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

At present no good method of assisting the right ventricle of the heart exists. This paper presents a new and effective approach to assisting the right ventricle of the heart which can be utilized independently or during cardiac surgery. Through implementation of this method, and timed inflation and deflation of several types of balloon catheters in the pulmonary artery, distal pulmonary arterial flow is augmented with subsequent unloading of the right side of the heart. This approach will be of great benefit in the treatment of atherosclerotic and congenital heart disease as well as in many cases of pulmonary hypertension.
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PMID:A new right ventricular cardiac assist device. 53 40

Calibrated jugular pulse tracings and cardiac catheterisation were performed on 50 consecutive patients with organic heart disease. Twenty normal adults had calibrated jugular pulse tracings and served as controls. The height of the jugular 'A' and 'V' waves was quantified as a percentage of a known displacement, rendering measurements independent of the amplification used in recording technique. A close correlation existed between the size of the calibrated jugular 'A' and 'V' waves and the actual magnitude of the right intra-atrial pressure changes (A wave, r = 0.72; V wave, r = 0.80). Patients who were free of pulmonary hypertension or tricuspid disease had calibrated 'A' and 'V' waves similar in height to the control population. An enlarged 'A' wave was usually associated with conditions restricting flow into the right ventricle. An enlarged 'V' wave generally indicated tricuspid regurgitation. These changes are often subtle and are not apparent in conventional venous tracings or at the bedside. We conclude that the calibrated jugular pulse tracings can accurately separate normal from abnormal venous waves and expand the diagnostic potential of the jugular pulse.
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PMID:Clinical assessment of calibrated jugular pulse recording. 63 84

On 33 patients with mitralic heart disease (III and IV class N.Y.H.A.) we have carried out polimechanical investigations (ecg, fcg, x-ray examination, external heart impulse record) and the following parameters was determined: 1) interval Q-I sound; 2) interval II sound-OS; 3) Wells's index; 4) Q-I sound/II sound-OS ratio; 5) duration of electromechanical systole of right ventricle; 6) duration of external heart impulse; 7) relative amplitude of E and E1 as percentage of amplitude from E point to nadir point; 8) relaxation isovolumetric time of right ventricle; 9) medium value of pulmonary capillary pressure, total pulmonary resistances, and area of mitral valve. The results demonstrate that there is a correlation between these parameters and the pulmonary blood pressure, whose value is possible to determine as well as haemodynamic investigation. The data indicate validity of non invasive techniques in detecting pulmonary hypertension in mitralic valve diseases.
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PMID:[Diagnosis of pulmonary hypertension by means of noninvasive techniques (author's transl)]. 64 86

The oto-vertebral syndrome is a rare combination of malformations of the ears, spinal anomalies, and congenital heart disease. The syndrome appears to be caused by early embryonic exogenous damage during the 6th or 7th week of embryonic development. The case is reported of a 28-year-old man with bilateral aplasia of the external ear, bilateral aplasia of the ear canal, hypoplasia of the mandibula, severe thoracic scoliosis, and ventricular septal defect with pulmonary hypertension. He was admitted with dyspnea on exertion, syncope, and severe cyanosis. Cardiac catheterization revealed severe pulmonary hypertension with moderate right-to-left and slightly left-to-right shunt (Eisenmenger syndrome). Right and left ventricular function, as evaluated by angiocardiography, was slightly reduced. Because of the severe hemodynamic alterations, symptomatic therapy with digitalis, repeated venesection, and anticoagulation was initiated.
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PMID:[The oto-vertebral syndrome]. 70 8

Congenital heart lesions are found in 0.8% of all newborns; four-fifths of them are correctable. Two thirds of all surgical procedures are done in acyanotic malformations, mainly in septal defects, patent ductus arteriosus, coarctations of the aorta and valvular stenosis. Within the last twenty years corrective repair has been established with good results in these lesions. Therapeutic problems still remain in cases of late diagnosis and in some rare and complex anomalies like malformations of the aortic arch, of the coronary arteries, in some types of aortopulmonary window and atrioventricular canal. Surgery becomes urgent in babies suffering from severe heart disease because of progressive pulmonary hypertension, inadequate growth or severe heart failure (despite intensive medical treatment). For certain lesions corrective repair (patent ductus arteriosus, coarctation) is definitely indicated, for others (ventricular septal defect, atrioventricular canal) urgent palliation or early total repair is debatable. In most patients with uncomplicated lesions treated in time during childhood a low operative mortality below 1% was observed. A higher mortality rate was found (10 to 50%) in patients with pulmonary artery disease or associated pulmonary lesions. A significantly higher mortality could also be observed in the advanced age group (4.7%) and in infants below one year of age (11,5%), underlining the important point of the age at operations. Recurrence of lesions occured in 1% of our patients after closure of ventricular septal defects, reconstructions of mitral valve disease and early corrected coarctations. Nevertheless, most of these patients can expect a normal growth, life span and ability to work.
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PMID:[Surgery of congenital acyanotic cardiac malformations (author's transl)]. 72 Oct 31

In young children with congenital heart disease the pulmonary circulation is exposed to abnormal haemodynamic conditions before it is fully developed. In the newborn infant the persistence or development of pulmonary hypertension rapidly leads to structural change. The speed with which an increase in muscularity can develop has hitherto been underestimated. In most children dying in early infancy with congenital heart disease and pulmonary hypertension the presence of thick walled small arteries is due not to persistence of the high wall thickness of foetal life, but to a rapid postnatal response of the pulmonary circulation to pulmonary hypertension. In older patients with a ventricular septal defect, aged between 3 months and 4 years, the presence of pulmonary hypertension has been shown to interfere with the growth and development of the pulmonary circulation, judging this by reduction in size and multiplication of intra-acinar arteries and an increase in muscularity of both pre and intra-acinar arteries and veins. In these patients elevation of pulmonary vascular resistance was associated with failure of the intra-acinar pulmonary circulation to develop normally and not with obliterative pulmonary vascular disease. Recent studies indicate that growth and development of the peripheral pulmonary circulation can be quantitated in lung biopsies taken from infants and young children with congenital heart disease. It should therefore be possibe to correlate structure and function at a critical period of lung development, before the changes of obliterative pulmonary vascular disease are established.
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PMID:The pulmonary circulation in congenital heart disease. II. Pulmonary hypertension. 72 Oct 42

The basic features of Goldenhar syndrome are preauricular appendices, epibulbar dermoids, vertebral and cardiac anomalies, and hypoplasia of the lungs. The syndrome appears to be caused by early damage during the first or second month of embryonic development. Prognosis is most often determined by the underlying heart disease. In the present study a 24-year-old female student is reported who exhibited a preauricular appendix on the right side, severe thoracic scoliosis, aplasia of the middle and lower lobes of the right lung, dextropositio cordis and an atrial septal defect with severe pulmonary hypertension. Cineangiocardiography revealed a mitral valve prolapse with slight mitral regurgitation and a dilated right ventricle with severe tricuspid regurgitation. Left and right ventricular function was slightly to moderately reduced. Selective coronary arteriography revealed a coronary fistula from an atrial branch of the left coronary artery to the right atrium. Symptomatic therapy with digitalis, anticoagulation and repeated venesection was initiated because of the severe hemodynamic findings. However, the patient developed syncope at increasingly frequent intervals and died 3 months after the initial examination.
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PMID:[Goldenhar syndrome]. 76 Jan 85

Two neonates with the most severe form of persistent fetal circulation are described. Their presentation mimicked severe congenital heart disease. As well as persistent pulmonary hypertension and right-to-left shunting through the ductus arteriosus, they had poor myocardial contractility and atrioventricular valve regurgitation. Associated acidaemia was extreme. They survived with medical management, and the functional abnormalities resolved.
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PMID:Persistent fetal circulation. Two cases with myocardial dysfunction and severe acidosis. 76 97

The problems associated with the ventilation of children who have congenital heart disease with left to righ shunts and pulmonary hypertension are more likely to be acquired than due to the congenital malformation. Haemodynamic, angiographic, bronchoscopic and bronchographic studies demonstrated that ventilation problems arose because of compression of the bronchus by the pulmonary artery. The bronchial compression should be treated by surgery to the heart defect without removing the lung. The intervention should be early to obtain maximum benefit and to avoid irreversible damage to the bronchus.
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PMID:[An explanation of ventilation problems in congenital heart disease with left to right shunt]. 88 70

The coincidence of pulmonary hypertension and pulmonary vascular disease was investigated in 186 infants and children with congenital heart disease and left to right shunts. The correlation between pulmonary hypertension and pulmonary vasculopathy was highly significant. Hemodynamic pulmonary hypertension is completely suppressed by early pulmonary artery banding or total correction. Even pulmonary vascular alterations can be reversed by these measures.
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PMID:[Pulmonary hypertension and histological findings before and years after surgical treatment of congenital heart disease (author's transl)]. 92 71


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