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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac and pulmonary disease are so closely interrelated that it is often difficult to determine in young infants which is the primary offender. As illustrated in these case reports, failure to recognize the true nature of the disease process may lead to unnecessary procedures and delays which can be life-threatening. Statistically, the wheezing infant very likely is suffering from primary pulmonary disease; however, congenital cardiac abnormalities can cause pulmonary symptoms which completely dominate the clinical picture and lead to erroneous diagnoses. Although rare, the basis of cough and wheezing may be a vascular ring which encircles and compresses the trachea. Lesions associated with large left-to-right shunts, such as ventricular septal defect and patent ductus arteriosus, also can cause cough and wheezing because of bronchial compression by a large tense pulmonary artery and a distended left atrium. These same lesions also produce isolated left ventricular failure with pulmonary venous congestion and episodes of cough and wheezing. Anomalous pulmonary venour return, cor triatriatum, supravalvular mitral ring, or mitral stenosis are other lesions which can cause cough and wheezing secondary to pulmonary venous obstruction.
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PMID:Cardiac disease in the wheezing child. 83 90

Cough and wheezing are common findings in left heart failure. However, it is still questionable whether nonallergic bronchial hyperresponsiveness, the hallmark of asthma, is also associated with this condition. In 12 subjects with acute decompensation of chronic postischemic LV failure, we assessed the PC20 methacholine during an episode of acute LV failure and after five to 15 days of intensive diuretic therapy. Weight, arterial blood gases, plethysmographic lung volumes, and expiratory flows were also measured on both visits. Extravascular lung water was estimated indirectly with a radiologic score. During acute decompensation, six subjects had significant airway obstruction and eight had a PC20 less than or equal to 16 mg/ml (significant bronchial hyperresponsiveness). After diuretic therapy, subjects improved significantly, losing an average of 2.2 kg, but they still had chronic LV failure and evidence of an obstructive breathing defect. Although mean PC20 was unchanged, three subjects had significantly improved PC20 after treatment. We conclude that: (1) left ventricular failure is often associated with mild bronchial hyperresponsiveness, although it is not excluded that smoking and the resulting possibility of bronchial obstruction can also play some role; and (2) acute treatment does not generally alter bronchial responsiveness to methacholine, suggesting that chronic LV failure can cause chronic changes to the airways.
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PMID:Bronchial hyperresponsiveness to inhaled methacholine in subjects with chronic left heart failure at a time of exacerbation and after increasing diuretic therapy. 237 98

Cardiac asthma has been used as a synonym for episodes of cough, dyspnea, and wheezing caused by left ventricular dysfunction. The similarity of the terms bronchial asthma and cardiac asthma, and the observed symptoms of each disease implies a common pathophysiology. Bronchial asthma is characterized pathologically by airway narrowing, inflammation, edema, and obstruction by mucus. Bronchial asthma is defined as increased responsiveness of the tracheobronchial tree, which is manifested clinically as reversible expiratory airflow obstruction. The classic symptoms of bronchial asthma are cough, dyspnea, and wheezing. Cardiac asthma produces the same symptoms, but the pathophysiology producing these symptoms is not well described. We describe two patients with cardiac asthma who failed to demonstrate airway hyperresponsiveness to nonspecific bronchoprovocation testing and we postulate that these patients' symptoms were produced exclusively by left ventricular failure.
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PMID:Normal airway responsiveness to methacholine in cardiac asthma. 269 Jul 10

The radiologic appearance of atypical cardiogenic pulmonary edema (ACPE) is presented in 10 cases admitted from 1983 to 1985, with age ranges from 74 to 89, and with diagnosis of ischemic heart disease, with myocardial infarction in 50% of them. Clinically they had asthenia, adynamia and anorexia in 80%, cough and weight loss in 50%. All of them had tachycardia, pulmonary rales and 50% pericardial rub. ECG showed in 80% anterior subepicardial ischemia, 60% posteroinferior subepicardial ischemia, 60% bifascicular block, and 50% left anterior fascicular block. Chest films were interpreted at first as pulmonary fibrosis in 90% of the cases with superior lobe involvement in 50%. Heart enlargement was present in 50%. A chronic lung disease was disclosed on clinical and pulmonary physiological grounds. It is concluded that asthenia, adynamia and anorexia were atypical manifestations of heart failure in the elderly. Silent myocardial infarction was observed in half of our patients and it was complicated with pericardial involvement in 50%. Irregular distribution of fluids in pulmonary edema was attributed to anatomic changes in elder lung. These atypical behaviour of pulmonary edema, has been misinterpreted on radiologic basis with pulmonary infection, tumours, metastasis or fibrosis. Those radiologic changes disappeared or improved in 72 hrs. with treatment of left ventricular failure.
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PMID:[Radiologic characteristics of cardiogenic pulmonary edema in the elderly]. 296 66

The demographics and natural clinical history of canine congenital subaortic stenosis (SAS) were evaluated by retrospective analysis of 195 confirmed cases (1967 to 1991), 96 of which were untreated and available for follow-up evaluation. Of these, 58 dogs had left ventricular outflow systolic pressure gradients available for assessment of severity. All 195 dogs were used for demographic analysis. Breeds found to be at increased relative risk included the Newfoundland (odds ratio, 88.1; P < .001), Rottweiler (odds ratio, 19.3; P < .001), Boxer (odds ratio, 8.6; P < .001), and Golden Retriever (odds ratio, 5.5; P < .001). Dogs with mild gradients (16 to 35 mm Hg) and those that developed infective endocarditis or left heart failure were diagnosed at older ages than those with moderate (36 to 80 mm Hg) and severe (> 80 mm Hg) gradients. Of 96 untreated dogs, 32 (33.3%) had signs of illness varying from fatigue to syncope; 11 dogs (11.3%) developed infective endocarditis or left heart failure. Exercise intolerance or fatigue was reported in 22 dogs, syncope in 11 dogs, and respiratory signs (cough, dyspnea, tachypnea) in 9 dogs. In addition, 21 dogs (21.9%) died suddenly. Sudden death occurred mainly in the first 3 years of life, primarily but not exclusively, in dogs with severe obstructions (gradient, > 80 mm Hg; odds ratio, 16.0; P < .001). Infective endocarditis (6.3%) and left heart failure (7.3%) tended to occur later in life and in dogs with mild to moderate obstructions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The natural clinical history of canine congenital subaortic stenosis. 788 29

Brucella endocarditis was diagnosed in a 21-year-old itinerant farm worker hospitalized for acute pulmonary edema. History taking revealed cough, fever and sweating one month earlier which had been treated with antibiotics. At admission, echography showed lesions on the aortic valve and hemocultures identified Brucella meltensis. On day 7 of specific treatment with doxycycline (200 mg/day) and rifamycine (1200 mg/day), and despite digitalics and diuretics, left ventricular failure rapidly worsened, leading to cardiac arrest and death before emergency surgery could be performed. Autopsy showed occlusive vegetations on the aortic valves facing the right coronary ostium, deep ulceration of the valsava sinus with abscess formation and fibrino-hemorragic pericarditis involving both the anterior and posterior walls of the epicardium. Gram negative germs were evidenced in the abscess alone. This case emphasizes the potentially rapid destructive effect of Brucella melitensis and confirms that surgery is the safest therapeutic alternative for aortic valve localizations. Surgery should be performed without delay.
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PMID:[Brucella pancarditis with fatal outcome]. 866 92

A 75-year-old man was admitted to the hospital due to acute onset of a dry cough and dyspnea on exertion. Arterial blood gas analysis showed hypoxemia (PaO2 = 63 Torr) on room air. Chest radiography and computed tomography showed diffuse bilateral infiltrates. Adult respiratory distress syndrome was diagnosed from the findings described above and from the lack of evidence of left heart failure. Diffuse alveolar damage was confirmed at autopsy. During the course of his illness, the patient underwent bronchoalveolar lavage five times. The recovered fluid had high concentrations of interleukin-8 (IL-8), with a maximum of 6260 pg/ml and a minimum of 190 pg/ml, and these values correlated with the number of polymorphonuclear cells in the fluid. Levels of leukotriene B4, another chemotactic factor for PMN, in the lavage fluid were not high. We conclude that IL-8 was a major chemoattractant for PMN in the alveoli of this patient.
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PMID:[High concentrations of interleukin-8 in bronchoalveolar lavage fluid from a patient with adult respiratory distress syndrome]. 875 13

To determine whether a relationship exists between bronchial hyperreactivity and cardiac asthma, which is commonly observed in patients with left heart failure, a methacholine inhalation test was performed in 15 patients with stable left ventricular failure (LVF) and 10 normal subjects. The subjects were divided into 3 groups based on symptoms of nocturnal coughing and/or wheezing in acute exacerbation of LVF. Group A consisted of 8 patients with nocturnal coughing and/or wheezing. Group B consisted of 7 patients without such symptoms, and Group C consisted of the 10 age-matched normal controls. Eleven of the 15 patients with LVF showed a significant increase in respiratory resistance in the methacholine inhalation test, as opposed to none of the normal subjects. The median cumulative dose which produced a 35% decrease in respiratory conductance (PD35Grs) was significantly lower in Group A than in Group B (1.45 log units and 1.90 log units, respectively, p < 0.05). The results of pulmonary function tests were not significantly different between Groups A and B. The minimum cumulative dose required to initiate a decrease in respiratory conductance from the baseline, as an index of bronchial sensitivity to methacholine, was significantly correlated with DLCO/VA (r = 0.710, p < 0.01). We conclude that bronchial hyperreactivity is responsible for cardiac asthma and that it might be related to pulmonary interstitial changes in stable patients with non-valvular LVF.
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PMID:Relationship between bronchial hyperreactivity and symptoms of cardiac asthma in patients with non-valvular left ventricular failure. 899 83

Primary sarcomas of the great vessels are rare, but the most common site is the inferior vena cava. Herein are reported five new cases arising from the pulmonary veins with clinicopathologic correlation and comparison to previously reported cases. All new cases occurred in women ranging in age from 23 to 64 years at diagnosis (mean, 56 years). They had symptoms suggestive of left heart failure, including three patients with dyspnea, one with hemoptysis, and one with cough. Three cases showed tumor extension along the pulmonary veins into the left atrium. Tumors ranged in size from 2.8 to 7 cm in greatest dimension. Histologically, all were leiomyosarcomas. They were highly cellular tumors. Three cases had predominantly spindle cell morphology and two were predominantly epithelioid; one had foci of calcification. Most showed extensive necrosis. All tumors were reactive with antibodies to actin and desmin. Two cases were reactive with antibodies to MIC-2 (dotlike); two cases showed reactivity to keratin antibodies; and two showed reactivity for estrogen, progesterone receptor protein, or both. None were positive for antibodies to S-100 protein. All cases were treated with surgical excision. Follow-up ranged from 2 months to 21 years (mean, 4.8 years). Two patients were alive and well; two were alive with metastases; and one died of disease. Pulmonary vein sarcomas represent intermediate- to high-grade leiomyosarcoma. Although often lethal, complete surgical excision can lead to long-term survival. They occur predominantly in women and may express hormone receptors. Therefore, hormonal manipulation may offer promise as adjuvant therapy.
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PMID:Leiomyosarcoma of the pulmonary veins. 1047 68

National and international societies have issued guidelines on the management of heart failure: The European Society of Cardiology, WHO, ACC/AHA Task Force Report, US Department of Health and Human Services, German Society of Cardiology. The therapeutic approaches to heart failure have undergone considerable changes during the last few years. The guidelines have to be updated almost yearly due to new results from prospective randomized studies. Although an agreement could be reached with respect to general measures and drug treatment, no agreement on mechanical devices, pacemakers and surgical interventions has been reached. The basis for medical treatment of chronic heart failure depends on diuretics, digitalis, ACE inhibitors, and beta-blockers. Calcium antagonists and other positive inotropic drugs, other than digitalis, should be avoided as far as possible. Thiazides, loop diuretics and aldosterone antagonists are needed for acute and chronic treatment of heart failure, alone or in combination (diuretic resistant heart failure!). Digitalis glycosides are needed in patients with atrial fibrillation with a fast ventricular rate or atrial flutter and in patients with systolic dysfunction, large hearts and symptomatic failure class NYHA III and IV. However, digitalis does not convert atrial fibrillation to sinus rhythm. Today there is no question that ACE inhibitors improve the prognosis of all patients with heart failure in all stages, if ejection fraction is reduced. Therefore, most patients after myocardial infarction or after having experienced pump failure due to myocarditis or cardiomyopathy are treated with ACE inhibitors and diuretics. The beneficial effects of ACE inhibitors seem to be most pronounced the worse the situation is. Relative risk reductions (mortality!) between 10% and 40% have been published depending on the severity of symptomatic left ventricular dysfunction. Those patients with high absolute risk have more to gain than those with low risk for any given "risk reduction", of course. Recent studies also indicate that most high risk cardiac patients profit from ACE inhibitors even if pump function is normal (i.e., patients with coronary heart disease, diabetes mellitus, cerebral vascular disease, hypertension) (15). AT1 antagonists can substitute for ACE inhibitors, if the latter are not tolerated due to cough. Up to now, beta-blocking agents apart from diuretics seem to be the best investigated drugs in heart failure. Large controlled studies with bisoprolol, carvedilol and metoprolol in addition to diuretics, digitalis and ACE inhibitors convincingly yielded positive results in chronic left ventricular failure patients. Reduction of mortality by 35% and even of sudden cardiac deaths by 40% have been proven beyond doubt. Thus, heart failure patients today should also receive beta-blocking agents in all stages of the disease. In the era of controlled prospective studies (evidence-based medicine), physicians are well advised to use only drugs that have been proven beneficial in large controlled studies.
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PMID:The management of heart failure--an overview. 1119 49


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