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

Congestive heart failure (CHF) is characterized by activation of (i) vasopressor and antinatriuretic influences (ii) and by counter-activation of vasodilator natriuretic systems. The former comprise the sympathoadrenal, renin-angiotensin-aldosterone and arginine vasopressin systems, and possibly endothelin and withdrawal of endothelium dependent relaxing factor respectively. The latter include the prostaglandins (PGE-2, PGI-2), dopamine and atrial natriuretic factor. The response of the kidney to chronic heart failure, i.e. vasoconstriction and antinatriuresis, resembles the renal reaction to volume depletion. The adverse renal effects of ACE inhibitors in some patients with advanced congestive heart failure may be explained by lowering of renal perfusion pressure and dependence of glomerular filtration rate on angiotensin II.
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PMID:The kidney in congestive heart failure. 191 36

The paper confirms the value of captopril in a sample group of 20 elderly patients (mean age 72.9 years) affected by overall cardiac decompensation in more or less clinically evident phases. All patients were randomly selected and received ACE-inhibition treatment for six months; doses of 25 mg or 50 mg captopril were given twice a day and all other drugs were suspended except for digitalis which was used by all patients without success. During the course of the trial the most important clinical results were the reduction of systemic blood pressure due to the diminution of peripheral resistance, the reduction of postload and ventricular filling pressure, and the consequent improvement of cardiac decompensation. All elderly patients treated in this manner experienced a stable improvement in the quality of life, with a considerable reduction in the consumption of diuretics to which they are particularly vulnerable. Following a broad ranging comparison with other reports, the Authors conclude that captopril is a geriatric drug which should be used as early as possible during the phases of latent cardiac insufficiency or at the first signs of a hypertensive crisis.
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PMID:[Captopril in heart failure in the elderly]. 192 93

One hundred and sixty four (164) patients were evaluated. Sixty (60) with Sickle cell disease (SSHg.) and ninety seven (97) with Trait (ASHg.); seventeen (17) were normal control group. The study confirmed that the incidence of cardiomyopathy in Trait (ASHg.) is greater than reported by other clinical investigations. Cardiac arrhythmia, atrial fibrillation, premature ventricular contractions, bundle branch blocks, and T and ST modifications with sub epicardial isquemia were most significant electrocardiographics changes. The possibility of myocardial infarction in SS patients with low or normal hemoglobin is significant. M-Mode and 2-D echo, demonstrated similar end diastolic volumes in AS and SS patients in which cardiomyopathy were diagnosticated. Patients with cardiac failure, treated with cardiotonics, diuretics and ACE were compensated most frequently. To prevent hemosiderosis, antioxydant (alfatocoferol and Ubiquinones) were used with satisfactory response.
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PMID:[Echocardiographic assessment of patients with sickle cell anemia]. 192 6

Inhibitors of angiotensin-converting enzyme are used commonly nowadays for the treatment of hypertension and cardiac failure. Over the past two years, shortly after the introduction of this type of drug the occurrence of acute renal failure mainly in elderly patients has been reported. The authors have insisted that strict control of renal function and electrolytes are necessary before and after administration of an ACE inhibitor. Particular caution is needed in patients with severe atherosclerotic disease, especially if bilateral (or unilateral in patients with a single kidney) renal arterial stenosis is present or suspected. Considering these limitations ACE inhibitors remain well tolerated and beneficial cardiovascular drugs.
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PMID:[Converting enzyme inhibitors and acute renal insufficiency--precautions to be taken]. 192 94

In the treatment of heart failure-also in the aged-digitalis preparations remain indispensable. At the present time, in particular in combination with diuretics and ACE inhibitors, they are experiencing a revival in the treatment of severe stages (NYHA stages III and IV). In addition, a spectrum of newly developed positive inotropic substances of various classes is now available. Among the catecholamines, apart from dopamine, dobutamine and their derivatives, new drugs with a beta-adrenergic agonistic effect are presently undergoing clinical testing. Another heterogeneous group of substances combine positive inotropic with vasodilatory properties. In this connection, mention might be made of the phosphodiesterase inhibitors, the H2 receptor antagonists, and certain catecholamine derivatives. However, digitalis remains the only substance that can be given orally over the long-term without tolerance developing. Particular aspects of the use of digitalis in geriatric patients are discussed.
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PMID:[Positive inotropic substances. Possible use in heart failure in the aged]. 193 36

ACE inhibition may be useful in several manifestations of ischaemic heart disease, such as heart failure due to ischaemic cardiomyopathy. Recent evidence suggests that these effects may also be present in normotensive patients with ischaemic heart disease without heart failure. Theoretically, converting-enzyme inhibition, through coronary and systemic vasodilating effects and negative inotropic properties, should have a favourable effect on the myocardial oxygen supply/demand ratio and, hence, affect the incidence and severity of myocardial ischaemia. It is doubtful, however, whether these cardiac and extracardiac properties of ACE inhibitors really underlie its potential antiischaemic effects, at least in the average patient with ischaemic heart disease without concomitant heart failure and hypertension. Recent animal and human studies indicate that converting-enzyme inhibitors may modulate myocardial ischaemia by reducing ischaemia-induced circulating neurohumoral activation. It has been shown that, depending on the severity of ischaemia, the circulating renin-angiotensin system may become activated together with an increase in circulating catecholamine levels. ACE inhibition suppresses this neuroendocrine stimulation during ischaemia and modulates subsequent systemic and, presumably, also coronary vasoconstriction. In addition to these effects on circulating neurohormones, ACE inhibition could affect myocardial ischaemia through a number of local actions, e.g. modulation of tissue (cardiac) angiotensin II formation and bradykinin breakdown, stimulation of prostaglandin synthesis and, in the use of sulphydryl compounds, by affecting EDRF formation. Whether ACE inhibitors have clear antiischaemic effects in all clinical conditions is uncertain. Their efficacy to limit exercise-induced ischaemia has been questioned. In contrast, pacing-induced ischaemia in patients at rest is clearly prevented by ACE inhibition. This differential effect may be related to a more pronounced difference in circulating neurohormones during exercise per se. It also suggests that ACE inhibitors may be particularly useful as (additional) antiischaemic therapy in patients with angina at rest, e.g. unstable angina and the acute phase of myocardial infarction.
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PMID:Neurohumoral activation during acute myocardial ischaemia. Effects of ACE inhibition. 197 98

There are two goals in the management of chronic heart failure: relief of symptoms and prolongation of life. Until recently, pharmacological interventions were tested primarily in order to evaluate their effects on exercise capacity and clinical symptoms. However, two multicenter trials have now provided evidence that treatment of chronic heart failure is able to improve mortality. Indeed, prolongation of life without improving symptoms is not desirable. The two classic keystones of therapy in heart failure, diuretics and digitalis, remain powerful agents to relieve symptoms. However, their impact on survival remains elusive, since no controlled studies are available which address this question with adequate sample size. Vasodilators such as the combination of hydralazine and isosorbide dinitrate and ACE-inhibitors, however, have been shown to improve survival in patients with moderate to severe chronic heart failure. In contrast, prazosin failed to be effective in this respect. More sophisticated questions emerge, in particular, do ACE-inhibitors or vasodilators, effectively interfere with the progression of the disease? May early treatment be preventive and retard the course of heart failure? Several large scale multicenter trials are now under way to address these issues.
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PMID:[Chronic heart failure: improvement of the prognosis by therapy?]. 197 16

Cardiac muscle cell hypertrophy, hyperplasia of connective tissue, abnormal peripheral circulation and metabolic changes in the cardiac fibre and in the smooth muscle cell as a consequence of mechanic overload are described in variable proportions in heart failure. These changes in turn are essential factors for progression of the disease. Results of early drug intervention in patients with few or no symptoms suggest that decrease of mechanic overload by vasodilator therapy slows down the progression of the disease. In late stages, treatment with diuretics and vasodilators improves the symptoms and the outcome of heart failure. Diuretics alone and inotropic positive substances bring about some improvement of symptoms and maximal oxygen consumption, but they have no favourable effect on the outcome. Positive inotropic substances remain restricted to late forms of heart failure, in which they seem to ameliorate symptoms but have a rather unfavourable effect on the outcome. The role of diuretics, ACE inhibitors and digoxin is well defined. This is not the case for newer calcium-channel blockers from the dihydropyridine group, of beta blockers, of phosphodiesterase inhibitors and of substances with partial beta agonist and partial beta blocking activity. These drugs must still be classified as experimental agents for the treatment of heart failure.
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PMID:[Current problems of pharmacotherapy--heart failure]. 197 5

The role of ACE-inhibition for the treatment of congestive heart failure has been established over the last decade. In patients with moderate and severe congestive heart failure long-term beneficial effects on symptoms may be achieved in 60-70%. Mortality is significantly improved in patients with congestive heart failure functional class NYHA IV. Therefore, ACE-inhibitors are superior to other vasodilators. Hypotension represents an important side effect of ACE-inhibitors. It is predominantly due to either inhibition of systemic and/or local angiotensin II formation or to reduce degradation of bradykinin. If the activity of the renin-angiotensin system is stimulated, as in severe congestive heart failure and/or by diuretic pretreatment, the risk for the occurrence of hypotension is therefore increased. With respect to these risk factors, small doses of ACE-inhibitors should be administered initially, e.g. captopril 6.25 mg or enalapril, 2.5 mg. Recently, two large trials demonstrated the safety of enalapril, a long-acting ACE-inhibitor, regarding the occurrence of hypotension in patients with congestive heart failure. The overall incidence of hypotension is about 2-4% in mild to moderate and about 5-8% in severe heart failure. Reduction of the dosage of the ACE-inhibitor or the diuretic drug usually results in normalization of blood pressure, allowing continuation of therapy with ACE-inhibitors.
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PMID:[Side effects of vasodilator therapy in heart failure: risk of hypotension with ACE inhibitors]. 202 38

In 33 patients with heart failure (NYHA II-III) the 24-h blood pressure was examined during the titration of two ACE-inhibitors. Blood pressure was measured by the oscillometric method using the blood pressure monitor 90202 from SpaceLabs, Inc.. All patients received an additional therapy either with captopril (group A, n = 17) or enalapril (group B, n = 16) in random order. Serum-electrolytes, serum- and urine-creatinine, and plasma-renin- activity were measured before and during therapy with both ACE-inhibitors. 24-h blood pressure measurements were taken before and on the first and fifth days of the treatment with ACE-inhibitors. Neither group was different with respect to the degree of heart failure, the concomitant medication, and the 24-h profiles of blood pressure and heart rate. The mean initial dose of captopril was 9.2 +/- 1.2 mg which was titrated to a mean daily dose of 40.7 +/- 3.3 mg given three-times daily. Each patient of group B received an initial dose of 2.5 mg enalapril and a mean maintenance dose of 8.4 +/- 0.9 mg once daily. The first dose effect on blood pressure was similar with captopril and enalapril with a maximal decrease of systolic and diastolic blood pressure of 8/8 mmHg (after 1 h) in group A and of 9/7 mmHg (after 4 h) in group B. The 24-h blood pressure values on day 5 were consistently below the pretreatment values (p less than 0.005) but heart rate was not significantly affected by either ACE-inhibitor. Neither group differed significantly during ACE-inhibition in their 24-h blood pressure and heart rate profiles.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Enalapril versus captopril in heart failure--effect on blood pressure and kidney function]. 202 41


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