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)

On the patients with moderate and severe heart insufficiency haemodynamic, clinical and electrocardiographic examinations were carried out. After the application of digitoxin at the beginning in the majority of cases no favourable effects on clinical and haemodynamic findings could be proved. In 2 patients with cor pulmonale even a drastic deterioration with increase of the pulmonary pressure and formation of a pulmonary oedema developed. The temporary analysis of the systole and the estimation of the glycoside level did not give any reliable references. The recompensation began only after 2-3 days. In 5 out of 10 patients in whom the cardiac rhythm was continuously controlled by means of a tape storage device, after the application of digoxin ventricular extrasystoles appeared. Also in these cases increased as well as subtherapeutic digoxin-plasma levels were present. In 2 patients with hypertrophic obstructive cardiomyopathy the infundibular gradients were considerably increased by strophantin. The causes of the different reaction patters are to be sought in disease-specific peculiarities, in the degree of severity of the heart insufficiency, in the speed of the flooding of glycoside and several extracardiac factors.
...
PMID:[Dangers of rapid digitalization]. 9 71

Cardiology was diagnosed by means of clinical, radiographic, electrocardiographic phonocardiographic, angiocardiographic, and pathological findings in 271 or 3,745 cats necropsied from January 1962 to April 1974. The affected cats can be divided into three groups on the basis of the gross and microscopic pathological lesions: 1)endocarditis and myocarditis in 20 young cats; 2)endomyocardial fibrosis and left ventricular hypertrophy in 182 cats; and 3)myocardial degeneration and biventricular dilatation in 69 cats. Of 271 affected cats, thromboembolus was observed in the aorta, and in the carotid, femoral, iliac, renal, pulmonary, and hepatic arteries in 104 instances. The important aspects of cardiomyopathy in cats appears to be the reduced diastolic compliance of the thick left ventricle, resulting in poor fillin. Resistance to ventricular inflow raises the diastolic pressure and causes compensatory left atrial enlargement. A pathogenesis for the onset of clinical signs at any stages as the cause of the heart disease is postulated on the basis of stress causing tachycardia and poor left ventricular filling. Acute left-sided failure with pulmonary edema may be precipitated. Approximately one-fourth of the cats have enlargement of all cardiac chambers, typical of congestive cardiomyopathy. On the basis of the close similarily to cardiomyopathy in man, the cat could serve as a suitable animal model for a conservation of time and effort in the attack against this disorder. There is a need for coordinated research programs for utilizing the multiple avenues of approach such as: epidemiological, clinical, biochemical, pathological, ultrastructural, virological, and immunological.
...
PMID:Feline cardiomyopathy. 12 93

Clinical studies have long suggested the presence of a specific cardiomyopathy in sickle cell anemia secondary to intracoronary thrombosis and subsequent infarction. Fifty-two autopsy patients were studied (48 with SS hemoglobin, 4 with S-C or S-Thal hemoglobin) to ascertain the range of cardiac pathologic abnormalities associated with this disease. The average age was 17 years (range 1 month to 48 years). Renal failure and infection were the most common causes of death; the former was a more common cause in adults than in children. Right and left ventricular hypertrophy and dilatation were the most common abnormal pathologic findings. No evidence of recent or remote myocardial infarction, coronary thrombosis or arteritis was noted in any patient. Eight patients who were studied with postmortem coronary arteriograms exhibited markedly increased coronary arterial caliber with no evidence of atherosclerosis. Seventeen of the 52 patients studied had clinical evidence of congestive heart failure before death. Of these 17 patients, 7 had moderate to severe left ventricular hypertrophy associated with chronic renal failure and hypertension, 2 had right ventricular hypertrophy with organized pulmonary thrombosis, 2 had rheumatic mitral valve disease and 2 died during the second trimester of pregnancy. Two of the 17 patients thought to have pulmonary edema before death in fact had aspiration pneumonia and hemorrhagic pneumonitis, respectively. The data suggest that cardiac dysfunction in sickle cell anemia can usually be explained by the adverse effect of coexisting disease on the diminished cardiac reserve of chronic anemia. The data do not support the concept of a specific "sickle cell cardiomyopathy".
...
PMID:Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia. 15 Jul 86

Three patients presented with severe congestive cardiomyopathy of unknown cause. All three had a profound depression of serum phosphorus levels resulting from the chronic ingestion of large quantities of a phosphorus-binding antacid. Results of physical examination and echocardiograms were consistent with cardiomegaly and severe myocardial dysfunction, and chest films showed enlargement of the cardiac silhouette with interstitial pulmonary edema. Serum phosphorus was restored to normal levels, and within 2 to 5 weeks the results of physical examination and echocardiogram of each patient returned to normal. We conclude that these patients had reversible hypophosphatemic cardiomyopathy and show the importance of inorganic phosphorus in myocardial metabolism and function. Serum phosphorus measurements should be a part of the routine evaluation of patients with congestive cardiomyopathy because, at least in some patients, hypophosphatemia appears to be a reversible cause of this disorder.
...
PMID:Reversible severe congestive cardiomyopathy in three cases of hypophosphatemia. 634 61

This report describes a patient with hypertrophic obstructive cardiomyopathy complicated by acute aortic and probably mitral valvular incompetence caused by endocarditis due to Staphylococcus aureus. Following the onset of valvular insufficiency, this patient developed hypotension and pulmonary edema and eventually underwent cardiac surgery in an attempt to control these complications. We review the unique pathophysiology of hypertrophic obstructive cardiomyopathy and its alterations in the presence of acute valvular incompetence and analyze the limitations of medical management of cardiac decompensation in patients with this combination of cardiac abnormalities. The possible need for early surgery in such patients is examined.
...
PMID:Acute valvular insufficiency complicating hypertrophic obstructive cardiomyopathy. 57 Apr 72

Thirty-four cats with primary myocardial disease were studied. The cats were divided into two groups, depending on the clinical, hemodynamic, angiocardiographic, and pathologic findings. Group A consisted of those cats with hypertrophic cardiomyopathy and Group B consisted of those cats with congestive cardiomyopathy. Similarity in the characteristics of cardiomyopathy in the human cat was found. Both Group A and Group B consisted predominantly of mature adult male cats. The most common presenting signs were dyspnea and/or thromboembolism, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (Group A) or without (Group B) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (Group A) or left ventricular dilatation (Group B). Some cats in Group A also had evidence of left ventricular outflow obstruction. The principal pathologic findings in these cats were left atrial dilatation, symmetric hypertrophy or asymmetric septal hypertrophy of the left ventricle (Group A), and dilatation of the four cardiac chambers (Group B). Aortic thromboembolism was commonly observed in both groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat is similar to the two most common forms of cardiomyopathy in the human (hypertrophic cardiomyopathy, with and without obstruction, and congestive cardiomyopathy).
...
PMID:Primary myocardial disease in the cat. A model for human cardiomyopathy. 84 11

An 18-year-old man developed acute pulmonary edema following heroin overdose. Two days after initial improvement, there was recurrence of hypotension and pulmonary edema with severe hypoxemia refractory to mechanical ventilatory support utilizing positive and end-expiratory pressure. Cardiac catheterization revealed elevated pulmonary capillary wedge pressure suggestive of left ventricular failure. The use of digitalis and diuretics resulted in prompt clinical improvement and ultimate recovery. Evidence is presented indicating that this patient represents an uncommon but important syndrome of acute cardiomyopathy with left ventricular failure which complicates the clinical course of certain cases of heroin overdose. Its physiologic diagnosis is of obvious importance in the choice of proper therapy, thereby increasing the patient's chances of recovery.
...
PMID:Acute cardiomyopathy with recurrent pulmonary edema and hypotension following heroin overdosage. 124 68

A 36-year-old black multipara at 32 weeks gestation was referred with apparent peripartal cardiomyopathy. Upon arrival, she was found to be in pulmonary edema; and shortly thereafter developed cardiopulmonary arrest. She failed to respond to initial attempts at cardiopulmonary resuscitation but subsequently responded after Caesarean section and pericardiocentesis. This case exemplifies the unique aspects of performing cardiopulmonary resuscitation on a gravid female in the latter part of pregnancy and that Caesarean section should be considered an integral part of the resuscitative protocol when standard protocols fail.
...
PMID:Cardiopulmonary arrest in pregnancy: the role of caesarean section in the resuscitative protocol. 146 32

Acute non-ischaemic mitral regurgitation (MR) has recently generated considerable interest because of its causal relationship to ruptured chordae tendineae and infective endocarditis, advances in its diagnosis by echo Doppler studies, and its management by afterload reduction and reconstructive surgery. It is fundamentally different from chronic MR because the previously normal, unprepared left ventricle (LV) and left atrium (LA) confront a sudden dramatic increase in volume. As the normal-sized left atrium suddenly receives a marked regurgitant flow, its pressure rises and is transmitted into the pulmonary capillaries causing pulmonary congestion and oedema. At onset, the LV function is usually well preserved and the pulmonary oedema does not reflect LV failure. In acute MR, the LV empties into the left atrium, thus reducing its radius and its systolic pressure, resulting in a decline in wall tension according to Laplace's law. With a reduction in LV wall tension, there is a marked increase in contractile shortening with marked increase in total LV output. The left ventricle may fail early in acute severe MR because it is forced to dilate rapidly before hypertrophy can occur, whereas in chronic MR both the LV diastolic volume and mass increase proportionately. With chronic persistence of MR, LV dysfunction and failure occur as a manifestation of the 'cardiomyopathy of overload'. Fortunately because of the low energy cost per unit of work in shortening, as opposed to that used for tension development, there is only a slight increase in myocardial oxygen consumption in acute MR. In patients with LV failure secondary to acute MR, the ejection fraction may be only slightly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Left ventricular function in acute non-ischaemic mitral regurgitation. 193 16

Fifty-two cases of acute phase subarachnoid hemorrhage were studied by brain CT scanning to determine the presence and incidence of ischemic myocardial disorder, the relationship between ischemic change and severity, disease prognosis, and the relationship between acute phase circulatory dynamics and so-called neurogenic pulmonary edema. In all cases, ECGs were carried out and CPK-MB determined. Some of the patients underwent Tl myocardial scintigraphy, echocardiography, cardiac catheterization, as well as circulatory dynamic investigation (by Swan-Ganz catheter) and arterial blood gas analysis. In 31 of the 52 cases (59.6%), 3-day ECG series revealed ischemic changes. These findings were backed up by other cardiac function tests, thus suggesting that myocardial ischemia was present. Results in cases undergoing cardiac catheterization revealed that the myocardial ischemic changes were not due to organic constriction of the coronary artery. Included in those cases in which ECG markedly changed and CPK-MB rose substantially were many patients for whom the prognosis was poor. Evaluation of respiratory function and circulatory dynamics in cases of so-called neurogenic pulmonary edema seemed to indicate decline in cardiac function owing to myocardial ischemic change. This could account for onset of symptoms. These findings support the need for adequate circulatory management in cases of acute subarachnoid hemorrhage with pulmonary edema and/or changes on ECG. In such cases, concurrent catheterization and cerebral angiography (cerebro-cardiac catheterization: CCC) proved effective for evaluating cardiac function and determining whether heart disease was also present.
...
PMID:[Ischemic myocardial disorder in acute phase subarachnoid hemorrhage: clinical study of 52 patients]. 204 49


1 2 3 4 5 6 7 8 9 10 Next >>