Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, the effects of forearm static exercise were determined on local blood flow and oxygen consumption in 15 normal individuals (NL) and their responses were compared with ten patients in congestive heart failure (CHF). Forearm blood flow was determined by a plethysmographic technique before and during 15% of maximum voluntary contraction of the forearm. Regional arterial and venous oxygen contents were sampled and forearm oxygen consumption calculated by the Fick principle. At rest, forearm blood flow was less in patients with heart failure than in normal individuals; however, this was compensated for by an increased oxygen extraction, thus maintaining forearm oxygen consumption at a normal level. In contrast, during static exercise, forearm blood flow failed to rise normally with heart failure (NL 9.31; CHF 4.35 ml/min-100 ml, P less than 0.001) and the increased oxygen extraction was not sufficient to maintain a normal forearm oxygen consumption (NL .82; CHF .44 ml/min-100 ml, P less than 0.01). Therefore, patients with congestive heart failure demonstrate regional circulatory and metabolic abnormalities during static exercise that are comparable to those present during dynamic exercise. Because of a limited ability of their skeletal muscle resistance vessels to respond to dilator stimuli, they have an attenuation of their exercise hyperemia which leads to an earlier shift to anaerobic metabolism.
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PMID:Impaired forearm oxygen consumption during static exercise in patients with congestive heart failure. 94 78

Controversy exists regarding the relative safety of intravenously administered lidocaine and procainamide to patients with acutely impaired hemodynamics. Accordingly, their effects were studied in 15 such patients, 14 with acute myocardial infarction and one with cardiomyopathy and severe congestive heart failure. All had elevated levels of pulmonary capillary wedge pressure (greater than 15 mm Hg) and/or low cardiac index (less than 2.5 liters/min/m2). Patients were given lidocaine, a 100 mg bolus followed by a 3 mg/min infusion and, after at least a 30 minute recovery period, procainamide, a 100 mg bolus over 2 minutes followed by a 20 mg/min infusion for 20 to 25 minutes. Hemodynamic measurements were compared early and late in the infusion of each drug. Small, clinically insignificant differences were observed in the hemodynamic responses to the drugs, and no clinically significant deterioration occurred with either. Conventional therapeutic doses of intravenous procainamide can be administered by this regimen, to patients with acute myocardial infarction complicated by cardiac failure or low cardiac output, without producing deleterious hemodynamic effects.
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PMID:Comparative effects of lidocaine and procainamide on acutely impaired hemodynamics. 95 94

Ventricular septal defect repair had been performed in 57 infants ages 21 days to 21 months and under 10 kg in weight using profound hypothermia-circulatory arrest technics. Severe congestive heart failure was the indication for operation in all but two infants under 6 months of age, and in those under 3 months there was usually an associated moderate or large sized atrial septal defect or patent ductus arteriosus or a coarctation. In infants over 6 months controlled heart failure was accompanied by failure to thrive and often recurrent respiratory infections. The main indication for surgery in three infants was repeated severe respiratory infections and in 7 infants, ages 10-15 months, an elevation of pulmonary vascular resistance of 6 units M2 or more. There were two hospital deaths among the 49 infants without coarctation (ages 6 and 20 months) and two among the 8 with coarctation. Postoperative respiratory and other complications were uncommon. On late review there was no significant residual VSD amongst the 11 recatheterized patients. Psychometric studies in 19 children who had reached the age of three to four years gave no evidence of cerebral damage due to the circulatory arrest period. In view of these results palliative pulmonary artery banding is no longer performed for VSD in infancy unless there is a Swiss cheese septum or an associated severe coarctation.
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PMID:Repair of ventricular septal defect in the first two years of life using profound hypothermia-circulatory arrest techniques. 96 2

In a series of 128 consecutive patients dying from severe megaloblastic anaemia, over half the deaths occurred within one week of hospitalisation and one third were sudden and unexpected. Congestive cardiac failure was extremely common in these patients and was often associated with pleural effusions. Just over half the patients were examined at autopsy and of these 42% had pleural effusions and 15% had pericardial effusions. The cause of the latter is unclear as is their clinical significance, nevertheless this condition has not previously been reported in the megaloblastic anaemias and may well play a part in the fatal outcome in such patients. Blood transfusion was administered to over half the patients, usually in the form of whole blood. It is recommended that transfusions be used sparingly, and consist of cells or preferably exchange transfusion, the latter being of particular value in the elderly or in those with pre-existing cardiac failure.
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PMID:Deaths from severe megaloblastic anaemia in hospitalised patients. 100 63

It was established by means of radioimmunoassay that the blood concentration of Digoxin in patients with congestive heart failure depends not only on the dose of the drug given, but also on the stage of cardiac insufficiency. With equal daily doses, higher Digoxin concentrations were observed in patients with more severe cardiac insufficiency. The analysis of the obtained data has demonstrated that in 75% of the patients with signs of digitalis intoxication the concentration of Digoxin in blood exceeded 2.5 ng/ml. In animal experiments it was established that a distinct reduction of the toxic threshold took place in rabbits with acute myocardial infarction, acute pulmonary embolism, congestive cardiac failure, this threshold being determined by the amount of intravenously injected Strophantin that causes persistent ventricular tachycardia.
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PMID:[Digitalis poisoning, risk factors and digitalis intolerance]. 101 87

In 20 normal persons and in 57 patients with heart diseases with functional class I-IV (according to the classification of the New York Heart Association) the 24 hour urinary excretion of the catecholamines adrenaline, noradrenaline and dopamine and of the O2-methylated degradation products metanephrine and normetanephrine was determined. The 3 catecholamines and the 2 O-methylated derivatives were measured simultaneously using chromatographic extraction and purification (Bio-Rex 70) and selective flurometric determination. The following results could be obtained: 1. The urinary excretion of noradrenaline increased with increasing severity of the heart disease. 2. In patients with severe congestive heart failure (functional class IV) in addition the adrenaline excretion in addition the adrenaline excretion increased significantly. 3. There was no relationship between the urinary excretion of dopamine and the severity of the heart disease. 4. The ratio of noradrenaline excretion to dopamine excretion increased with increasing severity of the heart disease, indicating an increased activity of dopamine-mu-hydroxylation in patients with congestive heart failure. 5. The excretion of the O-methylated degradation products metanephrine and normetanephrine in normal persons and in patients with heart diseases paralleled the excretion of the corresponding catecholamines adrenaline and noradrenaline. This indicates, that increased excretion of noradrenaline and adrenaline (Class IV) in patients with heart failure was not due to impaired catecholamine-degradation but indead to increased catecholamine-release indicating increased sympatho-adrenergic activity. These results show in addition that also in patients with heart failure O-methylation represents still the main degradation step for the inactivation of the circulating catecholamines. 6. The relationship of toal excretion of 0-methylated derivates to total excretion of adrenaline and noradrenaline, however, decreased with increasing severity of heart disease, indicating a relative impairment of O-methylation under the condition of severe congestive heart failure.
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PMID:[Urinary excretion of the catecholamines adrenaline, noradrenaline and dopamine as well as the derivatives metanephrine and normetanephrine in heart disease patients]. 101 4

An elderly female with an acute episode of congestive heart failure, unaccompanied by any periods of hypotension, developed fulminant hepatic failure with an accompanying coagulopathy. Attempts to establish an etiology for her acute hepatic insufficiency, other than cardiac failure, proved negative. Fulminant hepatic failure as a consequence of congestive heart failure, without prolonged periods of hypotension preceding alteration in hepatic function, has not heretofore been described. Liver function is adversely effected in congestive heart failure. Hepatic ammonia clearance is impaired in cardiac failure and may be diminished to the point of resulting in hepatic encephalopathy. Coagulopathy is a frequent concomitant of fulminant hepatic failure. Establishing a clear etiology for a coagulopathy in the face of concomitant liver disease is difficult, thus making any therapeutic intervention fraught with peril.
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PMID:Fulminant hepatic failure secondary to congestive heart failure. 101 98

Continuing evaluation of coronary care is necessary to determine its present effectiveness and to establish direction in the effort to decrease mortality after myocardial infarction. Data have been collected on 157 consecutive patients diagnosed as having myocardial infarction who were admitted to the coronary-care unit at St. Joseph's Hospital and Medical Center, Phoenix, Ariz. The hospital is a teaching hospital with a 560-bed capacity. Data sheets were completed on each patient at the time of transfer from the coronary-care unit. The accumulated data were processed by a computer at the end of a 13-month period. The overall mortality for the group was 16.5 per cent. The factors which were found to have a significant effect on mortality were: (1) location of infarction, (2) presence of heart failure, (3) occurrence of cardiogenic shock, (4) age, and (5) the presence of intraventricular conduction defect. In 19 of the 26 deaths after myocardial infarction, the terminal event was associated with congestive heart failure, pulmonary edema, or cardiogenic shock. Three patients died of resistant arrhythmia, four of ventricular rupture. These figures indicate that arrhythmia is not a primary cause of death after myocardial infarction and that attention must also be directed to the early diagnosis and treatment of left ventricular failure if coronary care survival rates are to improve.
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PMID:Continuing evaluation of coronary care. 103 78

1. We investigated the haemodynamic effects of intravenously administered hydrallazine, diazoxide and nitroprusside and orally administered minoxidil to determine whether vasodilators (such as nitroprusside) which do not increase cardiac output might be better treatment for hypertensive complications associated with, or caused by, myocardial failure than those that do. 2. Hydrallazine and diazoxide caused increases in heart rate, cardiac output, cardiopulmonary blood volume, the ratio of cardiac output to cardiopulmonary volume, and pulmonary artery pressure. Nitroprusside, although decreasing pressure and vascular resistance, caused no significant change in the other functions except for reducing pulmonary artery pressure. Minoxidil, when given orally, had the potential for causing pulmonary hypertension. This seemed explained by increased flow (hyperdynamic type) in some but by congestive cardiac failure in others; the latter condition was probably intensified by the marked fluid retention that the drug can cause. 3. On the basis of these results a classification of vasodilators was constructed which depends on the presence or absence of a venodilating effect. Vasodilators which produce no (or little) venodilatation, increase heart rate, cardiac output, cardiopulmonary blood volume and pulmonary artery pressure. In this class are diazoxide, hydrallazine and minoxidil. Those that cause venodilatation do not stimulate the heart nor do they cause pulmonary hypertension. Nitroprusside and nitroglycerine are drugs of this type. 4. These results suggest that drugs producing both venodilatation and arteriolar dilatation may be more specific therapy for hypertensive complications associated with cardiac failure than those that cause only arteriolar dilatation.
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PMID:Vasodilating drugs: contrasting haemodynamic effects. 107 83

1. The chronic administration of minoxidil, 0-024-0-212 mmol (5-40 mg) daily, to fifty-two severely hypertensive patients resulted in an average reduction of mean arterial pressure from 170 to 111 mmHg. 2. Haemodynamic studies in twelve of these patients indicated that the rise in pulmonary arterial pressure in patients without heart failure appears to be a direct result of a disproportionately large increase in cardiac output with respect to a relatively small decrease in pulmonary vascular resistance. Anti-hypertensive treatment of patients with congestive heart failure resulted in a decrease in mean pulmonary arterial pressure.
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PMID:Treatment of severe hypertension with minoxidil and its effects on systemic and pulmonary haemodynamics. 107 85


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