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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lung biopsy specimens were taken from 39 infants younger than 12 months of age with congenital heart disease and severe pulmonary hypertension (Pp/Ps greater than or equal to 0.75) accompanied by respiratory distress. The pathological change in lung specimens and clinical courses were compared. These 39 infants underwent surgical treatment of patent ductus arteriosus (PDA), seven patients; ventricular septal defect (VSD), 13 patients; and complex heart anomaly, 19 patients. The common pathological findings of the lung specimens taken from these infants were lymphoid cellular infiltration and thickening of the alveolar septum, which we have called "septitis" in the present study. In most cases pulmonary vascular obstructive change was within Grade 2 of the Health-Edwards criteria. Septitis was classified into three categories: mild, moderate, and severe. Only three of the 19 infants with severe septitis survived postoperatively, whereas 10 of the 12 infants with moderate septitis and all eight with mild septitis could be successfully weaned. The cause of septitis remains unidentified. We have found the patient's age and pulmonary hypertension to be closely related to the grade of septitis in this study. Septitis plays a much more important role than pulmonary vascular obstructive change in the prognosis of pulmonary hypertensive heart disease in early infancy.
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PMID:Lung pathology in infants with severe pulmonary hypertension and cardiac disease. 43 Nov 7

Alongside reversible secondary pulmonary arterial hypertension accompanying neonatal respiratory distress, there are primary PAH leading to the persistence of the foetal circulation. This is a true functional neonatal heart disease which may occur alone or be seen in association with another form of neonatal distress such as respiratory distress secondary to the inhalation of amniotic fluid. Any neonatal hypoxaemia irreductible by classical methods should suggest the possibility of persistent pulmonary arteriolar vasoconstriction and lead, in the absence of systemic hypotension, to the administration of vasodilators. These data remain in the preliminary stage and further studies, in particular pharmacological, of these drugs are necessary.
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PMID:[The persistence of foetal circulation. Neonatal pulmonary arterial hypertension. Favourable action of tolazoline (author's transl)]. 71 66

Five term and two premature newborn infants were referred for respiratory distress and congestive heart failure, and were found to have electrocardiographic Q or ST-T abnormalities suggesting ischemia. Echocardiographic and/or hemodynamic assessment excluded anatomic heart disease in six infants. In three infants, moderate or severe hemodynamic impairment within 36 hours of age was suggested by these studies. Myocardial perfusion images in all patients showed very poor myocardial uptake of thallium 201, compatible with global myocardial ischemia. Infants of similar age with myocarditis, or with congenital heart disease and congestive failure, had normal myocardial uptake. Rapid clinical improvement occurred within three to seven days. Two to five months later, all infants were well. Two had persistent electrocardiographic abnormalities but repeat thallium 201 imaging in six demonstrated almost normal myocardial uptake. These data provide further evidence that perinatal respiratory distress may be associated with myocardial dysfunction and congestive heart failure in some infants without anatomic heart disease, and suggest that myocardial dysfunction in these infants is associated with global myocardial ischemia, most of which is transient. The timing and nature of the insult causing the ischemia are unclear.
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PMID:Transient myocardial ischemia of the newborn infant demonstrated by thallium myocardial imaging. 76 22

The indices of P a-A CO2, P A-a O2 and VD/VT were evaluated in a group of children treated with controlled ventilation (IPPV) for: pneumonia, congenital heart disease, respiratory distress syndrome or central nervous system diseases. The P A-a O2 index is regarded as the most useful one, since it enables the possibility to select a F IO2 value for obtaining an optimal P aO2. For calculation of VD/VT according to Bohr's formula during connection of the child to respirator P ECO2 was determined planimetrically from the capnographic curve. P a-A CO2 was recognized as a less useful index and difficult to interpret.
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PMID:Evaluation of P a-A CO2, P A-a O2 and VD/VT measurements during controlled respiration in children. Preliminary communication. 79 76

A detailed study was made of 150 women delivered of their infants within 72 hours of an amniocentesis where the lecithin/sphingomyelin (L/S) ratio was 2.0 or greater. There were nine neonates with respiratory distress (6.0 per cent). There were two neonatal deaths, both due to severe congenital heart disease. A mature amniotic fluid L/S ratio predicts a newborn infant who will not have respiratory distress syndrome (RDS) in most pregnancies. There is a significantly increased risk of RDS in neonates with a mature L/S ratio if the mother has insulin-dependent diabetes or if there is a resulting low Apgar score. The method of delivery (cesarean section or vaginal) does not affect the frequency of RDS where the L/S ratio is 2.0 or more.
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PMID:Respiratory distress syndrome with mature lecithin/sphingomyelin ratios: diabetes mellitus and low Apgar scores. 98 67

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

Serum digoxin concentration and half-life were radioimmunologically determined in 9 mature newborns after 7 days medication with digoxin. The newborns were in respiratory distress treated with continuous positive airway pressure or were suspected to have serious congenital heart disease. Loading dose was 26 mug/kg body weight intravenously and 35 mug/kg body weight orally, respectively. Maintenance dose corresponded to 1/8th of the digitalization dose twice daily. The serum digoxin level 12 h after the last dose varied between 1.4 and 2.5 ng/ml (mean 2.0 ng/ml, Sx=0.4). The serum half-life of digoxin varied between 21.7 and 42.4 h (mean 30.0 h, Sx=7.7). The mean serum half-life of digoxin of 30 h attained values found in adults without renal disease. This suggests that the serum digoxin levels of newborns which are usually higher if compared with those of adults result from higher digoxin doses per unit body weight and not from diminished digoxin elimination.
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PMID:Serum digoxin concentration and half-life in newborn. 127 93

A clinical scoring method for assessing adult respiratory distress and the need for mechanical ventilation was matched against simultaneous blood-gas analysis in 27 patients with grave heart disease. The results showed little correlation between the two. Possible reasons for this are discussed.
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PMID:A clinical scoring system for adult respiratory distress. Preliminary report of its use in heart disease. 127 7

A neuropathologic study in 190 consecutive autopsies of patients with congenital cardiopathy was performed: 116 cases underwent a surgical procedure (S group) and the remaining 74 were non-surgical (NS group). Neuropathologic alterations were observed in 71 cases (41 in the S group and 30 in the NS group). However, most of the 129 cases with a normal examination had died in the first 72 hours either after surgery or the clinical events responsible for the death. Almost all the neuropathologic alterations were hypoxic ischemic. Infarctions, single or multiple, were found in 41 cases (23 in the S and 18 in the NS group). An embolic mechanism could be detected in 12 cases. Diffuse hypoxic changes were present in 17 cases (10 in the S and 7 in the NS group). Hemorrhages were found in 11 (6 in the S and 5 in NS group), 4 of which were related to a disseminated intravascular coagulation. In 17 cases (5 in the NS and 12 in the S group), the picture was of a periventricular leukomalacia. All these cases concerned children under 6 months of age. In 7 cases inflammatory alterations were present (diffuse micro-abscesses in 6 and a frontal lobe abscess in 1). Almost all cases in both groups presented clinical complications, isolated or associated, potentially harmful to the brain, as cardiac arrest, cardiac low output, hypoxemia, and respiratory distress. If was impossible to determine in each case the magnitude of the factor or factors responsible for the correspondent pattern of neuropathologic damage. There was no difference as to the neuropathologic pattern between congenital cardiopathies leading to increased or decreased pulmonary blood flow.
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PMID:[Neurologic changes in congenital heart diseases: a neuropathologic study]. 130 82

Renal cortical necrosis, renal medullary necrosis, and combined renal cortical-medullary necrosis result from renal ischemia without vascular occlusion. Renal hypoperfusion and ischemic injury in infants have been ascribed to massive blood loss, hemolytic disease, septicemia, and severe hypoxemia. In a postmortem study we identified 82 cases among 1,638 autopsies during the 20 years between 1970 and 1989 in infants 3 months old or less at the time of death. The frequency of renal necrosis in autopsy cases increased significantly during the last 6 years of the study. The distribution of the renal lesion was cortical in 28, medullary in 23, and combined in 31. Forty infants carried diagnoses of congenital heart disease, 17 of asphyxial shock, 9 of sepsis, 3 of infectious myocarditis, 9 of major malformations, 4 of anemic shock, 1 of vascular malformation, and 1 of gastroenteritis and dehydration. A significantly higher proportion of babies with congenital heart disease had cortical involvement. Comparison of clinical characteristics revealed a significantly higher frequency of prematurity, respiratory distress syndrome, bleeding diathesis, and possibly sepsis in the children with congenital heart disease, suggesting that these factors are important in the pathogenesis of the renal lesion. Fourteen infants underwent cardiac catheterization; there was no demonstrable association between the renal lesions and the use of radiographic contrast medium. We conclude that severe congenital heart disease itself is a risk factor for life-threatening renal cortical and medullary necrosis.
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PMID:Renal cortical and renal medullary necrosis in the first 3 months of life. 148 35


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