Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-three patients (mean age 62 +/- 1 years) were treated for ventricular septal defect (VSD) secondary to myocardial infarction. Whenever possible, operation was postponed until six weeks post-onset chest pain. However, hemodynamic instability, evidenced by cardiogenic shock, refractory pulmonary edema, or a rising blood urea nitrogen (BUN) forced operation in 21 patients within 21 days post-infarct (Group I). In seven patients operation was performed three to six weeks post-infarct (Group II). In only eight patients could operation be delayed beyond six weeks post-infarct (Group III). Clinical deterioration, once begun, progressed rapidly, and could be reversed only temporarily by intra-aortic balloon pumping, used in 26 patients for safe conduct of cardiac catheterization and for peri-operative hemodynamic support. Hospital survival was achieved in 24 of the 36 operated patients (66%). In Group I patients, ten of 21 survived. In Group II, six of seven survived. In Group III, eight of eight patients survived. There have been five late deaths with a mean follow-up of 41 months in survivors. Improved survival has been achieved recently by the greater use of prosthetic material to replace necrotic muscle and by a transinfarct incision regardless of infarct location. Operative mortality before 1973 was 47%; mortality after 1973 was only 18%, with a concomitant reduction of mortality (30%) even in Group I patients.
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PMID:Surgery for post-myocardial infarct ventricular septal defect. 30 10

A patient experienced episodic pulmonary edema accompanying nocturnal angina pectoris. The symptoms were provoked at cardiac catheterization by atrial pacing. Simultaneous onset of chest pain, shortness of breath, and sudden appearance of a large V wave in the pulmonary artery wedge pressure contour confirmed acute mitral valve regurgitation. Rapid reversal of these changes after nitroglycerin administration supported "papillary muscle dysfunction" as the explanation for these hemodynamic changes.
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PMID:Severe papillary muscle dysfunction substantiated by atrial pacing during cardiac catheterization. 40 54

Accidental acute mercury vapor poisoning in three persons is reported. Three hours after exposure, symptomatology began by chills, vomiting, diarrhea and chest pain. Two patients, respectively 67 and 77 year old, presented severe pulmonary edema, then neurological symptoms with tremor and coma. This toxic pulmonary edema, which entailed artificial ventilation, was followed in both cases by an acute interstitial pulmonary fibrosis which led to death respectively after six and sixteen days. In the third case (a thirty eight year old patient) a skin rash, erythematous and pustuliform was observed. Analysis for total mercury by flameless atomic absorption showed very high mercury levels in blood and urine of the three patients. The effect of treatment by Dimercaptopropanol on renal excretion of mercury was studied. Optic and electron microscopy of the lung of the two patients who died showed the pulmonary changes of acute interstitial fibrosis.
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PMID:Accidental acute mercury vapor poisoning. 50 88

The purpose of the study was to determine the proportion of patients with acute myocardial infarction (AMI) for whom an early programme of mobilization, independent of sex and age was possible, and the main reasons for delay of mobilization. Mobilization according to the programme (sitting on day 2 and standing on day 3) succeeded for 49% of the 241 patients alive and conscious after the 1st day, and there were no significant difference with regard to age and sex. The main reasons for delayed mobilization were prolonged chest pain, conduction disturbances and pulmonary oedema. Discharge on day 10 was feasible for 58% of the 241 patients alive and conscious after the 1st day. The mean hospital stay of the patients discharged later than that was 17.3 days. The reasons for the delayed discharge were delayed mobilization, chest pain persisting while in the ward, reinfarction, social, and other reasons. Early programmed mobilization was thus feasible for almost half the patients, and mobilization had been started in over 90% of the patients by the 5th day. Nevertheless, the remarkably high proportion of readmissions (13.3% of all discharged patients) and reinfarctions (6.9%) within the 30 days following discharge may indicate disadvantages in the early mobilization of some patients.
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PMID:Feasibility of early mobilization after acute myocardial infarction. 74 33

The experience of a group of nine men employed in a manufacturing plant, who developed attacks of illness during the course of working with polytetrafluoroethylene (PTFE), is reported. The cause was presumed to be the inhalation of fumes from PTFE-contaminated cigarettes. Eight of the nine employees reported chest pain, shortness of breath, and cough. One had documented pulmonary edema. In view of the potential seriousness of the respiratory complications reported by use and by others we raise the question whether "polymerfume fever" is an adequate or appropriate term to apply to the human inhalation reaction to pyrolysis products of PTFE. Under some conditions of PTFE use, special precautions need to be taken, in addition to those usually recommended, to prevent exposure of to this substance.
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PMID:Pulmonary problems associated with the use of polytetrafluoroethylene. 90 44

We report the case of a previously healthy 56-year-old male who suddenly developed severe chest pain and pulmonary edema. Cardiac catheterization and angiography revealed an aneurysm of the noncoronary sinus of Valsalva which had ruptured into the left atrium. This was confirmed at operation and it was noted that there were no signs of bacterial infection or rheumatic valve disease. We therefore concluded that the aneurysm was of congential origin. A successful repair of the defect was carried out and the patient made a satisfactory recovery. There are only 3 other reported cases of rupture of a congenital sinus of Valsalva aneurysm into the left atrium, and in only one case did the aneurysm originate from the noncoronary sinus and this patient had associated rheumatic aortic and mitral valve disease. We have received the classification of sinus of Valsalva aneurysms, the associated congenital and acquired defects and the presenting features of unruptured and ruptured aneurysms.
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PMID:Ruptured sinus of Valsalva aneurysm with aortic-left atrial fistula. 118 73

Epidemiologic investigations have provided a portrait of the potential candidate for coronary heart disease. This is important because studies of the evolution of coronary disease in the general population reveal that it is a common disease that frequently attacks without warning, can be silent in its most dangerous form and can present with sudden death as the first symptom. Progress in identifyin- persons in jeopardy and the factors needing correction makes it theoretically possible to interrupt the chain of factors that eventuate in this disease. Coronary disease does not really begin with crushing chest pain, pulmonary edema, shock, angina or ventricular fibrillation, but rather with more subtle signs like a poor coronary risk profile. The risk factors can be treated quantitatively as ingredients of a cardiovascular risk profile and their joint effect estimated. An efficient practicable set of variables for this purpose is a casual blood test for cholesterol and sugar, a blood pressure determination, an electrocardiogram and a cigarette smoking history. With this set of variables the risk of coronary heart diseases can be estimated over a 30-fold range and 10 percent of the asymptomatic population identified in whom 25 percent of the coronary disease, 40 percent of the occlusive peripheral arterial disease and 50 percent of the strokes and congestive heart failure will evolve. The periodic use of the electrocardiogram at rest and after exercise in persons with a poor risk profile can demonstrate persons with asymptomatic ischemic cardiomyopathy due to advanced coronary artery disease. Most cases of angina pectoris or myocardial infarction represent medical failures; the conditions should have been detected years earlier for preventive management. About 30 percent of patients with infraction will shortly experience new angina, have an annual death rate of 4 percent and a fourfold increased risk of sudden death. Reinfarction will occur at an annual rate of 6 percent, and half the recurrences will be fatal. Congestive heart failure must be expected at 10 times and strokes at 5 times the rate found in the general population. Although no major innovations are required to identify candidates for coronary disease and to estimate their risk, we have much to learn about motivating changes in behavior to control risk factors. Approaches to prevention of coronary heart disease include public health measures to alter the ecology in favor of cardiovascular health, preventive medicine directed at highly vulnerable candidates and hygienic measures initiated by an informed public in its own behalf.
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PMID:Some lessons in cardiovascular epidemiology from Framingham. 124 56

Over the span of two or three days in August, 1972, in two separate communities in eastern Massachusetts two men, one aged 39, the other 66, each without previous overt heart disease, were stung by wasps. Each went into shock rapidly after an interval of over a half-hour developed chest pain and, later, sequential electrocardiographic changes diagnostic of acute myocardial infarction. Each survived; each had normal electrocardiograms before the sting. Though preexistent coronary artery disease can be excluded in neither, the view is favored that acute myocardial infarction in each was caused by deficient coronary perfusion secondary to anaphylactic shock induced by the wasp stings. An intriguing case was just recently reported58 of a 62-year-old man with previous angina who developed pulmonary edema but no chest pain following wasp sting and went on to show rapidly reversed electrocardiographic changes attributable to subendocardial ischemia or infarction. In a sense, this sequence fills the gap as an intermediate phase between the normal and the two individuals described here who developed pain after anaphylactic shock, then proceeded, perhaps through this phase, to develop transmural infarction.
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PMID:Acute myocardial infarction following wasp sting. Report of two cases and critical survey of the literature. 125 36

To elucidate the clinical characteristics of pulmonary edema in unstable angina, 120 patients with unstable angina who admitted to the hospital within 6 hours after the onset of chest pain were studied. The criteria for the diagnosis of pulmonary edema included interstitial pulmonary edema and diffuse alveolar edema. Pulmonary edema was present in 24 patients. In these patients, the duration of chest pain was relatively longer, and the incidences of diabetes mellitus, emergency coronary revascularization and multiple-vessel coronary artery disease were higher than in those without pulmonary edema. In addition, in-hospital mortality rate in patients with pulmonary edema was higher than in those without it (21 vs 1%, p < 0.001), which is probably due to a large area of myocardial ischemia. For these patients, therefore, early diagnosis and appropriate therapy to save viable segments of the myocardium are mandatory.
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PMID:[Clinical characteristics of pulmonary edema in patients with unstable angina]. 134 24

Of 113 methyl isocyanate (MIC)-exposed subjects studied initially at Bhopal, India, 79, 56, 68, and 87 were followed with clinical, lung function, radiographic, and immunologic tests at 3, 6, 12, 18, and 24 months. Though our cohort consisted of subjects at all ages showing a varied severity of initial illness, fewer females and young subjects were seen. Initially all had eye problems, but dominant symptoms were exertional dyspnea, cough, chest pain, sputum, and muscle weakness. A large number showed persistent depression mixed with anxiety, with disturbances of personality parameters. The early radiographic changes were lung edema, overinflation, enlarged heart, pleural scars, and consolidation. The persistent changes seen were interstitial deposits. Lung functions showed mainly restrictive changes with small airway obstruction; there was impairment of oxygen exchange. Oxygen exchange improved at 3-6 months, and spirometry improved at 12 months, only to decline later. The expiratory flow rates pertaining to large and medium airway function improved, but those for small airways remained low. There were changes of alveolitis in bronchoalveolar lavage fluid on fiber optic bronchoscopy, and in 11 cases positive MIC-specific antibodies to IgM, IgG, and IgE were demonstrated. On follow up, only 48% of the subjects were clinically stable, while 50% showed fluctuations. Thirty-two percent of the subjects had lung function fluctuations. Detailed sequential behavior over 2-4 years was predicted for dyspnea, forced vital capacity, maximum expiratory flow rate (0.25-0.75), peak expiratory flow rate, VO2, and depression score. A model for clinical behavior explained a total variance of 52.4% by using the factors of cough, PCO2 and X-ray zones in addition to above five parameters. The behavior of the railway colony group (1640 patients) revealed a similar pattern of illness. When this observed pattern of changes was transferred to the affected Bhopal city sections (with an equitable age-sex distribution), our model results were again validated. Thus the picture of MIC-induced disease seems similar despite the differences for age-sex and initial severity of illness in our cohort and in the population of Bhopal city as predicted by our model.
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PMID:Sequential respiratory, psychologic, and immunologic studies in relation to methyl isocyanate exposure over two years with model development. 139 63


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