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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 40-year-old woman was admitted because of increasing exertional dyspnea. Right heart failure was suggested by the presence of hepatomegaly, pretibial edema and also echocardiographic findings. Physical examination and echocardiography showed no evidence of valvular disease or congenital heart disease except for right ventricular dilatation and tricuspid regurgitation. The ventricular septum deviated toward the left ventricle throughout the cardiac cycle, but left ventricular function was preserved. Severe pulmonary hypertension averaging 44 mmHg was revealed by cardiac catheterization. Digital subtraction angiography and pulmonary blood flow scintigraphy showed no evidence of pulmonary artery embolism, and no interstitial pulmonary lesions that might have caused pulmonary hypertension were recognized. Hypergammaglobulinemia suggested an autoimmune disorder, and signs of systemic lupus erythematosus (SLE), such as pleural effusion, proteinuria, lymphocytopenia, LE cell phenomenon and antinuclear antibodies were present. Several autoimmune diseases are known to be causative factors of pulmonary hypertension. However, only ten cases of SLE complicated by pulmonary hypertension have been reported the present one. These cases were characterized by a high incidence of Raynaud's phenomenon and positivity for anti-RNP antibody. In our present case, SLE activity was suppressed using prednisolone, but pulmonary hypertension persisted and the patient eventually died due to right cardiac failure. Judging from the clinical course of the ten reported cases of SLE-pulmonary hypertension, there seems to be no hope of improving the pulmonary hypertension once it has become established. Therefore it is important to detect and cure pulmonary hypertension as early as possible.
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PMID:[A case of lupus erythematosus preceded by right heart failure due to pulmonary hypertension]. 174 69

Excess fatigue is a common symptom of many chronic cardiovascular disorders with low cardiac output. Impairment of skeletal muscle function due to metabolic alterations seems to play a major role. In heart failure fatigue is a predominant symptom. It may be an early symptom on diseases with slow but progressive inhibition of blood flow, i.e. in constrictive pericarditis, pulmonary hypertension or mitral valve stenosis. Excess fatigue as a precursor of myocardial infarction is being discussed. Finally fatigue may be a limiting side effect of diuretic and beta-blocking agents.
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PMID:[Cardiovascular causes of abnormal fatigability]. 175 69

The article deals with experience in the first transplantation of a heart-lung complex in the USSR. The recipient was a 34-year-old male with dilation cardiomyopathy. It was decided to perform the transplantation because the terminal stage of cardiac failure and secondary pulmonary hypertension developed (cardiac index 1.3 l/m, pressure in pulmonary artery 80/50 mm Hg, resistance of pulmonary vessels 10.4 units after Wood). The heart and lung were transplanted from a 19-year-old male who died from a craniocerebral injury. Cyclosporine, metipred , imuran, dopamine in small doses, cardiotonics, and antibiotics were given in the postoperative period; the patient was kept on artificial respiration for 48 hours. For up to 10 days the patient's condition was relatively stable and his consciousness was clear. Bilateral pneumonia developed, however, from which he died on the 12th postoperative day. The article discusses organizational problems and some questions of immunosuppressive therapy, immunological monitoring, and the management of patients after transplantation of a heart-lung complex.
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PMID:[Transplantation of the heart-lung complex (the first clinical experience)]. 177 Jul 47

In examination of 817 patients with closed chest injury and multiple trauma 57% of them were found to have obvious or latent hemopleuritis. According to the character of the primary damage and the developing pathophysiological changes, 3 forms of hemopleuritis were revealed: cardiac, pulmonary, and abdominal. A single complex of symptoms forms finally: pulmonary hypertension, venous stasis in the lungs, right-ventricular cardiac insufficiency. As a result, venous blood escapes through the lymph nodes, mainly those of the right lung, and together with the lymph flows in the dilated lymph vessels of the lungs into the pleural cavity. The differential-diagnostic signs of each form of hemopleuritis are pointed out, the prognostic criteria of their development are revealed, and the pathogenetically substantiated therapy is determined.
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PMID:[Hemopleuritis in closed thoracic injuries and multiple trauma]. 178 50

In order to estimate the efficacity of prostaglandine E1 (PGE1) to dilate the obstruction in coarctation of the aorta (CoAo), we studied 16 full term neonates with heart failure. Over the 16 neonates, there was 5 with isolated CoAo and 11 with an intracardiac shunt. Over the 11 neonates, 7 had pulmonary hypertension. PGE1, at a dose of 0.05 microgram/kg/min associated to the classical treatment of heart failure were given on the 6 day of life. Effects of PGE1 were evaluated on clinical basis (presence of femoral pulse, blood pressure), echocardiographical basis (ductus arteriosus and aortic isthmus diameter) and morphological basis. In 15 neonates, the ductus arteriosus was open, in all cases CoAo diameter was the same. In 7 neonates with pulmonary hypertension, femoral pulse appeared. In conclusion, PGE1 increases post ductal perfusion by a right to left shunt through the ductus arteriosus, only in cases where pulmonary hypertension is present. No direct action on the aortic isthmus was observed.
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PMID:[Effects of PGE1 in neonatal aortic coarctation]. 179 57

In spite of good long-term results, heart transplantation continues to carry a significant risk of hospital mortality (about 10%). Among cardiac deaths, right-heart failure due to an elevated pulmonary vascular resistance represents a main contributing factor. Since no quantitative data on the hemodynamic situation early after transplantation are available, we monitored 27 heart transplant patients during the first four postoperative days. Data derived from right-heart catheterization, dosages of catecholamines and vasodilative substances were measured at 2, 4, 16, 24, 48, 72, and 96 h after the operation. Oxygen consumption and serum lactate levels were determined until 48 h postoperatively. During that time cardiac output remained constant (2 h: 6.6 +/- 1.4 l/min). The dosage of catecholamines was highest immediately after transplantation (2 h: 0.229 +/- 0.136 micrograms adrenaline/kg/min) and could be reduced thereafter. Highest values of pulmonary vascular resistance were obtained 2 h postoperatively (160 +/- 48 dyn.s.cm-5). This early postoperative situation may result in the development of right-heart failure as observed in two patients who died despite the use of prostacycline on the third and eighth postoperative days. To counteract the systemic vasodilative side-effects of prostaglandins, temporary atrial pacing seems to be useful. In our study atrial stimulation led to an increase of cardiac output and a moderate elevation of mean arterial blood pressure. Only a poor correlation between pre- and postoperative (2-h) pulmonary vascular resistance data could be observed. In most patients the pulmonary vascular resistance decreased during the postoperative course. This was not the case in patients with fixed pulmonary hypertension. We, therefore, conclude that preoperative diagnostics should be refined to recognize patients at risk in order to reduce postoperative mortality.
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PMID:[Hemodynamic characteristics of heart transplant patients in the early postoperative period]. 179 10

We examined 3 infants with persistent pulmonary hypertension. They also showed signs of heart failure. The signs of cardiac dysfunction noted in the acute phase were resolved after treatment with catecholamines and vasodilators. Contrary to the general concept that transient myocardial dysfunction is secondarily caused by persistent pulmonary hypertension, left myocardial dysfunction accompanied pulmonary hypertension and was followed by right myocardial dysfunction. High blood concentration of thromboxane B2 was reported in 2 neonates with persistent pulmonary hypertension. We considered thromboxane A2 as a possible cause of coronary spasm, resulting in myocardial ischemia.
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PMID:[Three infants with severe myocardial ischemia diagnosed by echocardiography: investigation of the cause of transient myocardial dysfunction]. 181 78

The purpose of the study was to elaborate criteria for the assessment of the severity of pulmonary hypertension and cor pulmonale in patients with chronic bronchitis and to give rationale for expert medical evaluation of the working capacity of such patients. 94 patients (89 males and 5 females) aged 20 to 60 with chronic bronchitis were examined. Basing on the clinical, x-ray, ECG, VCG and echocardiography data, the gravity of cor pulmonale was assessed by the degree of right ventricular hypertrophy (absent, mild, marked, dramatically marked), changes in the right ventricular echo dimensions and the stage of heart failure, and by the lung vital capacity (in percent of the predicted value). The rationale for expert medical evaluation of patients with associated cor pulmonale and chronic bronchitis is described.
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PMID:[The medical disability evaluation of patients with pulmonary hypertension and cor pulmonale]. 182 62

Partial airway obstruction due to the enlargement of the tonsils and adenoids is a well recognized clinical entity, but cardiorespiratory changes due to chronic obstruction have infrequently been reported. Four children with severe nasopharyngeal obstruction due to tonsil and adenoid hypertrophy, who developed pulmonary hypertension and cardiac failure, were studied. Relief of upper airway obstruction by adenotonsillectomy resulted in a regression of the presenting signs and symptoms.
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PMID:Pulmonary hypertension due to chronic upper airway obstruction: a clinical review and report of four cases. 184 74

Male broilers of two genetically related stocks with divergent growth rates and feed conversion ratios were used to study metabolic backgrounds on the occurrence of pulmonary hypertension, heart failure, hypoxemia, and ascites in poultry. An experiment with a 2 x 2 x 2 x 2 factorial split-plot arrangement of treatments with 96 groups of 12 broilers was performed. Effects of stock and environmental factors such as ambient temperature, dietary fat, and dietary energy on performance, energy metabolism, oxygen consumption, hematocrit values, and mortality were investigated in broilers from 1 to 5 wk of age. Dissimilar responses of the two stocks to environmental factors reflected genotype by environment interactions and revealed metabolic disorders related to heart failure and ascites. The results indicated that in the stock with the lower feed conversion ratio, a fast protein accretion was achieved together with a reduced ability to convert chemical energy to metabolic heat and to deposit body fat directly from ingested fat. Birds with a low feed conversion ratio show less flexibility in metabolic adaptation to a changing environment, which can account for the development of ascites.
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PMID:Ascites in broilers. 1. Experimental factors evoking symptoms related to ascites. 185 84


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