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)

Reactive airway disease has only rarely been associated with pulmonary hypertension. We treated two patients with congenital heart disease and asthma who had increased pulmonary arterial pressure at cardiac catheterization. Pulmonary hypertension could not be explained solely by the cardiac lesion, nor by respiratory mechanical factors, as the patients did not have wheezing during the catheterization study. After long-term treatment with bronchodilators, corticosteroids, and oxygen, and coincident with improvement in the airway disease, there was catheterization-proved diminution of pulmonary hypertension. Whether asthma and pulmonary hypertension were causally linked is unknown, but further work seems indicated to elucidate the relationship between bronchoconstriction and pulmonary vasoconstriction. Furthermore, aggressive management of even mild reactive airway disease may be warranted in patients with pulmonary hypertension, regardless of apparent cause.
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PMID:Pulmonary hypertension and asthma in two patients with congenital heart disease. 275 75

Airway reactivity is associated with rapid decline in pulmonary function with age or packyears of smoking in otherwise normal subjects. Because heterozygotes for cystic fibrosis (CFHZ) have a higher prevalence of airway reactivity than do controls, we tested the hypothesis that CFHZ have a more rapid decline in pulmonary function with age or packyears of smoking than do controls. We performed spirometry on 280 parents of children with CF and 280 age-matched control parents of children with heart disease. The ALA-DLD-78 questionnaire was also administered to these volunteers. Although the CF parents report wheezing apart from a cold more frequently than control parents, they show no greater decline of pulmonary function (FEV1, FEF25-75%, or FEV1/ht3) with age or packyears of smoking than do controls. The complaint of wheezing apart from a cold contributes significantly to the variance of FEV1 and FEF25-75% even when the effects of height, age, packyears of smoking, sex, and CF heterozygosity are controlled. The hypothesis that obligate heterozygotes for CF have increased age- or smoking-related decline in airflow is not supported by these data. Instead, the results suggest that any pulmonary function abnormalities associated with CF heterozygosity are small and not clinically significant and that CF heterozygosity per se is not a major risk factor for development and progression of obstructive airways disease.
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PMID:Pulmonary function in obligate heterozygotes for cystic fibrosis. 319 30

Parents of children with cystic fibrosis have been reported to have a high prevalence of increased airway reactivity, but these studies were done in a select young, healthy, symptomless population. In the present study respiratory symptoms were examined in 315 unselected parents of children with cystic fibrosis and 162 parents of children with congenital heart disease (controls). The cardinal symptom of airway reactivity, wheezing, was somewhat more prevalent in cystic fibrosis parents than in controls, but for most subgroups this increased prevalence did not reach statistical significance. Among those who had never smoked, 38% of obligate heterozygotes for cystic fibrosis but only 25% of the controls reported wheezing (p less than 0.05). The cystic fibrosis parents who had never smoked but reported wheezing had lower FEV1 and FEF25-75, expressed as a percentage of the predicted value, than control parents; and an appreciable portion of the variance in pulmonary function was contributed by the interaction of heterozygosity for cystic fibrosis with wheezing. For cystic fibrosis parents, but not controls, the complaint of wheezing significantly contributed to the prediction of pulmonary function (FEV1 and FEF25-75). In addition, parents of children with cystic fibrosis reported having lung disease before the age of 16 more than twice as frequently as control parents. Other respiratory complaints, including dyspnoea, cough, bronchitis, and hay fever, were as common in controls as in cystic fibrosis heterozygotes. These data are consistent with the hypothesis that heterozygosity for cystic fibrosis is associated with increased airway reactivity and its symptoms, and that the cystic fibrosis heterozygotes who manifest airway reactivity and its symptoms may be at risk for poor pulmonary function.
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PMID:Pulmonary abnormalities in obligate heterozygotes for cystic fibrosis. 343 35

Carcinoids are solid tumours arising from enterochromaffin cells, usually of the gastrointestinal or respiratory tract. They are fairly common, and in autopsy series have been present in up to 1% of cases. In contrast the carcinoid syndrome--the combination of flushing, diarrhoea, wheezing and heart disease due to release of vasoactive substances from these tumours--is rare. One estimate is that in a population of 250 000 over 10 years only two new cases would arise (Linell and Mansson, 1966).
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PMID:Carcinoid syndrome. Medical management. 374 26

Bronchiolitis, a lower respiratory tract illness most often caused by respiratory syncytial virus, generally affects children under two years of age, commonly during the winter months. Necrosis of epithelial cells in the small airways leads to inflammation and airway obstruction, causing decreased oxygen saturation, with cough and wheezing. Hospital admission should be considered for children with pulse oximetry levels less than 95 percent at rest. Treatment consists of humidified oxygen, intravenous hydration and administration of nebulized albuterol. Infants with mild disease who are identified early in the course of illness should be reevaluated in 24 hours. Infants with congenital heart disease, bronchopulmonary dysplasia or a history of prematurity, who are at high risk for severe disease, should be treated with ribavirin.
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PMID:Bronchiolitis. 784 31

Abnormal enlargement or malposition of any vascular structure or mass adjacent to the airway can cause extrinsic airway compression. In children with previous surgery for congenital heart disease, mass effect from prosthetic devices or alteration in the anatomic position of normal structures can lead to extrinsic airway compression. Because many children have complex medical problems after cardiac surgery, wheezing may be attributed to cardiac causes and airway compression may not be investigated. Furthermore, the distal airway compression seen in these children often is not visualized on chest radiographs. MR imaging can be useful in evaluating extrinsic airway compression in these patients. We present the MR imaging of two patients with symptomatic extrinsic airway compression secondary to pulmonary arterial conduits.
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PMID:Extrinsic airway compression secondary to pulmonary arterial conduits: MR findings. 912 90

When infants with recurrent wheezing have a clinical course inconsistent with asthma, an extensive list of alternative diagnoses needs to be considered. Anatomic malformations, such as congenital heart disease, laryngotracheomalacia, and diaphragmatic hernia, should be considered for immediate medical stabilization and early surgical correction. Life-threatening infections such as bacterial epiglottitis, retropharyngeal cellulitis, and viral myocarditis require prompt intervention. A careful history and physical examination reveal important diagnostic clues that, in this case, prompted a directed evaluation to rule out common masqueraders of asthma such as foreign body aspiration, cystic fibrosis, gastroesophageal reflux, viral pneumonitis, or pulmonary tuberculosis. On occasion, such a search is unrevealing and a diagnostic challenge remains. In those situations, judicious use of modern technology to scrutinize anatomic (high-resolution computed tomography) and functional (infant pulmonary function tests) pathology, and justifiable invasive procedures such as bronchoscopy and lung biopsy, uncover the true diagnosis, allowing for optimal management.
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PMID:A wheezy infant unresponsive to bronchodilators. 916 57

The group of angiotensin-converting enzyme (ACE) inhibitors is one of the drugs of choice for the treatment of hypertension and congestive heart disease. However, it has been reported that in some of patients ACE-inhibitors induce hyperreactivity of the airways with occurrence of a persistent dry cough, dyspnoe and wheezing. We supposed that the mechanism of these hyperreactivity is connected to accumulation of bradykinin, tachykinins and other inflammatory mediators in the airways. Increased local concentration of inflammatory neuropeptides stimulates bronchial C fibres and rapidly adapting receptors and provoke the cough reflex. Inflammatory processes in the airways could be followed by contraction of airway smooth muscle. In this study, our aim was to measure the changes of the number and intensity of mechanical induced cough in cats, which were treated for days with enalapril (5 mg/kg b.w.). After 15 days of treatment the reactivity of the lung and tracheal smooth muscles to the bronchoconstrictor mediator histamine was estimated. As to our finding 15 days of administration of enalapril results in significant increase of cough parameters measured with a more significant sensitivity of the laryngopharyngeal part. In the experimental animals we observed increased reactivity of bronchial smooth muscle to histamine after 15 days of enalapril treatment. The reactivity of the lung smooth muscle to the histamine was not significantly changed. These results confirmed the increased cough sensitivity and increased bronchial reactivity after enalapril treatment. These experimental animal model may be useful for the investigation of the pharmacological minimization of respiratory adverse effect of ACE-inhibitors.
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PMID:ACE-inhibitors and defence reflexes of the airways. 1043 7

RSV is the most important respiratory pathogen in infants and young children. About 1% of primary RSV infections result in hospitalization. The virus is spread by large droplets of secretions or contact with contaminated secretions. Infants infected with RSV may demonstrate poor feeding, rhinorrhea, apnea, lethargy, wheezing, and respiratory distress. Diagnosis may be made by clinical signs and symptoms (especially those observed during epidemics), by chest radiographs showing hyperinflation, or by rapid antigen detection with immunofluorescence of nasopharyngeal aspirates. Risk factors for severe disease accompanied by complications include chronic heart disease, chronic lung disease, immunodeficiency, HIV, and prematurity. Immunity is incomplete and of short duration, and reinfection is common. Treatment remains supportive and consists of oxygen administration, hydration, and diligent monitoring. Use of corticosteroids, bronchodilators, antibiotics, and ribavirin is controversial and is dependent largely on physician preference. Use of ribavirin should be reserved for patients who have severe underlying conditions associated with increased mortality rates. Intravenous RSV Ig has been replaced by palivizumab, which is generally recommended for infants at high risk for severe RSV, including those with a history of prematurity and those with chronic lung disease.
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PMID:RSV infection in infants and young children. What's new in diagnosis, treatment, and prevention? 1060 68

Cardiac malformations involving low-pressure chambers (i.e., either of the atria) are more often diagnosed later in life than lesions that involve high-pressure systems such as ventricular septal defects or persistent ducti arteriosi. Patients with congenital heart disease involving the atria may present only symptoms suggesting lung disease. We report on a child with recurrent episodes of wheezing, which did not respond to albuterol nebulizations and intravenous corticosteroids; he was subsequently found to have cor triatriatum. When a patient suffers from recurrent episodes of lower pulmonary infection and wheezing, despite appropriate management for asthma, less common (including cardiac) causes should be considered.
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PMID:Wheezing as the sole clinical manifestation of cor triatriatum. 1101 37


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