Infectious agents in coronary atheromas: a possible role in the pathogenesis of plaque rupture and acute myocardial infarction

Higuchi, Maria de Lourdes; Ramires, José Antônio Franchini

doi:10.1590/s0036-46652002000400007

Cited by 17 publications

(13 citation statements)

References 31 publications

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“…On one hand, as we have described in the aortae, previous researches of our laboratory have shown that even people without atherosclerosis can present some amount of bacteria in coronary arteries. Regarding the arteries, it was shown significant differences between the groups with and without atherosclerosis and between stable and unstable plaques [4][5][6][7]. These points strengthen PIRES, LJT ET AL -Morphometrical quantification of Chlamydia pneumoniae and Mycoplasma pneumoniae in human atherosclerotic abdominal aortic aneurysms the necessity of a quantitative method to better analyze the role of both Chlamydia and mycoplasma in the diseases.…”

Section: Discussionmentioning

confidence: 74%

“…Among others [3], the Chlamydia pneumoniae attracted the attention of many authors who believed in the role of the infectious agents in this disease, including the coronary arteries. Regarding the arteries, previous studies carried out in our laboratory have revealed not only the presence of this kind of bacterium, but also the Mycoplasma pneumoniae [4][5][6][7]. Such studies have found the Mycoplasma pneumoniae in almost all atheromas (atheromata), but the development of plaque instability is highly believed to be correlated with a large amount of both bacteria.…”

Section: Introductionmentioning

confidence: 82%

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Quantificação morfométrica de Chlamydia pneumoniae e Mycoplasma pneumoniae em aneurismas de aorta abdominal humana

Pires¹,

Gutierrez²

2007

Rev Bras Cir Cardiovasc

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RBCCV 44205-908Quantificação morfométrica de Chlamydia pneumoniae e Mycoplasma pneumoniae em aneurismas de aorta abdominal humana Morphometrical quantification of Chlamydia pneumoniae and Mycoplasma pneumoniae in human atherosclerotic abdominal aortic aneurysms Abstract 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.Descriptors: Aorta, pathology. Aortic aneurysm, abdominal. Chlamydophila pneumoniae. Mycoplasma pneumoniae. Atherosclerosis. Autopsy. Rev Bras Cir Cardiovasc 2007; 22(3): 322-331 PIRES, LJT ET AL -Morphometrical quantification ofChlamydia pneumoniae and Mycoplasma pneumoniae in human atherosclerotic abdominal aortic aneurysms

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Section: Discussionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 82%

Quantificação morfométrica de Chlamydia pneumoniae e Mycoplasma pneumoniae em aneurismas de aorta abdominal humana

Pires¹,

Gutierrez²

2007

Rev Bras Cir Cardiovasc

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“…Solid line corresponds to activation (→) or inhibition (-<) events. participation of mycoplasmas in vulnerable plaques by their entering the subendothelial space and creating conditions that favor fat accumulation, dysfunction of the immunological and endothelial response, inflammation and increasing apoptosis, all of which are fundamental ingredients for plaque rupture (13,14,21). The bacteria induce depression in the immune response (27), mainly of T cells through possible mechanisms of apoptosis (22) with a reduction in the CD4 T cells, which may be a facilitating mechanism for other infections.…”

Section: Discussionmentioning

confidence: 99%

“…These are organisms with one common feature -an ability to persist -but of quite different biology. These infections (in particular, mycoplasma infections) were shown to be essential factors in the development of atherosclerosis, plaque destabilizing and acute myocardial infarction (AMI) (13,14). Infectious agents biasing hemostasis and the vascular system may promote atherogenesis and AMI according to the known immune and biochemical mechanisms of reactivity to infectious agents (18,27,30).…”

Section: Introductionmentioning

confidence: 99%

The Pattern of Acute Myocardial Infarction in People with Opportunistic Infections

Arleevskiy

Чернова

Saphin

et al. 2007

Acta Med. (Hradec Kralove, Czech Repub.)

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Summary: First comparative analysis for some hemocoagulation reactions, immune state of acute myocardial infarction has been done in two groups of patients -with mycoplasma infections and without one. Postinfarction complications in the groups were observed. Atherosclerotic plaques of the patients were also studied on a presence of mycoplasmas and a content of strontium and zinc. A tendency to a mild pattern of acute myocardial infarction was observed in patients with mycoplasma infections. The role of mycoplasmas in atherogenesis and acute myocardial infarction is discussed.

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“…2 C pneumoniae is postulated to contribute to the pathophysiology of atherosclerosis, including an increase in intimamedia thickness and plaque size and a progressive reduction in luminal diameter. 3 In animal models, C pneumoniae infection causes a profound increase in intima-media thick-ness and atherosclerosis but does not increase the frequency of plaque rupture or thrombogenicity. 4 Therefore, PAD might represent a better population in which to study the impact of antibiotic therapy directed against C pneumoniae.…”

Section: Clinical Perspective P 458mentioning

confidence: 99%

Anti-Chlamydial Antibiotic Therapy for Symptom Improvement in Peripheral Artery Disease

Jaff

Dale²,

Creager

et al. 2009

Circulation

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Background-A potentially strong association exists between Chlamydia pneumoniae and atherosclerosis, but the clinical benefits of antibiotic therapy have not been demonstrated. Preliminary studies of antibiotic therapy in peripheral artery disease have shown a decreased need for revascularization and improved walking ability. The objective of this phase-III trial was to assess the effect of a potent anti-Chlamydial agent, rifalazil, on peak walking time in patients with symptomatic peripheral artery disease. Methods and Results-Patients with intermittent claudication secondary to peripheral artery disease who were seropositive for C pneumoniae were randomized to 25 mg rifalazil once weekly for 8 weeks or matching placebo. Two hundred ninety-seven patients were enrolled from 3 countries and were followed up for 1 year. The meanϮSD ankle brachial index at baseline was 0.63Ϯ0.16. The primary end point, change from baseline in log peak walking time on a graded treadmill, was assessed 180 days after randomization. Secondary end points included changes in claudication onset time and quality of life, assessed with the Walking Impairment Questionnaire and the Short Form Medical Outcomes 36. No benefit of rifalazil therapy was found in the primary or any secondary end point among this cohort of patients with peripheral artery disease. The group treated with rifalazil improved their peak walking times by 23% (95% confidence interval, 15 to 31) from baseline to day 180, whereas the placebo group improved by 18% (95% confidence interval, 11 to 26; Pϭ0.38). Peak walking time, claudication onset time, Walking Impairment Questionnaire, and Short Form Medical Outcomes 36 showed no treatment-by-time interaction during the 360-day study period. Thirty-two adjudicated cardiovascular events occurred, 16 in each treatment group. Conclusions-Rifalazil did not improve exercise performance or quality of life in patients with intermittent claudication.No safety concerns were identified. Given the very small effect size, it is unlikely that larger studies would demonstrate a symptomatic benefit of this therapy in peripheral artery disease. (Circulation. 2009;119:452-458.)

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Infectious agents in coronary atheromas: a possible role in the pathogenesis of plaque rupture and acute myocardial infarction

Cited by 17 publications

References 31 publications

Quantificação morfométrica de Chlamydia pneumoniae e Mycoplasma pneumoniae em aneurismas de aorta abdominal humana

Quantificação morfométrica de Chlamydia pneumoniae e Mycoplasma pneumoniae em aneurismas de aorta abdominal humana

The Pattern of Acute Myocardial Infarction in People with Opportunistic Infections

Anti-Chlamydial Antibiotic Therapy for Symptom Improvement in Peripheral Artery Disease

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