scholarly journals The Role of Chlamydophila (Chlamydia) Pneumoniae in the Pathogenesis of Coronary Artery Disease

Chlamydia ◽  
10.5772/30456 ◽  
2012 ◽  
Author(s):  
Miroslaw Brykczynski
2009 ◽  
Vol 2009 ◽  
pp. 1-5 ◽  
Author(s):  
Hem Chandra Jha ◽  
Pragya Srivastava ◽  
Rakesh Sarkar ◽  
Jagdish Prasad ◽  
Aruna Singh Mittal

Plasma inflammatory markers have been shown to be predictors for cardiovascular risk, however, there is no study where the levels of plasma circulatory markers have been evaluated in coronary artery disease patients (CAD pts) positive forC. pneumoniaeIgA and high sensitive C-reactive protein (hsCRP) which may help in better understanding of disease pathogenesis. A total of 192 patients and 192 controls attending the Cardiology Outpatient Department of Safdarjung Hospital were enrolled. The levels of plasma circulatory inflammatory markers were evaluated by ELISA. The levels of circulatory plasma markers (IL-4, IL-8, IL-13, ICAM-1, and VCAM-1) were significantly higher, whereas, levels of IL-10 and IFN-γwere significantly lower in CAD pts compared to healthy controls. The levels of IL-4, IL-8, and ICAM-1 (P=.007, .015, and .048) were significantly higher, however, IL-10 and IFN-γwere significantly lower (P<.001,<.001) inC. pneumoniaeIgA positive CAD pts. The levels of IL-4, IL-8, IL-13, ICAM-1, and VCAM-1 were higher but not significant and levels of IL-10 and IFN-γwere significantly (P<.001,<.001) lower in hsCRP positive CAD pts. Our study suggested that circulatory cytokines, namely, IL-4, IL-8, and adhesive molecules like ICAM-1 were enhanced after infection withC. pneumoniaewhereas in contrast to this IL-10 and IFN-λwere lowered. Suggesting the important role of these cytokines in progression of CAD.


2004 ◽  
Vol 4 (1) ◽  
pp. 19-22
Author(s):  
Mateja Legan ◽  
Olga Vraspir-Porenta ◽  
Darja Kese ◽  
Ruda Zorc-Plesković ◽  
Marjeta Zorc

BACKGROUND AND PURPOSE: To investigate the histopathologic characteristics of atherosclerotic lessions in diffuse coronary artery disease and to evaluate the possible inflammatory role of chronic infection with Chlamydia pneumoniae (CP).MATERIALS AND METHODS: For 10 patients (males, mean age 61 years) who were surgically treated for grave diffuse coronary artery disease, histomorphological analyses of endarterectomized segments of the coronary arteries were performed. Serological analyses for the detection of CP antibodies in peripheral blood were done, preoperatively.RESULTS AND CONCLUSIONS: Diffuse and concentric atherosclerotic changes from VI to VIII stage according to the Stary classification were found. Immunohistochemical methods revealed infiltrates of T-lymphocytes (80% of cases), B-lymphocytes (40% of cases) and macrophages (80%). Using the nuclear marker for proliferation activity MIB-1, single MIB-1 positive cells were found in 40% of cases. Features of arteriologenesis and vasculitis of newly formed arterioles (as well as thickening of the wall of newly formed arterioles) were found in the vessel wall of 8 patients, 7 of them had chronic infection with CP (preoperative micro-immunofluorescent test results: 1:32<IgG ≥1:512 and IgA≥32), one had passed CP infection (1:32 ≤IgG<1:512, IgA negative). These features were absent in 2 patients, both recovered from CP infection and had not the chronic CP infection at the time of surgery. DNA of Chlamydia pneumoniae was detected using the polymerase chain reaction (PCR) method in the vessel wall of 3 patients who were chosen randomly for this method. This study suggests an inflammatory and proatherogenic role of CP in a high grade atherosclerotic coronary artery wall in diffuse coronary artery disease.


2011 ◽  
Vol 5 (08) ◽  
pp. 580-586 ◽  
Author(s):  
Mehvash Haider ◽  
Meher Rizvi ◽  
Abida Malik ◽  
Mohammad Azam ◽  
Mohammad Urooj Rabbani

Introduction: We evaluated the role of inflammation and acute or persistent Chlamydia pneumoniae infection in coronary artery disease (CAD).      Methodology: The study involved 63 cardiovascular disease patients diagnosed with angina and myocardial infarction (MI) and 40 healthy controls. ELISA was performed for detection of C. pneumoniae IgA antibodies and for quantitative analysis of IFN-γ. PCR was performed for detection of the C. pneumoniae 16 SrRNA gene in blood. Results: C. pneumoniae IgA antibodies were detected in 66.66% cases and 41.37% controls. Of IgA seropositive cases 71.43% were MI patients, 61.90% were stable angina patients, and 64.29% unstable angina patients. Of 40 patients whose PCR was done 32.5% were positive of which 76.92% were IgA seropositive. Traditional risk factors were not significantly associated with CAD. The mean value of IFN-γ in cases was 32.12pg/ml and 11.32pg/ml in controls. Elevated IFN-γ was observed in 76.92% of C. pneumoniae IgA seropositives with a mean value of IFN-γ in angina patients of 3.39pg/ml, in unstable angina of 12.91 pg/ml and in MI patients of 23.89 pg/ml. IFN-γ levels in cases who were positive for C. pneumoniae infection by serology and PCR was 55.21 pg/ml. Conclusion: C. pneumoniae infection was significantly associated with CAD risk. The role of acute or persistent infection in progression of CAD to adverse clinical outcome was evident by a high percentage of seropositives among PCR positives. Although IFN-γ alone had a role to play in development of CAD, its values were further enhanced due to recurrent C. pneumoniae infection.


2006 ◽  
Vol 3 (2) ◽  
pp. 68-72
Author(s):  
Jennifer Mieres ◽  
Leslee J Shaw ◽  
Robert C Hendel ◽  
D Douglas Miller ◽  
Robert Bonow ◽  
...  


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 469-P
Author(s):  
MILOS MRAZ ◽  
ANNA CINKAJZLOVA ◽  
ZDENA LACINOVÁ ◽  
JANA KLOUCKOVA ◽  
HELENA KRATOCHVILOVA ◽  
...  

Author(s):  
Г.А. Березовская ◽  
Е.С. Клокова ◽  
Н.Н. Петрищев

Гены тромбообразования и фолатного обмена играют важную роль в развитии и прогрессии ишемической болезни сердца (ИБС). Однако о возможной роли полиморфных маркеров в рецидиве ИБС после чрескожного коронарного вмешательства (ЧКВ) известно недостаточно. Цель исследования: Оценить роль генетических факторов системы тромбообразования и фолатного обмена (полиморфных маркеров генов F5, F2, F13A1, PAI1, HPA1, MTHFR, FGB ), в возобновление клиники ИБС после ЧКВ. Методика: Исследование проводили с использованием выборки из 90 больных ИБС в возрасте от 40 до 75 лет: 75 пациентов после планового ЧКВ (60 мужчин и 15 женщин) и 15 лиц после экстренного ЧКВ (12 мужчин и 3 женщины). Молекулярно-генетическое исследование было выполнено с помощью комплекта реагентов «Сердечно-сосудистые заболевания СтрипМетод»® (ViennaLab Diagnostics GmbH, Австрия), выявляющие следующие варианты: F5, F2, F13A1, PAI1, HPA1, MTHFR, FGB . Результаты: В результате исследования была показана ассоциация полиморфного маркера G103T ( Val34Leu ) гена F13A1 (фактор свертываемости крови 13, субъединица A1) с развитием рецидивирующего состояния ИБС после ЧКВ. Выявлены статистически значимые различия в распределении частот генотипов полиморфного маркера Val34Leu гена F13A1 . Показано, что частота генотипа Val/Val у пациентов с осложнениями была выше, чем у пациентов без таковых: 0,700 и 0,400 соответственно (c = 7,78; p = 0,020), при этом генотип Val/Val проявил себя как фактор риска развития осложнений: ОШ = 3,50 (95%ДИ 1,37-8,93). При сравнении аллелей выявили, что частота аллеля L у больных с осложнениями была ниже, чем у лиц без таковых: 0,167 и 0,375 соответственно (p = 0,004), и носительство аллеля L уменьшало вероятность развития осложнений: ОШ = 0,33 (95%ДИ 0,15-0,72). Заключение: Носительство варианта 34V гена F13A1 , кодирующего A-субъединицу фактора свёртывания 13, предрасполагает к возобновлению клинических проявлений ИБС после ЧКВ. Genes of thrombosis and folate metabolism play an important role in development and progression of coronary artery disease (CAD). However, a possible role of polymorphic markers in CAD relapse following percutaneous coronary intervention (PCI) is not sufficiently understood. Background. Reports have indicated an association of genetic factors generally related with thrombophilia and recurrence of symptoms for coronary artery disease (CAD) following a percutaneous coronary intervention (PCI) due to restenosis and in-stent thrombosis. However, the relapse can also be caused by progression of atherosclerosis and endothelial dysfunction in unoperated blood vessels. Aim: To assess the role of genetic risk factors involved in thrombosis and folate metabolism (polymorphic markers of F5, F2, F13A1, PAI1, HPA1, MTHFR, and FGB genes) in recurrence of CAD symptoms after PCI. Methods: The study included 90 patients with CAD aged 40-75; 75 of these patients had undergone elective PCI (60 men and 15 women) and 15 patients - emergency PCI (12 men and 3 women). Molecular genetic tests were performed using a CVD StripAssays® reagent kit (ViennaLab Diagnostics GmbH, Austria) to identify the following genetic variations: F5, F2, F13A1, PAI1, HPA1, MTHFR, and FGB . Results: The study results showed a significant association of the G103T ( Val34Leu ) polymorphism in the F13A1 gene with relapses of IHD after PCI. Significant differences were found in genotype distribution frequencies of the Val34Leu polymorphism in the F13A1 gene. The frequency of Val / Val genotype was higher in patients with complications than without complications, 0.700 and 0.400, respectively (c = 7.78, p = 0.020). Furthermore, the Val/Val genotype can be classified as a risk factor for complications (OR = 3.50; 95% CI, 1.37-8.93). The L allele frequency was lower in patients with complications than in those without complications (0.167 and 0.375, respectively, p = 0.004), and carriage of the L allele reduced the likelihood of complications (OR = 0.33; 95% CI 0.15-0.72). Conclusion: Carriage of the 34V variant in the F13A1 gene that encodes the coagulation factor XIII A subunit predisposes to a relapse of CAD symptoms after PCI.


Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 737
Author(s):  
Marko Kumric ◽  
Josip A. Borovac ◽  
Tina Ticinovic Kurir ◽  
Dinko Martinovic ◽  
Ivan Frka Separovic ◽  
...  

Coronary artery disease (CAD) is widely recognized as one of the most important clinical entities. In recent years, a large body of accumulated data suggest that coronary artery calcification, a process highly prevalent in patients with CAD, occurs via well-organized biologic processes, rather than passively, as previously regarded. Matrix Gla protein (MGP), a vitamin K-dependent protein, emerged as an important inhibitor of both intimal and medial vascular calcification. The functionality of MGP hinges on two post-translational modifications: phosphorylation and carboxylation. Depending on the above-noted modifications, various species of MGP may exist in circulation, each with their respective level of functionality. Emerging data suggest that dysfunctional species of MGP, markedly, dephosphorylated-uncarboxylated MGP, might find its application as biomarkers of microvascular health, and assist in clinical decision making with regard to initiation of vitamin K supplementation. Hence, in this review we summarized the current knowledge with respect to the role of MGP in the complex network of vascular calcification with concurrent inferences to CAD. In addition, we discussed the effects of warfarin use on MGP functionality, with concomitant implications to coronary plaque stability.


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