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)

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

The long-term prognosis in severe congestive heart failure is very poor. Therapeutic regimens, in order to improve prognosis, should directly or indirectly influence the compensatory systems that are activated, ACE-inhibitor therapy has emerged as an important regimen in this context. In the CONSENSUS-trial (3), we could demonstrate that the addition of enalapril to conventional therapy in severe CHF significantly improved survival. The experience from this study forms the background for the recommendations in this work. 253 patients with severe heart failure (New York Heart Association (NYHA) Classification functional class IV) were randomized at 35 Scandinavian centers to placebo (n = 126) or enalapril (n = 127), in addition to their conventional therapy. The treatment dose of enalapril varied between 2.5 and 40 mg daily (man 18.3 mg). Blood samples for measurement of serum electrolytes and serum creatinine were taken repeatedly during follow-up. There seems to be about a 10% increase in creatinine within 2 weeks of initiating enalapril therapy. This increase seems to be independent of baseline creatinine level. Adverse experience regarding serum creatinine was reported in 22 placebo-treated patients and in 51 patients in the enalapril group. This reporting was based upon the investigators' feelings of significant importance of the observation and not on symptomatology. This was the main reason for permanent withdrawal in 2 and 7 patients, respectively. During initiation of enalapril therapy the blood pressure response is important after the very first dose, but for renal function the response may not appear until several days later. However, in most patients there are no problems with starting enalapril.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of ACE-inhibition on renal function in severe congestive heart failure. 202 43

Infectious heart diseases in childhood are--with less than 1% of hospital admissions--rare, but serious diseases. Among several causes of myocarditis in our region virus myocarditis plays the most important role. Besides of the acute course an autoimmune mediated chronic myocarditis and the transition to dilated cardiomyopathy are observed. The patho-histological assessment depends also on subjective influences. Clinical diagnosis is based on cardiac symptoms (Adams-Stokes, congestive heart failure, LV-dilatation), ECG-changes with increased enzyme levels and positive virus-serology or endomyocardial biopsy. Immunoserology and -histology as well as in-situ-hybridization can support diagnosis, echocardiography and eventually heart catheterization exclude other causes. In respect to therapy, ACE-inhibitors are a substantial improvement of conventional therapy of heart failure, while immunosuppressive therapy of chronic myocarditis has to assessed.
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PMID:[Myocarditis in childhood]. 202 60

A prospective study was carried out to investigate the effects of the ACE inhibitor captopril on glucose tolerance in 14 elderly patients, aged 76 to 89 years, who had co-incident cardiac failure and stable Type II diabetes mellitus. Patients were maintained on their diet and diabetic therapy and were given 12.5 mg captopril twice daily. Clinical findings, including signs of cardiac failure, body weight and blood pressure, biochemical profile and chest X-ray appearance were documented at each visit. Blood glucose tolerance testing was carried out immediately before starting captopril and again 28 days later. A reduction in symptoms of heart failure occurred in all patients and 5 of them reduced their New York Heart Association grade of heart failure. Significant improvement in glucose tolerance occurred in all patients. Four were able to reduce hypoglycaemic therapy and 1 was able to stop his hypoglycaemic agents. This potentially valuable additional benefit of captopril in improving glucose tolerance has not yet been shown to occur with other ACE inhibitors.
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PMID:Effects of captopril on glucose tolerance in elderly patients with congestive cardiac failure. 204 97

It is now established that ACE-inhibitors are effective in the treatment of severe chronic heart failure; in addition to digitalis and diuretics. Furthermore, recent studies suggest, that beneficial effects of ACE-inhibitors can be expected in patients with moderate heart failure: when combined with diuretics. In atrial fibrillation, the combination with digitalis is recommended. Up to now, there is no clear evidence that monotherapy with ACE-inhibitors is superior to first line therapy with diuretics or digitalis. Nevertheless, initial (and limited) experience favors the use of ACE-inhibitors to prevent progressive LV-dysfunction following myocardial infarction. Based on experimental data, several additional mechanisms of action (besides unloading the heart) have been proposed; which may open up new indications for ACE-inhibition, such as antiarrhythmic, antiischemic or antiproliferative effects (including decreased incidence of coronary restenosis following angioplasty). If confirmed by clinical studies, the indications for ACE-inhibitors will expand considerably, putting emphasis on prevention of occurrence and progression of heart failure rather than treatment of very late stages of chronic heart failure. Yet, the Consensus trial demonstrated a significant impact of these agents on mortality in the latter patient population.
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PMID:[The role of ACE-inhibition in the therapy of chronic heart insufficiency]. 213 55

Sudden death has been shown to be due in the majority of cases to ventricular arrhythmia. Left ventricular hypertrophy (LVH) may be implicated in the aetiology of some arrhythmia and sudden death. Recent evidence suggests that the relationship between LVH and arrhythmia may be complex and that there may be an interaction with serum potassium levels. ACE inhibitors have been shown to be anti-arrhythmic in heart failure. Although other vasodilators have been shown to be anti-arrhythmic, ACE inhibitors also raise serum potassium levels and this may therefore be of importance to their anti-arrhythmic activity. In LVH, their antiarrhythmic potential may be greatest in those who are potassium depleted.
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PMID:ACE inhibitors and the heart: hypertrophy reversal and antiarrhythmic effects. 214 90


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