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

Changes in vasomotor tone in cardiac failure are related to the severity of the cardiac failure. The causative factors include dysfunction of the baroreceptor reflex, abnormal stimulation of the normal physiological regulators of cardio-circulatory function such as the sympathetic nervous and the renin-angiotensin-aldosterone system, and certain local factors characteristic of cardiac failure such as salt and water retention at vascular wall and interstitial level or changes in the metabolism of certain tissues. These changes are variable according to the region perfused and their interaction results in preferential redistribution of blood flow to the coronary and cerebral circulations at the expense of other regions such as the splanchnic and cutaneous vessels. In addition, they play a key role in the adaptive peripheral mechanisms to left ventricular failure and to the modulation of the vascular effects of drug therapy. An improvement in our understanding of these mechanisms and their consequences is important from the physiopathological, prognostic and therapeutic points of view.
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PMID:[Mechanisms and consequences of changes of the vasomotor activity in cardiac insufficiency]. 205 35

It is not completely clear if the renal sympathetic nerves are essential for normal renal function, however, it has been reasonably well established that the renal nerves can influence renal function under experimental conditions. These influences are manifested as changes in sodium excretion, urine flow, renin release, renal blood flow and glomerular filtration rate. Under conditions of stress the renal nerves can have powerful influences on renal function and, as a result, on systemic hemodynamics. Because renal sympathetic outflow is under central control, the reflex modulation of renal nerve activity is an extremely important factor in the control of salt and water balance. We have shown that cardiac and arterial baroreflex control of renal nerve activity is abnormal in chronic congestive heart failure. The mechanisms for this abnormality can reside in any arm of the reflex arc. The evidence from this and other laboratories has clearly implicated the afferent limb of these reflexes as being abnormal. Experiments done in anesthetized dogs with pacing induced heart failure have indicated that the central component of these reflexes are probably normal. The experiments described above cannot differentiate between abnormal afferent mechanisms and abnormal end organ responses to renal nerve stimulation. Several humoral mechanisms may be operative in heart failure to modulate renal nerve activity. These include bradykinin, prostaglandins and the renin-angiotensin aldosterone axis. Future work should be directed towards a further understanding of the role played by these and other humoral factors in the control of renal sympathetic outflow in heart failure.
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PMID:Reflex control of renal sympathetic nervous activity in heart failure. 206 56

The evolution of our understanding of the pathogenesis and therapy of heart failure can be described in terms of three paradigms that have also proven useful in describing the development of knowledge of cardiovascular regulation and the actions of angiotensin II. Organ physiology, the first paradigm, viewed the variable performance of the heart in terms of length-dependent changes in myocardial contractile function (Starling's Law), and angiotensin II as a pressor factor that elevated blood pressure. This paradigm focused treatment of heart failure on the major circulatory abnormalities: salt and water retention and vasoconstriction. According to the second paradigm, cell biochemistry, regulation of cardiac performance reflected altered calcium fluxes and changing myocardial contractility, and the clinical effects of angiotensin II as arising from altered calcium fluxes involved in the control of smooth muscle tension. Following this second paradigm, treatment of heart failure focused on powerful inotropic agents designed to increase myocardial contractility. The third paradigm, gene expression (molecular biology) describes what is probably the most primitive, and almost certainly the most complex of these regulatory mechanisms. Altered gene expression explains long-term regulation of cardiac performance in terms of adaptive changes in the architecture and composition of the heart, and key effects of angiotensin II as arising from increased protein synthesis and promotion of cell growth. In the case of heart failure, this third paradigm may explain the accelerated deterioration of the hypertrophied, failing heart as being due to altered myocardial cell growth composition. While the useful life of the normal human heart appears to be at least 80-90 years, overload-induced hypertrophy may reduce the heart's life span to about 5 years. This unwelcome consequence of myocardial hypertrophy may arise from the expression of fetal isoforms of key muscle proteins, a hypothesis that is supported by evidence that deterioration of the failing heart can be alleviated by the converting enzyme inhibitors which have important effects to inhibit cellular growth.
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PMID:Is heart failure an abnormality of myocardial cell growth? 207 54

The diagnosis of cardiac failure carries practical and psychological consequences which may require the patient to change his way of life. In addition to compliance to therapy which is the basis of clinical stability, the patient must understand a number of realities: violent physical exercise may be forbidden but regular daily physical exercise is to be recommended (with intermittent rest periods) as it increases the patient's comfort, although a beneficial effect on the prognosis has not yet been demonstrated. In addition, a reduced salt intake should be recommended although strict restrictions are no longer necessary with the ready availability of diuretics; the patient should also be taught to titrate his diuretic therapy with respect to alimentary intake and daily weight changes. Finally, instructions should be given about intercurrent conditions (infection, paroxysmal arrhythmias, hypertensive crises) which may decompensate stable patients and lead to a relapse of congestive heart failure. The patient and his family must know how and whom to contact immediately in case of an emergency.
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PMID:[What patients with cardiac insufficiency should know and why?]. 212 19

Left ventricular failure results from many myocardial diseases: the symptoms of left ventricular failure are the consequence of adaptations which the left ventricle and circulatory system activate to counteract the initial myocardial disease. The aims of treatment of cardiac failure are diverse depending on whether treatment is directed to correct the initial myocardial disease, its myocardial consequences, its circulatory consequences or, more simply, the patient's symptoms. The ideal treatment of cardiac failure would include a drug acting on the cause, a drug restoring left ventricular contraction and relaxation adapted to the conditions of cardiac load, a drug correcting regional blood flow disturbances and a drug relieving symptoms related to salt retention. An ideal drug for chronic left ventricular failure does not exist, and so treatment is a composite effort. Should it be in first intention? This is the current trend.
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PMID:[Treatment of chronic left ventricular insufficiency]. 212 20

Antihypertensive drugs have been of major benefit to people with moderate or severe hypertension and have contributed enormously to fundamental physiological knowledge. Antihypertensive therapy in milder hypertension reduces the incidence of stroke by 40% or more, may reduce myocardial infarction and prevents progression to more severe hypertension or heart failure but is being criticised as not cost-effective. Much of this criticism is based on deductions from inappropriate data. Nevertheless, it is likely that money is in some cases being wasted on the treatment of people who were not truly hypertensive in the first place. It is also likely that drug dosage is often unnecessarily high. Clearly it is vital that treatment is delivered as economically as possible. A reduction in the prevalence of hypertension would be the best way to reduce costs. Obesity and a high alcohol intake are associated with a higher blood pressure at any age. A high salt intake throughout life appears to be associated with a rise in blood pressure in the second half of life and may well be the main factor in hypertension. A radical rethinking of the method of pricing of medical care should be considered, so as to provide incentives to people to adopt life-style measures that lead to avoidance of hypertension (and other cardiovascular risk factors) or, in established hypertension, to a reduction in the need for medication.
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PMID:Managing hypertension: drugs, life-style manipulation or benign neglect? Medical, ethical and economic considerations. 175 Sep 10

The failing heart is unable to provide some organs, notably the brain and the myocardium, with the amount of blood flow they require. To this myocardial inadequacy and resulting "circulatory insufficient" the body reacts by setting in action compensatory mechanisms which are "intracardiac" first (Starling's heterometric regulation, ventricular hypertrophy), then neurohormonal, with the activation of vasoconstrictor systems (noradrenergic system, renin-angiotensin-aldosterone system, arginine-vasopressin system) counterbalanced by the activation of vasodilator systems (vasodilator prostaglandins, atrial natriuretic factor and kinins). However, the vasoconstrictor systems outweigh the vasodilator systems. They create an excessive arterial and venous vasoconstriction, together with water-and-salt retention, which leads to an increase of left ventricular work during both systole and diastole and to a gradual worsening of the heart failure. The present-day treatment of heart failure aims at reducing the water-and-salt retention and at restoring the balance between the vasoconstrictor and vasodilator systems.
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PMID:[General physiopathology of chronic left ventricular insufficiency]. 214 35

General considerations in planning therapy of heart failure include identification of the cause, rapidity of onset, and the age of the patient. Neonates and young infants with acute onset heart failure frequently develop acidaemia, respiratory compromise or failure, and metabolic derangements such as hypoglycaemia, hypocalcaemia or hypomagnesaemia. These complications require early recognition and urgent therapy. The diagnosis of heart failure in neonates with ductal dependent congenital cardiac lesions (such as coarctation of the aorta, hypoplastic left heart syndrome or pulmonary valve atresia) allows the early institution of alprostadil (prostaglandin E1) therapy to maintain patency of the ductus arteriosus, which stabilises these infants before surgical therapy. Classic therapy for infants with heart failure due to a large left-to-right shunt consists of salt restriction, diuretics and digoxin. If this treatment is inadequate an angiotensin converting enzyme (ACE) inhibitor (e.g. captopril) is added to therapy. The question then arises whether captopril and diuretics should be the initial therapy and digoxin added if this treatment fails. Acute heart failure may occur in the immediate postoperative period after cardiac surgery or may complicate acute overwhelming infections. Therapy consists of volume loading, vasodilator or inotropic agents. Heart failure due to various forms of chronic dilated cardiomyopathy usually responds to treatment with salt restriction, diuretics, digoxin and captopril. Acute deterioration requires treatment with vasodilators and/or inotropic agents. Heart failure in fetuses may occur from sustained supraventricular tachyarrhythmias, and may respond to treatment of the mother with antiarrhythmic agents such as digoxin or procainamide.
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PMID:New drug approaches to the treatment of heart failure in infants and children. 218 7

Horses suffering from trauma, sepsis, and severe burns need 12% to 16% of protein (dry matter basis) in their diet. Since reduced appetite may be a problem, relatively energy dense (greater than 2 Mcal DE/kg) feeds should be offered. In hepatic failure, maintenance protein requirements (8% on a dry matter basis for adult horses) should be met with feeds that are high in short branched-chain amino acids and arginine but low in aromatic amino acids and tryptophan (for example, milo, corn, soybean, or linseed meal) in addition to grass hay. Vitamins A, C, and E should also be supplemented. In cases with renal failure, protein, calcium, and phosphorus should be restricted to maintenance or lower levels. Grass hay and corn are the best feeds for horses with reduced renal function. Do not offer free-choice salt to horses with dependent edema from uncompensated chronic heart failure. Following gastrointestinal resection, legume hay and grain mixtures are the feeds of choice. Horses with diarrhea should not be deprived or oral or enteral alimentation for prolonged periods of time. Liquid formulas may be used if bulk or gastrointestinal motility are a problem. Apple cider vinegar and a high grain diet may reduce the incidence of enteroliths in horses prone to this problem. Pelleted feeds will reduce fecal volume and produce softer feces for horses that have had rectovaginal lacerations or surgery. Horses with small intestinal dysfunction or resection should be offered low residue diets initially, but long-term maintenance requires diets that promote large intestinal digestion (alfalfa hay, vegetable oil, restricted grain). Geriatric horses (greater than 20 years old need diets similar to those recommended for horses 6 to 18 months old.
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PMID:Clinical nutrition of adult horses. 220 96

The increased neuroendocrine activity in patients with congestive heart failure appears to be a generalized attempt to maintain blood pressure at the expense of reduced cardiac performance and salt and water retention. It is likely that baroreceptor dysfunction contributes to increased sympathetic nervous system activity in patients with congestive heart failure. The usual tonic inhibitory messages emanating from baro- and mechanoreceptors in the great vessels and heart fail to adjust sympathetic traffic from the brain to the periphery, leading to uninhibited sympathetic tone. Arginine vasopressin and plasma renin activity may be increased secondarily; however, plasma renin activity activation could also be induced by a low-salt diet and diuretic use. Preliminary baseline data indicate that patients with left ventricular dysfunction (ejection fraction less than or equal to 35%) but no or very mild symptoms of heart failure have increased plasma levels of norepinephrine, atrial natriuretic factor and arginine vasopressin, while plasma renin activity is normal, suggesting that neuroendocrine activity contributes to the pathogenesis of congestive heart failure. Neurohormones such as angiotensin II may alter gene expression, leading to changes in the shape and size of the cell. Remodeling of the heart and blood vessels is associated with both heart failure and hypertension. Angiotensin-converting enzyme inhibitors have been demonstrated to retard or reverse the remodeling process under certain experimental conditions. Studies are currently under way to test this possibility in patients.
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PMID:Neuroendocrine activity in congestive heart failure. 222 Jun 3


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