scholarly journals Chlamydia pneumoniae and Atherosclerosis: Critical Assessment of Diagnostic Methods and Relevance to Treatment Studies

2002 ◽  
Vol 15 (1) ◽  
pp. 1-20 ◽  
Author(s):  
Jens Boman ◽  
Margaret R. Hammerschlag
Keyword(s):  
Chlamydia Pneumoniae ◽  
Vascular Tissue ◽  
Diagnostic Methods ◽  
Immunocytochemical Staining ◽  
Infectious Agents ◽  
Serologic Marker ◽  
Increased Risk ◽  
Adverse Cardiac Outcome ◽  
Cardiac Outcome ◽  
Progression Of Atherosclerosis

SUMMARY A number of studies have found that inflammation of the vessel wall plays an essential role in both the initiation and progression of atherosclerosis and erosion and fissure and the eventual rupture of plaques. Chlamydia pneumoniae is one of the infectious agents that have been investigated as possible causes of this inflammation. Initial studies of the association of C. pneumoniae and cardiovascular disease (CVD) were seroepidemiologic, and these were followed by studies in which the organism was identified in vascular tissue from patients with CVD by electron microscopy, PCR and immunocytochemical staining (ICC). C. pneumoniae has also been isolated by culture from vascular tissue in a small number patients. However, no single serologic, PCR, or ICC assay has been used consistently across all studies. The assays used are also not standardized. Recent studies of serologic and PCR assays for diagnosis of C. pneumoniae infection have suggested that there may be substantial interlaboratory variation in the performance of these tests. It now appears that some of the inconsistency of results from study to study may be due, in part, to lack of standardized methods. Although initial seroepi-demiologic studies demonstrated a significantly increased risk of adverse cardiac outcome in patients who were seropositive, subsequent prospective studies found either small or no in-creased risk. In addition to the lack of consistent serologic criteria, recent evaluations have demonstrated inherent problems with performance of the most widely used serologic methods. Most importantly, we do not have a reliable serologic marker for chronic or persistent C. pneumoniae infection.

Role of Chlamydia pneumoniae in atherosclerosis

2008 ◽  
Vol 114 (8) ◽  
pp. 509-531 ◽  
Author(s):  
Caroline Watson ◽  
Nicholas J. Alp
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Cardiovascular Events ◽  
Chlamydia Pneumoniae ◽  
Attributable Risk ◽  
Future Research ◽  
Infectious Agents ◽  
Contributory Factors ◽  
Progression Of Atherosclerosis

Cardiovascular disease, resulting from atherosclerosis, is a leading cause of global morbidity and mortality. Genetic predisposition and classical environmental risk factors explain much of the attributable risk for cardiovascular events in populations, but other risk factors for the development and progression of atherosclerosis, which can be identified and modified, may be important therapeutic targets. Infectious agents, such as Chlamydia pneumoniae, have been proposed as contributory factors in the pathogenesis of atherosclerosis. In the present review, we consider the experimental evidence that has accumulated over the last 20 years evaluating the role of C. pneumoniae in atherosclerosis and suggest areas for future research in this field.

scholarly journals Infectious Agents Are Not Necessary for Murine Atherogenesis

2000 ◽  
Vol 191 (8) ◽  
pp. 1437-1442 ◽  
Author(s):  
Samuel D. Wright ◽  
Charlotte Burton ◽  
Melba Hernandez ◽  
Heide Hassing ◽  
Judy Montenegro ◽  
...  
Keyword(s):  
Chlamydia Pneumoniae ◽  
Viral Infections ◽  
Infectious Agent ◽  
Infectious Agents ◽  
Germ Free ◽  
Atherosclerotic Lesions ◽  
Apo E ◽  
Microbial Agents ◽  
Progression Of Atherosclerosis

Recent work has revealed correlations between bacterial or viral infections and atherosclerotic disease. One particular bacterium, Chlamydia pneumoniae, has been observed at high frequency in human atherosclerotic lesions, prompting the hypothesis that infectious agents may be necessary for the initiation or progression of atherosclerosis. To determine if responses to gram-negative bacteria are necessary for atherogenesis, we first bred atherosclerosis-prone apolipoprotein (apo) E−/− (deficient) mice with animals incapable of responding to bacterial lipopolysaccharide. Atherogenesis was unaffected in doubly deficient animals. We further tested the role of infectious agents by creating a colony of germ-free apo E−/− mice. These animals are free of all microbial agents (bacterial, viral, and fungal). Atherosclerosis in germ-free animals was not measurably different from that in animals raised with ambient levels of microbial challenge. These studies show that infection is not necessary for murine atherosclerosis and that, unlike peptic ulcer, Koch's postulates cannot be fulfilled for any infectious agent in atherosclerosis.

Pathogens and atherosclerosis: Update on the potential contribution of multiple infectious organisms to the pathogenesis of atherosclerosis

2011 ◽  
Vol 106 (11) ◽  
pp. 858-867 ◽  
Author(s):  
Lee Ann Campbell ◽  
Michael Rosenfeld
Keyword(s):  
Cardiovascular Disease ◽  
Influenza A ◽  
Chlamydia Pneumoniae ◽  
Acute Phase Proteins ◽  
Experimental Studies ◽  
Epidemiological Studies ◽  
Potential Contribution ◽  
Infectious Agents ◽  
Or Groups ◽  
Increased Risk

SummaryIt is currently unclear what causes the chronic inflammation within atherosclerotic plaques. One emerging paradigm suggests that infection with bacteria and/or viruses can contribute to the pathogenesis of atherosclerosis either via direct infection of vascular cells or via the indirect effects of cytokines or acute phase proteins induced by infection at non-vascular sites. This paradigm has been supported by multiple epidemiological studies that have established positive associations between the risk of cardiovascular disease morbidity and mortality and markers of infection. It has also been supported by experimental studies showing an acceleration of the development of atherosclerosis following infection of hyperlipidaemic animal models. There are now a large number of different infectious agents that have been linked with an increased risk of cardiovascular disease. These include: Chlamydia pneumoniae, Porphyromonas gingivalis, Helicobacter pylori, influenza A virus, hepatitis C virus, cytomegalovirus, and human immunodeficiency virus. However, there are significant differences in the strength of the data supporting their association with cardiovascular disease pathogenesis. In some cases, the infectious agents are found within the plaques and viable organisms can be isolated suggesting a direct effect. In other cases, the association is entirely based on biomarkers. In the following review, we evaluate the strength of the data for individual or groups of pathogens with regard to atherosclerosis pathogenesis and their potential contribution by direct or indirect mechanisms and discuss whether the established associations are supportive of the infectious disease paradigm. We also discuss the failure of antibiotic trials and the question of persistent infection.

scholarly journals POS1065 CIRCULATING ENDOTHELIAL CELLS AS A MARKER OF CARDIOVASCULAR DISEASES IN PATIENTS WITH PSORIATIC ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 811.1-811
Author(s):  
S. Smiyan ◽  
A. Bilukha ◽  
B. Koshak
Keyword(s):  
Endothelial Cells ◽  
Cardiovascular Risk ◽  
Psoriatic Arthritis ◽  
Cardiovascular Diseases ◽  
Endothelial Damage ◽  
Diagnostic Methods ◽  
Circulating Endothelial Cells ◽  
Control Group ◽  
Cardiovascular Morbidity And Mortality ◽  
Increased Risk

Background:Psoriatic arthritis (PsA) is a chronic inflammatory joint disease which develops in patients with psoriasis. Mortality among patients with PsA is 1.28 times higher than population levels and in most cases it is caused by cardio-vascular diseases (CVD). Those patients have increased risk of clinical and subclinical CVD, mostly due to endothelial dysfunction (ED) and accelerated atherosclerosis. Elevated levels of circulating endothelial cells (CEC) have been described in different cardiovascular pathologies, suggesting their potential use as diagnostic biomarkers for dysfunction of endothelium.Objectives:To identify the potential role of circulating endothelial cells as a marker of cardiovascular diseases in patients with psoriatic arthritis.Methods:In total, ninety-four patients with PsA, who fulfilled the disease criteria (CASPAR) were examined using standard diagnostic methods (including C-reactive protein (CRP), lipid profile) and evaluation endothelium-dependent vasodilation in response to reactive hyperemia (EDVD). Circulating endothelial cells were determined in the peripheral venous blood samples by flow cytometry and counted according to a standardized protocol using a fluorescence microscope after acridine orange labeling. The control group, which were consisted from thirty healthy adults were also examined.Results:CEC were quantified in patients with PsA (7,15 ± 0,19 cells mL−1) and in the control group (4,05 ± 0,11 cells mL−1). Comparing two groups of patients, endothelial circulating cell level was significantly different (p = 0.0001). Finally, we analyzed the relationship between CEC count, comorbidities, cardiovascular risk factors and EDVD in patients with PsA. Increased CEC levels were associated with obesity (r=0,62), duration of disease (r=0,65), age (r=0,67), increased CRP (r=0,76), high blood pressure (r=0,87) and decreased EDVD (r=–0,91).Conclusion:CEC counts were significantly higher in patients with PsA, positively correlated with the main factors of CVD, and another specific marker of ED - EDVD. Elevated CEC levels were also associated with high concentrations of CRP, which plays a direct role in promoting vascular inflammation, vessel damage and clinical CVD events. In conclusion, increased CEC counts provide a direct proof of endothelial damage in patient with PsA and a clinically informative diagnostic tool for endothelial damage in pre-symptomatic CVD. As CEC are one of the most sensitive biomarker for ED, further efforts should concentrate on improving the sensitivity of its detection in order to increase diagnostic sensitivity.References:[1]Maura Farinacci, Thomas Krahn, Wilfried Dinh, et al. Circulating endothelial cells as biomarker for cardiovascular diseases. Res Pract Thromb Haemost, Vol. 3, Issue, 2019, P.49-58;[2]C. Horreau, C. Pouplard, E. Brenautet, et al. Cardiovascular morbidity and mortality in psoriasis and psoriatic arthritis: a systematic literature review. J Eur Acad Dermatol Venereol, Vol. 27, Issue 3, 2013, P.12-19;[3]Frank Verhoeven, Clément Prati, Céline Demougeot, Daniel Wendling. Cardiovascular risk in psoriatic arthritis, a narrative review. Joint Bone Spine, Vol. 87, Issue 5, 2020, P.413-418;Disclosure of Interests:None declared.

scholarly journals Early chronic pancreatitis: is a clinical diagnosis possible?

2019 ◽  
Vol 44 (3) ◽  
pp. 33-41
Author(s):  
N. B. Gubergrits ◽  
N. V. Byelyayeva ◽  
A. Ye. Klochkov ◽  
G. M. Lukashevich ◽  
V. S. Rachmetova
Keyword(s):  
Chronic Pancreatitis ◽  
Diagnostic Criteria ◽  
Pancreatic Insufficiency ◽  
Exocrine Pancreatic Insufficiency ◽  
Diagnostic Methods ◽  
Test Results ◽  
International Consensus ◽  
Financial Costs ◽  
Increased Risk ◽  
Antifibrotic Drugs

A “fatal chain” in pancreatology is discussed in the present article; peculiar attention is paid to an early chronic pancreatitis (CP), being one of the little-studied “links” in this range and corresponding to the latent period of CP(persistence of inflammation with the presence of biomarkers of CP, which does not meet the diagnostic criteria of proven or late CP, as well as the appearance of signs of exocrine pancreatic insufficiency in the form of reduced functional test results to 70% of normal). Features of the different stages of the pancreatic diseases’ course are presented, substantiatinganeed for a practical identification of the “early CP” diagnosis: "for" - the possibility of timely diagnosis, the identification of patients with an increased risk of prostate cancer; "against": the lack of specific antifibrotic, anti-inflammatory therapy, an increase in financial costs, no impact on the clinical outcome.Advantages and disadvantages of using the “early CP” diagnosis in practice are considered. The authors cite the provisions of the International Consensus on early CP, and list the current diagnostic criteria for this diseaseelaborated by the Japanese Pancreas Society. Advantages and disadvantagesof the instrumental and laboratory diagnostic methods are analyzed, including probable early CP biomarkers (interleukin-8, prostaglandin E2). The most suitable therapeutic tactics for management of patients with early CP are presented, including correction of the exocrine and endocrinepancreatic function, as well as the use of antifibrotic drugs.

Fetal growth restriction: unresolved issues of risk stratification, early diagnosis, and obstetric management

2021 ◽  
Vol 20 (5) ◽  
pp. 76-86
Author(s):  
N.M. Podzolkova ◽  
◽  
Yu.V. Denisova ◽  
M.Yu. Skvortsova ◽  
T.V. Denisova ◽  
...  
Keyword(s):  
Early Diagnosis ◽  
Risk Stratification ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Diagnostic Methods ◽  
Growth Potential ◽  
Increased Risk ◽  
Obstetric Management ◽  
Language Literature

Fetal growth restriction (FGR) refers to pregnancy complications associated with an increased risk of perinatal morbidity and mortality and is defined in the Russian-language literature as the fetal size and weight retardation in relation to the norm for a given gestational age, and in the English-language literature – as the inability of the fetus to realize its genetically determined growth potential. FGR is the cause of 43% of stillbirths of unspecified etiology, and some cases remain undiagnosed even in high-risk populations due to the lack of universal diagnostic standards for this pathology. The review presents a critical analysis of the existing definitions of FGR, the latest data on risk factors, an assessment of diagnostic methods for its early and late forms, the prospects of using biomarkers and instrumental methods of examination in predicting adverse perinatal outcomes, and an algorithm for the management of pregnancy complicated by FGR. For a more complete coverage of the literature and deeper understanding of the nosology, attention is focused on FGR that is not accompanied by preeclampsia and other hypertensive disorders, which occur in about 30% of cases. Key words: placental insufficiency, fetometry, percentile, pulsatility index, fetal growth restriction For citation: Podzolkova N.M., Denisova Yu.V., Skvortsova M.Yu., Denisova T.V., Shovgenova D.S. Fetal growth restriction: unresolved issues of risk stratification, early diagnosis, and obstetric management. Vopr. ginekol. akus. perinatol. (Gynecology, Obstetrics and Perinatology). 2021; 20(5): 76–86. (In Russian). DOI: 10.20953/1726-1678-2021-5-76-86

Abstract 5108: Microalbuminuria is Associated with Progression of Coronary Atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA)

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Andrew P DeFilippis ◽  
Holly J Kramer ◽  
Ronit Katz ◽  
Nathan Wong ◽  
Alain Bertoni ◽  
...  
Keyword(s):  
Lipid Lowering ◽  
Albumin Creatinine Ratio ◽  
Ethnic Study ◽  
Median Increase ◽  
Increased Risk ◽  
History Of ◽  
Relationship Of ◽  
The Relationship ◽  
Progression Of Atherosclerosis

Background: Microalbuminuria (MA) is associated with an increased risk of cardiovascular disease (CVD) but the mechanism by which microalbuminuria imparts this increased risk is not known. In this study we assessed the relationship between MA and the development and progression of atherosclerosis by measuring the incidence of new CAC and the progression of existing CAC in individuals free of clinical CVD. Methods : The Multi-Ethnic Study of Atherosclerosis (MESA) is a prospective cohort study of 6,814 participants free of clinical CVD at entry who underwent assessment of coronary artery calcification (CAC) by computerized tomography at baseline. Overall, 6,775 individuals had data available on urinary albumin creatinine ratio (UACR); 1,109 individuals were excluded for missing data or macroalbuminuria (UACR≥300 mg/g). Incident CAC was defined as detectable CAC at follow-up among those with CAC=0 at baseline, and absolute CAC score change among those with CAC>0 at baseline. Relative risk (RR) regression adjusted for covariates; and multivariable adjusted median regression was employed to assess the independent relationship of MA with CAC incidence and progression. Results : Of the 5,666 subjects (mean age 62±10 years, 48% males), baseline MA was seen in 424 (7%) participants, who were more likely to have CAC compared to those with normal UACR (62% vs. 48%, p<0.0001). During a mean follow-up of 2.4±0.8 years, those with MA were more likely to develop CAC (28% vs. 15%, p<0.0001) and they had a higher absolute median increase in CAC (47 vs. 29 Agatston Units, p<0.0001). After adjustment for age, gender, ethnicity, site, follow-up duration, diabetes, hypertension, smoking, family history of heart attack, total cholesterol, lipid lowering medications and body mass index; MA was associated with incident CAC (RR 1.65; 95%CI 1.41–2.48) among those with CAC=0 at baseline. Among those with CAC>0 at baseline, MA was associated with a median increase in CAC of 7.93 (95%CI 0.38 –15.47) Agatston Units in multivariable adjusted analyses (variables noted above). Conclusion : MA is independently associated with development of incident CAC and progression of CAC in an asymptomatic multi-ethnic population, and may in part explain its associated increased risk of CVD.

Abstract 2125: P Wave Morphology Is a Predictor of Poor Cardiac Outcome and Death in MADIT II Patients

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Fredrik Holmqvist ◽  
Pyotr G Platonov ◽  
Scott McNitt ◽  
Slava Polonsky ◽  
Jonas Carlson ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Death ◽  
P Wave ◽  
Wave Duration ◽  
P Wave Duration ◽  
Increased Risk ◽  
All Cause Mortality ◽  
Wave Morphology ◽  
Cardiac Outcome ◽  
Madit Ii

The objective of the present study was to non-invasively analyse atrial electrophysiology to identify markers associated with increased risk of mortality and deterioration of heart failure in a high-risk population with advanced CHF and a history of acute myocardial infarction. Patients included in MADIT II with sinus rhythm at baseline were studied (n=802). Unfiltered and bandpass filtered signal-averaged P waves were analyzed to determine orthogonal P wave morphology, P wave duration and RMS20. The association between P wave parameters and data on the clinical course and cardiac events during a mean follow-up of 20 months was analyzed. P wave duration was 139±23 ms and the RMS20 was 1.9±1.1 μV. None of these parameters were significantly associated with poor cardiac outcome. Differences in P wave morphology were independently predictive of non-sudden cardiac death (HR 2.66; 95% CI 1.41–5.04, P=0.0027). In addition, in univariate analyses differences in P wave morphology were found to be associated with an increased risk of all-cause mortality (HR 1.35; 95%CI 1.01–1.81, P=0.042) and cardiac death (HR 1.54; 95%CI 1.10 –2.16, P=0.011) (figure ) In the present study the value of analyzing the P wave morphology in patients with previous myocardial infarction and CHF is demonstrated. Changes in P wave morphology were shown to be independently predictive of increased risk of non-sudden cardiac death. Furthermore, statistically significant associations between P wave morphology changes and all-cause mortality, cardiac death and CHF hospitalization was demonstrated.

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