miological studies have reported positive associations between the risk of coronary heart disease (CHD) and plasma fibrinogen levels. Fibrinogen is the major coagulation protein in blood by mass, the precursor of fibrin, and an important determinant of blood viscosity and platelet aggregation. [38][39][40][41] Because fibrinogen levels can be reduced considerably by lifestyle interventions that also affect levels of established risk factors (such as regular exercise, smoking cessation, and moderate alcohol consumption), there is interest in the possibility that measurement (or modification) of fibrinogen may help in disease prediction or prevention. [38][39][40]42 A meta-analysis of published data from 18 such studies, involving about 4000 CHD cases, indicated a relative risk of 1.8 (95% confidence interval [CI], 1.6-2.0) per 1-g/L increase in plasma fibrinogen level. 43 However, such analyses are not able to provide detailed assessments of the nature of any independent association of fibrinogen level with CHD or with other vascular and nonvascular outcomes. [43][44][45] This meta-analysis differs from previous analyses in several ways that should increase its reliability and scientific value. First, it is large and comprehensive: the data comprise 6944 first nonfatal myocardial infarction (MI) or stroke events and 13 210 deaths (cause-*The Authors/Writing Committee, Authors/Members, and Other Members of the Fibrinogen Studies Collaboration are listed at the end of this article.

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Two chronic infections, HSV-1 and Cpn, increase the risk of coronary heart disease. The effect is emphasized in subjects with ongoing inflammation, denoted by increased CRP levels.

Objective-We analyzed the association of coronary heart disease (CHD) and serology of periodontitis in a random sample (nϭ1163) of men (aged 45 to 74 years) by determining serum IgG-antibodies to Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. Methods and Results-CHD (nϭ159) was more prevalent among edentulous than dentate subjects (19.8% and 12.1%, Pϭ0.003). In the dentate population, CHD was more common among subjects seropositive for P. gingivalis compared with those seronegative (14.0% and 9.7%, Pϭ0.029). Accordingly, CHD was more prevalent in subjects with a high combined antibody response than those with a low response (17. 4% and 11.1%, Pϭ0.026). When adjusted for age and several CHD risk factors, the subjects with a high combined antibody response had an odds ratio of 1.5 (95% CI, 0.95 to 2.50, Pϭ0.077) for prevalent CHD. In a linear regression model, the combined antibody response was directly associated with prevalent CHD (Pϭ0.046) and inversely with serum HDL cholesterol concentration (Pϭ0.050). Key Words: atherosclerosis Ⅲ cardiovascular diseases Ⅲ antibodies Ⅲ infection Ⅲ inflammation R ecent evidence suggests that chronic infectious diseases increase atherogenesis and risk for CHD. 1 Periodontitis is a persistent bacterial infection causing chronic inflammation in periodontal tissues. This common disease is characterized by the formation of deep periodontal pockets and destruction of connective tissue attachment and alveolar bone and may eventually lead to tooth loss. 2 The systemic immunological response to periodontitis can be measured as elevated serum antibody levels against certain periodontopathogenic bacteria. 3 The most important pathogens responsible for periodontitis are gram-negative bacteria, particularly Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. 4 They exhibit interspecies differences in virulence characteristics, such as leukotoxin production, endotoxin activity, and capability to adhere and invade host cells. 5,6 Both pathogens have been found in atherosclerotic plaques, 7 and certain clones of A. actinomycetemcomitans may also exert a particular potency to cause nonoral infections. 8 The aim of this crosssectional study was to investigate in a random populationbased sample whether serum antibodies to periodontal pathogens are associated with CHD. The associations between antibodies to periodontal pathogens and established risk factors of CHD were also studied. Conclusions-In MethodsThe participants of the Finnish Platelet Aggregation and Inflammation Study (PAIS) are a subsample of a large population-based risk factor study, which was conducted in Finland in 1997. 9 The PAIS sample originally comprised 2000 men aged 45 to 74 years from eastern and southern Finland. From the 1163 men included in the present analyses, 159 (14%) were classified as CHD patients on the basis of the register of the National Social Insurance Institution on persons entitled to special reimbursement for CHD drugs. To receive the special reimbursement, the diagnosi...

In a prospective cohort of healthy middle-aged men, the presence of a high aCL antibody level is an independent risk factor for myocardial infarction or cardiac death. Antibodies to cardiolipin and oxidized LDL may, at least in part, represent cross-reactive antibody populations.

Periodontitis, a consequence of persistent bacterial infection and chronic inflammation, has been suggested to predict coronary heart disease (CHD). The aim of this study was to investigate the impact of periodontitis on HDL structure and antiatherogenic function in cholesterol efflux in vitro. HDL was isolated from 30 patients (age 43.6 ؎ 6.1 years, mean ؎ SD) with periodontitis before and after (3.2 ؎ 1.4 months) periodontal treatment. The capacity of HDL for cholesterol efflux from macrophages (RAW 264.7), HDL composition, and key proteins of HDL metabolism were determined. After periodontal treatment, phospholipid transfer protein (PLTP) activity was 6.2% ( P Ͻ 0.05) lower, and serum HDL cholesterol concentration, PLTP mass, and cholesteryl ester transfer protein activity were 10.7% ( P Ͻ 0.001), 7.1% ( P ‫؍‬ 0.078), and 19.4% ( P Ͻ 0.001) higher, respectively. The mean HDL 2 /HDL 3 ratio increased from 2.16 ؎ 0.87 to 3.56 ؎ 0.48 ( P Ͻ 0.05). HDL total phospholipid mass and sphingomyelin-phosphatidylcholine ratio were 7.4% ( P Ͻ 0.05) and 36.8% ( P Ͻ 0.001) higher, respectively. The HDL-mediated cholesterol efflux tended to be higher after periodontal treatment; interestingly, this increase was significant ( P Ͻ 0.05) among patients whose C-reactive protein decreased (53.7% reduction, P ‫؍‬ 0.015) and who were positive by PCR for Actinobacillus actinomycetemcomitans . These results suggest that periodontitis causes similar, but milder, changes in HDL metabolism than those that occur during the acute-phase response and that periodontitis may diminish the antiatherogenic potency of HDL, thus increasing the risk for CHD. -Pussinen, P. J., M. Jauhiainen, T. Vilkuna-Rautiainen, J. Sundvall, M. Vesanen, K. Mattila, T. Palosuo, G. Alfthan, and S. Asikainen. Periodontitis decreases the antiatherogenic potency of high density lipoprotein.

Objective-In periodontitis, overgrowth of Gram-negative bacteria and access of lipopolysaccharide (LPS) to circulation may activate macrophages leading to foam cell formation. We investigated whether periodontal treatment affects proatherogenic properties of low-density lipoprotein (LDL) and, thus, macrophage activation. Methods and Results-LDL was isolated and characterized before and after treatment from 30 systemically healthy patients with periodontitis. Production of cytokines and LDL cholesteryl ester (LDL-CE) uptake by macrophages (RAW 264.7) was determined. Baseline periodontal variables correlated positively with serum LPS and C-reactive protein concentrations, as well as macrophage cytokine production and LDL-CE uptake. LPS concentration correlated positively with serum concentration of oxidized LDL and cytokine production. Higher cytokine production and LDL-CE uptake were induced by LDL isolated from patients with elevated number of affected teeth before treatment. Patients with serum LPS concentrations above the median (0.87 ng/mL) at baseline had higher serum high-density lipoprotein (HDL) cholesterol (baseline versus after treatment,

Background: Periodontitis is associated with elevated levels of C-reactive protein and fibrinogen and it may be a coronary heart disease risk factor. We wanted to study if treatment of periodontitis can decrease the levels of these inflammatory markers.