RESUMO
BACKGROUND: Pathogens causing chronic infections may promote atherosclerosis. The aim of our study was to evaluate the association of Chlamydia pneumoniae (Cp) and cytomegalovirus (CMV) infection and of inflammatory activation with premature myocardial infarction (MI). METHODS: Specific anti-Cp and anti-CMV immunoglobulin G (IgG), fibrinogen, white blood cells (WBC), and C-reactive protein (CRP) were measured in 120 post-MI patients
Assuntos
Infecções por Chlamydia/complicações , Chlamydophila pneumoniae/imunologia , Infecções por Citomegalovirus/complicações , Citomegalovirus/imunologia , Infarto do Miocárdio/etiologia , Adulto , Idade de Início , Anticorpos Antibacterianos/análise , Anticorpos Antivirais/análise , Biomarcadores , Proteína C-Reativa/análise , Infecções por Chlamydia/imunologia , Infecções por Citomegalovirus/imunologia , Feminino , Fibrinogênio/análise , Humanos , Imunoglobulina G/análise , Inflamação/diagnóstico , Inflamação/imunologia , Leucócitos/imunologia , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/imunologia , Fatores de Risco , Testes SorológicosRESUMO
To investigate the relationship among lipids, coagulation and thrombosis in the absence of atherosclerosis, spontaneous or dietary-induced hyperlipidemic (FHL) rats were studied. FHL showed higher levels of coagulation factors VII, IX, X, VIII and XII and a shortening of the occlusion time (OT) of an artificial arterial prosthesis as compared with normolipidemic (FNL) animals. Damage of abdominal aorta of FHL was followed by increased fibrin deposition in the vascular intima as compared to FNL. After 5 months of cholesterol-rich diet FNL showed increased cholesterol, triglycerides and factor II, VII, IX, X, XII levels. A significant shortening of the OT and increased fibrin deposition was also observed. Two-month diet withdrawal restored the initial condition. Warfarin treatment, at a dose decreasing vitamin K-dependent factor to levels found in FNL, prolonged the OT and reduced fibrin deposition, without modifying F XII or changing lipid profile. An increase in the activated form of F VII was observed. In contrast, no difference was found in F VII clearance. High lipid levels favour the process of thrombus formation by increasing the activation of vitamin K-dependent coagulation factors. Low-dose warfarin treatment reverts the prothrombotic effect of hyperlipidemia.
Assuntos
Anticoagulantes/uso terapêutico , Fatores de Coagulação Sanguínea/análise , Modelos Animais de Doenças , Hiperlipidemias/complicações , Trombofilia/etiologia , Trombose/etiologia , Varfarina/uso terapêutico , Administração Oral , Animais , Anticoagulantes/administração & dosagem , Aorta Abdominal/patologia , Aorta Abdominal/cirurgia , Doenças da Aorta/sangue , Doenças da Aorta/etiologia , Doenças da Aorta/patologia , Doenças da Aorta/prevenção & controle , Fatores de Coagulação Sanguínea/fisiologia , Prótese Vascular , Colesterol na Dieta/administração & dosagem , Dieta Aterogênica , Ativação Enzimática , Fator VII/metabolismo , Hipercolesterolemia/complicações , Hipercolesterolemia/genética , Hiperlipidemias/etiologia , Hiperlipidemias/genética , Hipertrigliceridemia/complicações , Hipertrigliceridemia/genética , Complicações Pós-Operatórias/sangue , Complicações Pós-Operatórias/etiologia , Complicações Pós-Operatórias/patologia , Complicações Pós-Operatórias/prevenção & controle , Ratos , Ratos Endogâmicos , Ratos Sprague-Dawley , Trombofilia/sangue , Trombofilia/tratamento farmacológico , Trombose/sangue , Trombose/patologia , Trombose/prevenção & controle , Vitamina K/fisiologia , Varfarina/administração & dosagemRESUMO
Coronary artery disease (CAD) is a multifactorial disease influenced by both genetic and environmental determinants. Coagulation activation plays a key role in thrombus formation and variation in its factors has been associated with the risk of CAD. The levels of these factors are genetically determined and polymorphisms in their genes can also be responsible for disease development. Three polymorphic alleles of coagulation factor VII (FVII) gene have been associated with a protective effect on the risk of familial myocardial infarction. Their distribution in Europe covaries across populations with the rate of myocardial infarction mortality, being higher in countries (like Italy, Spain, Greece) at low risk. These polymorphisms are major determinants of FVII variability in humans. They can also determine the response of FVII to environmental stimuli. Indeed, they modulate the association between triglycerides or smoking and FVII, while a gender-dependent regulation of FVII, probably related to sexual hormones, has also been described. Interestingly, lowering the plasma levels of FVII with low dose warfarin to the same low normal range as that associated with the 'protective' genotypes, results in protection against ischaemic heart disease, reducing mortality in high risk men. Journal of Human Hypertension (2000) 14, 369-372
