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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study of factors predicting mortality was performed in 201 patients with dilated cardiomyopathy (163 men, 38 women, mean age: 48 +/- 11 years) by multivariate analysis (Cox Model) of 51 clinical, electrocardiographic, echocardiographic and haemodynamic parameters, 56 patients died during follow-up (mean follow-up: 57.1 +/- 29.9 months). 5 year survival was 77 +/- 3%. The following parameters were independent predictors of mortality: first symptom: pulmonary oedema, peripheral oedema, syncope; duration of symptoms at the time of inclusion; end systolic left ventricular volume; end diastolic left ventricular diameter; pulmonary artery systolic pressure; and their combination had the most accurate predictive value for death. A quantitative score (s) was calculated and used to define three subgroups: A:s less than or equal to 4.5; B: 4.5 less than s less than 6; C:s greater than or equal to 6. Five-year survival was 90 +/- 5% in group A; 84 +/- 4% in B and only 53 +/- 7% in C. In conclusion, overall survival was good in this population of all stage dilated cardiomyopathy; factors related to clinical severity, left ventricular dilation, systolic pulmonary artery pressure and duration of symptoms defined a subgroup of patients with poor prognosis.
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PMID:Factors predicting mortality in idiopathic dilated cardiomyopathy. 222 8

The beneficial effects of physiologic dual-chamber (DDD) pacing in the treatment of end-stage idiopathic dilated cardiomyopathy were evaluated in 16 patients in whom conventional drug therapy had failed. Candidates for cardiac transplantation as well as patients not accepted for transplantation participated. During DDD pacing at an atrioventricular delay of 100 ms, left ventricular ejection fraction increased from 16.0 +/- 8.4 to 25.6 +/- 8.6% (p less than 0.001) accompanied by a striking improvement in clinical symptoms, such as severe dyspnea at rest and pulmonary edema. The New York Heart Association class decreased from 3.6 +/- 0.4 to 2.1 +/- 0.5 (p less than 0.001). The decrease in cardiothoracic ratio from 0.60 +/- 0.06 to 0.56 +/- 0.05 (p less than 0.001) coincided with a decrease in left atrial and right ventricular echocardiographic dimensions, indicating a decrease in preload. Systolic blood pressure increased from 108 +/- 29 to 126 +/- 21 mm Hg (p less than 0.01) and diastolic blood pressure from 67 +/- 15 to 80 +/- 11 mm Hg (p less than 0.01). Normalization of heart rate was achieved. No major complications developed as a consequence of DDD pacing. All patients could be discharged from the hospital within 3 weeks after pacemaker implantation and return to a relatively normal life. Within 1 year after onset of DDD pacing only 4 of the patients died (from either sudden death or stroke). DDD pacing could represent an alternative approach to the management of chronic heart failure due to dilated cardiomyopathy, especially for heart transplant candidates and patients who are not accepted for cardiac transplantation, but no longer respond to drug therapy.
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PMID:Usefulness of physiologic dual-chamber pacing in drug-resistant idiopathic dilated cardiomyopathy. 237 55

The regulation of water and electrolyte homeostasis is multifactorial and includes the heart and kidneys as important regulatory centers. Within the heart, a recently discovered hormone, atrial natriuretic factor (ANF), has been implicated in the maintenance of water and salt balance. Primarily found in mammalian atria, ANF has been detected in low amounts in several tissues, including lungs. A disorder of the ANF system has been demonstrated in genetically cardiomyopathic hamsters, a model for human congestive cardiomyopathy. Atrial ANF gene expression and storage are decreased during development of this disease, while paradoxically, circulating levels of ANF are increased. We have hypothesized that an extracardiac source may contribute to ANF production in these pathological conditions. In this paper we provide evidence that ANF synthesis is stimulated in the lungs of hamsters during development of cardiomyopathy as revealed by increased ANF mRNA and peptide levels. Furthermore, we show that ANF synthesized in lungs is secreted and has identical chromatographic and biological properties to circulating ANF. The increased production of ANF in lungs may be physiologically important in preventing pulmonary edema. Alternatively, during cardiac dysfunction, lungs may play a compensatory role by increasing their contribution to plasma ANF levels.
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PMID:Lung is an important source of atrial natriuretic factor in experimental cardiomyopathy. 252 13

Intravenous isosorbide-5-mononitrate (IS-5-MN) was administered to 24 patients, mean age 73, with severe respiratory distress after pulmonary edema and acute left heart failure. The condition was due to ischemic cardiopathy in 18 patients (4 with acute myocardial infarctions), congestive cardiomyopathy in 3, hypertensive cardiopathy in 2, and mitral valvular disease in 1. Therapy consisted of an intravenous (i.v.) bolus dose of IS-5-MN, followed by a continuous infusion (mean 8 mg/hour over 24 hours) of i.v. furosemide and additional oxygen. Clinical data were recorded as well as blood gas values and repeated chest radiographs. All patients survived and improved markedly; only 6 needed mechanical ventilation. Most patients had fast respiratory relief, with no untoward reaction, except a brief decrease of blood pressure in a ventilated patient taking morphine. These data indicate that i.v. IS-5-MN is effective and safe for the management of severe acute cardiogenic pulmonary edema.
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PMID:Emergency treatment of severe cardiogenic pulmonary edema with intravenous isosorbide-5-mononitrate. 334 37

Furazolidone (FZ)-induced congestive cardiomyopathy was diagnosed as the cause of high mortality and unthriftiness in two flocks of white pekin ducklings. Cumulative mortality at 7 weeks of age was 10.0-14.4%. Samples of FZ-supplemented feeds fed to flocks 1 and 2 from day 1 to day 14 had 140 and 150 mg FZ/kg, respectively. Both flocks had various degrees of water restriction. Clinically, the ducklings had dyspnea, incoordination, and abdominal distention. Necropsy findings included pulmonary edema and congestion, ascites, atrophic congested livers covered with sheets of fibrin, and cardiac enlargement with biventricular dilatation. Cardiac alterations were minimal by light microscopy. Ultrastructurally, scattered myocytes had myofibrillar lysis. These outbreaks occurred following intake of FZ at therapeutic dosages and emphasize the high susceptibility of young ducklings to FZ cardiotoxicity.
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PMID:Furazolidone-associated cardiomyopathy in two Indiana flocks of ducklings. 367 32

Thirty-four men with left ventricular mechanical dysfunction were admitted to an intensive care unit with either an acute myocardial infarction (Group 1, n = 18) or worsening of clinical respiratory signs and symptoms in the setting of a chronic congestive cardiomyopathy (Group 2, n = 16). On admission, all individuals had pulmonary venous hypertension classified as at least Grade 3 by standard radiographic criteria. In each subject, mean pulmonary capillary wedge pressure (mm Hg), extravascular lung water (EVLW) (ml/kg), and chest radiographs were serially evaluated. In the patients in whom pharmacologic therapy successfully returned left ventricular filling pressures to near normal levels (less than or equal to 15 mm Hg), the chest radiograph returned to its baseline level (defined by the discharge radiograph) later in the patients with chronic heart failure (5.1 +/- 1.0 days) than in the patients with acute myocardial infarctions (2.1 +/- 1.2 days, p less than 0.01). Radiographic changes in extravascular water (interstitial and alveolar edema) mirrored changes in EVLW, although EVLW was initially greater in Group 2 (16.3 +/- 1.8 ml/kg) than in Group 1 (10.7 +/- 1.3 ml/kg, p less than 0.01). In the patients in whom filling pressures either worsened or changed less than 3 mm Hg, EVLW and chest radiographs did not markedly change. It is concluded that changes in radiographic pulmonary edema mirror changes in indicator-dilution measurements of EVLW. Radiographic phase lag represents a slow decline in EVLW after therapy for heart failure, which is prolonged in patients with chronic failure and greater EVLW.
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PMID:Chest radiographs in congestive heart failure: response to therapy in acute and chronic heart disease. 333 Jun 19

Extravascular lung water was assessed using a double-indicator dilution technique (thermal-green dye) in 15 men who had radiographic and clinical evidence of cardiogenic interstitial and alveolar pulmonary edema. Eight patients had suffered an acute myocardial infarction and seven had a history of chronic congestive cardiomyopathy and worsening of previous clinical signs and symptoms. At the same level of pulmonary capillary wedge pressure and similar arterial oxygen tensions extravascular lung water was significantly greater in the group with chronic congestive cardiomyopathy (p less than .05). The two groups did not differ with respect to systemic arterial pressure, resistance, or cardiac index.
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PMID:Extravascular lung water in patients with congestive heart failure. Difference between patients with acute and chronic myocardial disease. 634 31

Left ventricular (LV) diastolic dysfunction is the first discernible manifestation of heart disease in hypertensive patients. Arterial hypertension with LV hypertrophy leads to reduced preload followed by impaired cardiac output (systolic dysfunction stemming from primary diastolic dysfunction). Diastolic dysfunction leads more often than systolic dysfunction to hypertensive heart failure and is in many cases clearly distinguishable from heart failure with low ejection fraction (EF). Mortality due to heart failure from impaired inotropism is higher than mortality due to diastolic dysfunction, but morbidity is lower. Hypertensive cardiomyopathies can be divided into 4 ascending categories, according to the pathophysiologic and clinical impact of hypertension on the heart: Degree I: LV diastolic dysfunction with no associated LV hypertrophy Degree II: LV diastolic dysfunction with echocardiographic LV hypertrophy Degree IIA: Normal exercise capacity in terms of maximal oxygen consumption Degree IIB: Impaired exercise capacity in terms of maximal oxygen consumption Degree III: Congestive heart failure (severe dyspnea and radiographically determined pulmonary edema with normal (> or = 50%) EF Degree IIIA: LV mass/volume ratio > 1.8 with little or no myocardial ischemia Degree IIIB: LV mass/volume ratio < 1.8 with significant myocardial ischemia Degree IV: Profile of dilated cardiomyopathy; LV hypertrophy and impaired EF (< 50%).
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PMID:Congestive heart failure due to hypertensive ventricular diastolic dysfunction. 749 17

Cardiogenic shock is a syndrome of different etiologies resulting in the inability of the heart to provide adequate O2 delivery to peripheral organs and tissues with or without signs of severe pulmonary congestion or pulmonary edema. Clarification of the underlying etiologies is essential for prognosis and therapy. Depending on the various etiologies, the therapeutic procedure may be totally different. Furthermore, it is decisive to differentiate between an acute shock (e.g., acute myocardial infarction) and the development of a cardiogenic shock state on the basis of preexisting chronic congestive heart failure (e.g., congestive cardiomyopathy). Whenever possible the underlying disease should be treated causally (e.g., PTCA or thrombolytic therapy in AM, lysis in acute pulmonary embolism) in addition to symptomatic pharmacologic treatment with vasodilators and/or inodilators. In myogenic cardiogenic shock, the treatment with inotropic drugs (with and without vasodilatory potency) and, if necessary, in combination with additional vasodilators may be life-saving. At present, there is no alternative to catecholamines in the acute state with apparent hemodynamic instability. Catecholamines still represent the initial first line treatment. A Swan-Ganz catheter is mandatory in such situations. In view of the rapid beta 1-receptor down-regulation induced by endogenous catecholamines, long-term administration of exogenous catecholamines (adrenalin, dopamine, dobutamine), seems essentially problematic, since these compounds intensify and accelerate this process.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Therapy of cardiogenic shock]. 786 6

To further define the prognosis and identify clinical findings predictive for survival in dogs with dilated cardiomyopathy (DCM), we performed Kaplan Meier survival analysis of 37 dogs with idiopathic DCM. Survival analysis showed that the 50% probability of survival occurred at 2.3 months. Probability of survival at 1 year was 37.5% and at 2 years was 28%. Bivariate Cox proportional hazard ratios identified pleural effusion and pulmonary edema, both signs of congestive heart failure, as independent prognostic indicators for dogs with DCM (P < .01). Hazard ratios for these prognostic indicators were 2.354 and 3.291, respectively. Multivariate Cox stepwise regression identified pleural effusion, left ventricular free-wall thickening fraction, ventricular ectopy, and weight loss as significant prognostic indicators for dogs with DCM. Because of the retrospective nature of this study, the effects of different drug treatments were not evaluated. The type of cardiac-related death, progressive failure versus sudden death, was not addressed in this study and requires further evaluation.
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PMID:Idiopathic dilated cardiomyopathy in dogs: survival and prognostic indicators. 789 57


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