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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine cases of the combination of coarctation of the aorta and mitral stenosis were evaluated over a seven-year period. Symptoms did not usually cause distress in infancy, but began subtly with pneumonia or cardiac failure at about 2 years of age. Important clues were differences in blood pressure between the arms and legs, paroxysmal dyspnea, congestive heart failure, right ventricular hypertrophy, and left atrial enlargement. Cardiac catheterization studies showed elevated right ventricular and main pulmonary artery wedge pressures. These features in patients with coarctation of the aorta should suggest associated mitral valve disease. The importance of demonstrating associated valvular lesions, particularly mitral stenosis, is emphasized. Two of our children had successful repair of the coarctation of the aorta and mitral stenosis simultaneously. In a third child, resection of the coarctation was followed in six years by mitral valve replacement.
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PMID:Associated coarctation of the aorta and mitral valve disease: nine cases with surgical correction of both lesions in three. 12 22

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".
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PMID:Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia. 15 Jul 86

Among the causes of death of 43 scoliotics were 5 directly due to complications of congenital heart disease. Over half (57.9%) of the remaining 38 died of cardiac or respiratory causes. The paralytic scolitoics tended to die of pneumonia or respiratory failure, while the nonparalytic scoliotics died of cardiac failure. Right ventricular hypertrophy was present in 65% of the 17 subjects examined postmortem. Electrocardiographic evidence of right ventricular hypertrophy correlated well with the postmortem findings. The vital capacity was less than 1.75 liters in 84% of the dead subjects. The case records of a further 719 living scoliotics were examined for evidence of congenital heart disease. This was found in: 34 (4.5%) of the whole group of 762, 6.9% of the congenital ; 3.4% of the idiopathic scoliotics; 22.7% of those with Marfan's syndrome.
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PMID:Causes of death, right ventricular hypertrophy, and congenital heart disease in scoliosis. 15 77

In order to facilitate for the general physicians the making of a suitable selection of babies who are in the most urgent need of specialized treatment at cardiac centres, simple methods for diagnosing and qualifying congenital cardiovascular diseases were elaborated. The following "minor" criteria were taken for suspecting a CHD: 1) cardiorespiratory distress following birth, 2) sequentially repeated Apgar score below normal, 3) "pneumonia" symptoms with respiratory distress, dyspnoea and cyanosis, attacks of unconsciousness, 4) feeding difficulties, failure to thrive, inexplicable irritability, 5) presence of other congenital anomalies. The almost certain presence of serious heart disease should be recognized in children, showing the following "major" symptoms: 1) permanent cyanosis, pallor or greyish colour, 2) cardiorespiratory failure (resembling usually symptoms of pneumonia), 3) ECG patterns indicating ventricular hypertrophy signs, 4) other significantly abnormal ECG patterns (e.g. AV and intraventricular conduction disturbances), 5) cardiac enlargement and lung vascularity abnormalities in chest X-rays, 6) weak, or impalpable arterial, particularly femoral pulses, femoral arterial pressures significantly lower, than at upper extremities, bounding pulses and high-pressure amplitude in arms and legs, 7) abnormal heart sounds and pathologic heart and vascular murmurs. A diagnostic "key", based upon evaluation of the "major criteria" facilitates the diagnosis and differentiation of the most important CHD's at neonatal and infantile age. When using this "key" one should keep in mind the relative frequency of incidence of particular lesions. The initial diagnoses by the above "key" were verified in 354 patients by cardiovascular catherisation, angiocardiography, surgical exploration, and for by autopsy. The diagnoses were perfectly accurate in 83.6% cases, in further 11.3% cases being also accurate but were supplemented by some details, and had to be corrected in only 5.1% cases.
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PMID:[Congenital heart diseases in newborns and infants; early detection, differentiation and accuracy of clinical diagnoses (author's transl)]. 122 66

Increased pulmonary arterial pressures as a result of pulmonary disease are described in two cows with chronic pneumonia and one cow with acute pneumonia. Based on clinical signs of congestive right heart failure, increased pulmonary arterial pressure, and right ventricular hypertrophy, cor pulmonale was diagnosed in one cow. Two cows had increased pulmonary arterial pressure and signs of right heart insufficiency, but right ventricular hypertrophy was not identified. Two of the cows had ventral edema and exercise intolerance. All cows had jugular venous distention and increased right atrial and pulmonary arterial pressures. Peripheral arterial PaO2 was decreased in two cows, and not measured in the third cow. Although an uncommon cause of congestive heart failure in cattle at low altitudes, pulmonary hypertension should be considered in cattle with clinical right heart failure.
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PMID:Pulmonary hypertension and cardiac insufficiency in three cows with primary lung disease. 138 97

A 64-year-old man underwent cardiac transplantation for long-standing severe dilated cardiomyopathy. Postoperative complications included primary cytomegalovirus (CMV) infection with several episodes of moderate acute rejection and severe pneumonia. Six months after transplantation, an endomyocardial biopsy specimen revealed focal necrotizing myocarditis with intranuclear inclusions consistent with CMV. The patient subsequently developed fulminant pneumonia and died 7 months after transplantation. Postmortem examination revealed that the cause of death was acute necrotizing bronchopneumonia due to Staphylococcus aureus, with underlying CMV pneumonitis. The transplanted heart had left ventricular hypertrophy with multiple organizing myocardial infarcts, moderate coronary atherosclerosis, and organizing thrombi of the left atrium. Characteristic inclusions of CMV were identified, predominantly within endothelial cells, in the left coronary artery, left ventricular endocardium, and myocardium. With in situ hybridization, the presence of CMV was verified in the inclusions, as well as in many fibroblasts without inclusions. In situ hybridization is warranted in myocardial biopsy specimens when suspicious inclusions or infiltrates are present, to confirm CMV infection, so that appropriate therapy can be initiated.
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PMID:Cytomegalovirus endomyocarditis in a transplanted heart. A case report with in situ hybridization. 185 May 89

199 out of 509 foxes culled in a rabies control scheme, were shown to be infected with the metastrongylid parasite Angiostrongylus vasorum. Pathological lesions associated with angiostrongylosis in the fox are described and compared to reported lesions of A. vasorum infection in the dog. The lesions observed in the foxes seemed to be less severe and mainly confined to the ventral parts of the lung lobes which showed granulomatous pneumonia. Right ventricular hypertrophy of the heart was present in all infected foxes. It is believed that the fox population represents an important reservoir of A. vasorum.
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PMID:Pathology of naturally acquired Angiostrongylus vasorum infection in the red fox (Vulpes vulpes). 192 94

Eight children with human immunodeficiency virus (HIV) infection had symptomatic cardiac dysfunction. The median age was 1.4 years (range 0.2 to 7.9 years). All had hepatosplenomegaly, fever, pneumonia with tachypnea, and tachycardia ascribed to infection and anemia. An S3 gallop was present in six of eight. All had normal creatine phosphokinase values. Chest x-rays did not aid in the diagnosis of cardiac dysfunction. ECG showed flattened T waves in five of eight with left ventricular hypertrophy, right ventricular hypertrophy, or both in seven of eight. Results of echocardiography showed decreased left ventricular function in all eight, despite anemia, with dilated left ventricular myopathy in six, concentric left ventricular wall thickening in two of eight, an enlarged right ventricle in two, and pericardial fluid in three. Medical therapy improved cardiac function in all. All patients subsequently died of noncardiac causes. Results of autopsies on four of eight patients showed focal myocarditis in two (with cytomegalovirus inclusions in one) and dilated cardiomyopathy in two others. We conclude: (1) Preexistent hepatosplenomegaly, fever, infection, and anemia result in physical findings that mimic findings of heart failure, thereby masking the occurrence of cardiac dysfunction; (2) an S3 gallop may indicate the presence of impaired heart function when other clinical signs are masked; (3) confirmation of cardiac compromise may be accomplished by noninvasive evaluation with echocardiography and (4) medical therapy can improve cardiac dysfunction in HIV-infected children.
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PMID:Symptomatic cardiac dysfunction in children with human immunodeficiency virus infection. 252 16

We report 30 patients with exogenous lipoid pneumonia due to vegetal oil. This was employed in most of the cases during the first month of life for digestive tube symptomatology; clinical manifestations began three months following administrations, as a pneumonia or bronchopneumonia with a respiratory distress syndrome of variable severity. 60% of the thorax x-ray studies were abnormal, the main finding was opacity. One patient has alterations of the mechanics of deglutition; seven had gastroesophageal reflux. Arterial gasometry showed hypoxaemia and increase of alveolo-arterial gradient of oxygen in all. Ten patients died and all the survivors were reevaluated in september, 1988; 18 had normal physical findings. Thorax x-ray studies in 13 patients had right reticulate infiltration and 6 right apical opacity; ECG showed right ventricular hypertrophy in 3. Perfusion pulmonary gamagram with technetium 99 was abnormal in 5. Gastroesophageal reflux was evident in 2. Five were under treatment for several causes. Diagnosis and treatment is discussed.
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PMID:[Exogenous lipoid pneumonia]. 260 74

Alveolar septal fibrosis, the main residual feature in the "healed" stage of bronchopulmonary dysplasia (BPD), was the consistent finding in 28 infants who died at 3 to 40 months of age, all having had moderate to severe BPD in the neonatal period. The cause of death in 68 per cent of the cases was progressive respiratory failure related directly to the residual changes. An additional 18 pe cent of the infants died of pneumonia superimposed on the long-standing healed bronchopulmonary dysplasia. Cardiomegaly was present in 84 per cent of the cases; biventricular hypertrophy was present in 29 per cent of the cases, right ventricular hypertrophy alone in 21 per cent, and left ventricular hypertrophy alone in 21 per cent. Evidence of pulmonary hypertensive vascular disease was found in 68 per cent of the cases. The pulmonary changes of alveolar septal fibrosis are strikingly variable within individual infants, with moderate or severe fibrosis in one area and normally inflated or hyperinflated lung in the adjacent sublobule or lobe. It is postulated that this variability may be related to a protective effect of necrotizing bronchiolitis (a prominent feature of the acute stages of BPD), whereby the occlusion of the bronchioles shields the distal sublobule from the high oxygen tensions and ventilatory pressures used in treating BPD.
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PMID:Pathologic features of long-standing "healed" bronchopulmonary dysplasia: a study of 28 3- to 40-month-old infants. 363 56


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