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

Heart failure is a syndrome of breathlessness, fatigue and oedema. The effects of ageing on myocardial function and the prevalence of often multiple cardiac pathologies makes heart failure a disease of the elderly, usually characterized by primary or secondary myocardial systolic dysfunction. Appropriate treatment, which requires precise diagnosis, involves correction of precipitating or aggravating factors and the rational use of drug therapy. Diuretics and ACE inhibitors offer a combination of both symptom control and improvement in prognosis. Other agents such as digoxin, xamoterol and nitrates may be particularly useful in the treatment of patients with associated problems such as atrial fibrillation and angina. Because both ageing and heart failure may alter pharmacokinetics and pharmacodynamics, safe and effective treatment of heart failure in the elderly requires understanding of the clinical pharmacology of the drugs used.
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PMID:Treatment of heart failure in the elderly. 240 42

The prevalence of coronary artery disease shows no signs that it is declining, yet mortality is decreasing and advanced methods of treatment are creating a large population of individuals with a substantially damaged left ventricle. Clinical observations and experimental data provide convincing evidence that postischemic damage is progressive even in the absence of a fresh ischemic insult. Any intervention capable of preventing or limiting this progression can reasonably be expected to make a strong favorable impact on the prevalence and severity of heart failure, defined as symptomatic ventricular dysfunction. Preliminary data indicating that this desirable result can be achieved by the administration of ACE-inhibiting drugs to patients soon after the onset of acute Q-wave myocardial infarction are encouraging, but recommendations for a major change in current clinical practice will have to await the results of major multicenter trials now in progress.
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PMID:Long-term pharmacological prevention of heart failure after myocardial infarction. 248 35

The data herein presented provides persuasive evidence that in addition to diuretics, and probably digitalis (since all studies have included subjects taking this drug) patients with congestive heart failure should also be placed on a vasodilator regimen to slow the progression of the syndrome and to reduce its mortality. Firm recommendations for the choice of drug and the selection of patients likely to benefit from this treatment must await the results of further studies. At present, ACE inhibitors are preferred because they are usually better tolerated than conventional vasodilators and are clinically more effective. In regard to the question of when to begin vasodilator it is noteworthy that neurohormonal activation may occur early in the course of the disease, even before symptoms appear. If so, perhaps vasodilators should be initiated even in the asymptomatic stage of left ventricular dysfunction to prevent the progressive dilatation and deterioration that lead to clinical heart failure. The just published study of the efficacy of captopril in preventing the progression of left ventricular dilatation in patients with a recent anterior, transmural myocardial infarction supports this view. Further, ongoing studies, will help place these issues in their proper perspective.
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PMID:The medical treatment of congestive heart failure. 248

Despite a well-established rationale for pharmacologically induced arterial and venous vasodilatation in congestive heart failure, the clinical usefulness of long-term vasodilator therapy without concomitant converting-enzyme inhibition generally has been disappointing. With the exception of nitrates and, possibly, the combination of nitrates and hydralazine, the use of converting-enzyme inhibitors in many aspects appears preferable in the majority of patients. This article reviews the pathophysiology of inappropriate vasoconstriction in heart failure, the cellular mode of action of the various vasodilators, hemodynamic effects with respect to the peripheral site of action, clinical usefulness and limitations of different vasodilators, and the various determinants of clinical efficacy. Finally, an attempt is made to assess when and how to introduce vasodilator treatment with and without concomitant ACE inhibition.
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PMID:Vasodilator therapy without converting-enzyme inhibition in congestive heart failure--usefulness and limitations. 248 35

The decline of the use of digitalis for the treatment of congestive heart failure was due to the introduction of oral diuretic therapy, the recognition of the frequency of digitalis induced arrhythmias and the uncontrolled observations that digitalis could frequently be withdrawn from patients with a history of heart failure without recurrence of heart failure. Subsequently, it has been well documented that digitalis has chronic beneficial hemodynamic effects in patients with chronic congestive heart failure. Moreover, digitalis has been shown to improve hemodynamics when added to other drugs including diuretics, ACE inhibitors and vasodilators. It is concluded that digitalis is a mild inotropic agent that is still a primary drug for the treatment of mild to moderate acute or chronic left ventricular failure.
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PMID:The use of digitalis for the treatment of congestive heart failure: a tale of its decline and resurrection. 248 99

1. The effects of heart failure due to chronic myocardial infarction on the responsiveness to injected angiotensin I and ACE inhibition by intravenous cilazapril (1 mg kg-1) were evaluated. 2. For this purpose one group of 17 rats with a 4-week old myocardial infarction was compared with a group of 10 sham operated rats. 3. Heart failure increased markedly the responsiveness of the renal and mesenteric vascular beds to ACE inhibition which produced a vasodilation in these two vascular beds. 4. This increased responsiveness was most likely due to a stimulation of the renin-angiotensin system without any change of sensitivity to angiotensin I of the renal and mesenteric vascular beds. 5. Cilazapril produced the same level of ACE inhibition in both groups of rats.
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PMID:Effects of chronic heart failure on the responsiveness to angiotensin I and to angiotensin converting enzyme inhibition with cilazapril in rats. 252 30

The chronic reserve for the secretion of atrial natriuretic factor (ANF) was studied in conscious dogs with an arteriovenous (a-v) fistula, a model of high-output heart failure. After the first 7 days of marked sodium retention after creation of the a-v fistula, the animals regained sodium balance for the subsequent 3 wk. This compensatory natriuresis occurred in the presence of significant increases in right atrial pressure and was associated with marked and sustained elevations in plasma ANF and with the return of plasma renin and aldosterone to base-line values. The cardiac reserve for ANF secretion was further evaluated in these dogs with compensated high-output heart failure during additional progressive elevations in cardiac filling pressures induced by 3 wk of deoxycorticosterone acetate (DOCA) administration. During the DOCA regimen, plasma ANF increased an additional twofold from its high base line. Arterial blood pressure increased by 6-12 mmHg, and plasma renin activity was suppressed. However, the animals consistently retained sodium, and the high plasma levels of ANF were unable to counterbalance the sodium-retaining actions of DOCA. After termination of DOCA, the dogs exhibited a marked natriuresis, and all the hemodynamic and hormonal parameters returned to pre-DOCA control levels. This longitudinal study demonstrates that the cardiac reserve for chronic ANF secretion is well maintained in dogs with an a-v fistula during progressive cardiac volume overload. The present results suggest that the ANF endocrine system may represent one chronic compensatory mechanism to achieve sodium balance in heart failure when there is concomitant normalization of the renin-aldosterone system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:DOCA administration and atrial natriuretic factor in dogs with chronic heart failure. 252 18

The hypertensive damage to the target organ "heart" comprises the sum and interactions of the cardiac organ manifestations of arterial hypertension such as myocardial hypertrophy and disease of large and small coronary arteries. As the prognosis of arterial hypertension is determined, to a considerable extent, by these cardiac complications, the aim of treatment of hypertensive heart disease is reversal of the myocardial hypertrophy in order to prevent later progression to hypertensive failure. A further goal of therapy is reversal of hypertensive small coronary disease in order to improve the coronary reserve. While the evidence that regression of hypertrophy can be induced by suitable antihypertensive drugs (calcium channel blockers of the dihydropyridine type, ACE inhibitors, and sympathicolytic substances) is practically conclusive, clinical evidence of reversal of hypertensive small coronary disease has yet to be provided. Moreover, we do not know at present to what extent the prognosis of hypertensive heart disease can be improved by reversal of hypertrophy. Once the stage of hypertensive heart failure is reached, the principles of medical management of heart failure with digitalis, diuretics, and ACE inhibitors apply.
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PMID:[Treatment of myocardial and coronary effects of arterial hypertension]. 253 67

Alterations in the vasopressor system found in cardiac failure are part of compensatory measures that may modify pharmacologic-therapeutic response. Therefore, in 64 patients with dilated cardiomyopathy, we investigated its enhanced activity in different clinical stages of the disease as compared to normal controls. Patients in NYHA class II (n = 20) demonstrated increased activity of the sympathico-adrenal, renin-angiotensin-aldosterone, vasopressin, and atrial natriuretic factor systems, while maximum values were found in patients of NYHA class IV (n = 24). In these patients, noradrenaline was enhanced by a factor of 7, adrenaline by a factor of 2, plasma-renin-activity by a factor of 7, angiotensin II by a factor of 2.5, aldosterone by a factor of 5, vasopressin by a factor of 1.5, and ANF by a factor of 4 as compared to normal controls. Clinical NYHA classes correlated to a certain degree with the various plasma hormones. Patients treated with an aldosterone inhibitor in addition to digitalis and diuretics revealed significantly higher values for aldosterone, vasopressin, and angiotensin II as compared to those who received digitalis and diuretics alone. The addition of ACE-inhibitor therapy resulted in a decrease of angiotensin II, aldosterone, and vasopressin. Plasma catecholamines and ANF, however, did not change under the influence of cardiac medication. Diuretic treatment in NYHA class II patients reduced plasma volumes (p less than 0.01). Plasma volume in NYHA class IV patients only was found to be higher than in normal controls. Thus, analysis of the neurohumoral system can aid both in the identification of the clinical degree of dilated cardiomyopathy and in its optimal therapy.
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PMID:The vasopressor system in patients with heart failure due to idiopathic dilated cardiomyopathy--influence of the clinical stage of disease and of chronic drug treatment. 253 2

Enalapril provides significant haemodynamic, symptomatic and clinical improvement when added to maintenance therapy with digitalis and diuretics in patients with congestive heart failure [NYHA (New York Heart Association) classes II to IV]. These effects are not attenuated during long term therapy. More significantly, a clinical study demonstrated that enalapril reduces mortality when added to established therapy in patients with severe congestive heart failure (NYHA class IV) refractory to digitalis, diuretics and other vasodilators. Thus, ACE inhibitors such as enalapril offer a significant advance in the treatment of congestive heart failure. Because these drugs improve symptoms in patients with classes II to IV failure, and reduce mortality in patients with severe heart failure, they should be considered as first choice adjuvant therapy when a vasodilator is needed in addition to conventional treatment with digitalis and diuretics.
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PMID:Enalapril. An update of its pharmacological properties and therapeutic use in congestive heart failure. 253 90


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