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)

Although converting-enzyme inhibition is of established value in the management of patients with severe chronic congestive heart failure, troublesome adverse reactions occur frequently during the course of treatment and may cause physicians to interrupt effective therapy. The three most common adverse reactions that are seen in patients with heart failure following treatment with captopril and enalapril (symptomatic hypotension, functional renal insufficiency, hyperkalaemia) are predictable consequences of interfering with the homeostatic functions of the renin-angiotensin system, which evolved millions of years ago to preserve life in sodium-depleted states. It is not surprising, therefore, that these untoward effects can be prevented or reversed by increasing the dietary intake of salt or reducing the dose of concomitantly administered diuretics; their occurrence rarely requires discontinuation of drug therapy. Recognition of this link between sodium balance and the adverse effects of converting-enzyme inhibition is important, because most patients with severe heart failure who experience such untoward reactions can nevertheless be expected to improve clinically during long-term therapy, if effective treatment is not interrupted.
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PMID:Adverse effects of converting-enzyme inhibition in patients with severe congestive heart failure: pathophysiology and management. 302 72

Congestive heart failure is a clinical syndrome with inadequate cardiac output and increased venous pressure, characterized by hyperfunction of the sympatho-neuro-endocrine system, favoring maximal vasoconstriction in non-essential organs and retention of salt and water. Identification of the cause of heart failure and its correction is the best treatment. The suppression of precipitant factors is also essential. Traditionally the treatment of congestive heart failure is based on diuretics, restriction of salt intake, and digitalis. The conventional vasodilators are effective in the short term, but they have a marked tendency to tachyphylaxis. The inhibitors of angiotensin-converting enzyme are, through their specific action on neuro-endocrine dysregulation, the most important advance in recent years. Of the non-glycosidic inotropic agents used in severe heart failure, the new inhibitors of phosphodiesterase need further testing. In certain cases, permanent synchronous pacing has to be considered.
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PMID:[Pathophysiologic aspects and modern treatment of congestive heart failure]. 302 12

The emergence of diuretic drugs and angiotensin converting enzyme (ACE) inhibitors ranks amongst the major therapeutic advances of modern medicine. The discovery of these drug groups arose largely by chance, yet each has dramatically influenced the treatment of congestive cardiac failure and arterial hypertension. The central role which diuretics have had in the management of both oedema and hypertension hinges on their ability to induce a net renal excretion of solute and water by selective interference with either active or passive ion transport processes in different segments of the nephron. Irrespective of sites of action, the continued antihypertensive action of diuretics is characterized by a reduction in plasma volume and extracellular fluid (ECF) volume that lasts for as long as the diuretic is given. The mechanism of this effect remains unclear but may involve autoregulatory reactions that leave cardiac output unaltered but maintain a sustained reduction in total peripheral resistance. ACE inhibitors also lower blood pressure by decreasing total peripheral resistance, leaving cardiac output, plasma volume and ECF volume unchanged. The detailed way these haemodynamic changes are achieved remains unknown but inhibition of converting enzyme present not only in the kidney but also in many extrarenal tissue sites, appears important. In both hypertension and cardiac failure, however, the kidney acts as a key target organ for ACE inhibitors. The increased renal vascular resistance and inappropriate renal salt excretion are reversed with enhanced renal blood flow and saluresis. Both angiotensin II (AII) and vasopressin-mediated contraction of glomerular mesangial cells is inhibited, making glomerular filtration more efficient. Reduced aldosterone secondary to blockade of AII formation contributes to saluresis whilst encouraging positive potassium balance. ACE inhibition also impairs breakdown of kinins which may contribute to intrarenal and peripheral vasodilation either on their own or via release of prostaglandins and other vasoactive substances. The hypotensive actions of diuretics are potentiated by ACE inhibition primarily through blockade of AII formation and prevention of secondary aldosteronism. In combination, these drugs permit low doses to be used because of their synergistic effects. Caution has to be exercised whenever ACE inhibition is used, without and especially with diuretics, in the management of renovascular hypertension and other low-perfusion states. In these circumstances, AII plays an important autoregulatory role in preserving glomerular filtration through an increase in post-glomerular resistance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Evolution of diuretics and ACE inhibitors, their renal and antihypertensive actions--parallels and contrasts. 303 17

Dilated cardiomyopathy, owing to any cause, usually culminates in the clinical syndrome of congestive heart failure. Heart failure is characterized by exertional dyspnea and fatigue, but the precise mechanisms that produce these symptoms are still not clear. Sodium retention occurs early in heart failure, but this disturbance is dynamic in nature and is not always present in the patient. The mechanism of early salt and water retention in heart failure is not defined. Gross edema and ascites occur much later, undoubtedly owing to the convergence of a number of factors. The peripheral adaptations to heart failure include activation of the renin-angiotensin system and the sympathetic nervous system, and the release of AVP. The result is an increase in preload with a resultant increase in stroke volume for some patients, but the price is paid in the form of heightened impedance to ejection and circulatory congestion. The sympathetic nervous system disturbances in heart failure are striking, as disturbances in both circulating and myocardial NE levels are consistently found. Vasorelaxant and natriuretic hormones, as well as certain prostaglandins, may be released in an attempt to offset excessive "compensatory" pressor-sodium retentive mechanisms, but the net result seems to be excessive peripheral vasoconstriction and a downward spiral of deterioration in many patients. One would hope that an unraveling of the complex pathophysiology of heart failure would lead to therapy that would change the natural history of the disease. The results of the first V-HeFT trial give room for cautious optimism in this regard.
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PMID:Pathophysiology of congestive heart failure secondary to congestive and ischemic cardiomyopathy. 304 87

The diuretic effect of the supine position was evaluated in six patients with cirrhosis and ascites and six with congestive cardiac failure. After fasting overnight in bed the patients received bumetanide 1 mg intravenously and were then immediately randomly assigned to either bed rest in the supine position or normal daily activity in the upright position for the next six hours. Two days later the procedure was repeated, the patients being assigned to the other posture. The diuretic response was similar in patients with heart failure and cirrhosis, and was significantly greater in the supine than in the upright position: mean 1133 v 626 ml/6 h (p less than 0.01). The natriuresis was similarly larger during recumbency: mean sodium 96 v 45 mmol(mEq)/6h (p less than 0.01), and the excreted potassium in six hours was similar in both postures. The glomerular filtration rate was 100 and 66 ml/min (p less than 0.01) and heart rate 76 and 83 beats/min (p less than 0.01) in the supine and upright positions respectively. Plasma concentrations of noradrenaline, renin, and aldosterone were all raised even when the patient adopted the supine position, and a further significant rise was observed during the upright position. The results suggest that the attenuated response to intravenous bumetanide in the upright position and during normal daily activity may be due to the activation of several homeostatic mechanisms that may reduce the excretion of water and salt.
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PMID:Diuretic treatment in decompensated cirrhosis and congestive heart failure: effect of posture. 308 44

With the failure of the heart as a pump, there ensues a series of neurohumoral compensations that defend organ perfusion at the expense of alterations in cardiac filling pressures and the distribution of blood flow to various regional circulations. Activation of the sympathetic nervous system and the renin-angiotensin II-aldosterone system and increases in circulating arginine vasopressin maintain arterial blood pressure by producing systemic arteriolar vasoconstriction and the renal retention of salt and water. Constriction of the efferent arterioles in the kidney by angiotensin II and norepinephrine promotes reabsorption of glomerular filtrate in the peritubular capillaries and maintains glomerular filtration in the face of declines in glomerular plasma flow and the glomerular permeability-surface area ultrafiltration coefficient. In resting, sodium-replete, conscious animals and humans, pharmacologic inhibition of renal cyclo-oxygenase by nonsteroidal anti-inflammatory drugs has little or no effect on renal hemodynamics. However, electrical or reflex stimulation of the renal nerves, intrarenal infusion of angiotensin II, or infusion of arginine vasopressin stimulates the release of vasodilator prostaglandins from the kidneys. In sodium-depleted animals or humans, and when cardiac output decreases, there is an increase in total peripheral vascular resistance but little change in renal vascular resistance. Increased renal synthesis of vasodilator prostaglandins (presumably by the blood vessels) maintains renal blood flow despite increased release of renin and norepinephrine from the kidneys. In these situations, pharmacologic inhibition of renal cyclo-oxygenase is accompanied by marked reductions in renal blood flow and glomerular filtration rate. When this occurs in patients with advanced heart failure, reversible oliguric renal failure may result. In this setting, cyclo-oxygenase inhibition may also increase arterial pressure and induce additional depression of cardiac function. Recent data indicate that blood vessels have the capacity to synthesize the sulfidopeptide leukotrienes C4, D4, and E4, which can constrict peripheral and renal blood vessels and alter vascular permeability. The vascular cell types responsible for leukotriene C4 synthesis and the potential roles of these vasoactive eicosanoids in kidney and other regional circulations are currently under study.
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PMID:Prostaglandins in congestive heart failure and the effects of nonsteroidal anti-inflammatory drugs. 309 62

Atherosclerosis and hypertension are, by far, the most common cardiovascular diseases affecting women, and both are influenced by diet. Atherosclerosis occurs more commonly in men than women; generally women are 10 to 15 years older than men when symptoms develop. The prevalence of hypertension is about equal in the two sexes, particularly in middle aged and older persons. These cardiovascular diseases are major causes of death and disability in this country. Atherosclerosis results in myocardial infarction, thrombotic strokes, and claudication. Hypertension, when severe, damages small blood vessels, causing kidney failure, hemorrhage, strokes, and heart failure; when the condition is mild to moderate, it produces atherosclerosis. Nutritional factors are of primary importance in both atherosclerosis and hypertension. Risk factors for atherosclerosis related to nutrition are hypercholesterolemia, hyperglycemia-diabetes, and for hypertension, obesity, high salt intake, and excessive use of alcohol. Of all these risk factors, obesity seems to be the most important because it is strongly linked to hypertension and diabetes. Dietary intake of saturated fat is a potent factor in determining the blood cholesterol level, and reducing intake often decreases the level, thus lessening the risk of atherosclerotic complications. Although high salt intake and excessive alcohol use produce hypertension in susceptible people, less is known about the frequency of this adverse effect than is known about obesity.
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PMID:Nutrition and cardiovascular diseases of women. 312 Feb 15

Hypertension extracts a huge toll from the black community in terms of excess morbidity and mortality. The black hypertensive is more likely to die from the disease and to have stroke, end-stage renal disease or heart failure. Furthermore, contrary to previous beliefs, blacks are at least as likely to have coronary artery disease as whites. Although substantial overlap occurs, the black hypertensive is more likely to be volume-expanded, to have a lower plasma renin level, and to be classified, as salt-sensitive than is the white hypertensive. Decreased dietary potassium and calcium intake, altered intra-cellular handling of sodium and calcium, and psychosocial factors have also been implicated in the pathophysiology of hypertension in blacks.
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PMID:Profile of systemic hypertension in black patients. 328 50

Patients with heart failure should stop smoking, maintain an optimal weight and limit their intake of salt. Alcohol abuse should be avoided. The detection and early treatment of hypertension appears to have had a major impact in preventing heart failure. Diuretics revolutionized the treatment of congestive heart failure and their proper and appropriate use can alleviate peripheral and pulmonary oedema. Diuretics should not be overused and care should be taken to avoid hypokalaemia. Controversy surrounds the use of digoxin in patients in sinus rhythm; the drug should be used in patients in atrial fibrillation. The use of an inotropic drug may be harmful in the presence of coronary artery disease. A reduction in the current use of digoxin might be of benefit to many patients with heart failure. When the drug is prescribed it should be used in a therapeutic and not homeopathic dose. Recent interest has been directed toward the use of vasodilators and the angiotensin-converting enzyme inhibitors in patients with heart failure. In my opinion, these drugs should be used after patients have been treated with thiazide and loop diuretics. Vasodilators are particularly beneficial in acute heart failure or in patients with chronic heart failure when the symptoms are related to fluid overload and volume expansion. The cause of symptoms in patients with chronic heart failure optimally treated with diuretics is controversial. Shortness of breath may not be simply related to the left atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changing ideas in the treatment of heart failure--an overview. 330 Sep 78

Experimental and clinical experience with compounds containing antimony have shown that the trivalent compounds are generally more toxic than the pentavalent ones. APT can cause severe pain and tissue necrosis and is therefore not given by intramuscular or subcutaneous injection. APT has the actions and uses of AST, but it is less soluble and more irritating than the sodium salt which is therefore more suitable for intravenous use. Trivalent antimony compounds are toxic when used topically. Adverse effects are similar for all trivalent compounds, and include nausea, vomiting, weakness and myalgia, abdominal colic, diarrhoea, and skin rashes, including pustular eruptions. Hypersensitivity reactions also occur. Respiratory symptoms include cough, dyspnoea, and chronic lung changes. Cardiotoxicity is the most important and may produce arrhythmias, myocardial depression and damage, Stokes-Adams attacks, heart failure, and cardiac arrest. Hepatic damage and necrosis, as well as blood dyscrasias, may occur. Toxic effects on the kidney may follow chronic use. Continuous treatment with small doses of antimony may give rise to symptoms of subacute poisoning, similar to those of chronic arsenic poisoning, due to accumulation of antimony in the body, especially if trivalent compounds are used, because of their long biological half-lives. Reproductive disorders and chromosome damage have been reported; antimony compounds are, therefore, potentially toxic to reproduction and have mutagenic, and oncogenic potential. Antimony compounds should, therefore, not be used during pregnancy or in the presence of hepatic, renal, or heart disease. Pentavalent antimony preparations especially the organic compounds, together with non-metallic synthetic preparations, such as the diamidines, have now replaced APT for use in leishmaniasis. Because of the toxicity of antimony compounds, investigations have been undertaken to reduce their adverse effects by combining them with chelating agents. These preparations appear to have reduced the toxic effects of antimony without affecting the efficacy of the preparations. Liposome-encapsulated antimony products have, more recently, been shown to be much less toxic because of the reduced dose of the antimony compound required for effective therapy. The historical uses of antimony were based on the belief that the topical and systemic adverse effects, for example, skin eruptions and diarrhoea and vomiting, were signs that the condition being treated was responding by being brought to the surface to relieve congestion at the diseased area. There is no evidence in topical use, but there is evidence that such use can cause severe reactions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Toxicity of antimony and its compounds. 330 36


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