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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With the objective of determining if specific sexually transmitted diseases (STDs) are associated with prematurity (birth weight less than or equal to 2500 g and gestational age less than or equal to 36 weeks), a case-control study was conducted to evaluate women for serologic evidence of syphilis and human immunodeficiency virus infection and microbiologic evidence of cervical infection with Neisseria gonorrhoeae, Chlamydia trachomatis, and Haemophilus species and vaginal infection with genital mycoplasma, Streptococcus agalactiae, and Enterobacteriaceae. Gram stains of vaginal secretions were evaluated for bacterial vaginosis. Among 166 cases and 175 controls, infection with N. gonorrhoeae was associated with preterm birth. Four percent of controls and 11% of cases were infected with N. gonorrhoeae (odds ratio 2.9, 95% confidence interval 1.2-7.2). This association was independent of age, rupture of membranes, and hypertension. Other STDs were not associated with preterm birth. The attributable risk of gonococcal infection was 14%. Gonococcal infection appears to be responsible for a substantial proportion of premature births and is theoretically preventable by antenatal case detection and treatment.
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PMID:Maternal gonococcal infection as a preventable risk factor for low birth weight. 231 31

The author found that the onset of hypertension or hypotension is relatively often associated with infections or development of so-called "sneezing due to allergy to pollen or dust," with or without headache, or due to trauma to the occipital area of the head. Using the "Bi-Digital O-ring Test," it was possible to demonstrate that, among bacterial and viral infections, the most common cause of infection associated with the appearance of hypertension is chlamydia, herpes simplex virus, cytomegalovirus, or Epstein-Barr virus. Particularly chlamydia and/or herpes simplex virus, with or without coexistence of other microbes, is usually present at the heart representation area of the medulla oblongata, especially at the left ventricular representation area, often accompanied by upper respiratory infection, cephalic, cervical or facial pain, with or without coexisting genito-urinary infection. The left ventricular representation area of the medulla oblongata is usually located at the right side. In most hypertensive patients, the left ventricular representation area of the medulla oblongata is enlarged up to 3 or 4 times normal size. Sufficient antibiotic treatment of chlamydia with erythromycin sometimes eliminated severe hypertension which appeared after chlamydia infection. In the presence of viral infections, such as herpes simplex, which is also causing severe pain in the head or neck, oral administration of acyclovir, erythromycin, or EPA (Eicosa Pentaenoic acid)-DHA (docosa hexaenoic acid) Omega 3 fish oil often reduced associated intractable pain and hypertension toward the normal level. Thus, the author is proposing new possible mechanisms as among the causes of so-called essential hypertension as a result of microbial infection or trauma of the cardiovascular representation area, particularly that of the left ventricular representation area at the right side of the medulla oblongata.
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PMID:Microbial infection or trauma at cardiovascular representation area of medulla oblongata as some of the possible causes of hypertension or hypotension. 290 10

Several studies have implied an association between Chlamydia pneumoniae (C. pneumoniae) and cardiovascular disease. Our study was designed to determine whether this organism is associated with severe essential hypertension in a multiracial British population. Antibodies to C. pneumoniae were measured by microimmunofluorescence in 123 patients with chronic severe hypertension and 123 control subjects, matched for ethnic origin, age, sex, and smoking habit, admitted to the same hospital with various noncardiovascular, nonpulmonary disorders. Previous infection was defined by IgG 64 to 256, provided that there was no detectable IgM. Multiple regression analyses of matched and unmatched data were used to investigate the influences of antibody levels and potential confounding factors (ethnic origin, age, sex, smoking habit, diabetes mellitus, and social deprivation) on hypertension. A portion of the hypertensive patients underwent echocardiography, estimation of left ventricular mass index, and measurements of fibrinogen, D-dimer, and von Willebrand factor concentrations. Thirty-five percent of hypertensive patients and 17.9% of matched control subjects had antibody titers consistent with previous C. pneumoniae infection. The hypertensive patients differed significantly from their matched control subjects in their level of previous infection, with an odds ratio of 2.5 (95% confidence interval, 1.3 to 4.7). There were no significant differences in antibody levels between patients with left ventricular hypertrophy and those without it. Fibrinogen, D-dimer, and von Willebrand factor concentrations were not significantly associated with antibody levels. These data support an association of C. pneumoniae with severe essential hypertension. They provide no evidence of a predisposition to develop left ventricular hypertrophy in hypertensive patients with C. pneumoniae infection or of associations with hypercoagulability or endothelial dysfunction.
Hypertension 1998 Feb
PMID:Chlamydia pneumoniae antibodies in severe essential hypertension. 946 Dec 26

Although first suggested at the turn of the 20th century, there is a renewed interest in the infectious theory of atherosclerosis. Studies done in many laboratories around the world over the past several years have shown an association between markers of inflammation and coronary atherosclerosis with an exacerbation of the inflammatory process during acute myocardial ischemia, particularly in the early stages of reperfusion. It is also being recognized that the traditional risk factors, such as smoking, dyslipidemia, hypertension and diabetes mellitus, do not explain the presence of coronary atherosclerosis in a large proportion of patients. We believe that in certain genetically susceptible people, infection with very common organisms, such as Chlamydia pneumoniae or cytomegalovirus, may lead to a localized infection and a chronic inflammatory reaction. Persistence of infection may relate to the degree of inflammation and severity of atherosclerosis. Early trials with appropriate antibiotic agents in some patients with a recent history of acute myocardial infarction have led to very salutary results. If patients with an infectious basis of atherosclerosis can be identified, a therapy directed at eradication of the offending organism may be appropriate.
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PMID:Interactive role of infection, inflammation and traditional risk factors in atherosclerosis and coronary artery disease. 980 69

Traditional cardiovascular risk factors, such as smoking, hypercholesterolaemia and hypertension probably only explain about 50% of the prevalence and severity of coronary heart disease (CHD). The recent interest in the association between Chlamydia pneumoniae and the pathogenesis and progression of atherosclerotic diseases is based on several lines of evidence-seroepidemiological studies, pathological specimen examinations, laboratory-based experiments, animal models and more recently, pilot intervention trials with anti-chlamydial antibiotics (Table 1). Whether C. pneumoniae has a direct causal role in atherosclerosis (and its clinical sequelae), and whether antibiotics have a protective role in the secondary prevention of CHD remains unclear. The results from large scale, prospective antibiotic trials in CHD, currently in progress, should help to clarify these important issues.
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PMID:Chlamydia pneumoniae, antimicrobial therapy and coronary heart disease: a critical overview. 981 84

A review of the most important findings published during 1997 in cardiovascular papers is presented: Chlamydia pneumoniae was recognised as a potential risk factor for coronary artery disease (CAD) and possible pathogenic agent for valvular aortic stenosis. Valvular changes similar to the valvular disease reported after ergotamine and methylsergide were also detected in obese women treated with a combination of phentermine and fenfluramine. In CAD, several new laboratory methods were introduced for early diagnosis, such as serum troponin levels, and arbutamine and adenosine stress echocardiography. Laser transmyocardial revascularisation can be performed in patients unsuitable for PTCA and CABG. In patients with end-stage heart failure, implantable ventricular-assist devices can be used, and dynamic cardiomyoplasty or partial ventriculectomy may be useful temporary measures until a suitable heart donor is available. In pharmacotherapy, fluvastatin was registered as an antiatherosclerotic agent, and mibefradil and moxonidin in hypertension and angina. Digoxin was shown to reduce the number of hospitalisations in patients with CHF but still in sinus rhythm. In the future, several improvements in anti-thrombotic therapy are expected: antithrombins, platelet glycoprotein IIb/IIIa receptor blockers and tissue factor inhibitors are all potentially more potent than presently available drugs. Also, efforts are under way to introduce genes directly into the cells of the vascular wall to prevent atherosclerosis and restenosis, as well as to transform cardiac mesenchymal cells into the cardiac myocytes of hearts that have suffered large infarctions.
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PMID:[Cardiology in 1997]. 981 70

On the basis of several epidemiological investigations performed simultaneously in the eighties and then in early nineties, a presumption has been put forward that is a relationship between the incidence of arteriosclerosis, especially of the coronary arteries and the presence of antibodies against antigens of Chlamydia pneumoniae in the blood serum. These investigations revealed that an infections by Chlamydia pneumoniae is an independent risk factor in the development of arteriosclerosis as well as hypertension, cigarette smoking and increased level of lipids in the blood serum. The present work is a survey of the current literature on the subject of presumable role of these bacteria in the process of arteriosclerosis. Clinical and epidemiological reports have been presented and two investigations on the animal models using rabbits and mice have been discussed. On the basis of the presented studies, it can be observed that Chlamydia pneumoniae has a specific tendency to accumulate not only in the respiratory system, but also in the arteries affected by arteriosclerosis. However, studies of the relationship between an infections by these bacteria and development of arteriosclerosis are far from final explanation of this problem.
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PMID:[Chlamydia pneumoniae chronic infection in the development of arteriosclerosis]. 982 66

The association of Chlamydia pneumoniae with atherosclerosis of coronary and carotid arteries and the aorta has been demonstrated by seroepidemiology and by detection of the organism in atheromata. We investigated the frequency of C. pneumoniae seropositivity in patients with acute myocardial infarction (AMI). C. pneumoniae-specific antibodies were measured by the microimmunofluorescence test in 160 AMI patients and 160 control subjects matched for age and gender. The odds ratios (ORs) were 2.2 (95% confidence interval (CI), 1.2 to 3.9) for immunoglobulin (Ig)G and 2.7 (95% CI, 1.7 to 4.3) for IgA. After adjustment for other cardiovascular risk factors of age, gender, hypertension, diabetes, cigarette smoking and serum cholesterol, the ORs were essentially unchanged. This study confirmed that the observations of an association between antibody against C. pneumoniae and coronary heart disease in Western nations is also present in Japan. Our results are comparable to the previous seroepidemiological studies reporting ORs of 2.0 or greater.
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PMID:Association of chronic infection of Chlamydia pneumoniae and coronary heart disease in the Japanese. 986 50

The vascular endothelium is the inner lining of all blood vessels and serves as an important autocrine and paracrine organ, that regulates vascular wall functions. Because of its strategic location between the circulating blood and the vascular wall, the endothelium interacts with cellular and neurohumoral mediators, thus controlling vascular contractile state and cellular composition. The vascular endothelium maintains vascular homeostasis by modulating blood vessel tone, by regulating local cellular growth and extracellular matrix deposition and by controlling hemostatic as well as inflammatory responses. One of the best characterized and most important substances released from the endothelium is nitric oxide (NO). NO is a soluble gas which is continuously synthesized from the amino acid L-arginine in endothelial cells by the constitutively expressed nitric oxide synthase. The most important stimuli represent physical factors such as shear stress and pulsatile stretching of the vessel wall as well as circulating and locally released vasoactive substances. The endothelium can be seen as a biosensor, reacting to a large variety of stimuli and therefore maintaining adequate NO release. A large number of risk factors for atherosclerosis including hypercholesterolemia, systemic hypertension, smoking and diabetes have been associated with impaired endothelial NO-mediated vasodilation. "Endothelial dysfunction" is an early marker of atherosclerosis and may be closely related to the disease process. In acute coronary syndromes dysfunctional endothelium may trigger the devastating event of plaque rupture by promoting adhesion of leukocytes, vasoconstriction, activation of platelets and thrombos formation. Atherosclerotic blood vessels are further characterized by activation through zytokines and expression of cellular adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and endothelial-leukocyte adhesion molecule-1 (E-Selectin). After adhesion to the endothelium mononuclear cells migrate to the subendothelial space to take up oxidized LDL, thus transforming into foam cells, a hall mark of early atherosclerotic lesions. A number of conditions including infection with Chlamydia pneumoniae may cause continuous activation of the endothelium and inflammation of the vessel wall. Continuous endothelial dysfunction and activation, caused by risk factors and infection, represent the basis for atherogenesis and acute coronary syndromes.
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PMID:[Endothelial dysfunction--assessment of current status and approaches to therapy]. 1009 15

Pathologic findings and cross-sectional epidemiologic studies suggest that past infection with Chlamydia pneumoniae is associated with clinical and subclinical atherosclerotic disease, although evidence from prospective studies is still scarce. The association between chronic infection by C. pneumoniae and incident coronary heart disease (CHD) was investigated in a case-cohort study conducted among participants in the Atherosclerosis Risk in Communities Study who were free of CHD at the baseline examination (1986-1989). Levels of C. pneumoniae immunoglobulin G (IgG) antibodies in serum collected at baseline from 246 incident cases of CHD identified during follow-up (median, 3.3 years; maximum, 5 years) were compared with those from a stratified sample of the baseline cohort (n = 550). Among incident CHD cases, 65% had IgG antibody titers > or =1:64, compared with 55% of noncases (compared with negative IgG titers, the relative hazard of CHD was 1.6 (p < 0.01)). In multivariate analyses controlling for other risk factors (age, gender, smoking, serum cholesterol, hypertension, diabetes mellitus, and educational level), the above estimates were substantially reduced and became statistically nonsignificant (relative hazard = 1.2). A significantly increased CHD hazard associated with IgG antibody titers > or =1:64 was observed among nonsmokers, even after adjustment for other risk factors. Overall, these results do not provide strong support for the hypothesis that C. pneumoniae infection is a risk factor for clinical CHD. Studies with longer follow-up periods will be necessary to determine whether C. pneumoniae infection is involved as an etiologic factor in earlier phases of atherogenesis.
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PMID:Chlamydia pneumoniae infection and incident coronary heart disease: the Atherosclerosis Risk in Communities Study. 1041 59


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