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

Twenty-nine patients with severe heart failure (NYHA III) were randomly assigned to receive therapy with an angiotensin converting enzyme inhibitor (ACE inhibitor), either captopril or enalapril. The mean daily dosage of captopril was 56 +/- 5 mg and of enalapril 9.5 +/- 0.4 mg. After a mean of 8 +/- 1 days, the influence of both ACE inhibitors on hemodynamics and renal function was compared. The mean arterial pressure in the group treated with captopril (Group A) fell by 9 +/- 3 mmHg (p less than 0.01), and in the group treated with enalapril (Group B) it fell by 12 +/- 3 mmHg (p less than 0.001). The difference between the groups was not significant. Heart rate decreased in both groups; however, the change was significant (p less than 0.05) only in patients treated with enalapril (-11 +/- 3 bpm in Group B vs. -7 +/- 4 bpm in Group A). Stroke volume index increased by 6 +/- 3 ml/m2 in Group A (p less than 0.05) vs. 10 +/- 2 ml/m2 in Group B (p less than 0.01). The increase in stroke volume index was not significantly different between the two groups. Mean decreases in pulmonary artery and right atrial pressure were also comparable in both groups. Thus, hemodynamic improvements were similar during therapy with either captopril or enalapril. Serum sodium and potassium before therapy were 137 +/- 1 mmol/l and 4.1 +/- 0.1 mmol/l, respectively, in group A and 139 +/- 1 mmol/l and 4.0 +/- 0.1 mmol/l, respectively, in group B.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of captopril with enalapril in the treatment of heart failure: influence on hemodynamics and measures of renal function. 139 Mar 31

Angiotensin converting enzyme inhibitors (ACE-I) are widely used in patients with severe heart failure on the basis of the significant improvement in mortality in the CONSENSUS-I trial in patients with Class IV heart failure. Recent data from the 5-year clinical trial Studies of Left Ventricular Dysfunction (SOLVD) suggest a role for ACE-I in patients with mild to moderate heart failure as well as in those with asymptomatic left ventricular dysfunction. The SOLVD treatment trial in patients with a left ventricular ejection fraction (LVEF) less than or equal to 35% and treated for heart failure with conventional therapy including digitalis, diuretics, or vasodilators demonstrated that the addition of enalapril resulted in a significant reduction in mortality from heart failure as well as in the combined end point of death plus hospitalization from heart failure. These data suggest that ACE-I should be the base of therapy for patients with mild to moderate heart failure, as well as for those with severe heart failure.
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PMID:Congestive heart failure: new therapeutic strategies. 139 11

Congestive heart failure is a syndrome common in the United States, especially in elderly patients. The most common etiology is coronary artery disease. A number of general factors contribute to the heart failure syndrome, including loss of muscle, decreased myocardial contractility, pressure or volume overload, or restricted filling. All of these factors may play a role in a given patient as, for example, with coronary artery disease. Although systolic dysfunction with a reduced ejection fraction is the most common heart failure syndrome, up to 40% of patients may have a relatively preserved ejection fraction with diastolic dysfunction. As the heart begins to fail, a number of compensatory mechanisms are activated. These include increased heart rate, the Frank-Starling mechanism, increased catecholamines, activation of the renin-angiotensin system, and release of atrial natriuretic peptides. Although these mechanisms are initially helpful to the cardiovascular system, they frequently overshoot, initiating a vicious cycle. For example, with a decrease in cardiac output, there is a reflex increase in systemic vascular resistance in order to maintain perfusion pressure. This increase in resistance, however, acts as a load on the left ventricle and further reduces cardiac output. The best evidence for the existence of this vicious cycle is the beneficial change in hemodynamics produced by vasodilator drugs and the ACE inhibitors. Thus, an understanding of pathophysiology allows for the selection of rational therapy. An unresolved problem in heart failure patients is how best to reduce the high incidence of sudden death, which is one of the major challenges for the future.
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PMID:Pathophysiology of congestive heart failure. 139 15

During the past years, several large trials (Consensus, VHEFT I and II, SOLVD) have shown a significant reduction of mortality in patients with moderate and severe heart failure. However, despite effective treatment with vasodilators, digitalis and diuretics mortality in these patients remains unacceptable high. It seems logic, to state treatment at an earlier stage of the disease to achieve more benefit. The main early pathophysiological disturbance is left ventricular hypertrophy, resulting from hypertension, coronary artery disease, increasing age and obesity. On the long run, LVH may lead to diastolic and systolic heart failure, myocardial ischemia, arrhythmias and sudden death. With ACE-inhibitors LVH can be reduced within 1 month of treatment. The large SAVE- and SOLVD-prevention trials will show, whether this early intervention will improve proposis in patients with asymptomatic heart failure.
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PMID:[Early therapeutic intervention in heart failure]. 141 67

In a longitudinal study comprising a total of 18 patients, the paradoxical time course of hANP plasma levels, i.e. the reproducibility of the low levels previously reported in cases of extreme cardiac insufficiency after administration of amiodarone, was investigated over a period of 9 months. At the same time, the effect of the degree of cardiac insufficiency and arrhythmia on the secretion of hANP was observed. The patients had been admitted to hospital because of the diagnoses "cardiac insufficiency secondary to cardiomyopathy" or "Grade IVb arrhythmia according to Lown's classification". During in-patient treatment, antiarrhythmic therapy was commenced in all patients. Clinical examinations and determinations of humoral parameters during therapy showed a substantial number of patients, who exhibited no increase in hANP levels despite massive cardiac decompensation. As far as drug therapy of patients with severe arrhythmias secondary to congestive (dilated) cardiomyopathy is concerned, amiodarone has proved to be the drug of choice in combination with digitalis, ACE inhibitors and diuretics. There is a close correlation between the degree of cardiac insufficiency and plasma hANP levels.
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PMID:[Effects of treatment of arrhythmias requiring therapy in dilated cardiomyopathy with amiodarone on alpha human atrial natriuretic peptide]. 141 68

1. Intravenous ACE inhibitor therapy is of increasing importance in the treatment of patients with unstable heart failure after myocardial infarction. Available pharmacokinetic and concentration effect data with this route of administration are limited. 2. The pharmacokinetics and blood pressure responses to perindoprilat were studied during prolonged low dose (1 mg) infusions in eight normotensive salt replete male volunteers. 3. Subjects received randomised, single (subject) blinded therapy with saline placebo (30 ml) over 3 h or active treatment (1 mg in 30 ml) over 1 h, 3 h or 6 h by constant rate infusion. 4. Significant falls in blood pressure greater than placebo were noted with active infusions without changes in heart rate. Mean maximal plasma perindoprilat concentrations reflected the rate of infusion (1 h, 51.5 +/- 11.4 ng ml-1; 3 h, 30.4 +/- 8.4 ng ml-1; 6 h 19.0 +/- 4.0 ng ml-1) and mean maximal plasma ACE inhibition was less with slower infusions (1 h, 95.7 +/- 0.5%; 3 h 92.3 +/- 2.7%; 6 h 87.4 +/- 5.1%, P less than 0.013). 5. Concentration-time profiles showed a sigmoid drug accumulation profile with delay in the early accumulation of drug particularly during the 3 h and 6 h infusions. The pharmacokinetic data was assessed by statistical comparison of a hierarchy of standard compartmental models and non linear saturable binding models. A non linear model incorporating elements to describe both tissue and plasma binding of the drug provided the best fit to observed data. 6. Low dose constant rate infusions are a means of optimising intravenous ACE inhibitor therapy to allow individual dose titration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies with low dose intravenous diacid ACE inhibitor (perindoprilat) infusions in normotensive male volunteers. 141 73

Traditional therapy for heart failure (diuretics, digitalic compound, vasodilators, inodilatory ACE-inhibitors) cannot arrest the progressive overloading of the circulatory system so that it is inevitable that a refractory stage to all forms of treatment will be reached when more specialised techniques, such as heart transplant and ultrafiltration will be needed. The paper reports the results obtained in 13 patients in ultrafiltration treatment for refractory heart failure: in the majority of these, a marked improvement in general conditions (edema, dyspnea) was recorded together with a regression from class 5 to class 3 NYHA in 5 patients, and to class 2 for others. The ultrafiltration method in spite of not altering the prognosis which remains negative in these patients, allow those waiting for heart transplant to survive and may improve their chances of surviving heart surgery.
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PMID:[Use of ultrafiltration in refractory cardiac decompensation]. 146 35

Recent concepts about post-infarction left ventricular remodeling, which is the basis for heart failure in these patients, as well as its prevention by ACE inhibitors are briefly summarized. Those data were the rationale for the SAVE trial. The most important initial aspects of this trial (general objective, pre-specified endpoints, inclusion and exclusion criteria, etc.) are then described as well as the basal characteristics of the respective cohort. The most important results of the SAVE trial, now in press, are subsequently presented. Several clinical guidelines, derived from these results, are then suggested. Finally, some new questions, both clinical and pathophysiological, and originated by the results from the SAVE results, are commented.
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PMID:[The SAVE trial: rational basis, results, and reflections]. 147 63

In a retrospective study we analyse two populations of aged patients in congestive heart failure, one treated with ACE inhibitors other not and the other with conventional therapy. Both populations received the same medication (diuretics and digitalis) and are equivalent in age, sex distribution, NYHA functional class and echocardiographic left ventricular parameters. Comparing the mortality of the two populations at the first, second and third year of follow-up, a statistically significant reduction in mortality was found on the ACE inhibitors treated population, at the first year. However, this reduction did not reach statistical significance at second and third years. The results are similar to trials in which the effects of ACE inhibitors are studied on general populations in heart failure.
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PMID:[Effect of converting enzyme inhibitors in cardiac insufficiency mortality in the elderly]. 150 88

The effects of flosequinan and enalapril on exercise capacity (bicycle exercise duration), quality-of-life symptomatology (visual analogue scales) and New York Heart Association (NYHA) grading, were compared in 61 patients with chronic heart failure (NYHA, grade III). Bicycle exercise duration improved similarly with flosequinan (+27%) and enalapril (+18%); in patients completing the study, flosequinan produced a significantly greater increase in exercise time at week 12, compared with enalapril (P = 0.02). Improvements in visual analogue scores relating to general health, energy and vitality, ability to perform physical activities and breathing performance, were equivalent for both drugs. Changes in NYHA classification showed that 27 (55%) of 49 patients completing the study had improved by at least one NYHA grade (15 (68%) patients on flosequinan; 12 (44%) on enalapril). The overall safety and tolerability of the two treatments was similar; 18 patients reported adverse effects while on flosequinan, compared with 19 patients on enalapril. Neither treatment was associated with any clinically important changes in haematological or biochemical variables, although some treatment-related effects were observed. This study confirms that flosequinan achieved similar efficacy to enalapril in the symptomatic relief of chronic heart failure. The effect of flosequinan on survival in chronic heart failure has not been tested; pending such studies, our data suggest that it may prove a useful alternative therapy in patients where ACE inhibitors are contraindicated or poorly tolerated.
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PMID:A double-blind, parallel-group comparison of flosequinan and enalapril in the treatment of chronic heart failure. 150 60


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