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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A growing amount of clinical and experimental evidence suggests a link between infection and atherosclerotic diseases including both myocardial and cerebral infarction. A prime example is a greatly increased risk of stroke in septicaemic patients with and without endocarditis. Controlled clinical studies have recently shown, however, that certain other milder bacterial infections are also a risk factor for infarction. A preceding febrile respiratory infection was a major risk factor for stroke in young and middle aged patients. In patients with acute myocardial infarction Chlamydia pneumoniae and dental infections seem to be risk factors according to one controlled clinical study. Several possible mechanisms could explain the observed association of infection and infarction. For instance, infection causes a hypercoagulable state which increases the risk of thrombosis. In addition, infection has profound and harmful effects on prostaglandin and lipid metabolism. Infection may also have some role in the atherosclerotic process itself by inducing damage and inflammation in vascular endothelium in the presence of hypercholesterolemia. So far, however, little clinical evidence is available to suggest that by controlling infection the risk of infarction or development of atherosclerotic lesions might be reduced except in patients with endocarditis, where the risk of thromboembolic complications rapidly diminished when the infection is controlled with antimicrobial therapy.
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PMID:Infection as a risk factor for infarction and atherosclerosis. 175 23

Recommendations to Americans concerning dietary fat and heart disease began to appear in the late 1950s. This followed the publications of Gofman et al. (1950) and Keys (1953) relating to techniques for separating plasma lipoprotein fractions and the epidemiologic correlations between dietary fat, serum cholesterol and heart disease, respectively. Advice to the public after 40 years is similar to that given originally, namely, to reduce total fat, saturated fat and cholesterol intake, although cholesterol intake per se is not correlated strongly with cholesterolemia. Newer players on the heart disease stage are homocysteinemia, chlamydia infection and cytomegalovirus. These findings, when amplified, may alter the thrust of medical and dietary advice. In the meantime, since 1950, deaths from all causes in the U.S. (per 100,000, age-adjusted) have fallen by 40% and deaths from heart disease and stroke have fallen by 53 and 70%, respectively.
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PMID:History of recommendations to the public about dietary fat. 947 46

An increasing body of evidence has linked infections to atherosclerosis and thrombosis. Herpesviruses cause atherosclerosis in experimental animals. Herpesviruses can also be detected in atherosclerotic lesions in humans. Cytomegalovirus may play a role in arteriosclerosis in transplanted hearts, and this virus, together with tumor suppressor protein p53, can be found in restenosis lesions following angioplasty. Chlamydia pneumoniae and dental infections are associated with coronary heart disease in cross-sectional and longitudinal studies, and preceding respiratory infections are associated with ischemic stroke. Infections may favor formation of atherosclerosis and thrombosis by elevation of blood levels of fibrinogen, leukocytes, clotting factor, and cytokines and by alteration of the metabolism and functions of endothelial cells and monocyte macrophages. Low-grade infections may also be one of the causes of the inflammatory reaction observed in atherosclerotic lesions and acute ischemic symptoms, reflected in elevated levels of C-reactive protein. These observations warrant further studies in this field.
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PMID:Role of infection as a risk factor for atherosclerosis, myocardial infarction, and stroke. 952 51

On a variety of fronts, chronic bacterial infection is being found to be significantly associated with the development of atherosclerosis and the clinical complications of unstable angina, myocardial infarction, and stroke. Although for the most part, these are still just associations, and specific causative relationships on the par with that determined for Helicobacter pylori and peptic ulcer disease have not been determined. Further studies may well lead to a similar conclusion about these potential mechanisms whereby chronic infections may play a role in atherosclerosis on myocardial infarction. As in the case of Chlamydia pneumoniae, the affect may result from direct vessel wall colonization and infection. This local infection may either react directly on the vessel wall or indirectly through its initiation of a number of immunologic responses. In other cases, the influence of chronic infection on the progression of atherosclerosis may be related to an indirect affect of enhancing the chronic inflammatory response of the body. Even though the infectious agent may not directly infect the vessel wall it may have a critical affect acting from afar. There is a potential that chronic bacterial infection may aggravate pre-existing plaque by enhancing T cell activation as well as other inflammatory responses that may participate in the destabilization of the intimal cap resulting in plaque rupture, progression to acute ischemic syndromes, and ultimate enlargement of the atherosclerotic plaque. Consequently, chronic bacterial infection may play a role in the initiation, the progression, or the destabilization of atherosclerotic plaques. Further studies that are presently ongoing and planned for the near future are expected to not only further elucidate the pathophysiology related with the association between chronic bacterial infection and atherosclerosis but also evaluate whether antibiotic treatment may result in clinical benefit to the patient.
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PMID:Bacterial infections and atherosclerosis. 980 26

A growing amount of epidemiologic, experimental, and clinical evidence has linked infection as a risk factor to variousatherosclerotic diseases including acute myocardial infarction and cerebral infarction. Bacteremic infections with and without endocarditis carry a high risk for both stroke and acute myocardial infarction. During the last decade, chronic bacterial infections such as Chlamydia pneumoniae and dental infections have been associated as risk factors for various atherosclerotic diseases. These chronic bacterial infections are risk factors for acute cardiovascular events, but they may also have some role in the etiopathogenesis of atherosclerotic process itself. There are many known mechanisms that might explain the observed association of infection and atherosclerotic diseases, but it is probable that these mechanisms are complex and multifactorial and probably differ from infection to infection and from patient to patient. Infection theory is by no means against classic risk factor theory in the etiopathogenesis of atherosclerosis. Infection may also act as a synergistic risk factor together with classic risk factors in the development of various atherosclerotic diseases.
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PMID:Role of infections in atherosclerosis. 1053 42

The established risk factors for ischemic stroke do not sufficiently explain all clinical and epidemiological features of the disease, such as the winter peak of stroke incidence, the decline of stroke during this century and the time point of cerebral ischemia. A role of infectious disease as stroke risk factor may partly explain above features. Several case-control studies with both hospital and population control groups showed that acute infection within the preceding week and mainly respiratory infection of both viral and bacterial origin increase the risk of cerebral ischemia independent from other risk factors (odds ratio 2.9-14.5). Infection as a risk factor appears to be most important in young age groups. Infection may cause a procoagulant state and thus, trigger thrombosis and cerebral ischemia. There is increasing evidence for chronic infection as stroke risk factor. A case-control study indicated chronic and recurrent bronchitis to increase stroke risk. Two case-control and one cohort study showed that chronic dental infection, mainly parodontitis, is a risk factor for stroke. There are conflicting results on chronic infection with cytomegalovirus and insufficient evidence for a role of Helicobacter pylorii infection in pathogenesis of stroke. Seroepidemiological studies and analyses of carotid plaques indicate a role of Chlamydia pneumoniae in ischemic stroke. However, causality can not yet be inferred from present results. Acute and chronic infectious diseases are treatable and partly preventable conditions. Their recognition as stroke risk factors could therefore be important for stroke prevention.
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PMID:[Infection, atherosclerosis and acute ischemic cerebrovascular disease]. 1069 60

This review presents recent informations concerning the role of viral and bacterial (especially Helicobacter pylori and Chlamydia pneumoniae) infections in the development of ischaemic stroke. Among possible pathogenic pathways that link infections and stroke, the special attention is paid to the coagulation abnormalities and immunological reactions.
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PMID:[Infection as a likely risk factor for ischemic stroke]. 1073 40

We observed a lot of immune system disorders significantly influencing the development and clinical course of stroke. Depression of cell-mediated immune reactivity was observed in the early stage of stroke. It was manifested by the decrease of the number of T lymphocytes, depression in lymphocyte blastogenesis, diminished production of the migration inhibition factor and reduced delayed-type skin reactivity. Observed depression was probably caused by severe metabolic and endocrinological disorders often seen in the acute phase of the disease and related with increased patients' susceptibility to infections. Simultaneously we observed that the elevated total WBC was an independent stroke risk factor and predictor of 30-days stroke fatality. The activation of the adhesion molecules expression on granulocytes (CD18) and the increased cytokine production by leukocytes could favour leukocytes influence to the ischemic area and potentiate brain injury. The chronic inflammation could be also responsible for the development of vascular injuries leading to the ischemia. In our studies we demonstrated the high levels of antibodies to cardiolipins and heat shock proteins and the increased blood levels of immune complexes (i.c.). We observed the presence of Chlamydia pneumoniae and CMV antigens in isolated i.c. It suggests that different markers of chronic inflammation observed at very early stage of the disease are probably related with the chronic infection potentially leading to the development of atherosclerotic lesions and destabilization of atherosclerotic plaque.
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PMID:[The relationship between immunological parameters with etiopathogenesis and clinical course of stroke]. 1098 97

Atherosclerosis constitutes the most common medical and surgical problem. This can be manifested clinically as stroke, coronary artery disease, or peripheral vascular disease. In the present review the microscopic appearance of the normal arterial wall, the definition of atherosclerosis and the five theories of atherogenesis are described. These are: the lipid theory, the hemodynamic theory, the fibrin incrustation theory, the nonspecific mesenchymal hypothesis and the response to injury hypothesis. Based on the above theories the sequence of events in atherogenesis is analyzed. The classification of the atherosclerotic lesions according to Stary (types I-VI) and their characteristics appear in a table. The epidemiology and the role of the following risk factors are presented in detail: age, sex, lipid abnormalities, cigarette smoking, hypertension, diabetes mellitus, physical inactivity, alcohol consumption, obesity, and hemostatic factors. In addition, less common genetically determined associations like homocystinuria, Tangier disease, Hutchinson-Gilford syndrome (progeria), Werner's syndrome, radiation induced atherosclerosis and the implications of Chlamydia pneumoniae on the arterial wall are discussed.
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PMID:The genesis of atherosclerosis and risk factors: a review. 1122 92

Coronary heart disease is the primary cause of mortality in western countries. The well-established ("classical") risk factors cannot fully explain epidemiological variations of this disease. From several years infections have been linked to ischemic vascular events and recent studies pointed to the role of Helicobacter pylori (H. pylori), a spiral Gram negative bacterium, that chronically infects human stomach and is involved in the pathogenesis of gastritis and peptic ulceration. Systematic reviews of studies have suggested the existence of a possible weakly positive association between this bacterium and coronary heart disease, but this could be due to confounding bias and influenced by the degree of investigations heterogeneity. Experiments from animal studies demonstrated that H. pylori infection in mice induces the formation of platelet aggregates and in contrast to Chlamydia pneumoniae it has not been found in the plaque: therefore, the role of H. pylori, could be even more important in the acute phase of myocardial infarction. There is the need for extensive prospective studies to evaluate the incidence of these diseases in relation to the presence of H. pylori infection. Appropriately randomized studies employing an antibiotic treatment for patients affected by ischemic vascular disease will answer the question of whether H. pylori has a causal role in the pathogenesis of acute myocardial infarction and ischemic stroke.
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PMID:[Ischemic cardiovascular diseases. Correlation with Helicobacter pylori infection]. 1125 32


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