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

Systemic hemodynamic changes and noradrenaline concentrations in coronary sinus blood were studied at rest and during work before and after acute beta-receptor blockade. Patients with congestive cardiomyopathy were compared to patients with primary valvular diseases and to healthy subjects. Noradrenaline concentrations were higher in coronary sinus blood than in arterial blood and increased after beta blockade and during work. Noradrenaline concentrations were more increased in patients with more pronounced myocardial failure and did not seem to separate patients with congestive cardiomyopathy from those with valvular disease. Patients with congestive cardiomyopathy showed a good hemodynamic tolerance toward acute beta blockade.
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PMID:Effects of work and acute beta-receptor blockade on myocardial noradrenaline release in congestive cardiomyopathy. 4 91

The authors have developed a new method for the estimation of peroperative blood loss by measurement of the haematocrit of a fluid obtained by diluting the blood from swabs in a known volume of isotonic saline solution. This value, referred to a monogram, may be used to assess the volume of blood impregnating the compresses, in relation to the pre-operative or present haematocrit of the patient, by direct reading. The precision of the method is discussed. The results obtained justified its routine application in surgery in children, patients with cardiac failure and in all cases requiring precise compensation of per-operative blood loss.
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PMID:[New non-volumetric method for estimating peroperative blood loss]. 4 86

One hundred and nineteen episodes of accelerated ventricular rhythm (less than 125/min) were noted in 37 patinets with acute myocardial infarction during a 1 year period. The incidence was 12.7 per cent. Twenty-seven episodes of fast ventricular tachycardia (less than 125/min) were noted in 16 of these patients. Eighteen patients had anterior myocardial infarction and 19 inferior myocardial infarction. The mechanism of onset of accelerated ventricular rhythm was classified as escape in 65 episodes. Ventricular premature beats were noted close to episodes of accelerated ventricular rhythm in 31 patients and fast ventricular tachycardia in 14 patients. The morphology of accelerated ventricular rhythm was similar to the ventricular premature beats in 27 patients and similar to the fast ventricular tachycardia in 12. In 11 patinets the morphology of ventricular premature beats, accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm is a relatively common complication of both anterior and inferior myocardial infarction. The high incidence of concomitant fast ventricular tachycardia, the frequency of ventricular premature beats with similar morphology and coupling time, and the instances of two arrhythmias having common rate multiples, suggest that at least in some instances accelerated ventricular rhythm may represent an ectopic focus with exit block.
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PMID:Incidence and description of accelerated ventricular rhythm complicating acute myocardial infarction. 4 3

Propafenon (SA 79, Fenoprain, Baxarytmon) is a new antiarrhythmic agent with "quinidine-like" localanaesthetic direct membrane and beta adrenergic blocking actions. The drug was given to 50 patients with various types of cardiac arrhythmias. The effective and compatible dose was 70-140 mg administered intravenously in 1 to 3 minutes. Therapeutic success was observed in ectopic beats and paroxysmal tachycardias of both atrial and ventricular origin. Propafenon is effective on the sinus node, the atrial wall and the atrioventricular muscle; the rate of sinus node and ectopic pacemakers is lowered. The atrioventricular and intraventricular conduction time may be increased. Within the therapeutic dose Propafenon has only minimal cardiodepressive activity. Propafenon should not be given in patients with severe heart failure, hypotension and shock and atrioventricular block.
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PMID:[Propafenon, a new antiarrhythmic agent for the treatment of ectopic and rapid cardiac arrhythmias (author's transl)]. 4 83

To circumvent the decreased pulmonary blood flow associated with closure of the ductus arteriosus in newborns with heart defects, we infiltrated buffered formalin solution into the wall of that structure to delay its closure. In four infants with pulmonary atresia in whom shunts had been unsuccessful or were technically not feasible, this procedure produced rapid improvement of arterial oxygen tension that was maintained in three infants for one to nine months. The other died of complications of attempted shunt procedures. In an infant with interrupted aortic arch and a large ventricular septal defect, formalin infiltration of the ductus and pulmonary arterial banding alleviated cardiac failure and improved lower-body perfusion. Formalin infiltration of the ductus is an effective palliative technic for treating certain congenital cardiac defects. No adverse effects have been noted.
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PMID:Formalin infiltration of the ductus arteriosus. A method for palliation of infants with selected congenital cardiac lesions. 4 92

Six patients whose standare electrocardiograms showed multiform ventricular ectopic rhythm were studied. All patients had advanced organic heart disease and a significant intraventricular conduction defect (left bundle branch block in five and right bundle branch block plus left anterior hemiblock in one). The ventricular arrhythmia was generally resistant to antiarrhythmic therapy. Five of the six patients died after 2 to 6 months form the period of observation from terminal heart failure. None died suddenly. The ventricular arrhythmia did not seem to be directly related to mortality in any patient. Critical analysis of several long rhythm strips in each case revealed that discharge from multiple ventricular parasytolic foci shared in the multiform ventricular activity. The concurrent discharge of a minimum of three parasytolic foci and a maximum of six foci was found in the same case with a total of 24 parasystolic foci in the six patients. There was a remarkable constancy of the QRS configuration of all parasytolic foci over periods of observation of up to 16 months. However, 22 out of 24 parasystolic rhythms showed significant variation in the apparent rhythm or the administration of drugs. Fourteen parasytolic foci showed evidence of exit block, some of which were exaples of a rapid parasystole with a high degree of exit block. The study suggests that multiform ventricular ectopic rhythm may, in part, be due to the concurrent discharge of multiple parasystolic foci.
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PMID:Multiform ventricular ectopic rhythm. Evidence for multiple parasystolic activity. 4 29

Mitochondrial calcium uptake, but not binding, like microsomal calcium uptake in failing human hearts, was less than the control values for dog, rabbit, and hamster hearts. Decrease in mitochondrial calcium binding and uptake was observed in genetically myopathic hamsters (BIO 14.6) at early, moderate, and late stages of congestive heart failure. Inhibitors of mitochondrial calcium transport, Dicumarol, dinitrophenol, and sodium azide, were found to produce a rapid fall in contractility of the isolated rat heart. Inability of rat hearts to generate contractile force on perfusion with Na+- or K+-free medium was associated with an increase in mitochondrial calcium uptake. A dramatic increase in mitochondrial calcium uptake was observed on perfusing rat hearts with control medium after CA++-free medium. No change in mitochondrial calcium uptake was noted in acute ischemic dog myocardium or hypoxic rat heart in which contractile force was severely depressed. Both mitochondrial calcium transport and contractility were decreased on perfusing rat hearts with substrate-free medium; however, the change in calcium uptake was secondary to the fall in contractile force. Decrease in pH, ATP:ADP ratio, ATP6AMP ratio, and K+:Na+ ratio were found to reduce the dog heart mitochondrial calcium uptake. It is likely that various factors such as pH, ATP:ADP ration, ATP:AMP ratio, and K+ :Na+ ration, in addition to damage in mitochondrial structure, play an important role in inhibiting mitochondrial calcium transport in failing hearts. The results also suggest that alterations in mitochondrial calcium transport are dependent upon the degree and type of heart failure.
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PMID:Role of mitochondrial calcium transport in failing heart. 5 79

Nine Cooperstown beagles of known DL-A genotypes were exposed to supralethal total-body irradiation and received bone-marrow allografts from DL-A-identical donors. Four to 5 months later, the resulting chimeras received orthotopic cardiac allografts from their corresponding donors of marrow. Six chimeras died of operative complications in the immediate postoperative period. The other 3 chimeras survived from 173 to 547 days; 1 dog died at 173 days as a result of right-sided heart failure, secondary to stenosis at the site of the pulmonary artery anastomosis. The other two recipients continue to be active and healthy at 545 and 547 days. The results indicate that dogs can be rendered specifically tolerant to orthotopic cardiac allografts by supralethal total-body irradiation and the transplantation of marrow obtained from the prospective allograft donor.
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PMID:Allogeneic unresponsiveness to orthotopic cardiac transplants in DL-A-identical radiation chimeras. 5 25

In exsudate cells separated from serous body cavities of 29 tumour patients and 30 patients with inflammatory and congestive effusion in cardiac failure or liver cirrhosis respectively the activities of acid and alkaline phosphatase were determined. In addition to sudanophilia the cell content of glycogen and that of ribonucleinic acid were evaluated. By means of cytochemical findings it could be found that an increase of unspecific esterase, acid phosphatase and ribonucleic acid in atypical cells points to a malignous ethiology of the exudate.
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PMID:[Cytochemical tests on sediment cells of malignant and benign exudates]. 5 3

In 59 digitalized and 3 non digitalized patients the effect of digitalis during the 1st to 4th days after transmural myocardial infarction was controlled. Rhythm disturbances in acute myocardial infarction may arise secondary to a complicating cardiac failure and may be influenced by digitalis. In 9 of 17 cases (53 p.c.) with ventricular or supraventricular extrasystoles daily doses of 0,4 mg beta-Methyldigoxin or 0,4 mg Digoxin i.v. resulted in undisturbed sinus rhythm. In two cases supraventricular tachycardia and extrasystoles with rapid ventricular rate were abolished by 1,2 mg beta-Methyldigoxin within 12 hours, in three other cases an improvement was recorded. Dysrhythmias or other complications did not occur in previously non digitalized patients. When the antiarrhythmic effect of digitalis cannot be obtained cardiodepressive complications by treatment with typical antiarrhythmic agents are diminished. In patients on digitalis and in cardiogenic shock, digitalization should be performed carefully. Intoxication leads to a diminution of cardiac output and to cardiac dysrhythmias.
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PMID:[The antiarrhythmic effect of digitalis in acute myocardial infarction with cardiac failure (author's transl)]. 5 51


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