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

Children with cyanotic congenital heart disease had a decreased glomerular filtration rate (71-8 +/- 18-9 ml/min per 1-73 m2) measured by endogenous creatinine clearances, compared with children who had had complete corrective surgery, children with noncyanotic heart disease, and normal children. There was a significant correlation between low glomerular filtration rate and haematocrit values above 50%. Daily urinary sodium excretion was reduced in the cyanotic patients.
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PMID:Abnormal renal functions in cyanotic congential heart disease. 100 86

Round heart disease in turkey poults has been associated with high levels of dietary salt and when it occurs in the field recommendations often include a reduction in the level of dietary salt. Poults fed diets containing up to 1.5% salt and 1.5% sodium did not exhibit signs of round heart disease. A high mortality rate occurred with poults fed a salt-free diet. Post-mortem analysis generally revealed enlargement of the kidneys with urates; exudate was present in both abdominal and thoracic air sacs. Growth trials indicated that in order to maintain an optimum feed:body weight gain ratio, corn-soybean diets should contain at least 0.1--0.2% supplemental salt, and at least 0.2--0.3% salt when growth rate is considered. Minimum salt levels could not be reduced further by adjustment of the total dietary sodium:chloride ratio to unity.
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PMID:Dietary salt and round heart disease in turkey poults with a note on the minimum level of supplementary salt necessary in corn-soybean diets. 103 22

During 76 extracorporeal circulations (CEC) carried out for open heart operations using an identical protocol, the authors carried out renal function tests from the time of administration of the anesthetic to the post-operative period. Various periods may be distinguished: pre-operative, anesthesia induction (CEC 1, CEC 2) post induction (CEC 1, post CEC 2) finally, the post-operative period (post-operative 1 to 4). As far as renal hemodynamics are concerned, the authors made the following observations: constant reduction in thiosulphate clearance and endogenous creatinine clearance, which reflect glomerular filtration. Reduction in PAH clearance, which reflects renal perfusion. Taking into consideration changes in the hematocrit, one may consider that there is a reduction in renal blood flow at all stages of anesthesia. Taking into consideration concomitant variations in blood pressure, one may calculate that intrarenal resistances are increased. The diuresis/minute increases in very great proportions during induction of anesthesia. Plasma osmolality also increases, urinary osmolality becomes reduced and osmolar clearance rises. The ratio between osmolar clearance and creatinine clearance rises. The clearance of free water rises from negative values. The serum sodium becomes slightly reduced, and sodium diuresis increases. Serum potassium becomes slightly reduced and urinary potassium rises. The interpretation of these phenomena is difficult and should take into consideration the experimental conditions. Comparison with published results shows that there are definite differences depending on whether pure or diluted blood is used. It is however, possible to seek the role of the anesthetic, the thoracotomy or the extracorporeal circulation itself and its load, quite independent of prior changes due to decompensation or not of the congenital heart disease, whether or not it has been treated. The study of these changes in renal function permits one to understand better the precariousness of renal perfusion during extracorporeal circulation, imperfectly corrected by osmotic diuresis and responsible for transient and reversible renal hypofunction, liable to lead however, in cases of complications and prolonged low blood flow, to organic renal failure.
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PMID:[Renal functions and extracorporeal circulation]. 110 26

Intrarenal distribution of blood flow was measured by the 133xenon washout curve in 33 patients with heart disease. Plasma renin activity and sodium concentration were also measured on the day when the xenon study was performed. The patients were divided into three groups according to cardiac index: Group I whose cardiac index showed higher than 3.50 1/min/M2, BSA, group II whose index ranged from 2.50 to 3.50, and group III who had lower than 2.50. Total renal blood flow was significantly decreased in group II (p less than 0.001), as compared with normal controls. The percents of the total renal blood flow supplied to component I decreased significantly in group I, II (p less than 0.05) and group III (p less than 0.01). The flow rate in component I decreased significantly only in group II (p less than 0.05) and group III (p less than 0.01). There was a significant increase in the percent distribution of component II in group II (p less than 0.05) and in group III (p less than 0.01). The flow rate of component II showed a slight increase in group I and III. The study of autoradiographs done in dogs with heart failure demonstrated that component I corresponded to a cortical area having a relatively faster flow rate, whereas component II corresponded to the cortical area which was perfused more slowly. Accordingly, component III indicated outer medulla. There was no apparent relation between intrarenal distribution of blood flow and plasma renin activity although the latter tended to be elevated in patients treated with diuretics. In view of the data available it was concluded that outer cortical as well as outer medullary blood flow are decreased in chronic congestive heart failure and that there is no apparent correlation between outer cortical flow and plasma renin activity.
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PMID:Intrarenal distribution of blood flow and renin in chronic congestive heart failure. 111 37

Changes of the mineral concentrations of the heart muscle can point at disturbances of myocardial metabolism. Disturbances of heart muscle with functional loss and without coronary or inflammatory heart disease are called myocardosis, especially cardioplegic myocardosis after open-heart surgery with extracorporal bypass. 30 dogs were examined in three groups varying the method of induced cardiac arrest: 1. ischemic cardiac arrest by clamping the ascending aorta, 2. functional cardiac arrest by electrically induced fibrillation and 3. ischemic cardiac arrest and in addition injection of a Mg-aspartate-procain-solution. Sodium, potassium, magnesium, calcium, copper and zinc were analyzed by atomic absorption spectrophotometry. Specimens from the left and right ventricular wall were examined before and after extracorporal circulation. After a recovery period for one hour the dogs were killed and specimens from the right and left ventricular wall and from the basis and apex of the interventricular septum were taken and reduced to ashes with mineral acids. In all animals changes of the mineral content were most marked after the recovery period. In all forms of cardiac arrest mineral metabolism showed monotone reactions: water content increased, potassium and magnesium decreased. Variations of mineral concentrations were more expressed in the right ventricular wall than in the left. Animals with cardiac arrest by electrically induced fibrillation indicated the smallest deviations from the basic values. The comparison of the values of dogs with sufficient circulation at the end of the experiments and those dogs with medicamentally or mechanically supported circulation at this time showed a more increased water content and simultaneously a decrease of all cations in the group with supported circulation. The decrease of the osmolality of the cations seems to be the metabolic answer to the increased cardioplegic damage of heart muscle.
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PMID:[Myocardial electrolytes in "cardioplegic" myocardosis (author's transl)]. 122 Jun 68

Sodium and potassium levels in plasma and leucocytes and the sodium efflux rate constants of leucocytes were measured in patients with congenital heart disease not on treatment, patients with valvular heart disease being treated with digoxin and conventional diuretics, and patients with valvular heart disease receiving digoxin and either conventional diuretics or triamterene or both. The group being treated with digoxin and conventional diuretics showed low cellular potassium levels, low sodium efflux rate constants, and a rise in cellular sodium levels. Patients given triamterene showed a rise in potassium levels in plasma and cells and in the sodium efflux rate constant.
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PMID:Effect of triamterene on leucocyte sodium and potassium levels in heart disease. 126 55

Graves' disease is an autoimmune disorder that comprises the triad of diffuse toxic goiter, ophthalmopathy, and infiltrative dermopathy, although all three are not necessarily present in a given patient. The manifestations of Graves' disease vary, depending on the patient's age and other factors. Choice of therapy is influenced by the patient's age, history of heart disease, pregnancy status, expectations, and preferences. Most patients are treated with either radioactive iodine (sodium iodide I 131 [Iodotope]) or the antithyroid drugs propylthiouracil or methimazole (Tapazole). Antithyroid drugs may be more effective in producing long-term remission if levothyroxine sodium (Levothroid, Levoxine, Synthroid) is added to the regimen after the patient becomes euthyroid. Hypothyroidism occurs in many patients following 131I therapy but is also seen in a substantial number of patients who have been treated with thyroidectomy and even in some who have taken antithyroid drugs. Long-term follow-up is necessary, regardless of type of initial treatment, and should include an annual physical examination and measurement of serum concentrations of thyrotropin and the free thyroxine index, both of which should be maintained in the normal range.
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PMID:Intervention in Graves' disease. Choosing among imperfect but effective treatment options. 128 Aug 17

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

Our purpose in this article is to examine the hypothesis that both myocardial disease and ischemia can alter the electrophysiologic function of the ion channels responsible for the cellular electrical activity of the heart. Changes in the intracellular and extracellular milieus occur during ischemia and can alter the electrophysiology of several species of ionic channels and the cellular electrophysiologic activity of cardiac myocytes. Included are 1) changes in extracellular [K+] and pH and in intracellular [Na+], [Ca2+], and pH; 2) accumulation of noxious metabolic products such as lysophosphatidylcholine; and 3) depletion of intracellular ATP. Finally, ischemia or disease (e.g., hypertrophy) can alter the electrophysiology of at least two types of K+ channels, the A-like channels underlying the transient outward current and the inward rectifier, by mechanisms that apparently do not involve alteration of either the intra- or extracellular milieus. Findings suggest that the expression of cardiac A-like channel function can be altered by hypertrophy and that at least one intrinsic conductance property of the inward rectifier can be altered by ischemia. We speculate that the control of expression, function, and regulation of cardiac ion channels can be affected at the molecular level by heart disease and myocardial ischemia.
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PMID:Connections: heart disease, cellular electrophysiology, and ion channels. 137 69

The renin-angiotensin system (RAS) plays a major role in the control of blood pressure and cardiovascular homeostasis and is involved in the pathogenesis of a number of cardiovascular disorders. The efficacy of angiotensin-converting enzyme (ACE) inhibitors in the treatment of hypertension and congestive heart failure has led to the widespread clinical use of ACE inhibitors in primary or secondary prevention of heart disease. The demonstration of the expression of the components of the RAS in several extrarenal tissues, as well as local generation of angiotensin II, has confirmed the existence of a tissue RAS that may serve organ-specific functions and act independently from the plasma RAS. The concept of paracrine/autocrine functions of the local RAS has changed our understanding of the functions of the RAS and suggests that tissue ACE inhibition may be of greater importance than inhibition of circulating ACE in the treatment of congestive heart failure and other cardiovascular disorders. Whereas the circulating endocrine RAS appears to be responsible for mediation of acute effects, the tissue RAS seems to be involved in more chronic situations, such as secondary structural changes of the cardiovascular system, and therefore could contribute to the pathogenesis of hypertension as well as other cardiovascular disorders, such as cardiac hypertrophy, coronary artery disease, and atherosclerosis. Several experimental and clinical findings suggest that reversal of cardiovascular structural changes secondary to cardiovascular disease and enhancement of renal sodium excretion by ACE inhibitors are important long-term antihypertensive actions possibly mediated by inhibition of the tissue RAS.
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PMID:Effects of angiotensin-converting enzyme inhibitors on tissue renin-angiotensin systems. 141 88


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