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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mortality from ischaemic heart disease was studied in a prospective cohort of 1725 shipyard workers exposed to asbestos. The analyses were stratified for age and smoking habits and restricted to men. In agreement with other findings, men with impaired lung function had a significantly higher risk (relative risk (RR) = 3.5) of dying from ischaemic heart disease than men with normal lung function. Men with asbestosis or suspected asbestosis had a significantly higher risk (RR = 3.1) of dying from ischaemic heart disease than men without asbestosis. Thus asbestosis or suspected asbestosis also seemed to be a risk factor for ischaemic heart disease. This finding was independent of respiratory function. There was no increased risk for ischaemic heart disease in men with compared with men without pleural plaques. Men with production of phlegm or sputum and wheezing or whistling had no increased risk for ischaemic heart disease compared with men without these symptoms. In the group with normal lung function men with dyspnoea had a significantly higher risk of dying from ischaemic heart disease than men without dyspnoea. The findings for men with asbestosis or suspected asbestosis indicated a further risk factor besides impaired lung function, in persons exposed to asbestos. Perhaps this risk factor is due to lesions of the pericardium with consequences for heart function.
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PMID:The importance of lung function, non-malignant diseases associated with asbestos, and symptoms as predictors of ischaemic heart disease in shipyard workers exposed to asbestos. 839 71

Asthma is a chronic inflammatory disease of the airways that may affect individuals at any age, and can be especially challenging to diagnose and treat in the elderly. The hallmarks of asthma--bronchial hyperreactivity and reversible airflow obstruction--lead to symptoms of intermittent wheezing, dyspnoea and cough. Occasionally, atypical symptoms such as chest pain or tightness occur and may mimic other diseases more common in the elderly, such as ischaemic heart disease. It is therefore important to use objective measures such as spirometry or bronchoprovocation testing to make a diagnosis. In recent years, trends in the treatment of asthma have changed from reliance on shorter-acting bronchodilating drugs to long term preventative therapy with inhaled corticosteroids. In some elderly asthmatic patients, symptoms may be mild and intermittent, and treatment with an inhaled beta 2-adrenergic agent may be all that is required. Most, however, experience persistent symptoms, and pharmacological therapy should begin with daily inhaled corticosteroids and be increased in a stepwise fashion according to the patient's needs. In such patients, short-acting beta 2-agonists should be continued as needed for acute symptomatic relief. Longer-acting beta 2-agonists, oral theophylline and inhaled anticholinergic therapy may be useful. When symptoms are more severe and potentially life-threatening, oral corticosteroids should be given. Since elderly patients are more likely to develop complications of asthma therapy and more likely to manifest adverse interactions with other therapeutic agents, more intense monitoring of asthma treatment is required in dealing with this population.
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PMID:Drug treatment of asthma in the elderly. 888 79

A 61-year-old woman with chronic asthma sustained an episode of dyspnea and chest heaviness and was brought to the emergency department. Her examination revealed tachypnea, tachycardia, hypotension, and diffuse prolonged respiratory wheezing. Arterial blood gas analysis showed severe hypoxemia and hypercapnia. A 12-lead electrocardiogram showed marked, downsloping ST-segment depression, with deep, negative T waves in leads I, II, III, and aVF and precordial leads V3-V6. After 15 minutes of therapy with oxygen, beta-agonists, and corticosteroids, the electrocardiographic abnormalities subsided and 2 hours later they had disappeared. Subsequent coronary angiography and ventriculography revealed normal coronary arteries and good left ventricular ejection fraction. It is concluded that an acute asthmatic paroxysm may produce transient myocardial ischemia even with angiographically documented normal coronary arteries.
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PMID:Acute, reversible myocardial ischemia in a patient with an asthmatic attack. 891 9

Chronic dyspnea is shortness of breath that lasts more than one month. The perception of dyspnea varies based on behavioral and physiologic responses. Dyspnea that is greater than expected with the degree of exertion is a symptom of disease. Most cases of dyspnea result from asthma, heart failure and myocardial ischemia, chronic obstructive pulmonary disease, interstitial lung disease, pneumonia, or psychogenic disorders. The etiology of dyspnea is multifactorial in about one-third of patients. The clinical presentation alone is adequate to make a diagnosis in 66 percent of patients with dyspnea. Patients' descriptions of the sensation of dyspnea may be helpful, but associated symptoms and risk factors, such as smoking, chemical exposures, and medication use, should also be considered. Examination findings (e.g., jugular venous distention, decreased breath sounds or wheezing, pleural rub, clubbing) may be helpful in making the diagnosis. Initial testing in patients with chronic dyspnea includes chest radiography, electrocardiography, spirometry, complete blood count, and basic metabolic panel. Measurement of brain natriuretic peptide levels may help exclude heart failure, and D-dimer testing may help rule out pulmonary emboli. Pulmonary function studies can be used to identify emphysema and interstitial lung diseases. Computed tomography of the chest is the most appropriate imaging study for diagnosing suspected pulmonary causes of chronic dyspnea. To diagnose pulmonary arterial hypertension or certain interstitial lung diseases, right heart catheterization or bronchoscopy may be needed.
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PMID:Causes and evaluation of chronic dyspnea. 2296 29

The information on night-time symptoms in chronic obstructive pulmonary disease (COPD) is sparse. We investigated the prevalence of night-time dyspnoea in 6616 individuals with COPD recruited from the general population in the Copenhagen area, Denmark, and described characteristics and prognosis of subjects with this symptom. The prevalence of night-time dyspnoea was 4.3%: 2.1% in Global Initiative for Chronic Obstructive Lung Disease (GOLD) group A, 12.9% in GOLD B, 2.6% in GOLD C and 16.3% in GOLD D. Compared with individuals without night-time dyspnoea, those with night time dyspnoea had lower forced expiratory volume in 1 s, higher daytime dyspnoea scores (modified Medical Research Council scale) and more wheezing, more often had chronic mucus hypersecretion, ischaemic heart disease and atrial fibrillation, and more often reported stress, nervousness and tiredness. After adjustment for age and sex, the presence of night-time dyspnoea was associated with future COPD exacerbations (hazard ratio (HR) 2.3, 95% CI 1.7-3.0), hospital admissions due to COPD (HR 3.2, 95% CI 2.3-4.4) and mortality (HR 1.7, 95% CI 1.2-2.3). Prevalence of night-time dyspnoea in COPD increases with disease severity according to both spirometric and clinical GOLD classification, and is associated with presence of daytime respiratory symptoms and cardiac comorbidities. Night-time dyspnoea is a significant predictor of poor prognosis in individuals with COPD.
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PMID:Prevalence of night-time dyspnoea in COPD and its implications for prognosis. 2488 Oct 57

Asthma is a chronic inflammatory disorder of the airways related to the obstruction of reversible airflow. Asthma presents as recurrent attacks of cough and dyspnea. Poor control causes recurrent admissions to the ICU, and mortality is related to poor drug compliance and follow-up. Angina pectoris is a syndrome of recurrent chest discomfort related to myocardial ischemia. The presence of these two disorders rarely has been reported. We reported a 12-year-old boy who was referred with exacerbation of asthma and developed angina pectoris during hospitalization. He had labored breathing and diffuse wheezing. During treatment of the asthma, the patient developed severe chest pain due to shunt formation and coronary hypoxia, caused by the sole administration of ventolin, since oxygen had been disconnected. After receiving appropriate therapy, both his asthma and angina recovered, and, to date, he has not experienced angina pectoris again.
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PMID:Severe angina pectoris in asthma attack: a case report. 2750 77