Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 560 patients with serologically confirmed Mycoplasma pneumoniae infection, 25 (4.5%) had carditis (19 perimyocarditis, 6 pericarditis). During the acute phase 9 patients required intensive care. After an average of 16 months follow-up 11 patients with no previous signs of heart disease still had cardiac symptoms or signs. Thus carditis associated with M. pneumoniae infection is a serious disease, having cardiac sequelae more often than has hitherto been supposed. The pathogenesis of the carditis associated with M. pneumoniae infection is discussed, including the possibility that in some cases the elevated titre in the complement fixation test is non-specific. A summary is given of the 33 cases previously presented in the literature.
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PMID:Carditis associated with mycoplasma pneumoniae infection. 11 88

Virological examination of 385 patients with suspected heart disease and 26 with Bornholm disease over a period of 6 years suggested that Coxsackie group B virus infections were associated with at least half the cases of acute myocarditis and one third of the cases of acute non-bacterial pericarditis. Complement-fixation tests revealed only a few cardiac illnesses associated with other infections (influenza and Mycoplasma pneumoniae). No evidence of infection was found in chronic cardiac disease.
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PMID:A six-year study of coxsackievirus B infections in heart disease. 452 4

Severe CAP is a life-threatening condition defined by the presence of respiratory failure or symptoms of severe sepsis or septic shock. It accounts for approximately 10% of hospitalized patients with CAP. The majority of patients with severe pneumonia have underlying comorbid illnesses, with COPD, alcoholism, chronic heart disease, and diabetes mellitus being the most frequent. S. pneumoniae, Legionella spp, GNEB (especially K. pneumoniae), H. influenzae, S. aureus/spp, Mycoplasma pneumoniae, respiratory viruses (especially influenza viruses), and P. aeruginosa represent the most important causative organisms of severe CAP. Rapid initiation of appropriate antimicrobial treatment is crucial for a favorable outcome. Initial antimicrobial treatment should be based on an epidemiological (empiric) approach. Microbial investigation may be helpful in the individual case but is probably more useful to define local antimicrobial policies based on local epidemiologic and susceptibility patterns. Mortality rates range from 21% to 54%. The most important prognostic factors include general health state of the patient, appropriateness of initial antimicrobial treatment, and the existence of bacteremia, as well as factors reflecting severe respiratory failure, severe sepsis, septic hypotension or shock, and the extent of infiltrates in chest radiograph. Initial antimicrobial treatment should consist of a second (or third) generation cephalosporin and erythromycin. Modifications of this basic regimen should be considered in the presence of distinct comorbid conditions and risk factors for distinct pathogens. Promising new approaches of nonantimicrobial treatment, including noninvasive ventilation, treatment of hypoxemia, and immunomodulation, are under investigation.
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PMID:Severe community-acquired pneumonia. 1051 5

Among the multiple factors involved in the pathophysiology of heart disease, infections have been proposed to play a role in atherosclerosis with most of the available evidence implicating Chlamydia pneumonia, influenza virus and Mycoplasma pneumoniae. Based on a model case presentation, we speculate that in the absence of traditional risk factors and in the context of an ongoing respiratory infection caused by a pro-inflammatory pathogen (M. pneumoniae) along with a past positive serologic history for potentially proven atherogenic microorganism (C. pneumoniae) and infection may elicit potentially pathogenic events on vascular wall cells and leukocytes of atheromatous lesions, supporting the hypothesis that such infections may potentiate atherosclerotic cardiovascular disease (CVD).
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PMID:Infectious atherosclerosis: is the hypothesis still alive? A clinically based approach to the dilemma. 2121 37