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

Under ether anesthesia electrocardiograms were derived from Syrian hamsters (strain BIO 8262) suffering from cardiomyopathy and muscular dystrophy. In addition, ventricular weights and body weight were determined. Young hamsters -- not yet showing morphological signs of the cardiomyopathy with the exception of possible left ventricular hypertrophy -- demonstrated only a longer ventricular activation time than normal hamsters. With the onset of cardiac necrotization left axis deviation in frontal plane projection and right bundle branch blocks are developing in the cardiomyopathic hamsters followed by first degree atrioventricular conduction defects. During the late stage of the cardiomyopathy left bundle branch blocks are additionally arising, while left ventricular hypertrophy is disappearing. Since no overt heart failure is occurring in this strain of cardiomyopathic hamsters, gradual development of high degree conduction defects is assumed to terminate their lives. The electrocardiographic pattern of the hamster cardiomyopathy fits partly into that of human primary as well as secondary cardiomyopathy. Nevertheless, it seems to form an entity of its own, as arrhythmias, higher degree atrioventricular conduction disturbances, typical signs of ventricular or septal hypertrophy, abnormal P and Q waves, ST segment and T wave changes are lacking.
Basic Res Cardiol
PMID:Electrocardiographic changes in cardiomyopathic Syrian hamsters (strain BIO 8262). 14 76

A study of 44 Nigerians with heart muscle disease defined as congestive cardiac failure and cardiac enlargement of unknown cause with a presenting diastolic blood pressure of not more than 100 mm Hg has shown 20 were alcoholics. 12 of these belonged to the high socioeconomic class. 17 were thiamine deficient; 11 of these consumed alcohol excessively and 8 of the 11 belonged to the high socioeconomic class. Only 3 alcoholics were identified in 52 controls. None of the 3 patients was thiamine deficient but 10 others were. Only 1 patient with heart muscle disease had a reversible high output cardiac failure. The mean serum albumin of the patients with heart muscle disease was significantly lower than controls. There was no significant difference between the mean levels of serum potassium in the study group and controls. It is concluded that chronic alcoholism is not rare among Nigerians with heart muscle disease. Although there is no convincing evidence to show that malnutrition or thiamine deficiency could in themselves cause the chronic myocardial failure seen in heart muscle disease, they could be conditioning factors which increase the susceptibility of the heart to other injurious agents.
Eur J Cardiol 1979 Sep
PMID:Heart muscle disease among adult Nigerians: role of nutritional factors in its aetiology. 15 80

Of a total sixtytwo patients covering all the spectrum of genetic ASH, who were studied by heart catheterization, M-mode echocardiography and phonomechano cardiography, five patients (four with the obstructive variety of the disease) showed clinical evidence of chronic congestive heart failure with ankle edema and hepatomegaly (group I). Their data were compared with those of fifteen "obstructed" patients who were not in heart decompensation (group II). No statistically significant differences were found between groups I and II in terms of L.V. internal transverse dimensions and in terms of L.V. systolic function. Conversely a statistically significant difference was found between the two groups in terms of left atrial and right ventricular dimensions (P less than 0,001), which were markedly increased in groups I. These findings strongly suggest that in patients with ASH and congestive heart failure there is a reduction in L.V. compliance (or distensibility), whereas L.V. systolic function is essentially preserved. The persistence of severe L.V. outflow obstruction in four patients of I group gives further confirmation to these observations. The use of beta-blockers (in association or not with cardiac glycosides) seems therefore to preserve its validity in the treatment of patients with ASH and heart failure, particulary when severe L.V. outflow obstruction is present. Cardiac glycosides are indicated in the forms with little or no obstruction to L.V. ejection.
G Ital Cardiol 1979
PMID:[Congestive heart failure in genetic hypertrophic cardiomyopathies (ASH) (author's transl)]. 16 Mar 52

The hemodynamic effects of tazolol, a new long-acting beta-stimulating drug, were studied in dogs with acute pump failure caused by experimental myocardial infarction and the results were compared with the actions of isoproterenol given in small and large doses. Tazolol produced a significant and sustained increase in cardiac output and stroke volume, while causing a decrease in peripheral resistance and mean aortic pressure. Heart rate was only modestly increased. Compared with isoproterenol at equivalent doses. tazolol appeared to cause less S-T segment elevation at the margin of infarction. The increase in double product (systolic pressure X heart rate) produced by tazolol was also considerably less than that of isoproterenol. Tazolol may prove to be a useful addition to the drugs available for the treatment of myocardial failure of various causes. It is now being studied in patients with heart failure due to coronary artery disease.
Am J Cardiol 1975 May
PMID:Circulatory effects of tazolol in experimental myocardial infarction. 23 34

Circulatory behavior in chronic, severely anaemic patients on volume loading is not precisely known. Twenty young male subjets with hook-worm anaemia, (Hb 2 to 5 gm %), without any complications were transfused with 300 or 600 ml of whole blood at 3 6 or ml/mt. Haemodynamic study was done before and immediately after. Blood volume was low, intracardiac pressures normal or minimally abnormal, cardiac output raised and vascular resistances low. After transfusion, there was a small but significant rise in arterial and mixed venous oxygen content, oxygen transport, heart rate, pulmonary wedge and mean polmonary arterial pressures and fall in % coeffcient of oxygen utilisation. Central venous pressures rose only with bigger transfusion. Change in cardiac output was related to the output before transfusion. Three subjects with cardiac index above 7 1/min had a fall and 6 of 7 below 7 1/min. a rise. Fall is perhaps related to the rise in blood oxygen content. It is argued that it is not an index of cardiac failure, as is often believed. Changes in pulmonary pressures are more sensitive than central venous pressure. One of our subjects died suddenly a day after uneventful study. Existing knowledge of haemodynamic status in severe anaemia and the change on transfusion helps little in explaining such deaths and others due to pulmonary oedema during or shortly after small to large transfusions. Further work in this field aiming to study changes in myocardial function and dynamic pressure volume relation in the vascular system is required.
Acta Cardiol 1977
PMID:Haemodynamic changes with blood transfusion in chronic severe anaemia. 30 Sep 64

Although postoperative constrictive pericarditis is rare, the diagnosis should be considered when unexplained right-sided heart failure develops after cardiac surgery. Within a 6 week interval, evidence of constrictive pericarditis developed in three patients who had recently undergone myocardial revascularization. One patient presented with biventricular failure, pericardial effusion and suspected tamponade. Severe constrictive pericarditis was demonstrated at subsequent operation. An apparent postpericardiotomy syndrome preceded evidence of right heart failure in the other two patients. Etiologic considerations include the possibility that pericardial irrigation with povidone-iodine (Betadine) solution may have contributed to subsequent fibrosis.
Am J Cardiol 1979 Jul
PMID:Constrictive pericarditis after myocardial revascularization: report of three cases. 31 49

160 consecutive CCU-treated AMI patients below 66 yr were investigated for ventricular ectopic beats (VEB) by 6-h telemetry prior to discharge and after 1 yr. During the follow-up year 11 patients died suddenly and 20 suffered reinfarction. By stepwise discriminant analysis three independent prognostic parameters were found: (1) radiologic cardiomegaly; (2) severe VEBs prior to discharge; (3) diabetes mellitus. Previous infarct, angina, functional class II to IV, smoking, higher age and radiologic cardiomegaly were significantly more frequent in patients with VEBs prior to discharge. History of heart failure, functional class deterioration, higher age, male sex, large first infarct, VT or VF in CCU, transmural infarction, radiologic cardiomegaly were more frequent in patients with severe VEBs prior to discharge. VEB severity increased significantly during the follow-up year in survivors without reinfarction. This increase occurred in patients with previous infarction, angina pectoris, higher age and heart failure.
Eur J Cardiol
PMID:Ventricular arrhythmias after an acute myocardial infarction. Prognostic weight and natural history. 35 1

To evaluate the antiarrhythmic efficacy of the new beta adrenergic blocking agent acebutolol, 15 monitored patients with supraventricular arrhythmias received, in double-blind fashion, an intravenous infusion of either acebutolol or saline solution after a control period. Patients treated with saline solution demonstrated no change (P greater than 0.05) in heart rate or arterial blood pressure or conversion to sinus rhythm. After administration of acebutolol, significant (P less than 0.05) reductions in heart rate were noted at 5 minutes. Peak reduction occurred at 10 to 30 minutes and correlated with maximal acebutolol plasma concentrations, antiarrhythmic activity persisted for 24 hours. Mild reductions in systolic blood pressure were observed in the majority of patients. Two patients with atrial fibrillation and one with multifocal atrial tachycardia had conversion to sinus rhythm. Frequent premature atrial complexes noted in one patient were greatly suppressed after administration of the drug. In the nine patients with clinical evidence of chronic obstructive lung disease acebutolol was well tolerated. Adverse reactions were limited to transient dyspnea in one patient with prior heart failure and a decrease in systolic blood pressure to less than 90 mm Hg in three patients who remained asymptomatic. In the patients studied, acebutolol was an effective agent for the treatment of supraventricular arrhythmias and appeared to be of special value in those with chronic obstructive lung disease.
Am J Cardiol 1979 Sep
PMID:Effective treatment of supraventricular arrhythmias with acebutolol. 38 21

The effect on the left ventricle of changes in the state of the arterial vasculature is best identified by utilizing calculations of pulsatile rather than steady flow phenomena. Impedance is the most satisfactory term to describe this effect. The normal ventricle compensates for changes in impedance largely by changes in preload, but the damaged heart loses this compensatory ability and its stroke volume becomes inversely related to outflow resistance. Patients with heart failure behave in a similar fashion and pharmacologic vasodilation may induce marked improvement in left ventricular pump function. Inappropriate vasoconstriction in heart failure may result from stimulation of the sympathetic or renin-angiotensin system. Early experience with converting enzyme inhibitors suggests that blockade of the formation of angiotensin II may be a useful means of treating some patients with heart failure.
Am J Cardiol 1979 Oct 22
PMID:Role of vasoconstrictor mechanisms in the control of left ventricular performance of the normal and damaged heart. 38 61

Patients with severe left ventricular failure generally have both reduced cardiac output and increased pulmonary and systemic venous pressures. A study was therefore made of the use of combined vasodilator therapy with nonparenterally administered nitrates, which act primarily on venous capacitance vessels and thus reduce preload, and orally administered hydralazine, which acts on arteriolar resistance vessels and thus reduces afterload. Twelve patients with chronic refractory heart failure were given these drugs individually and in combination during continuous hemodynamic monitoring. Heart rate and arterial pressure did not change significantly. Nitrates significantly reduced filling pressures of both ventricles without affecting cardiac index. Hydralazine did not alter filling pressures but dramatically increased cardiac index. The hemodynamic effects of each drug were additive during combined therapy, resulting in a 36 percent (28 to 18 mm Hg) mean decrease in left ventricular filling pressure and a 58 percent (2.1 to 3.3 liters/min per m(2)) mean increase in cardiac index. The seven patients who have continued to receive combined therapy for 3 to 10 months have shown sustained clinical improvement.
Am J Cardiol 1977 Nov
PMID:Hemodynamic advantage of combined administration of hydralazine orally and nitrates nonparenterally in the vasodilator therapy of chronic heart failure. 41 64


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