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 76-year-old man was referred to our hospital with complaints of productive cough, dyspnea and peripheral cyanosis. The chest X-ray film indicated the pulmonary emphysema and acute bronchitis, but no abnormal intracardiac calcification. The electrocardiogram revealed a peaked P-wave, complete left bundle branch block, and ventricular premature contraction. Chest tomography demonstrated abnormal intracardiac calcium deposition in the right heart region. Two-dimensional echocardiography revealed the tricuspid annular calcification in the postero-lateral portion, showing a synchronous movement with tricuspid annular motion throughout the cardiac cycle. The size of calcification was 10 x 14 mm. The tricuspid valve showed no significant regurgitation. Left ventricular dilatation, associated with mild mitral regurgitation and impairment of systolic function (EF = 49%) was revealed by echocardiography. Serum examination revealed positive in Wassermann reaction. This case of tricuspid annular calcification might be caused by atherosclerotic degenerative change related to the aging process, or by an unknown mechanism related to pulmonary emphysema.
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PMID:[A case of tricuspid annular calcification]. 179 47

This is a case report presenting interesting findings on two-dimensional and Doppler echocardiograms due to multiple pulmonary thromboses. A 67-year-old woman had a history of surgery for colon polyps in August, 1986. After surgery, she suffered from tachycardia and dyspnea, and was admitted to our hospital because of a loss of consciousness. Sinus tachycardia, complete right bundle branch block and T-wave inversion in leads III, aVF and V1-4 were observed on her electrocardiogram. Cardiomegaly was noted on her chest radiograph. On the third hospital day, echocardiography was performed. On two-dimensional echocardiography, marked right ventricular dilatation with hypokinesis of the wall, and a flattened interventricular septum were observed on the short-axis view, and M-mode echocardiograms showed disappearance of the E wave and delay of the opening of the tricuspid valve, resulting in a monophasic triangular pattern. Doppler echocardiography showed the tricuspid valve flow to be delayed, mainly observed during atrial systole. These findings indicate decreased right ventricular compliance. The patient died on the 6th hospital day, and multiple new and old thrombi were found in the pulmonary artery at autopsy.
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PMID:[Two-dimensional and Doppler echocardiographic findings of a sudden death case due to multiple pulmonary thromboses]. 322 15

Echocardiography provided the initial diagnosis of significant pulmonary hypertension, unrelated to left heart pathologic conditions, in 10 patients: four with acute pulmonary embolism; five with chronic pulmonary hypertension, primary in three patients and secondary to tumor emboli in the other two patients; and one with Eisenmenger's syndrome due to previously unsuspected atrial septal defects. Referral diagnoses were pericardial disease in five patients (including three with suspected tamponade), and right ventricular infarction versus pericarditis, atrial septal defect, dyspnea, inferoposterior infarction (by electrocardiography), and Ebstein's malformation in one patient each. The echocardiographic diagnoses were confirmed by lung scan (ventilation/perfusion mismatches were interpreted as high probability for pulmonary emboli in all four patients considered to have acute pulmonary emboli by echocardiographic study), pulmonary angiography (one patient), cardiac catheterization (four patients), and autopsy (three patients). No patient had evident aortic or mitral valvular, myocardial, or other left heart pathologic condition. In acute pulmonary embolism, mean right ventricular diameter was increased at 4.2 cm (range 3.2 to 6 cm) and right ventricular wall thickness was normal (mean 4.5 mm, range 3 to 5 mm). Moderate or marked right ventricular hypokinesis was noted in two patients each. Doppler examination, performed in three patients, revealed tricuspid regurgitation in all, with an increased flow velocity suggestive of mild to moderate systolic pulmonary hypertension (right ventricular minus right atrial pressures of 28 to 36 mm Hg). Patients with chronic pulmonary hypertension also had right ventricular dilatation (mean 4.4 cm diameter, range 3 to 5.4 cm) and hypokinesis (marked in four and moderate in one patient), but wall thickness was increased in all (mean of 9 mm, range 6 to 14 mm) and the flow velocities in the tricuspid regurgitant jets, detected by Doppler in all patients, suggested higher right ventricular minus right atrial pressures of 44 to 104 mm Hg (mean 64 mm Hg). The single patient with Eisenmenger's syndrome had right ventricular dilatation (3.2 cm), hypertrophy (10 mm), and hypokinesis (mild). Only the patient with Eisenmenger's syndrome had Doppler or contrast echocardiographic evidence for an intracardiac or extracardiac shunt. In the absence of left heart pathologic conditions, right ventricular dilatation and hypokinesis strongly suggest pulmonary arterial or primary right ventricular disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Echocardiographic recognition of pulmonary arterial disease and determination of its cause. 334 42

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

To contribute for making early diagnosis and treatment of acute pulmonary embolism (APE), we investigated on clinical pictures of 225 patients with APE. Common underlying factors were heart disease, prolonged bed rest, post-surgical state, thrombophlebitis, malignant tumor and post-catheterization state in this order. Dyspnea, chest pain, tachycardia and shock were frequently seen as initial symptoms and signs. Blood screening showed leukocytosis, hypoxemia, hypocapnia and elevated serum LDH. Electrocardiographic findings highly demonstrated were ST.T abnormalities, such as T inversion with ST elevation in V1-3, ST depression in V4-6 and sinus tachycardia. Chest X-rays showed diminished pulmonary vascular marking and pulmonary artery dilation. Right ventricular dilatation were frequently seen on 2-dimensional echocardiograms. Pulmonary artery pressure were elevated up to 49/20 (30) mmHg. Twenty-five percent of the patients died, and the recurrence was seen in 4%. Thus, as soon as APE is suspected by above clinical findings, definitive diagnosis should be obtained by the lung perfusion scan and pulmonary arteriography, then oxygen and thrombolytic agents should be given immediately to prevent the fatal outcome.
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PMID:[Early diagnosis and management of acute pulmonary embolism: clinical evaluation those of 225 cases]. 835 37

Although the results of intracardiac repair for pulmonary stenosis or atresia are generally good, some patients develop symptoms due to to pulmonary regurgitation and right ventricular dilatation. Implantation of a pulmonary homograft may have a beneficial effect on these symptoms. Twenty-seven patients with symptoms due to pulmonary regurgitation and right ventricular dilatation were reoperated. The indication for surgery was dyspnea in 19, arrhythmia in five and both symptoms in three patients. The arrhythmia was supra-ventricular in four, ventricular in two and both supra-ventricular and ventricular in another two patients. A cryopreserved pulmonary homograft was implanted in the right ventricular outflow tract. Mean interval between intracardiac repair and homograft implantation was 15.6 years. Mean age at homograft implantation was 23.0 years. Concomitant procedures were performed in 18 patients. There were two early deaths (7%). Replacement of the homograft was necessary in one patient, 21 months after insertion. This patient had residual pulmonary stenosis immediately after surgery. On mid-term follow up (mean 36 months) all patients with dyspnea as indication for operation improved, except one with right and left ventricular dysfunction. Only two of eight patients with arrhythmia improved. On echocardiography, pulmonary regurgitation decreased in all patients. Right ventricular dilatation decreased in only 14 patients (52%). We conclude that pulmonary regurgitation after transannular patching can be treated with implantation of a cryopreserved pulmonary homograft with acceptable mortality and low morbidity. Clinical improvement results from reduction of the right ventricular volume overload rather than from decline in right ventricular dilatation. Arrhythmia as the only indication for operation is controversial.
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PMID:Pulmonary homograft insertion after repair of pulmonary stenosis. 855 80

Exophthalmos and clinical signs of heart failure occurred sporadically in 3- to 12-month-old cotton rats (Sigmodon hispidus) in a colony originally derived from three male and four female littermates. Macroscopic lesions in severely affected animals included subcutaneous edema, hydrothorax, right ventricular dilatation, unilateral or bilateral atrial thrombosis, and exophthalmos. Hearts from 17 cotton rats that were found dead or were euthanatized because of exophthalmos or dyspnea and 33 control cotton rats were examined microscopically. Myocardial lesions were present in 46 of 46 cotton rats > or = 1 month of age and consisted of multifocal cardiac myocyte necrosis, mineralization, and mononuclear inflammatory cell infiltration. Cotton rats > 5 months of age also had foci of interstitial fibrosis and myocyte atrophy. Twelve of 24 (50%) necropsied cotton rats had chronic pulmonary congestion, and livers from eight of 24 (33%) had chronic periacinar congestion and atrophy. Thrombi were present in one or both cardiac atria in nine of 50 (18%) hearts, and in at least one orbital venous sinus in 14 of 24 (58%) necropsied cotton rats and in 12 of 14 (86%) with exophthalmos. Exophthalmos in this colony of cotton rats appears to have resulted predominantly from orbital venous sinus thrombosis caused by stasis of venous blood secondary to right heart failure associated with a heritable cardiomyopathy.
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PMID:Spontaneous cardiomyopathy and exophthalmos in cotton rats (Sigmodon hispidus). 881 34

Nitrates exert their anti-anginal activity by a number of mechanisms. By reducing venous return and left ventricular end-diastolic pressure they lower myocardial oxygen demand and at the same time enhance blood flow to the sub-endocardium. They also directly increase myocardial oxygen supply by dilating the coronary artery stenoses and increasing collateral blood flow. These pharmacodynamic attributes are clinically efficacious in all the ischaemic myocardial syndromes. In stable angina pectoris, nitrates reduce myocardial ischaemia and ischaemic pain and increase exercise tolerance. In unstable angina, nitrates similarly reduce electrocardiographic evidence of myocardial ischaemia and relieve anginal pain. Following acute myocardial infarction, nitrates reduce ventricular dilatation and by so doing reduce pulmonary congestion and mitral regurgitation. The weak anti-aggregatory effect of nitrates on platelets may also play an adjuvant role in their anti-ischaemic activity. Early small-scale studies with both intravenous and oral nitrates demonstrated a trend to reduced mortality and reinfarction in survivors of acute myocardial infarction. However, the later and larger ISIS-4 and GISSI-3 trials have not confirmed this trend possibly due to the smaller doses of nitrates used and the diluting effect of the widespread use of open-label nitrates in the placebo group. In patients with congestive heart failure, including those of ischaemic aetiology, nitrates together with hydralazine have clearly demonstrated a significant reduction in the medium term mortality risk. Nitrates have the undoubted ability, probably greater than any other single anti-anginal drug, to rapidly and often completely relieve the pain and breathlessness associated with myocardial ischaemia. They are haemodynamically efficacious in reducing dilatation of the ischaemic left ventricle and enhancing coronary blood flow to ischaemic areas. Although their preventative impact in survivors of acute myocardial infarction awaits clarification, they have been shown in combination with hydralazine to extend survival in patients with congestive heart failure, including those of ischaemic origin.
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PMID:Secondary preventive potential of nitrates in ischaemic heart disease. 896 Apr 45


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