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

Artificial subtraction of fluids and solutes was evaluated in the course of acute and chronic heart failure when it became refractory to standard intensive medical treatment. A group of 19 patients (mean age 57 years), 9 with ischemic, 2 amyloidotic, 4 valvular, and 4 idiopathic cardiomyopathy, were treated. In 17 patients extracorporeal ultrafiltration (UF) by means of a polysulfonate ultrafilter was adopted along 125 sessions (105 assisted by a roller pump and 20 as a slow continuous ultrafiltrate). In two patients continuous peritoneal dialysis was adopted. In every case UF was well tolerated. Ultrafiltrate volumes ranged from 1680 to 3500 ml for every session with corresponding Na losses ranging from 194 to 434 mEq/session. Improved clinical and functional status with reduction of edema was observed in 17 of 19 patients. In 12 patients UF could be discontinued due to restored response to diuretics; 5 of these patients could subsequently undergo heart surgery (1 transplant, 3 valve replacement, 1 coronary bypass). The remaining 7 patients survived on medical therapy alone for an average of 228 days. In 7 of 19 cases, UF could not be discontinued, and these patients died after an average of 23 days of treatment. In conclusion, UF proved to be effective in eliminating salt-fluid overload and restoring response to medical treatment. Patients who are potential surgical candidates seem to be the most suitable for UF.
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PMID:Ultrafiltration in the treatment of refractory congestive heart failure. 341 11

Treatment of heart failure comprises the use of diuretics, vasodilators and inotropic substances. Unloading of the heart and the circulation in hydropic states is classically achieved with diuretics. The retention of salt and water in chronic heart failure requires chronic treatment with diuretics. This mode of treatment is basic to all forms of hydropic heart failure. Inotropic substances such as digitalis glycosides, sympathomimetic amines or phosphodiesterase inhibitors have certain disadvantages: Inotropic stimulation increases energy demand of the working heart muscle. Most of the substances used today increase energy consumption inordinately, thereby decreasing economy of myocardial contraction. This aspect calls for caution in the application of these substances in chronic heart failure, although they seem indispensable (sympathomimetic amines) in acute hypotensive failure and shock. Digitalis glycosides, basically suited for longterm treatment, exert only mild inotropic effects. In addition inotropic stimulation brings with it arrhythmogenic effects. All inotropic substances can induce ventricular arrhythmias already at therapeutic levels. Vasodilating substances have found increasing acceptance as a particularly useful and safe group of drugs for the treatment of heart failure. Nitrates: With the different nitrate compounds and nitrate preparations an effective venodilation with preload reduction can safely be achieved. At higher doses, arteriolar also dilatation can be induced. Although tolerance may be a problem with chronic application, this can be avoided with prudent dosing. The strong venodilating property makes these drugs together with their rapid onset of action ideally suited for the treatment of acute heart failure with pulmonary congestion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of heart failure: status of therapy with vasodilator agents]. 343 15

Cardiac (or myocardial) failure, a major health problem, can be defined using physiologic criteria that consider the adequacy of O2 delivery relative to the body's O2 requirements. In clinical terms, cardiac failure may be described in terms of its chronicity or the extent to which signs and symptoms of right- versus left-sided heart failure are dominant. Congestive heart failure is a clinical syndrome that consists of a constellation of signs and symptoms that arise from congested organs and hypoperfused tissues. Acute cardiac failure occurs because of a decrease in myocardial contractility that can be offset by the Frank-Starling mechanism. In chronic cardiac failure dilatation and myocardial hypertrophy serve to restore ventricular function. Other compensatory responses that are invoked include a salt avid kidney, which mediates an expansion of the intravascular space, and the activation of the adrenergic nervous and renin-angiotensin-aldosterone systems and an increase in circulating arginine vasopressin. The management of acute and chronic cardiac failure can be derived from an understanding of the pathophysiologic mechanisms responsible for their appearance and include improving cardiac performance, as well as the distribution of systemic blood flow to tissues based on physiologic priorities and moment to moment variations in O2 requirements.
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PMID:Pathophysiology of acute and chronic cardiac failure. 361 18

Central haemodynamics and regional blood flow were studied comprehensively in conscious New Zealand White rabbits before and during the development of chronic low output cardiac failure produced by administration of the anticancer agent adriamycin. After eight weeks of adriamycin treatment, cardiac index fell from 326(40 to 225(56) ml.min-1.kg-1. This was accompanied by an increase in heart rate and total peripheral resistance but no change in mean systemic blood pressure. Myocardial function was shown to be depressed by the measurement of Frank-Starling curves, the slopes of which were appreciably flatter in adriamycin treated rabbits. Regional blood flow (measured by the radioactive microsphere technique) was redistributed. There were decreases in renal, splenic, small gut, and skeletal muscle blood flow, whereas myocardial and cerebral blood flow were unchanged. There was an increase in total body exchangeable sodium, indicating some salt and water retention. Systemic toxic effects of adriamycin could be limited by treating the animals for eight weeks with adriamycin and then allowing a two week recovery period before haemodynamic study. This would appear to be the optimal dosage schedule.
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PMID:An experimental model of chronic cardiac failure using adriamycin in the rabbit: central haemodynamics and regional blood flow. 366 39

We have studied the efficiency of urea in the treatment of hyponatremia and hydrosaline retention in a 76-year-old man with chronic ischemic congestive heart failure. Since increase of furosemide worsened the hyponatremia (120 mmol/l), 30 g/day of urea was added and induced the following changes: progressive weight loss (6.5 kg in one week), increased diuresis (from 0.750 to 1.950 l/day), increased salt excretion (from 40 to 165 mmol sodium/day) and correction of the hyponatremia (120 to 136 mmol/l). Blood urea and creatinine serum concentrations rose moderately without significant change in creatinine clearance (32 to 38 ml/min). No adverse effects related to urea administration were observed. Urea intake seems to be useful in the management of hyponatremia in our patient with cardiac failure.
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PMID:Urea treatment for water retention in hyponatremic congestive heart failure. 366 93

Peripartum heart disease is reviewed in the light of reports in the literature and personal experience from the University College Hospital, Ibadan. It is concluded that it is worldwide in distribution but appears most commonly in multiparous black women with a low socioeconomic background. The clinical features are the same as those of dilated cardiomyopathy, with the exception of cases from Zaria, northern Nigeria, where heart failure may be induced by high salt and fluid intake. The possible causes of peripartum heart disease are reviewed. Glomerulonephritis, toxemia of pregnancy, and malnutrition have not been shown convincingly to be causal, and infection, hypertension, and alcoholism have been suggested. Hypertensive heart failure and toxemia of pregnancy can induce peripartum heart disease. It is concluded that the myocardial disorder in peripartum heart disease is probably the same condition as dilated cardiomyopathy, and that infection may be an important element. However, diverse other factors may also play a part.
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PMID:Peripartum heart disease. 384 85

Renal digoxin clearance was compared in patients suffering from atrial fibrillation with well preserved cardiac function (n = 9; salt intake +/- 170 mmol daily) and patients with chronic congestive heart failure (n = 10; salt intake 50 mmol daily and maintenance treatment with diuretics). There was no difference between the groups concerning digoxin dosage, creatinine clearance, diuresis or sodium excretion in the urine. Digoxin clearance in chronic heart failure proved to be significantly lower than in atrial fibrillation (48 +/- 21 vs 71 +/- 36 ml X min-1, p less than 0.05), and Cdig/Ccreat was similarly reduced at 0.73 +/- 0.15 compared to 1.09 +/- 0.27 (p less than 0.005). Steady state serum digoxin concentration was significantly higher in patients with congestive heart failure (1.44 +/- 0.47 vs 0.87 +/- 0.33 micrograms X 1(-1), p less than 0.01). Chronic congestive heart failure is a state with reduced digoxin clearance by the kidney, which could lead to digoxin intoxication not explicable by overdose, reduced renal function or the effect of interacting drugs.
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PMID:Decreased renal clearance of digoxin in chronic congestive heart failure. 400 28

Peripartum cardiac failure (PPCF) is common in Zaria, in northern Nigeria, but has not been described elsewhere in Nigeria except in Ibadan. The geographic origin of a series of 224 patients with PPCF was studied in Zaria, and a survey of the syndrome as seen in hospitals and by physicians in the northern states of Nigeria was carried out; information was also gathered from medical and nursing students from various tribal groups in the same area. It was found that PPCF is only common in the areas of Hausa majority, mostly around Zaria and Malumfashi, where the postpartum practices of taking hot baths, lying on a hot bed, and taking large amounts of kanwa (a lake-salt rich in sodium) are pursued with great vigour. These customs may impose a critical load on a vulnerable myocardium, and it seems that tribe and tradition could well explain the high incidence of PPCF around Zaria.
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PMID:Perpartum cardiac failure. An explanation for the observed geographic distribution in Nigeria. 454 86

Ten years of experience with three different converting enzyme inhibitors (CEI; teprotide, captopril and enalapril) in over 300 hypertensive patients reveals that CEI act largely to block renin-angiotensin mediated vasoconstriction. Thus, their effectiveness or lack of it is predicted by the baseline plasma renin measurement. Accordingly, responses to these pharmacological agents can be used to identify and quantify renin-mediated vasoconstriction in the spectrum of hypertensive diseases. The converse is also generally true. Patients failing to respond to CEI exhibit low renin values and their increased peripheral resistance appears related to other mechanisms, possibly involving a subtle increase in total body sodium. Thus, low renin states such as low-renin essential hypertension, primary aldosteronism, and anephric man exhibit little or no response to CEI. The relationship between the renin system activity and effectiveness of CEI reflects a specific interference with a particular pathogenic mechanism which is further supported by the fact that two other types of renin system inhibitors (beta-blockers and saralasin) are similarly effective or ineffective according to the operant renin profile also by studies in patients with congestive heart failure without hypertension in whom the same relationships can be demonstrated. Like hypertensives, heart failure patients exhibit a broad spectrum of renin activity values, and their pretreatment renin levels predict the responses to CEI. We have also found that plasma renin values in heart failure are dependent on sodium intake. When salt is administered, renin falls and patients then become unresponsive to CEI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Converting enzyme inhibition to identify and treat renin-mediated or sodium-volume related forms of increased peripheral resistance in hypertension and in congestive heart failure. 608 35

Angiotensin converting enzyme inhibitors are effective therapy in hypertension. They are particularly useful in severe drug resistant or accelerated hypertension, in renal hypertension and in hypertensive heart failure. Although their exact mode of action has not been determined it is a consequence of the inhibition of angiotensin converting enzyme. They offer distinct advantages over conventional drugs in the treatment of high blood pressure particularly as they have no central or autonomic side effects and as a consequence the patients feel well. There is no postural effect on blood pressure and patients retain their normal cardiovascular reflex mechanisms and sexual function. They are particularly useful when combined with diuretics or salt restriction as not only do they have additive hypotensive effects but angiotensin converting enzyme inhibitors prevent the secondary hyperaldosteronism and hypokalemia associated with diuretic administration. Lastly, unlike many other forms of treatment for hypertension, renal blood flow and renal function tend to be maintained with converting enzyme inhibitors. Their overall role in the management of hypertension has yet to be determined, and the ultimate incidence of adverse effects after prolonged therapy is not yet known. They are however, an exciting new development in the treatment of hypertension.
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PMID:Treatment of hypertension with angiotensin converting enzyme inhibitors. 609 8


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