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- Johansson, C.S., et al.
(författare)
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Periodontal conditions in patients with coronary heart disease : A case-control study
- 2008
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Ingår i: Journal of Clinical Periodontology. - 0303-6979 .- 1600-051X. ; 35:3, s. 199-205
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Tidskriftsartikel (refereegranskat)abstract
- Aim: This study examined periodontal conditions in patients with coronary heart disease (CHD) and subjects with no history of CHD. Material and Methods: Participants were 161 patients (40-75) with severe angina pectoris (diagnosed as CHD by coronary angiography) who subsequently underwent percutaneous coronary intervention and 162 control subjects with no history of CHD. Periodontal status was recorded. Bone loss was determined on radiographs. Periodontal disease experience was classified into five groups according to Hugoson & Jordan. Results: Periodontal disease experience groups 4 and 5 were more common in the CHD group (25%) compared with the control group (8%). The mean bone level (the distance from the CEJ to the most coronal level of the alveolar bone) was 3.0±1.0 mm in CHD subjects and 2.6±0.8 mm in controls. CHD patients had significantly lower numbers of natural teeth, higher numbers of periodontal pockets 4-6-mm and higher bleeding on probing (%). In a stepwise regression analysis, the factor periodontal disease experience groups 4+5 gave an odds ratio of 5.74 (2.07-15.90) for having CHD after controlling for smoking and age. Conclusion: Severe periodontal disease expressed by several clinical and radiographic parameters was more prevalent among subjects with CHD than among controls. Analysis, the factor periodontal disease experience groups 4+5 gave an odds ratio of 5.74 (2.07-15.90) for having CHD after controlling for smoking and age. © 2008 Blackwell Munksgaard.
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| 2. |
- Järemo, Petter, et al.
(författare)
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Elevated platelet reactivity in stable angina pectoris without significant coronary flow obstruction
- 2008
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Ingår i: Journal of Cardiovascular Medicine. - : Lippincott Williams & Wilkins. - 1558-2027. ; 9:2, s. 129-130
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND:There are many different causes of angina pectoris without significant coronary flow obstruction in major coronary arteries. Examples include Prinzmetal angina and small vessel atherosclerotic disease.METHODS:We investigated individuals with stable angina pectoris subject to elective coronary angiography. To keep the study group as homogeneous as possible, patients with diabetes mellitus were excluded. Subjects with normal coronary angiograms (n = 13) or insignificant (< 50%) coronary flow obstruction(s) (n = 4) were grouped together. The remaining cohort (n = 96) with at least one significant (> or = 50%) flow obstruction in at least one major coronary artery served as controls.RESULTS:Before angiography, platelet activity in vitro on stimulation with a thrombin-receptor activating peptide (TRAP-6) (57 micromol/l and 74 micromol/l) and ADP (1.7 micromol/l and 8.5 micromol/l) was determined. Angina pectoris individuals without significant flow obstruction in major coronary arteries had enhanced platelet reactivity both when stimulated with TRAP-6 and ADP (P < 0.01 for both TRAP-6 concentrations and P < 0.05 for both ADP concentrations, respectively.CONCLUSIONS:It is concluded that angina pectoris without significant flow impediment in major epicardial arteries is associated with augmented platelet reactivity.
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| 6. |
- Järemo, Petter, et al.
(författare)
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Letter: Elevated platelet density and enhanced platelet reactivity in stable angina pectoris complicated by diabetes mellitus type II
- 2009
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Ingår i: Thrombosis Research. - : Elsevier Ltd. - 0049-3848 .- 1879-2472. ; 124:3, s. 373-374
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- The prognosis of coronary heart disease (CHD) has changed for the better. Type II diabetes mellitus (T2DM) complicates CHD and is associated with less favorable prospects and higher rates of coronary recurrence.149 individuals below 75 years of age subject to elective coronary angiography to evaluate chest pain were consented. Patients were eligible if they did not have a history of rheumatic disease. 51 individuals treated medically for T2DM were compared with the remaining subjects (n = 98). Blood samples were obtained before elective coronary angiography.A special designed optical apparatus was used to analyze peak platelet density. Platelet bound fibrinogen after provocation reflecting the activation of the GPIIb-IIIa receptor i.e. platelet reactivity was determined with the use of a flow cytometer.T2DM is associated with augmented platelet density (p < 0.001).Diabetic platelets displayed enhanced reactivity when stimulating with higher concentrations ADP (8.5 μmol/l) (p < 0.01) and TRAP-6 (74 μmol/l) (p < 0.001).DTII patients with stable angina pectoris showed enhanced platelet density, augmented platelet reactivity and increased MPV. Platelets are more reactive in DTII. More aggressive platelets may offer a explanation as to why DTII has an impact upon the prognosis of CHD.
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| 7. |
- Kälvegren, Hanna, et al.
(författare)
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Chlamydia pneumoniae induces nitric oxide synthase and lipoxygenase-dependent production of reactive oxygen species in platelets — effects on oxidation of low-density lipoproteins.
- 2005
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Ingår i: Thrombosis and Haemostasis. - 0340-6245. ; 94:2, s. 327-335
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Tidskriftsartikel (refereegranskat)abstract
- There is increasing evidence that Chlamydia pneumoniae is linked to atherosclerosis and thrombosis. In this regard, we have recently shown that C. pneumoniae stimulates platelet aggregation and secretion, which may play an important role in the progress of atherosclerosis and in thrombotic vascular occlusion. The aims of the present study were to investigate the effects of C. pneumoniae on platelet-mediated formation of reactive oxygen species (ROS) and oxidation of low-density lipoprotein (LDL) in vitro. ROS production was registered as changes in 2´,7`-dichlorofluorescin- fluorescence in platelets with flow cytometry. LDL-oxidation was determined by measuring thiobarbituric acid reactive substances (TBARs). We found that C. pneumoniae stimulated platelet production of ROS.Polymyxin B treatment of C. pneumoniae, but not elevated temperature, abolished the stimulatory effects on platelet ROS- production, which suggests that chlamydial lipopolysaccharide has an important role. In hibition of nitric oxide synthase with nitro-L-arginine, lipoxygenase with 5,8,11-eicosatriynoic acid and protein kinase C with GF 109203X significantly lowered the production of radicals. In contrast, inhibition of NADPH-oxidase with di-phenyleneiodonium (DPI) did not affect the C. pneumoniae induced ROS-production. These findings suggest that the activities of nitric oxide synthase and lipoxygenase are the sources for ROS and that the generation is dependent of the activity of protein kinase C.The C. pneumoniae-induced ROS-production in platelets was associated with an extensive oxidation of LDL, which was significantly higher compared to the effect obtained by separate exposure of LDL to C. pneumoniae or platelets. In conclusion, C. pneumoniae interaction with platelets leading to aggregation, ROS-production and oxidative damage on LDL, may play a crucial role in the development of atherosclerotic cardiovascular disease.
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| 8. |
- Kälvegren, Hanna, et al.
(författare)
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Correlation between rises in Chlamydia pneumoniae-specific antibodies, platelet activation and lipid peroxidation after percutaneous coronary intervention.
- 2008
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Ingår i: European Journal of Clinical Microbiology and Infectious Diseases. - : Springer Science and Business Media LLC. - 0934-9723 .- 1435-4373. ; 27:7, s. 503-511
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Tidskriftsartikel (refereegranskat)abstract
- We recently showed that Chlamydia pneumoniae activates platelets in vitro, with an associated oxidation of low-density lipoproteins. The aim of this study was to investigate whether C. pneumoniae is released during percutaneous coronary intervention (PCI) and, thereby, causes platelet activation and lipid peroxidation. Seventy-three patients undergoing coronary angiography and following PCI or coronary artery bypass graft (CABG) and 57 controls were included in the study. C. pneumoniae antibodies, serotonin and lipid peroxidation were measured before and 24 h, 1 month and 6 months after angiography. The results show that serum C. pneumoniae IgA concentrations were significantly higher in patients than in the controls. Furthermore, in 38% of the C. pneumoniae IgG positive patients, the C. pneumoniae IgG concentration increased 1 month after PCI. The levels of C. pneumoniae IgG antibodies 1 month after PCI correlated with plasma-lipid peroxidation (r = 0.91, P < 0.0001) and platelet-derived serotonin (r = 0.62, P = 0.02). There was no elevation in the total serum IgG 1 month after PCI. In conclusion, the present results suggest that PCI treatment of coronary stenosis releases C. pneumoniae from the atherosclerotic lesions, which leads to platelet activation and lipid peroxidation.
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| 9. |
- Kälvegren, Hanna, 1978-
(författare)
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The Role of Chlamydia pneumoniae-induced Platelet Activation in Cardiovascular Disease : In vitro and In vivo studies
- 2007
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The common risk factors for atherosclerosis, such as obesity, high cholesterol levels, sedentary lifestyle, diabetes and high alcohol intake, only explain approximately 50% of cardiovascular disease events. It is thereby important to identify new mechanisms that can stimulate the process of atherosclerosis. During the past decades, a wide range of investigations have demonstrated connections between infections by the respiratory bacterium Chlamydia pneumoniae and atherosclerosis. Earlier studies have focused on the interaction between C. pneumoniae and monocytes/macrophages, T-lymphocytes, smooth muscle cells and endothelial cells, which are present in the atherosclerotic plaque. However, another important player in atherosclerosis and which is also present in the plaques is the platelet. Activation of platelets can stimulate both initiation and progression of atherosclerosis and thrombosis, which is the ultimate endpoint of the disease. The aim of the present thesis was to investigate the capacity of C. pneumoniae to activate platelets and its role in atherosclerosis.The results show that C. pneumoniae at low concentrations binds to platelets and stimulates platelet aggregation, secretion, reactive oxygen species (ROS) production and oxidation of low-density lipoproteins (LDL), and that these effects are mediated by lipopolysaccharide (LPS). Activation of protein kinase C, nitric oxide synthase and 12-lipoxygenase (12-LOX) was required for platelet ROS production, whereas platelet aggregation was dependent on activation of GpIIb/IIIa. Pharmacological studies showed that the C. pneumoniae-induced platelet activation is prevented by inhibitors against 12-LOX, platelet activating factor (PAF) and the purinergic P2Y1 and P2Y12 receptors, but not against cyclooxygenase (COX). These findings were completely opposite to the effects of these inhibitors on collagen-stimulated platelets. We also present data from a clinical study indicating that percutaneous coronary intervention (PCI or balloon dilatation) leads to release of C. pneumoniae into the circulation, which causes platelet activation and LDL oxidation.In conclusion, these data support a role for C. pneumoniae-induced platelet activation in the process of atherosclerosis. Stimulation of platelets by C. pneumoniae leads to release of growth factors and cytokines, oxidation of LDL and platelet aggregation, which are processes that can stimulate both atherosclerosis and thrombosis. Development of novel drugs that prevent C. pneumoniae-platelet interaction by inhibiting 12-LOX and/or PAF, may be important in the future treatment of cardiovascular disease.
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