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

Four serologically confirmed fatal cases of nephropathia epidemica (NE), the mild form of hemorrhagic fever with renal syndrome (HFRS) are described. All the patients had disseminated intravascular coagulation. Autopsies revealed hemorrhage and necrotic areas of their pituitary glands, myocarditis, venous congestion and hemorrhage of the kidneys as well as pulmonary edema and hemorrhage of the lungs in all patients. This report provides new evidence that NE can be a fatal disease.
 ...
PMID:Four fatal cases of nephropathia epidemica. 858 46

The direct toxic effect of alcohol and its metabolite acetaldehyde has been demonstrated both in laboratory animals and in humans. Alterations in the mitochondrial ultrastructure and the dilatation of the sarcoplasmatic reticulum have been shown after an acute infusion of alcohol in the heart. These changes correlate with decreased mitochondrial function, defects in protein synthesis and the occurrence of arrhythmias. The risk of developing alcoholic cardiomyopathy is related to both the mean daily alcohol intake and the duration of drinking, but there is much individual susceptibility to the toxic effect of alcohol. Most patients, in whom alcoholic cardiomyopathy develops, have been drinking over 80 g/d for more than 5 years. The clinical diagnosis of alcoholic cardiomyopathy reflects the coexistence of global myocardial dysfunction in a heavy drinker in whom no other cause for myocardial disease was found. In studies focussing on alcoholic cardiomyopathy the surprising histologic findings in endomyocardial biopsy in about 30% of all cases was myocarditis with a lymphocytic infiltrate in association with myocyte degeneration or focal necrosis. In myocarditis, the network of microtubules and intermediate filaments is also disrupted by the inflammatory reaction which involves resident cells (myocytes, fibroblasts, endothel cells) and systemic cells (granulocytes, macrophages, monocytes, lymphocytes). Changes in the cardiac cytoskeleton and the extracellular matrix may affect contractile function, since the cytoskeleton organizes the intra- and intercellular architecture. After all, in patients with alcohol abuse and myocarditis the immune functioning appears to be compromised. Several studies suggest that heavy drinking alters both lymphocyte and granulocyte production and function. Alcohol consumption per se might harm the immune system. Furthermore, the myocardial damage due to alcohol consumption could initiate autoreactive mechanisms comparable to those in viral or idiopathic myocarditis. Patients with alcohol abuse and myocarditis have a poor prognosis: signs of biventricular failure including tachycardia, hepatomegaly, and peripheral and lung edema are observed. These symptoms are as nonspecific as are various echocardiographic and electrocardiographic changes such as atrial and ventricular arrhythmias which may be associated both with myocarditis, alcoholic cardiomyopathy and acute effects of drinking without hemodynamic alterations. For the management of patients with alcohol abuse the prevention of further alcohol intake is mandatory to reverse the myocardial damage and the unfavorable predisposition for infection. Specific treatment of myocarditis is the second important option, and treatment of heart failure by reducing the size of the dilated heart and alleviating the signs and symptoms of heart failure is a logical third step.
 ...
PMID:[Alcohol and myocarditis]. 880 5

A review summarizing recent findings on the causes of the development, pathogenesis, diagnosis and treatment of acute cardiac failure. It is a condition when the heart is unable to pump blood in amounts needed for the metabolic activity of tissues. It may be the first manifestation of disease or acute deterioration of chronic heart failure. The most frequent causes of acute left-sided failure include acute myocardial infarction, arterial hypertension, valvular defects, myocarditis, toxic damage or metabolic myocardial disorders. In right-sided failure pulmonary embolism, extensive affections of the lungs and pleura, right ventricular infarction and affection of the pericardium predominate. The clinical picture of cardiac failure is due to a combination fo the basic disease, evoking causes, signs of an inadequate minute volume, transudation of fluids into the interstitium and the presence of compensating mechanisms. The diagnosis of cardiac failure is based on an analysis of subjective and objective clinical symptoms and other auxiliary examinations such as X-ray examination of the chest, electrocardiogram, echocardiography, examination of blood gases and other laboratory examinations. In right-sided insufficiency the examination is supplemented by pulmonary scintigraphy, possibly by catheterization of the right heart and pulmonary angiography. As to the differential diagnosis, we must differentiate from acute cardiac failure, asthma bronchiale, spontaneous pneumothorax, dyspnoea in neuroasthenic patients, non-cardiac pulmonary oedema. Treatment of cardiac failure involves lifestyle and dietary provisions, medicamentous treatment which has undergone great changes in recent years. Cardiac failure is controlled by reduction of the cardiac filling pressure and support of the efficiency of the cardiac pump (Inotropy) and control of excessive fluid and salt retention. Decisive for the subsequent development of the disease is diagnosis of the basic cardiac or non-cardiac disease and its aimed treatment. In uncontrolled cardiac failure mechanical support of cardiac activity and transplantation of the heart are options.
 ...
PMID:[Clinical aspects of acute heart failure]. 892 24

Cardiac failure is a syndrome which comprises ventricular dysfunction (confirmed by echocardiography) and compensating mechanisms (immediate activation of the sympathetic nerve and functioning of Starling's mechanism, within hours or days activation of RAAS within days or weeks hypertrophy of the heart). Cardiac failure develops rapidly either in a previously healthy subject (first extensive IM, diffuse myocarditis, acute aortic or mitral regurgitation) or in a damaged heart (IHD, KMP, defect) as a result of sudden excessive burdening (ischaemia, arrythmia, infection, surgery etc.) or spontaneously (end-stage). It is manifested above all by "backward" failure (pulmonary oedema). The pulmonary pressure must be rapidly reduced: i.v. nitrovasodilators act immediately, i.v. furosemide acts within 10-15 min. (in can, however, reduce the circulating volume which has not increased during the first failure). Also O2, anodynes. In the subacute stage (without any precise time limits) which may develop in serious cases from acute failure, or develop as a result of deterioration of chronic failure, in addition to congestion, symptoms caused by "forward" failure are in the foreground. These are symptoms caused by a reduced minute output and hyperfusion of tissue. It is indicated to administer substances which improve work tolerance, i.e. positive inotropics (digitalis, beta-agonist or phosphodiesterase inhibitors). If the blood pressure drops, a combination of dopamine and dobutamine should be administered; if the respiratory volume drops, artificial pulmonary ventilation, in case of persisting oedema continuous arteriovenous haemofiltration, in severe failure intraaorrtic balloon contrapulsation etc. In an irreversible state urgent or elective orthoptic transplantation of the heart should be considered. In chronic heart failure an important component of comprehensive treatment is in addition to treatment of congestion and hypoperfusion, prevention of "cardiovascular remodelling" by means of angiotensin convertase inhibitors etc. Which improve the quality of life and survival. Arrhythmias are an independent prognostic factor.
 ...
PMID:[Acute and chronic heart failure]. 924 65

A 48-year-old woman with no cardiovascular risk factors was admitted to the hospital because of acute dyspnea. At 27-year-old, she developed Hodgkin's disease, that was successfully treated with splenectomy, combined chemotherapy (nitrogen mustard, vincristine, procarbazine, prednisone-MOPP regimen) and radiotherapy (4500 rads). At 43-year-old the lymphoma relapsed and she had further chemotherapy with doxorubicin, bleomycin, vinblastina and dacarbazine. After this treatment, she had an episode of pulmonary edema, attributed to doxorubicin acute cardiotoxicity. She responded to digitalis and diuretics and was discharged with an electrocardiogram (ECG) showing left bundle branch block and a normal echocardiogram. The patient enjoyed good health for several years and 4 months before the present admission the ECG and echocardiogram were unchanged. On this admission there were signs of left ventricular failure with acute pulmonary edema, and a new soft apical murmur (3-4 Levine). The patient required endotracheal intubation and high doses of diuretics, digitalis and vasodilators. The cardiac enzymes were negative, the serial ECGs confirmed left bundle branch block, while the echocardiogram showed moderate to severe mitral regurgitation, akinesia of the interventricular septum and inferior wall with dilation of the left ventricle. A previous silent myocardial infarction was suspected. After recovery, she underwent cardiac catheterization confirming akinesia of the interventricular septum and inferior wall with moderate mitral regurgitation, while coronary angiography showed a critical ostial stenosis of the right coronary artery. In view of a dipyridamole-thallium scan negative for myocardial viability, reperfusion was not attempted. With changes in radiotherapeutic techniques, the incidence of radiation-induced heart disease (pericarditis, myocarditis, conduction abnormalities and, rarely, occlusive coronary artery disease) is declining. Nevertheless, after irradiation of the chest and mediastinum a longterm cardiological follow-up is useful in selecting patients at higher risk of radiation-induced coronary artery disease, who will eventually require coronary angiography and reperfusion intervention.
 ...
PMID:[Silent myocardial infarction in a patient treated with radiation therapy and polychemotherapy for Hodgkin's lymphoma]. 928 80

A 16 year old boy presenting with features of myocarditis and pulmonary oedema following scorpion sting developed hemiplegia with patchy vasculitic lesions on CT scan. The possible pathogenic mechanism is discussed.
 ...
PMID:Myocarditis and hemiplegia from scorpion bite--a case report. 935 96

Extracorporeal membrane oxygenation (ECMO) is used as circulatory support or bridge to transplantation in patients with severe left ventricular (LV) dysfunction. Left heart decompression is needed to reduce pulmonary edema, prevent pulmonary hemorrhage, and reduce ventricular distention that may aid in recovery of function. We reviewed our experience from November 1993 to December 1997 with 10 patients having severe LV dysfunction (7 myocarditis, 3 dilated cardiomyopathy) who required circulatory support with ECMO and who underwent left heart decompression with blade and balloon atrial septostomy (BBAS). Patients ranged in age from 1 to 24 years (median, 3 years). Indications for BBAS included left atrial/left ventricular distension (10), pulmonary edema/hemorrhage (9), or severe mitral regurgitation (2). BBAS was performed electively in eight patients and urgently in two patients. BBAS was performed while on ECMO in seven patients and pre-ECMO in three. A femoral venous approach was used in all patients. ECMO patients were fully heparinized. Transseptal puncture was required in nine patients while one patient had a patent foramen ovale. Blade septostomy was performed in all patients. Enlargement of the defect was then performed by stationary balloon dilation in nine and Rashkind balloon atrial septostomy in one. Balloon diameters ranged from 10 to 20 mm. Sequential balloon inflations were performed in some patients. Adequacy of the atrial septal defect (ASD) was confirmed by pressure measurement and echocardiography. Adequate left heart decompression was achieved in all patients. Pulmonary edema improved in nine of nine patients. Left atrial mean pressure fell from a mean of 30.5 mm Hg, (range, 12-50 mm Hg) to 16 mm Hg (range, 9-24 mm Hg). Left atrial to right atrial pressure gradient fell from a mean of 20 mm Hg pre-BBAS to 3 mm Hg post-BBAS. ASDs ranged in size from 2.5 to 8 mm (mean, 5.9 mm). Complications included needle perforation of the left atrium without hemodynamic compromise (one), ventricular fibrillation requiring defibrillation (one), and hypotension following BBAS which responded to volume infusion (two). Duration of ECMO ranged from 41 hr to 704 hr (mean, 294 hr). Seven patients survived and four patients had recovery of normal LV function. Of those who recovered, two had no ASD at follow-up while two ASDs are patent 14 days and 3 months post-BBAS. Three patients underwent successful cardiac transplantation. Three patients died, all of whom had multisystem organ failure with or without sepsis. A patent ASD was noted at transplant (three) or autopsy (two). No patient required a second BBAS. BBAS alleviates severe left atrial hypertension and pulmonary edema. In addition, BBAS avoids the potential bleeding complications of surgical left heart decompression. Stationary balloon dilation of the atrial septum is an effective alternative to Rashkind balloon septostomy in older patients. BBAS achieves left heart decompression that may permit recovery of LV function or allow extended ECMO support as a bridge to transplant.
 ...
PMID:Blade and balloon atrial septostomy for left heart decompression in patients with severe ventricular dysfunction on extracorporeal membrane oxygenation. 1034 39

A 65-year-old woman was admitted to the coronary care unit because of acute pulmonary edema. Immediate 2-dimensional and Doppler echocardiograms revealed extensive left ventricular wall motion abnormalities and left ventricular hypertrophy with extreme outflow obstruction. Although an ECG showed ST-segment elevation in the anterolateral leads, a coronary arteriogram revealed normal epicardial arteries. Heart failure was relieved after diminishing the dynamic outflow obstruction with disopyramide administration. An endomyocardial biopsy from the right ventricle on the 8th hospital day showed borderline myocarditis. Wall motion abnormalities gradually normalized within 2 weeks. It is speculated that her pulmonary edema would not have been relieved so readily without the immediate reduction in ventricular afterload by disopyramide. These clinical changes over time were observed with serial echo-Doppler examinations.
 ...
PMID:Dynamic outflow obstruction due to the transient extensive left ventricular wall motion abnormalities caused by acute myocarditis in a patient with hypertrophic cardiomyopathy: reduction in ventricular afterload by disopyramide. 1047 16

Myocarditis complicated with complete heart block is rare in childhood. We report a case of 4-year-old child presented with complete heart block which may have been caused by Mycoplasma pneumoniae. Under emergent temporal pacing, patient experienced cardiogenic shock with pulmonary edema eventually. The cardiopulmonary function was improved with atrial rhythm at the 6th hour later after intravenous infusion with high-dose gamma-globulin (IVIG). The IVIG therapy may have immunomodulatory effects and serve as a potential adjunctive therapy for fulminant myocarditis.
 ...
PMID:Intravenous gamma-globulin therapy in myocarditis complicated with complete heart block: Report of one case. 1172 11

Mycoplasma alligatoris was the suspected etiology of an epidemic of acute multisystemic inflammatory disease which emerged in captive American alligators (Alligator mississippiensis) in Florida (USA) in 1995. In an experimental inoculation study conducted from April through October 1999, 18 alligators were inoculated with 10(2), 10(4), or 10(6) colony forming units (CFU) of M. alligatoris by instillation into the glottis. As early as 1 wk post-inoculation (PI), mycoplasma were cultured from blood of three of six alligators inoculated with 10(6) CFU. Two of those died and the third was euthanatized within 4 wk PI. Necropsy gross findings included fibrinous polyserositis and polyarthritis. Histopathologic changes in affected individuals included pulmonary edema, interstitial pneumonia, pericarditis, myocarditis, meningitis, and synovitis. Mycoplasma were cultured quantitatively in high numbers from trachea, lung, coelomic cavity, liver, spleen, interior of pericardial sac, heart, blood, brain, and limb joints. In alligators inoculated with 10(6) CFU, heterophilia and moderate hyperglycemia peaked about 4 wk PI, and seroconversion occurred by 6 to 8 wk PI. Necropsy gross and histologic findings were generally unremarkable for the surviving alligators inoculated with 10(6) CFU, alligators inoculated with 10(2) or 10(4) CFU, and four uninoculated control alligators. Mycoplasma were not cultured at any time point from those alligators. The findings confirm that M. alligatoris can cause fulminant inflammatory disease and rapid death of alligators.
 ...
PMID:Pathology of experimental mycoplasmosis in American alligators. 1176 30


<< Previous 1 2 3 4 5 6 7 8 9 Next >>