Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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).
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PMID:Primary myocardial disease in the cat. A model for human cardiomyopathy. 84 11

A new clinical entity is described in which free aortic regurgitation from congenital aortic valve disease caused rupture of the chordae to the anterior leaflet of the mitral valve in 7 men aged 45 to 63 years (mean 52 years); 2 of the patients also had rupture of chordae to the posterior leaflet. Comparing these patients with those with ruptured mitral chordae in association with rheumatic heart disease and patients with spontaneous chordal rupture, differences were evident. No patient had a history of rheumatic fever and none had active infection. The typical clinical presentation was of acute mitral regurgitation into a small left atrium, with severe pulmonary oedema which was often resistant to medical treatment. The cause of chordal rupture in these patients was in part the result of progressive left ventricular dilatation, of direct trauma to the anterior cusp of the mitral valve, and possibly of a genetic factor. The anatomical features of both aortic and mitral valves are described, and in 3 histology of the mitral valve was available; 2 had myxomatous degeneration similar to that seen in patients with spontaneous chordal rupture, and in 1 there was degeneration of collagen tissue. All patients were treated surgically but the mortality was high (5 out of 7,70%). Early operation with replacement of the aortic and mitral valves is recommended if this high mortality is to be reduced.
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PMID:Congenital aortic valve disease with rupture of mitral chordae tendineae. 97 89

Mechanical ventilation is a valuable therapeutic option in left ventricular failure because of its effect on ventricular load. However, weaning cardiac patients form mechanical ventilation may result in severe pulmonary oedema, especially if it is not properly prepared. Some of the factors which contribute to pulmonary oedema are: 1) increased venous return due to the inversion ot the regime of inthrathoracic pressures and the release of catecholamines commonly observed during weaning, 2) reduction of left ventricular compliance due to myocardial ischemia, compression of the cardiac chambers by the lungs, ventricular interdependence in some cases and left ventricular dilatation in others, 3) increased left ventricular afterload due to negative intrathoracic pressures and increased systolic blood pressure. Of all the causes of unsuccessful weaning, left ventricular dysfunction should be carefully considered because its treatment alone may enable the patients to be taken off the ventilator. The authors report six cases of pulmonary oedema in coronary patients after discontinuing mechanical ventilation. The administration I.V. enoximone, a phosphodiesterase inhibitor, prevented acute left ventricular dysfunction in 5 of the 6 cases and enabled successful and definitive weaning from mechanical ventilation.
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PMID:[Left ventricular dysfunction while weaning from mechanical ventilation. Contribution of enoximone]. 214 40

Feline and canine cardiomyopathies (primary myocardial diseases) were reviewed and divided into three groups based on the clinical, hemodynamic, angiocardiographic, and pathologic findings: (1) feline and canine hypertrophic cardiomyopathy, (2) feline and canine congestive (dilated) cardiomyopathy, and (3) feline restrictive cardiomyopathy. All three groups consisted predominantly of mature adult male cats and dogs. Cardiomyopathy in the hamster and turkey was also reviewed. The most common presenting signs were dyspnea and/or thromboembolism in the cat, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (groups 1 and 3) or without (group 2) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end-diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (group 1), left ventricular dilatation (group 2), or midventricular stenosis (group 3). Some cats in groups 1 and 3 also had evidence of left ventricular outflow obstruction. The principal pathologic findings in all of the cats and dogs were left atrial dilation, hypertrophy, increased septal:left ventricular free wall thickness ratio with disorganization of cardiac muscle cells (group 1); dilatation of the four chambers with degeneration of cardiac muscle cells (group 2); and extensive endocardial fibrosis and adhesion of the left ventricle (group 3). Aortic thromboembolism was commonly observed in the cats of all three groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat or dog is similar to the three forms of cardiomyopathy in humans (hypertrophic, congestive, and restrictive).
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PMID:Animal models of primary myocardial diseases. 644 12

Selective beta-sympathomimetic drugs are frequently used for tocolysis. But, since these drugs exhibit some beta-1 activity as well, they may bring about pulmonary edema, myocardial ischemia, cardiac arrhythmia and others as side effects. A 29 year-old female with a triplet pregnancy had premature contraction at 26 weeks of gestation. High doses of IV ritodrine were given for tocolysis for 8 weeks until caesarean section. One hour after caesarean section at 35 weeks of gestation, she complained of dyspnea. Urinary output decreased and chest X-ray showed pulmonary edema. She was intubated and artificial ventilation with PEEP was performed in ICU. Echocardiogram showed left ventricular dilatation. ECG showed inverted T waves on all leads. We diagnosed her as suffering from acute heart failure, pulmonary edema and acute renal failure. Hemodialysis was performed for 6 hrs but PCWP was still 18 mmHg. So CVVH was added to hemodialysis. Five hrs after the start of CVVH, her symptoms gradually started to subside. Total fluid removal was 5.8 l over 16 hrs. Three days after admission she was extubated and five days later returned to her ward. We concluded that pulmonary edema, heart failure and renal failure were induced by the long-term high dose medication of ritodrine, resulting in volume overload and myocardial dysfunction.
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PMID:[Ritodrine induced pulmonary edema after caesarean section for a triplet pregnancy]. 793 76

Physiologic changes during pregnancy affect nearly every organ system. In the thorax, the diaphragm elevates as much as 4 cm because of displacement of the abdominal organs by the gravid uterus, resulting in lower lung volumes. Maternal blood volume and cardiac output increase approximately 45% by mid-pregnancy. Cardiac output can increase as much as 80% during vaginal delivery and up to 50% with cesarean section. These changes result in pulmonary vascular engorgement, progressive left ventricular dilatation, and mild hypertrophy (Fig. 1). Pregnant patients are also prone to a number of pulmonary insults, including infection, aspiration, and neoplastic disease. These abnormalities have several radiographic patterns: cardiogenic and noncardiogenic pulmonary edema, focal pulmonary abnormalities, and extraalveolar air. Radiologists must recognize not only the normal chest radiographic appearance in these patients but also the thoracic complications associated with pregnancy.
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PMID:Cardiopulmonary complications of pregnancy: radiographic findings. 827 29

The Epstein-Barr virus nuclear antigen-leader protein (EBNA-LP) is required for high efficiency B lymphocyte growth transformation by the virus. To test the potential contribution of EBNA-LP to tumorigenesis in vivo, we produced transgenic mice carrying an EBNA-LP cDNA construct, using the widely expressed metallothionein promoter. Expression of EBNA-LP was detected in liver, kidney, heart, lung and spleen. There were no apparent oncogenic consequences of EBNA-LP expression. Unexpectedly however, at ages ranging from about 4 months to over a year, transgenic mice developed symptoms of congestive heart failure, including left ventricular dilatation, right ventricular hypertrophy, left atrial thrombosis, pulmonary oedema and hydrothorax. Fibrillation was not apparent in the electrocardiograph; however a reduction in T-wave amplitude suggested that the development of an abnormality of ventricular repolarization may precede the manifestation of overt symptoms. The highly predictable development of dilated heart failure in these transgenic mice suggests they may be a useful model for the pathophysiological changes associated with human dilated cardiomyopathy.
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PMID:Dilated heart failure in transgenic mice expressing the Epstein-Barr virus nuclear antigen-leader protein. 839 79

Endocardial fibroelastosis is an uncommon congenital heart disease in dogs that may be manifested by signs of left-sided congestive heart failure. A three-month-old, male, Fila Brasileiro dog developed signs of generalised heart failure. Physical examination revealed normal temperature, ascites, and pale and cyanotic mucous membranes. The pup died just after radiography which revealed ascites, hepatomegaly, severe cardiac enlargement and pulmonary oedema. At necropsy, serosanguineous fluid in the thorax and abdomen, pulmonary oedema, right ventricular dilatation, hypertrophy and dilatation of the left ventricle, and mitral valve incompetence were observed. The histopathological examination demonstrated that the thickening of the endocardium of the left atrium and left ventricle was due to the presence of elastic and collagen fibres, although there were no signs of an inflammatory process.
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PMID:Endocardial fibroelastosis in a dog. 912 86

Autopsy findings in 10 cases of high-altitude pulmonary edema have been collected from published articles and personal observations. All cases were males with a mean age of 37 years (22-62). The altitude of occurrence was from 8400 to 17 500 feet. The mean combined lung weight in nine cases was 1682 g (1200-3000 g). Cerebral edema was present in five of eight cases. The most frequency pulmonary findings in addition to diffuse edema consisted of leukocyte infiltrates, alveolar hemorrhages, thrombi in small pulmonary arteries, and alveolar hyaline membranes. Pulmonary infarction was present in only one case. Right ventricular dilatation was commonly present. The left ventricle was normal. No significant coronary disease was present.
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PMID:Lung pathology in high-altitude pulmonary edema. 1199 Jan 62

Acute aortic insufficiency can now be diagnosed rapidly and accurately thanks to Doppler echocardiography. The etiologies include infectious endocarditis, aortic dissection, bioprosthesis degeneration and thoracic injury. The clinical diagnosis is substantiated by the particular etiological context, dyspnea and pulmonary edema being the main factors involved. Examination includes finding out whether there is a reduction in the first sound, S1 a generally brief apical diastolic murmur. Echocardiography detects the presence of aortic leakage, the acute character of which is confirmed by the findings of a premature closure of the mitral valve, the existence of telediastolic mitral leakage, a restriction in the transmitral flow, and finally, the absence of left ventricular dilatation. An emergency operation is recommended by most authors in the case of acute aortic leakage due to the major risk or mortality resulting from pulmonary edema, ventricular arrhythmias, electromechanical dissociation or cardiogenic shock.
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PMID:[Acute aortic insufficiency]. 1255 79


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