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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reiter's disease in a child, manifesting as circumscribed, thick, hyperkeratotic, rupioid lesions over the skin and later in the course of the disease developing pyopericardium and cardiac failure, is reported. Recovery of Chlamydia from the urethral discharge, too, was significant.
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PMID:Unusual manifestations of Reiter's disease in a child. 397 34

All series of infective endocarditis had a variable proportion of cases without an etiologic agent because all cultures were negative. New microbiologic techniques have permitted the discovery of the role of many microorganisms in infective endocarditis. C. burnetii is an increasing causative agent of subacute infective endocarditis. In the diagnosis, to the detection of antiphase-I antibodies, immunohistochemical, molecular techniques and cellular cultures have been added. Total cure is difficult to obtain. The combination of doxicicline plus ciprofloxacin for at least 3 years has been proposed as the treatment of choice. Surgery must be reserved for patients with cardiac insufficiency. Less than 2% of cases of acute brucellosis are complicate with infective endocarditis. Infective endocarditis produces serious and rapid valvular destruction with high mortality rates if valve surgery is not performed. For medical treatment at least 3 active agents are required. Bartonella has recently been described as an etiologic agent of infective endocarditis. It mainly affects to homeless people living in poor hygienic conditions. The aortic valve is most commonly involved and, frequently, valve insufficiency requires valve replacement. Blood culture isolation needs long incubation periods. Parenteral nutrition, immunosuppression, wide spectrum antibiotic regimens, intravenous drug addiction and cardiovascular surgery are risk factors previously described in the development of fungal endocarditis. C. albicans and Aspergillus spp. are most frequent etiologic agents. Infective endocarditis should be suspected in any patient with systemic fungal disease. Blood cultures are often negative except for Candida spp. Peripheral emboli and large vegetations are frequent. Mortality is high, antifungal therapy combined with surgery is the treatment of choice. Legionella, Mycoplasma, Chlamydia, Mycobacteria, viruses are potential agents of infective endocarditis, and difficult to diagnose because of special culture requirements. Epidemiological clues, serologic and molecular techniques and blood cultures could identify them.
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PMID:[Infective endocarditis caused by unusual microorganisms]. 965 53

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

Peripartum cardiac failure due to cardiomyopathy is common in sub-saharan Africa. The etiology is unknown. This study was performed in Niger to assess a possible relationship between peripartum cardiomyopathy and Chlamydia. A total of 50 African women presenting peripartum cardiomyopathy underwent testing for infection by Chlamydia pneumoniae, Chlamydia trachomatis, and Chlamydia psittaci. The inclusion criteria were cardiac failure during the last three months of pregnancy or first 6 months postpartum with echocardiographic evidence of dilated cardiomyopathy. Similar testing was carried out in a control group of 25 African women from the same geographical location without cardiac disease. Detection of specific IgG, IgA and IgM antibodies was performed using the microimmunofluorescence technique. The cut-off values were > or = 1/32 for specific IgG antibody and > or = 1/16 for specific IgA and IgM antibody. Statistical comparison of the patient and control groups was achieved using the chi 2 test. For Chlamydia pneumoniae, 48 patients (96 p. 100) versus 20 controls (80 p. 100) controls were positive for IgG antibodies (p < 0.025) and 39 patients (80 p. 100) versus 14 controls (56 p. 100) were positive for IgA antibodies (p < 0.05). No patient or control demonstrated IgM antibodies for Chlamydia pneumoniae. For Chlamydia trachomatis and Chlamydia psittaci, differences in positive rates were not statistically significant. This is the first study demonstrating infection in patients with peripartum cardiomyopathy. The possible role of Chlamydia pneumoniae is discussed.
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PMID:[Chlamydia infection and peripartum dilated cardiomyopathy in Niger]. 1110 Apr 38

The pathogenesis of primary pulmonary hypertension is still unclear. The case of a 68-yr-old female patient who complained of recurrent dizzy spells and collapses over a period of 6 weeks and died of global cardiac failure is presented. Autopsy revealed severe pulmonary hypertension, slight chronic bronchitis, and bronchiolitis as well as intra-alveolar accumulation of macrophages. Chlamydiae were detected within the pulmonary arteries and in intramural and intra-alveolar macrophages by immunofluorescence, confocal laser scanning microscopy, scanning and transmission electron microscopy. Nested-polymerase chain reaction (PCR) and nonradioactive deoxyribonucleic acid (DNA) hybridization of PCR products from pulmonary arteries revealed Chlamydia pneumoniae DNA. Chlamydia pneumoniae has already been detected in atherosclerosis and in pulmonary emphysema. It can induce proliferation of smooth muscle cells. Chlamydia pneumoniae might be relevant in aggravation of primary pulmonary hypertension and might perhaps be a trigger factor in some cases.
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PMID:Detection of Chlamydia pneumoniae in unexplained pulmonary hypertension. 1184 18

Patients hospitalized with community acquired pneumonia were studied prospectively in two hospitals located in the surroundings of Buenos Aires city. Fifty two patients from General Hospital Manuel Belgrano (HMB) were included from March 1998 to February 1999 and 23 patients from Hospital Dr A. Cetrangolo (HCET) for respiratory disease, were included from June 2000 to May 2001. Patients with lung tuberculosis, lung neoplasia and HIV infection were excluded. Clinical background, signs and symptoms were recorded. Microbiological examinations performed included bacteria, respiratory viruses and mycobacteria. Studies for "atypical" bacteria (Chlamydia spp., Coxiella burnetii, Mycoplasma pneumoniae and Legionella spp.) were carried out by serological methods. No differences in age and gender were observed between both groups. Most frequently observed comorbidities in the HMB group included COPD, diabetes and cardiac failure while in the HCET group these were COPD, asthma and lung fibrosis. Etiology was established in 48% and 65.2% of the patients in the first and second group, respectively. Most frequent agents were Mycoplasma pneumoniae, Streptococcus pneumoniae, influenza A and Legionella spp.; the last one was detected in 12% of the patients. Most of these patients were from HMB and presented a good outcome. Mortality was similar in both groups (13.3%). In the HBM group it was related to the presence of comorbidities in 7 out of 8 cases, and in the HCET group it was a consequence of the worsening of their chronic respiratory failure.
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PMID:[Community-acquired pneumonia in patients in 2 hospital populations]. 1267 53

It is known that local and systemic inflammatory processes play an important role in the genesis and development of atheroclerotic lesions and in the pathophysiology of acute coronary syndromes. This hypothesis is supported by findings of elevated parameters of the "inflammatory" reaction in the affected blood vessels but also in the blood of atherosclerotic patients. Known risk factors do not explain quite satisfactorily epidemiological cardiovascular phenomena and different manifestations of coronary heart disease. It is very probable that also Chlamydia pneumoniae is a risk factor. This assumption is based on evaluation of seroepidemiological data, examination of atherosclerotic plaques not only in humans but also in animal models with chlamydial infection. Based on retrospective and prospective evaluation of case-records the authors analyzed the incidence of cardiovascular complications in 83 patients with acute myocardial infarction (AIM), incl. 51 patients (31 men and 20 women, mean age 64.4 +/- 3.4 years who had a non-specific inflammation and chlamydial infection, and 32 patients (24 men and 8 women, mean age 64.7 +/- 3.6 years) who had chlamydial infections but no non-specific inflammation (in the blood). These patients were selected from all patients hospitalized during 1998-2001. When diagnosing acute myocardial infarction we applied WHO criteria, and the presence of at least two of three criteria was necessary: a history of prolonged (more than 20 min). stenocardia, electrocardiographic changes typical for ischaemia and/or necrosis and elevation of myocardial enzymes in serum, Non-specific inflammatory activity was present in patients (i.e. positive) if the following laboratory parameters were recorded: C-reactive protein > 5 mg/l assessed by the radial immunodiffusion method; fibrinogen > 4 mg/l assessed by the coagulation method according to Claus; leukocytes > 9.6 x 10(3)/microliter, leukocytes were counted automatically in a Coulter chamber; lymphocytes > 3.4 x 10(3)/microliter. Red cell sedimentation rate > 20 mm/hour. The activity was evaluated as positive when all parameters were elevated. The presence of chronic infection with Chlamydia pneumoniae was assessed qualitatively by antibody positivity (IgG) in serum using the microimmunoflurescent method (using a set from Labsystems Co.). The incidence of associated risk factors (obesity, smoking, diabetes, hyperlipidaemia and hypertension) is higher in the sub-group of patients with Chlamydia infections without inflammation, however, the difference is not statistically significant. The incidence of cardiovascular attacks was higher in the sub-group of patients with chlamydial infection and concurrent inflammation as compared with the sub-group of patients with chlamydial infection without inflammation. In case of re-infarction of the myocardium, a sudden cerebrovascular attack, death and arrhythmia the difference was statistically significant, while in case of cardiac failure and cardiogenic shock the difference was not significant. Patients with acute myocardial infarction with chlamydial infection and a concurrent non-specific inflammation had to be treated more often by combined (i.e. more intense) treatment, thrombolytic treatment, PTCA and surgery (bypass) of the coronary vessels as compared with patients with Chlamydia infections but without inflammation. The authors assume therefore that not only different risk factors but also the effect of non-specific inflammation and Chlamydia infection contribute towards the increased number of cardiovascular postinfarction complications. Therefore a therapeutic approach involving eradication of infection and suppression of the inflammatory reaction should be considered.
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PMID:[Effect of chronic Chlamydia infection with non-specific inflammation on cardiovascular complications in acute myocardial infarct]. 1272 71

We have to consider the exacerbation of chronic obstructive pulmonary disease(COPD) may be caused not only by infection, but also by acute exacerbation of chronic heart failure, pulmonary embolism, pneumothorax, or other cardiopulmonary complications. Because it is characteristic that the exacerbation of COPD is often recurensive, the most important thing is the administration during stable status. Approximately 40% of pathogens of the acute infectious exacerbation of COPD are Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, Pseudomonas aeruginosa, Staphylococcus aureus, and Echelisia coli. Also, approximately 15% is exacerbated by atypical pathogens such as Chlamydia pneumoniae and approximately 30% is by viral infection. We should contemplate the possibility of pathogens according to the statistics, when we choose antibiotics empirically.
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PMID:[Administration of acute exacerbation of chronic obstructive pulmonary disease]. 1467 28

We report a case involving a young female patient with Chlamydia pneumoniae myocarditis who required assist device therapy for acute heart failure. Early diagnosis was provided by endomyocardial biopsy, and tailored antibiotic therapy facilitated quick recovery of myocardial function. This is the first case to report detecting C pneumoniae as the pathogen responsible for fulminant myocarditis while the patient was still alive and to report long-term follow-up data.
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PMID:Early detection and successful therapy of fulminant chlamydia pneumoniae myocarditis. 1615 18

Cardiomyopathies are an important and diverse group of heart muscle diseases in which the heart muscle itself is structurally or functionally abnormal and in which coronary artery disease, hypertension, valvular and congenital heart disease are absent or do not sufficiently explain the observed myocardial abnormality. This often results in severe heart failure accompanied by arrhythmias and/or sudden death. Clinical and morphological diversity of cardiomyopathies can reflect the broad spectrum of distinct underlying molecular causes or genetic heterogeneity. In many cases the disease is inherited and is termed familial dilated cardiomyopathy (FDC), which may account for up to 30% of dilated cardiomyopathies (DCM). FDC is principally caused by genetic mutations in FDC genes that encode for cytoskeletal, nuclear and sarcomeric proteins in the cardiac myocyte. In addition, modifying genes, lifestyle and additional factors were reported to influence onset of disease, disease progression, and prognosis. The individual patient's phenotype may reflect a summation and/or interaction of the underlying mutation(s) with other genetic or environmental factors. During the last years major advances have been made in the understanding of the molecular and genetic basis of this type of disease. Nevertheless, much more progress in the identification of underlying mutations, susceptibility genes and modifier genes is important and indispensable for the development of new etiology-orientated forms of therapy. A pivotal role for autoimmunity in a substantial proportion of patients with DCM is supported by the presence of organ-specific autoantibodies, inflammatory infiltrates and pro-inflammatory cytotoxic cytokines. Furthermore, familial occurrence of DCM goes ahead with the presence of autoantibodies and abnormal cytokine profiles in first-degree relatives with asymptomatic left ventricular enlargement. These relatives suffer from a higher risk for the development of DCM after years. This suggests the involvement of a disrupted humoral and cellular immunity early in the development of the disease. There is reasonable clinical and experimental evidence, that DCM in addition may occur as late stage of cardiac infection and inflammation. The large spectrum of clinical forms depends on several factors such as genetic determinants of the infective agent, the genetics, age and gender of the host, and the host immunocompetence. In general, infectious agents, including viruses such as entero-, cytomegalo-, and adenoviruses, bacteria such as Borrelia burgdorferi or Chlamydia pneumoniae, protozoa and even fungi can cause inflammatory heart disease leading to DCM. The infectious agents most often identified in DCM nowadays are parvovirus B19, human herpesvirus 3, and Epstein-Barr virus. Persistence of these viruses within the myocardium is associated with reduction of ejection fraction after 6 months. For patients with suspected inflammatory heart disease the immunohistochemical detection of inflammatory infiltrates is related to poor outcome. Many faces of inflammatory heart disease coexist where different phases of the disease progress simultaneously: phase 1 is dominated by viral infection itself, phase 2 by the onset of (probably) multiple autoimmune reactions, and phase 3 by the progression to cardiac dilatation. Further investigations with regard to the etiology of structural heart diseases should include an intensive clinical investigation of the given patient. A possible family history including a pedigree should be ascertained and with regard to a possible inflammatory or viral heart disease, endomyocardial biopsies should be investigated by polymerase chain reaction and immunohistochemistry.
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PMID:[Familial predisposition and microbial etiology in dilated cardiomyopathy]. 1937 Mar 26


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