Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin-converting enzyme (ACE) inhibitors are considered as the cornerstone of the treatment of congestive heart failure with systolic dysfunction, proving beneficial in all grades of heart failure, from I to IV on the New York Heart Association scale. However, despite these positive results, a brief glance at the published mortality data or an hour spent in any heart failure clinic easily demonstrates that the problems of heart failure are far from being solved. Among the unresolved issues that will be addressed in this brief review are: the high incidence of deaths due to pump failure and sudden death in patients receiving ACE inhibitor therapy; methods of further improving exercise tolerance and quality of life, and, finally, current views regarding prevention of heart failure.
 ...
PMID:Improving patient care: some unresolved issues in heart failure. 806 6

Angiotensin-converting enzyme inhibitors are proved, effective agents for the treatment of hypertension and congestive heart failure. New data suggest that angiotensin-converting enzyme inhibitors may be effective therapy for patients following acute myocardial infarction. Results from clinical trials, such as the Survival and Ventricular Enlargement trial, have demonstrated that captopril attenuates left ventricular enlargement, minimizes and/or prevents the subsequent development of overt congestive heart failure, and improves survival in patients with asymptomatic left ventricular dysfunction after myocardial infarction. Clinical reinfarctions and need for subsequent revascularization procedures were also reduced with captopril. In the Acute Infarction Ramipril Efficacy study, patients with clinically evident heart failure following acute myocardial infarction who received ramipril demonstrated a significant reduction in mortality and cardiovascular events. The mortality benefit in this study was evident within 30 days, possibly reflecting differences in patients studied (ie, population with high-risk heart failure in the Acute Infarction Ramipril Efficacy study as opposed to population with asymptomatic left ventricular dysfunction in the Survival and Ventricular Enlargement trial). Contrary results have been reported in another major postmyocardial infarction trial, the Cooperative New Scandinavian Enalapril Survival Study, which evaluated enalaprilat/enalapril maleate in unselected patients with acute myocardial infarction. This article reviews the recent trials using angiotensin-converting enzyme inhibition after myocardial infarction and will explore the reasons why angiotensin-converting enzyme inhibition seems to be beneficial in this clinical setting.
 ...
PMID:Comparing angiotensin-converting enzyme inhibitor trial results in patients with acute myocardial infarction. 788 63

An understanding of the important role of neurohormonal compensatory mechanisms in heart failure has been translated into therapeutic options that can improve cardiac function, alter disease progression, and improve survival. Angiotensin-converting enzyme inhibitors are of proven benefit in this regard, and beta-adrenergic receptor antagonists are potentially another such class of agents. By inhibiting the myocardial effects of chronic adrenergic activation, beta blocking agents may improve left ventricular function or delay its deterioration in patients with heart failure. Aside from blocking beta-adrenergic receptors, other ancillary properties inherent in third-generation beta-blocking agents (such as vasodilation) may exert additional favorable effects. Clinical data generated in subjects with heart failure indicate that beta-antagonist therapy exerts its physiologic and clinical effects through neurohormonal antagonism, generally analogous to angiotensin-converting enzyme inhibitors. Virtually all controlled long-term studies show that beta-blocking agents improve cardiac function and hemodynamics in patients with chronic heart failure, but large-scale trials are needed to ascertain a favorable effect on the natural history of heart failure.
 ...
PMID:Pathophysiologic and pharmacologic rationales for clinical management of chronic heart failure with beta-blocking agents. 809 71

In order to evaluate changes in left ventricular volumes and regional left ventricular function after thrombolytic therapy in acute myocardial infarction serial two-dimensional echocardiography was performed during a follow-up of 2 years in 206 consecutive patients treated with streptokinase and adjunctive angioplasty in a randomized group of patients. Unexpected progressive left ventricular enlargement was detected both with and without angioplasty. In anterior wall infarction, end-diastolic volume index increased from 55 +/- 14 to 91 +/- 28 ml/m2 (+65%, P < 0.01) and end-systolic volume index increased from 31 +/- 11 to 55 +/- 23 ml/m2 (+79%, P < 0.01), whereas ejection fraction decreased from 45 +/- 9 to 41 +/- 7% (-9%, P = NS). Averaged regional anterior wall motion improved during the first 4 weeks (11 +/- 10 to 16 +/- 12%), but subsequently deteriorated (16 +/- 12 to 10 +/- 6, P < 0.05). The number of segments with pathological wall motion increased. Similar volumetric and regional wall motion data were demonstrated in inferior wall infarction. We believe this reflects a chronic ventricular remodelling phenomenon. This process takes place predominantly during the first 3 months, but continues over the whole follow-up period. Forty percent of the patients suffered symptoms of heart failure on long-term follow-up. Attenuation of progressive ventricular enlargement remains a therapeutic challenge in the long-term care of these patients. Angiotensin-converting enzyme inhibitors are promising agents in this regard.
 ...
PMID:Long-term follow-up of global and regional left ventricular function by two-dimensional echocardiography after thrombolytic therapy in acute myocardial infarction. 822 71

The renin-angiotensin system (RAS) is believed to play a central role in the pathophysiology of heart failure. However, there is a wide variability in plasma renin levels in patients with heart failure, and normal plasma renin activity has been documented in patients with mild or compensated disease. Recent evidence has demonstrated the existence of endogenous RAS in a number of tissues associated with cardiovascular homeostasis. It is possible that these tissue RAS are activated in the early stages of heart failure when plasma renin activity is normal, and therefore contribute to the progression of this condition. Angiotensin-converting enzyme (ACE) inhibitors reduce both circulating and tissue RAS activity. They are of symptomatic benefit and reduce the mortality associated with heart failure. A number of large studies initiated to investigate the effects of the ACE inhibitor enalapril in patients with all degrees of heart failure have been published recently. These studies show that addition of this drug to therapy significantly decreases patient morbidity and mortality, an effect which is most likely due to the suppression of circulating and tissue RAS activity this agent affords. The relationship of the profile of hormonal suppression seen with enalapril and drug dosage to observed beneficial effects on morbidity or mortality is unclear. Given the large range of alternative ACE inhibitors available, their variable structure, potency and duration of action, the potential for differences between agents needs further consideration. Although direct comparative studies are rare, there is a body of work suggesting that such differentiation may be present and may be of clinical significance.
 ...
PMID:Role of the circulating and tissue-based renin-angiotensin system in the development of heart failure: implications for therapy. 826 85

Angiotensin-converting enzyme (ACE) inhibitors, in conjunction with diuretic agents, have an established role in the management of moderate and severe heart failure due to left ventricular dysfunction. ACE inhibitor improves prognosis, symptoms and exercise performance. There have been some promising studies and one of the most widely quoted is the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS I), which demonstrated a 36% reduction in mortality with the ACE inhibitor, enalapril, versus placebo in patients with advanced heart failure. Over the last few years, we have received important information that seems to tell us that ACE inhibitors must be utilized if we hope to reduce mortality. An important topic is study the action of ACE inhibitors in improving prognosis, and the mechanism of the action.
 ...
PMID:[Effect of angiotensin-converting enzyme inhibitors in congestive heart failure]. 833 96

Angiotensin-converting enzyme (ACE) inhibitors improve survival in heart failure and delay progression to clinical heart failure in patients with left ventricular dysfunction after myocardial infarction. Increasing numbers of older patients are being considered for such treatment. However, there are reports of excessive and prolonged decreases in blood pressure (BP) after the first dose of some ACE inhibitors. We have studied the hemodynamics, pharmacokinetics, and neurohumoral responses to the first dose of oral captopril 6.25 mg, enalapril 2.5 mg, perindopril 2.0 mg, intravenous enalaprilat 1.5 mg, and perindoprilat 1.0 mg, compared with oral or intravenous placebo in 6 parallel groups of 12 elderly patients each with moderate-to-severe (New York Heart Association classes II-IV) heart failure. Oral dosing with active drugs led to different temporal responses. After captopril, there was an early short-lived decrease in BP. Enalapril led to a later long-lasting decrease, but perindopril was not different from placebo. Intravenous enalaprilat and intravenous perindoprilat each lowered BP to a similar extent. The doses of drugs used appeared to be comparable because plasma ACE inhibition was similar following perindopril or enalapril and also comparing perindoprilat and enalaprilat. These studies indicate that oral ACE inhibitors have different profiles of acute BP changes after the first dose. The explanation is not clear, but could include physicochemical differences in the interaction between prodrug ester and diacid metabolites leading to differences in tissue distribution and local enzyme inhibition.
 ...
PMID:Blood pressure response to the first dose of angiotensin-converting enzyme inhibitors in congestive heart failure. 839 82

Angiotensin-converting enzyme (ACE) inhibitors prevent the formation of angiotensin II in the circulation and a range of tissues. ACE inhibitors not only are effective, well-tolerated antihypertensive drugs but also improve symptoms and signs in patients with congestive cardiac failure. In addition, they improve long-term survival in these latter patients. Although ACE inhibitors are relatively free of side effects in patients with heart failure, hypotension after the first dose has been reported that may lead to symptomatic renal, cardiac, or cerebral hypoperfusion. Most reports have been uncontrolled and anecdotal. We report a double-blind placebo-controlled study in a parallel group of patients with cardiac failure (New York Heart Association classes II through IV). In total, 72 patients (6 groups of 12) were studied after either placebo, captopril, 6.25 mg, enalapril, 2.5, or perindopril, 2 mg orally, enalaprilat 1.5 mg, or perindoprilat, 1.0 mg intravenously. The blood pressure responses differed between the groups, with a short-lived early fall after captopril and a long-lasting fall after enalapril, whereas perindopril was no different from placebo. There was no significant difference between the two active intravenous regimens. Plasma ACE measurements suggested that the relative doses used were at least comparable. Further studies are in progress to investigate the mechanisms underlying the differential hemodynamic responses and also to explore the clinical relevance to safety and efficacy in the management of heart failure.
 ...
PMID:Angiotensin-converting enzyme inhibitors in heart failure: blood pressure changes after the first dose. 839 61

Inhibition of the renin-angiotensin system is being applied with considerable success to the treatment of hypertension and heart failure. Angiotensin-converting enzyme (ACE) inhibitors are the only currently available agents that can achieve this objective. In general, the major therapeutic effects of these agents in the treatment of mild to moderate hypertension or of heart failure are exerted on the vascular tissue through inhibition of the renin-angiotensin system and, secondarily, of the sympathetic nervous system. When cardiovascular functional reserve is diminished and autoregulation of regional and systemic blood flow is strained, however, ACE inhibitors may affect other organ functions (heart, kidneys, and possibly brain), hormones other than the renin system, and local tissue humoral systems. The interrelations between the renin-angiotensin system and several other vasoactive systems--including circulating and locally generated tissue hormones and centrally acting neurohormonal factors--are complex and unclear. A better understanding of these mechanisms and interrelations would allow for a more rational therapeutic use of these agents. Unknown also are the clinical effects of prolonged ACE inhibition. Whether the use of ACE inhibitors can provide primary cardiorenal protection requires proof through definitive clinical trials.
 ...
PMID:Long-range safety and protective benefits of angiotensin-converting enzyme inhibitors for hypertension. Do we need more clinical trials? 846 May 11

Angiotensin-converting enzyme (ACE) inhibitors are now widely prescribed for the treatment of hypertension and heart failure. Their increasing popularity is based on impressive results from studies of efficacy in clinical situations and the realisation that they may have advantages over conventional treatment. This review will highlight some of the recent advances in our knowledge of the role of ACE inhibitors and will develop a rational approach to prescribing.
 ...
PMID:ACE inhibition in the 1990s. 846 Dec 46


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>