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

Growth failure in infants with congenital heart disease was investigated by studies of food intake, change in body weight, oxygen consumption, carbon dioxide production, and lean body mass. Infants with congenital heart disease weighed less initially and gained less weight during observation than normal infants. The daily intake of calories per kilogram body weight was inadequate for some infants and considered generally adequate for others. Lean body mass was normal, and the quantity of oxygen used for metabolism was similar in both groups. Infants with congenital heart disease were not found to be hypermetabolic when oxygen consumption was related to lean body mass. The growth failure seen in these infants appears to be most appropriately related to inadequate calorie intake rather than to any other factor studied.
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PMID:Infants with congenital heart disease. Food intake, body weight, and energy metabolism. 113 Mar 44

The influence of thiopental (Trapanal) on coronary blood flow (MPF), myocardial oxygen consumption (MVO2), and general haemodynamics was investigated in seven patients without heart disease. Besides measurement of MBF, the amount of substrates (glucose, lactate, pyruvate and free fatty acids (FFA) was also determined in arterial and coronary sinus blood samples. Thiopental was given intravenously in a mean dose of 4 mg/kg b,w, MBF was measured by means of the argon method. After injection of thiopental, all seven patients showed a significant increase of MBF and MVO2, a fact which can essentially be explained by the increase of heart rate. The effects of thiopental on arterial concentrations, arterior-coronary substrate differences, myocardial uptake, and O2-extraction ratio of the different substrates are discussed.
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PMID:Effects of thiopental (Trapanal) on coronary blood flow and myocardial metabolism in man. 113 93

Resting oxygen uptake was determined by a diaferometer in 90 children with congenital heart disease and in 39 children without cardiac defects, both groups ranging in age from 1 month to 15 years. The children with cardiac defects were classified according to the kind of the defect. The values of all children were related to body surface area and in every case compared with standards of basal metabolic rate of Karlberg and Fleisch. Although there was a tendency to higher values of resting oxygen uptake in children with cardiac defects, a statistically definite difference to the standard values could not be established. The possibly influencing factors of oxygen uptake in children with cardiac defects, as weight reduction, sedation, heart dynamics and oxygen cost of breathing are discussed regarding the literature.
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PMID:[Oxygen consumption in infants and children with congenital heart defects]. 114 73

Seven infants under one month of age with controlled congestive heart failure showed a mean oxygen consumption of 9-4 +/- 1-6 SD ml/kg per min, a mean respiratory quotient of 0-71 +/- 0-05 SD, and a mean metabolic rate of 63 +/- 12 SD cal/kg per 24 h. This compares with a group of infants with congenital heart disease not in heart failure with Vo2 of 6-5 +/- 1-2 SD ml/min per kg, respiratory quotient of 0-80 +/- 0-11 SD, and basal metabolic rate of 45 +/- 8 SD cal/kg per 24 h. These differences are significant (P less than 0.001). The findings of a greater metabolic rate associated with congestive heart failure are thus extended to the newborn period.
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PMID:Metabolic rate of neonates with congenital heart disease. 116 66

Estimation of exercise tolerance in patients with heart disease and significant symptoms can usually not be expressed in terms of maximal oxygen uptake or power at a fixed heart rate calculated from a 'steady state' exercise test. The exercise tolerance can be expressed only by the maximal power developed, when limited by symptoms. For this purpose the level of tolerance is better assessed by a test with small increments and short duration of each work load. In clinical practice this type of almost continuous increase in load was found to be particularly useful in patients with ischaemic heart disease. Comparative studies showed that the work per heart beat at equal loads is significantly higher in the test with continuous increase in load than in the test with steps of 6 minutes duration, both in normal subjects and in heart patients. The difference, however, is small (7%) and for practical purposes these tests have equal validity as a measure of the circulatory capacity.
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PMID:Design of exercise test, with special reference to heart patients. 125 43

The optimum and critical hemoglobin concentrations are determined by the oxygen demand of the tissues and several oxygen transport parameters (i.e., blood flow, arterial oxygen saturation, oxygen affinity of hemoglobin, and the critical venous oxygen pressure). Most of the oxygen transport parameters change markedly during the first weeks after birth. Oxygen consumption and cardiac output in neonates are three times those of adults on a body weight basis. Due to the high oxygen affinity of fetal hemoglobin, the oxygen unloading capacity of hemoglobin in neonates is about 50% less than in adults. From oxygen transport parameters and oxygen consumption we have calculated the optimum and the critical hemoglobin concentrations for preterm and full-term neonates during the first weeks after birth. A hemoglobin concentration of 15 g/dl appears optimal for preterm and full-term infants at birth as well as for adults. The calculated minimum acceptable hemoglobin concentration is 6 g/dl for children and adults, 12 g/dl for preterm infants and 11 g/dl for full-term neonates at birth. Due to the postnatal decrease in oxygen affinity, the minimum acceptable hemoglobin concentration decreases by approximately 1 g/dl/week for the first 5-6 weeks until the minimum value of 6 g/dl for children and adults is reached. The minimum hemoglobin concentration should be 2 g/dl higher in patients who require increased oxygen or suffer from other serious disorders. A minimum hemoglobin concentration of 10 g/dl is recommended in children with leukemia or other oncological disease. In infants and children with chronic hypoxemia (cyanotic congenital heart disease) the minimum hemoglobin concentration should be increased by the percentage of arterial oxygen desaturation.
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PMID:[The critical hemoglobin value in newborn infants, infants and children]. 128 12

During aorto-biiliac by-pass, patients with heart disease are exposed at many haemodynamic problems. Mixed venous oxygen saturation monitoring help anesthetist along clamping and unclamping periods. This study concerning 13 patients with pre-operative NYHA class II and III congestive heart disease, discusses therapeutic algorithm especially for choosing inotropic or vasodilatator drugs.
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PMID:[Surgery of the aortic bifurcation and heart diseases: peroperative hemodynamics]. 130 43

Severity of illness and clinical characteristics of parainfluenza virus (PIV) infection were evaluated in 81 hospitalized children over a 4 year period. Fifty three patients were previously healthy and 28 had preexisting pulmonary abnormalities associated with bronchopulmonary dysplasia (BPD), congenital heart disease (CHD), asthma, or prematurity. When compared with formerly healthy children, the patients with preexisting pulmonary abnormalities were more likely to develop lower than upper respiratory tract illness (P less than 0.0001). In the lower respiratory tract infection group, patients with preexisting pulmonary abnormalities were sicker (P = 0.047), were hospitalized longer (P = 0.016), required more supplemental oxygen (P = 0.004), and were older (8.8 vs. 5.1 months) than previously healthy patients. Nosocomial infection occurred only in BPD patients. All these patients developed pneumonia. They were sicker (P = 0.0018), requiring more therapy (P = 0.0038) than other patients with preexisting pulmonary abnormalities and lower respiratory tract disease. Patients with BPD should be placed in protective isolation during PIV epidemics.
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PMID:Clinical characteristics of parainfluenza virus infection in hospitalized children. 132 98

Cigarette smoking causes significant exposure to nicotine, which increases heart rate, blood pressure, and thus myocardial oxygen demand, and to carbon monoxide, which decreases the oxygen-carrying capacity of the blood because of carboxyhemoglobin formation. Cigarette smoking also predisposes the patient to coronary vasoconstriction. Smoking cessation results in the early elimination of nicotine and carbon monoxide from the system and decreases the risks of ischemia based on these mechanisms. Over the long term, smoking cessation results in elimination of the increased risk of myocardial infarction in patients without previous heart disease as early as 2 years after smoking stops. In addition, for patients with known coronary artery disease, smoking cessation results in an increase in HDL level, which may result in a retardation of atherogenesis and reduced cardiovascular morbidity and mortality. It is important for all physicians to reiterate both the short- and long-term risks of cigarette smoking as well as the good news-that smoking cessation results in a substantial, if not complete, reversal of the risk of myocardial infarction and death, particularly for patients with established coronary artery disease. In light of those established facts, efforts to develop more effective methods to help patients quit smoking must be increased so patients can realize these important health benefits.
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PMID:Cardiovascular benefits of smoking cessation. 134 4

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.
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PMID:The effects of acute and chronic cocaine use on the heart. 134 9


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