis; Biomarker; Difference gel electrophoresis; Proteomics; Surface-enhanced laser desorption/ionization; Symptomatic patients
18.  Persistently elevated IgA antibodies to Mycoplasma pneumoniae in patients with internal carotid artery stenosis 
Background: It has been suggested that Mycoplasma pneumoniae may play a role in the development of atherosclerosis, but to date this association is still a matter of debate due to conflicting findings.
Methods: We have investigated the levels of specific IgA antibodies to M. pneumoniae in 91 patients with internal carotid artery (ICA) stenosis using a commercial kit (SeroMP™ IgA; Savyon Diagnostics, Israel; cut-off value: 20 binding units; BU). All patients underwent surgery for ICA stenosis. From each patient, the first serum sample (S1) was taken before surgery, and the second after an interval of 6 month (S2).
Results: The S1 seroprevalence was 18.7% (17/91). Thirteen of the 17 patients with positive S1 levels also remained positive after six month, whereby no decrease of IgA level was seen (median S1 level: 34 BU, range: 22–65 BU; median S2 level: 37 BU, range: 22–58 BU). Specifically, six of the patients showed an increased level after 6 months, and six a decrease, with the level remaining constant in one patient. In contrast, only 3 of the 74 S1 negative patients became positive for anti-M. pneumoniae IgA between the taking of the first and the second serum specimen (p<0.01). None of the assessed demographic factors or risk factors for atherosclerosis was associated with IgA seropositivity, neither were the degree CAVK or the degree of stenosis.
Conclusion: These findings cannot be explained throughout by the general seroprevalence, or by past respiratory tract infections with the pathogen, and therefore may suggest a role for M. pneumoniae in the development of atherosclerosis, since a chronic infection must be assumed.
PMCID: PMC3252649  PMID: 22242085
Mycoplasma pneumonia; IgA; atherosclerosis; stenosis; elevated antibodies; A. carotis interna
19.  Co-existing intracranial and extracranial carotid artery atherosclerotic plaques and recurrent stroke risk: a three-dimensional multicontrast cardiovascular magnetic resonance study 
As a systemic disease, atherosclerosis commonly affects intracranial and extracranial carotid arteries simultaneously which is defined as co-existing plaques. Previous studies demonstrated that co-existing atherosclerotic diseases are significantly associated with ischemic cerebrovascular events. The aim of this study was to investigate the characteristics of co-existing intracranial and extracranial carotid atherosclerotic plaques and their relationships with recurrent stroke by using 3D multi-contrast magnetic resonance (MR) vessel wall imaging.
Patients with recent cerebrovascular symptoms in anterior circulation and at least one carotid plaque were recruited. All patients underwent cardiovascular magnetic resonance (CMR) for brain and intracranial and extracranial arteries. Presence/absence of atherosclerotic plaque at each arterial segment was identified. The maximum wall thickness (Max WT), length, stenosis of each plaque was measured. The presence/absence of calcification, lipid-rich necrotic core (LRNC), and intraplaque hemorrhage (IPH) was assessed. Cerebral old and acute infarcts in anterior circulation were evaluated.
Fifty-eight patients (mean age: 58.0 ± 8.5 years old, 34 males) were recruited. Of the 58 patients, co-existing intracranial and extracranial carotid artery plaques were found in 45 patients (77.6%), of which 7 (15.6%) had first time acute stroke and 26 (57.8%) had recurrent stroke. For these 33 patients with stroke, the number of intracranial plaques (OR = 11.26; 95% CI, 1.27–100; p = 0.030) and co-existing intracranial and extracranial carotid artery plaques (OR = 2.42; 95% CI, 1.04–5.64; p = 0.040) was significantly associated with recurrent stroke. After adjusting for traditional risk factors, the number of co-existing plaques was still significantly correlated with recurrent stroke (OR = 3.31; 95% CI, 1.09–10.08; p = 0.035). No correlations were found between recurrent stroke and Max WT, length, stenosis, and compositions of plaques.
Co-existing intracranial and extracranial carotid artery plaques are prevalent in symptomatic patients and the number of co-existing plaques is independently associated with the risk of recurrent stroke.
PMCID: PMC5134005  PMID: 27908279
Intracranial artery; Carotid artery; Atherosclerosis; Cardiovascular magnetic resonance; Recurrent stroke
20.  The Impact of Expansive Arterial Remodeling on Clinical Presentation in Carotid Artery Disease: A Multidetector CT Angiography Study 
Atherosclerotic arterial remodeling has been described in the coronary circulation but has not been studied extensively for carotid atherosclerosis. The purpose of our study was to examine the association between carotid artery remodeling and clinical presentation in patients with significant stenosis by using multidetector row CT (MDCT).
One hundred eight patients with ≥50% stenosis (North American Symptomatic Carotid Endarterectomy Trial criteria) by MDCT angiography between January 2004 and June 2006 were identified. The study group included 37 symptomatic (65.9 ± 13.0 years; 12 women; stenosis, 81.5 ± 12.2%; 17 with stroke; 15 with transient ischemic attack; 5 with amaurosis fugax) and 71 asymptomatic patients (70.5 ± 10.5 years; 28 women; stenosis, 78.8 ± 11.1%). Remodeling ratio (RR) was calculated by dividing the outer vessel circumference at the site of greatest stenosis by a normal reference-segment vessel circumference. Maximum vessel thickness (MxVT) and eccentricity index (EI) of the plaque, defined as maximal thickness/minimal thickness at the site of greatest luminal narrowing, were also determined. Data were analyzed by using an independent t test.
The RR was significantly higher in symptomatic patients (1.64 ± 0.44) than in asymptomatic patients (1.41 ± 0.5) (P = .02). There was no significant difference in MxVT in symptomatic (5.9 ± 2.1 mm) and asymptomatic patients (5.6 ± 2.4 mm) (P = .45) and no significant difference in EI (symptomatic, 4.7 ± 2.7; asymptomatic, 4.3 ± 2.2; P = .38).
In this series of subjects with significant internal carotid artery stenosis, expansive carotid remodeling was significantly greater in patients with cerebral ischemic symptoms than in asymptomatic patients. The extent of expansive remodeling may indicate underlying atherosclerotic plaque vulnerability. MDCT has a role in the evaluation of carotid artery disease beyond examining luminal stenosis.
PMCID: PMC2955285  PMID: 17569959
21.  Distribution of Chlamydia pneumoniae DNA in Atherosclerotic Carotid Arteries: Significance for Sampling Procedures 
Journal of Clinical Microbiology  2003;41(4):1454-1457.
Despite extensive efforts to confirm a direct association between Chlamydia pneumoniae and atherosclerosis, different laboratories continue to report a large variability in detection rates. In this study, we analyzed multiple sections from atherosclerotic carotid arteries from 10 endartectomy patients to determine the location of C. pneumoniae DNA and the number of sections of the plaque required for analysis to obtain a 95% confidence of detecting the bacterium. A sensitive nested PCR assay detected C. pneumoniae DNA in all patients at one or more locations within the plaque. On average, 42% (ranging from 5 to 91%) of the sections from any single patient had C. pneumoniae DNA present. A patchy distribution of C. pneumoniae in the atherosclerotic lesions was observed, with no area of the carotid having significantly more C. pneumoniae DNA present. If a single random 30-μm-thick section was tested, there was only a 35.6 to 41.6% (95% confidence interval) chance of detecting C. pneumoniae DNA in a patient with carotid artery disease. A minimum of 15 sections would therefore be required to obtain a 95% chance of detecting all true positives. The low concentration and patchy distribution of C. pneumoniae DNA in atherosclerotic plaque appear to be among the reasons for inconsistency between laboratories in the results reported.
PMCID: PMC153859  PMID: 12682129
22.  Presence of Periodontopathic Bacteria DNA in Atheromatous Plaques from Coronary and Carotid Arteries 
BioMed Research International  2015;2015:825397.
Objectives. Interest in periodontitis as a potential risk factor for atherosclerosis and its complications resulted from the fact that the global prevalence of periodontal diseases is significant and periodontitis may induce a chronic inflammatory response. Many studies have analyzed the potential impact of the Porphyromonas gingivalis, major pathogen of periodontitis, on general health. The purpose of this study was to find the presence of the Porphyromonas gingivalis DNA in the atherosclerotic plaques of coronary and carotid arteries and in the periodontal pockets in patients with chronic periodontitis, who underwent surgery because of vascular diseases. Methods and Results. The study population consisted of 91 patients with coronary artery disease or scheduled for carotid endarterectomy. The presence of Porphyromonas gingivalis DNA in atheromatous plaques and in subgingival samples was determined by PCR. Bacterial DNA was found in 21 of 91 (23%) samples taken from vessels and in 47 of 63 (74.6%) samples from periodontal pockets. Conclusions. Porphyromonas gingivalis DNA is frequently found in atheromatous plaques of patients with periodontitis. That is why more research should be conducted to prove if this periopathogen may have an impact on endothelium of patients at risk of atherosclerosis.
PMCID: PMC4609377  PMID: 26504835
23.  Inflammatory markers in patients with internal carotid artery stenosis 
Available reports underline the significance of the inflammatory process in the development, progression and destabilisation of atherosclerotic plaques in the internal carotid artery (ICA). The aim of this study was to evaluate the relationship between the degree of ICA stenosis, ultrasound plaque morphology and serum concentration of selected inflammatory markers.
Material and methods
Sixty-five patients with ICA stenosis > 50% (39 symptomatic) and 30 healthy volunteers were enrolled in the study. Clinical, neurological examination and laboratory evaluation (leucocyte count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), fibrinogen, tumour necrosis factor-α (TNF-α), interleukins (1β, 6 and 10), anti-cytomegalovirus IgG antibody titre) were performed. Stenosis grade ≥ 70%, ulcerations on the plaque surface and a hypoechoic (or predominantly hypoechoic) structure of the plaque, obtained by colour-coded duplex examination, were accepted as the characteristics of unstable stenoses.
Unstable ultrasound features of ICA stenosis were found significantly more often in symptomatic than in asymptomatic patients (71.79% vs. 30.71% for stenosis degree ≥ 70%, p = 0.001 and 61.23% vs. 38.46% for unstable plaque morphology, p = 0.01). Patients with ICA stenosis had significantly higher serum concentrations of interleukin-6, fibrinogen, ESR and higher CRP values than the individuals from the control group (p = 0.001, p = 0.009, p = 0.036, p = 0.009 respectively). Patients with unstable plaques structure had significantly higher concentrations of TNF-α, interleukin-6, fibrinogen, higher number of leukocytes, monocytes and higher CRP values than patients with stable plaques (p = 0.008, p = 0.049, p = 0.012, p = 0.0002, p = 0.006, p = 0.0003 respectively). No significant differences in above-mentioned parameters between the groups with stenosis < 70% and ≥ 70% were found.
There is a relationship between the activity of the selected inflammatory markers in serum and atherosclerotic unstable internal carotid artery stenosis. There is no relationship between serum concentration of inflammatory markers and degree of carotid artery stenosis.
PMCID: PMC3648829  PMID: 23671435
atherosclerosis; artery stenosis; inflammatory markers
24.  Leukotriene B4 Levels in Human Atherosclerotic Plaques and Abdominal Aortic Aneurysms 
PLoS ONE  2014;9(1):e86522.
Leukotriene B4 (LTB4) has been associated with the initiation and progression of atherosclerosis and abdominal aortic aneurysm (AAA) formation. However, associations of LTB4 levels with tissue characteristics and adverse clinical outcome of advanced atherosclerosis and AAA are scarcely studied. We hypothesized that LTB4 levels are associated with a vulnerable plaque phenotype and adverse clinical outcome. Furthermore, that LTB4 levels are associated with inflammatory AAA and adverse clinical outcome.
Atherosclerotic plaques and AAA specimens were selected from two independent databases for LTB4 measurements. Plaques were isolated during carotid endarterectomy from asymptomatic (n = 58) or symptomatic (n = 317) patients, classified prior to surgery. LTB4 levels were measured without prior lipid extraction and levels were corrected for protein content. LTB4 levels were related to plaque phenotype, baseline patient characteristics and clinical outcome within three years following surgery. Seven non-diseased mammary artery specimens served as controls. AAA specimens were isolated during open repair, classified as elective (n = 189), symptomatic (n = 29) or ruptured (n = 23). LTB4 levels were measured similar to the plaque measurements and were related to tissue characteristics, baseline patient characteristics and clinical outcome. Twenty-six non-diseased aortic specimens served as controls.
LTB4 levels corrected for protein content were not significantly associated with histological characteristics specific for vulnerable plaques or inflammatory AAA as well as clinical presentation. Moreover, it could not predict secondary manifestations independently investigated in both databases. However, LTB4 levels were significantly lower in controls compared to plaque (p = 0.025) or AAA (p = 0.017).
LTB4 levels were not associated with a vulnerable plaque phenotype or inflammatory AAA or clinical presentation. This study does not provide supportive evidence for a role of LTB4 in atherosclerotic plaque destabilization or AAA expansion. However, these data should be interpreted with care, since LTB4 measurements were performed without prior lipid extractions.
PMCID: PMC3903534  PMID: 24475136
25.  Infectious burden and atherosclerosis: A clinical issue 
Atherosclerotic cardiovascular diseases, chronic inflammatory diseases of multifactorial etiology, are the leading cause of death worldwide. In the last decade, more infectious agents, labeled as “infectious burden”, rather than any single pathogen, have been showed to contribute to the development of atherosclerosis through different mechanisms. Some microorganisms, such as Chlamydia pneumoniae (C. pneumoniae), human cytomegalovirus, etc. may act directly on the arterial wall contributing to endothelial dysfunction, foam cell formation, smooth muscle cell proliferation, platelet aggregation as well as cytokine, reactive oxygen specie, growth factor, and cellular adhesion molecule production. Others, such as Helicobacter pylori (H. pylori), influenza virus, etc. may induce a systemic inflammation which in turn may damage the vascular wall (e.g., by cytokines and proteases). Moreover, another indirect mechanism by which some infectious agents (such as H. pylori, C. pneumoniae, periodontal pathogens, etc.) may play a role in the pathogenesis of atherosclerosis is molecular mimicry. Given the complexity of the mechanisms by which each microorganism may contribute to atherosclerosis, defining the interplay of more infectious agents is far more difficult because the pro-atherogenic effect of each pathogen might be amplified. Clearly, continued research and a greater awareness will be helpful to improve our knowledge on the complex interaction between the infectious burden and atherosclerosis.
PMCID: PMC4097149  PMID: 25032197
Infectious burden; Atherosclerosis; Bacteria; Virus; Pathogenetic mechanisms

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