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D Dimitroulis

Publications and source records attributed to D Dimitroulis.

4 recordsLinked to original sources
PubMed2006

Inflammation and Chlamydia pneumoniae infection correlate with the severity of peripheral arterial disease.

BACKGROUND: Our aim was to investigate the association of inflammation and Chlamydia pneumoniae infection with the presence and severity of peripheral arterial disease. METHODS: Twenty-eight patients whose initial claudication distance (ICD) in the traditional constant-load treadmill test was <200 m, underwent femoral endarterectomy as part of their interventional treatment (group A). Group B consisted of 23 patients whose ICD was >200 m and were put on medication and a daily exercise program. The control group consisted of 30 non-vascular patients of the Ophthalmology Department (group C). We measured the levels of C-reactive protein, fibrinogen, vascular cell adhesion molecule-1 and tumor necrosis factor-alpha, and the titers of IgA and IgG antibodies against C. pneumoniae in the serum of all the patients. Finally, the atheromas and vein segments of group A patients, were immunohistochemically (IHC) examined for the presence of C. pneumoniae. RESULTS: Peripheral arterial disease (PAD) patients, had significantly higher CRP (p=0.026) and anti-Cp IgA levels (p=0.001) when compared to control subjects, after a multiple linear regression analysis. The odds ratio for the prevalence of femoral atherosclerosis was 3.16 for IgA seropositive patients (CI 1.15-8.67). When comparing group A and group B patients, CRP (p=0.003) and IgA (p=0.011), were significantly correlated with severe PAD. Group A patients with positive immunohistochemical examination of the plaque, had higher anti-Cp IgA levels (p=0.023) and TNF-alpha values (p=0.031), compared to the IHC negative patients. C. pneumoniae was detected in 50% of the femoral atheromas, but in only 3.6% of the veins. CONCLUSION: This study supports the hypothesis that inflammation (CRP) and chronic C. pneumoniae infection (IgA seropositivity), have an important role in lower limb atherosclerosis and correlate with the severity of the disease.

Aged↗
PubMed2005

Inflammation and atherosclerosis.

PURPOSE: The aim of this article is to discuss the role of inflammation in atherosclerosis. SUMMARY: An initial chemical, mechanical or immunological insult induces endothelial dysfunction. This triggers a cascade of inflammatory reactions, in which monocytes, macrophages, T lymphocytes and vascular smooth muscle cells participate. Leukocyte adhesion molecules, cytokines, growth factors and metalloproteinases participate in all stages of atherogenesis. Almost all of the traditional risk factors for atherosclerosis are associated with and participate in the inflammatory process. Many infectious agents, mainly Chlamydia pneumoniae, have been proposed as potential triggers of the cascade. The immune system has been implicated in plaque formation, through the activation of cellular and humoral immunity against innate or microbial heat shock protein 60. Methods of detection of systemic or local plaque inflammation have been developed and research is being conducted on the potential use of anti-inflammatory and antibiotic drugs in atherosclerosis.

Atherosclerosis↗
PubMed2005

Long-term treatment of deep venous thrombosis with a low molecular weight heparin (tinzaparin): a prospective randomized trial.

OBJECTIVES: Evaluation of the effectiveness and safety of the low molecular weight heparin (LMWH) tinzaparin versus unfractionated heparin (UFH) followed by acenocoumarol in proximal deep venous thrombosis (DVT). DESIGN: Prospective, randomized clinical trial. MATERIAL AND METHODS: Consecutive patients (n=108) with acute leg DVT, confirmed by duplex, were randomized to either tinzaparin alone or UFH and acenocoumarol for 6 months. Patients were evaluated ultrasonographically at entry, 1, 3, 6 and 12 months. Thrombus regression, reflux distribution and the incidence of complications were studied. A cost-analysis, comparing the two treatments, was performed. RESULTS: The overall incidence of major events (mortality, DVT recurrence, pulmonary embolism, major bleeding, heparin-induced thrombocytopenia) was significantly different (p=0.035) in favor of tinzaparin (7 versus 17 events). The ultrasonographic clot volume score (an index of recanalization) decreased significantly in both treatment groups. However, tinzaparin produced significantly more extended overall recanalization from 3 months onwards (p<0.02). Thrombus regression was equivalent or in favor of tinzaparin in the different DVT subgroups and venous segments, but the statistical significance varied. Reflux showed non-significant differences overall or in subgroups. A cost-analysis resulted in favor of LMWH. CONCLUSIONS: A fixed daily dose of tinzaparin for 6 months was at least as effective and safe as UFH and acenocoumarol. Regarding major events and recanalization, there was a significant benefit in favor of tinzaparin. Long-term DVT treatment with tinzaparin could represent an alternative to conventional treatment.

Acenocoumarol↗