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

Proven cardiovascular benefit from angiotensin-converting enzyme (ACE) inhibition is a cornerstone of evidence-based medicine. The first study to show dramatic benefits from ACE inhibition was the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS-I), in which a 31% decrease in the rate of death was observed in patients with severe heart failure at the end of 1 year of enalapril treatment (p = 0.001). This result led to large long-term studies-including Survival and Ventricular Enlargement (SAVE), Acute Infarction Ramipril Efficacy (AIRE), Trandolapril Cardiac Evaluation (TRACE), and Study of Left Ventricular Dysfunction (SOLVD)-which verified that ACE inhibition decreases heart failure, myocardial infarction (MI), and mortality, and that striking benefit could be observed within 30 days. Short-term studies of patients in the acute phase of a heart attack verified that ACE inhibition provided rapid benefits. A meta-analysis of short-term (up to 8 weeks) studies of ACE inhibition (including CONSENSUS-II, Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico [GISSI]-3, International Study of Infarct Survival [ISIS]-4, and the Chinese Captopril Study [CCS]-1) demonstrated that post-MI risk was reduced by 10% within the first day of treatment. The immediacy of the benefit suggested that ACE inhibition not only improved cardiovascular function in failing hearts but also affected important mechanisms in patients without overt heart failure. Effects on more general mechanisms of heart disease suggested that patients with problems other than hypertension or heart failure might benefit from ACE inhibitors. The Heart Outcomes Prevention Evaluation (HOPE) study investigated the hypothesis that ACE inhibition would confer benefits to patients who were at high risk for cardiovascular events, but who were without left ventricular dysfunction or heart failure. Long-term reductions in MI, stroke, cardiac arrest, and heart failure, as well as improvements in mortality, were observed in this population after treatment with ACE inhibitors. Substudies of the HOPE study revealed that ACE inhibition reduced progression of atherosclerosis and improved myocardial remodeling. Taken together, these studies provide evidence that supports treatment of a broad population of patients at risk for cardiovascular events with ACE inhibitors. The next step is to combine ACE inhibition with other treatments to maximize patient benefit. The Ongoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial (ONTARGET) will compare the efficacy of an ACE inhibitor (ramipril) with an angiotensin receptor blocker (telmisartan), and determine whether these treatments in combination will further reduce morbidity and mortality from cardiovascular disease.
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PMID:Angiotensin II and trials of cardiovascular outcomes. 1183 5

Renovascular hypertension is usually caused by atherosclerotic narrowing of the origin of the renal artery and is much more common than is thought among patients with peripheral vascular disease, carotid stenosis or heart failure. Renovascular hypertension must be distinguished from renal artery stenosis. In true renovascular hypertension, the kidney takes charge of the blood pressure and will do what it takes to push blood pressure high enough to force blood through the blocked artery. This can be diagnosed with functional tests that measure glomerular filtration rate before and after blockade of the renin-angiotensin system with angiotensin converting enzyme inhibitors or antagonists of the AT(1) subtype of the angiotensin receptor. There is insufficient data on which to make evidence-based recommendations on the management of renovascular hypertension. Only two randomised trials exist of angioplasty versus medical therapy and of these the larger was severely contaminated by angioplasty among the group initially assigned to medical therapy. Only one trial exists of angiotensin converting enzyme inhibition versus alternative medical therapy. The drugs that are most effective in medical management of renovascular hypertension--angiotensin converting enzyme inhibitors and angiotensin receptor-1 blockers--tend to be avoided because of fear of a very rare complication (acute renal failure in patients with severe stenosis of both renal arteries, or the artery to a single remaining kidney). This fear is misplaced not only because it is rare (< 5% of patients with renovascular hypertension) but because it is reversible and treatable by revascularisation. Patients with renovascular hypertension should be evaluated by nuclear medicine differential glomerular filtration rate, enhanced by blockers of the renin-angiotensin system. If medical therapy is ineffective or causes severe impairment of renal function, revascularisation is required. Some experts favour surgical revascularisation because of occasional angioplasty failure and the risk of deterioration of renal function after angioplasty.
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PMID:Treatment options for renovascular hypertension. 1193 44

Renin-angiotensin blockade is an important component of management of heart failure in the 21st century. It can be achieved by angiotensin-converting enzyme inhibition (ACEI) and angiotensin receptor blockade (ARB). Neuro-hormonal activation was considered a necessary mechanism for survival of patients with left ventricular dysfunction in 1960s and 1970s. This has been proven to be incorrect, and in fact, there is a large and growing body of evidence showing the cardio-protective effects of RAS and other neuro-hormonal blockade.
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PMID:Ace inhibitors in cardiovascular diseases. 1195 89

Diastolic heart failure is defined clinically when signs and symptoms of heart failure are present in the presence of preserved left ventricular systolic function (ejection fraction >45%). The incidence and prevalence of primary diastolic heart failure increases with age and it may be as high as 50% in the elderly. Age, female gender, hypertension, coronary artery disease, diabetes, and increased body mass index are risk factors for diastolic heart failure. Hemodynamic consequences such as increased pulmonary venous pressure, post-capillary pulmonary hypertension, and secondary right heart failure as well as decreased cardiac output are similar to those of systolic left ventricular failure, although the nature of primary left ventricular dysfunction is different. Diagnosis of primary diastolic heart failure depends on the presence of preserved left ventricular ejection fraction. Assessment of diastolic dysfunction is preferable but not mandatory. It is to be noted that increased levels of B-type natriuretic peptide does not distinguish between diastolic and systolic heart failure. Echocardiographic studies are recommended to exclude hypertrophic cardiomyopathy, infiltrative heart disease, primary valvular heart disease, and constrictive pericarditis. Myocardial stress imaging is frequently required to exclude ischemic heart disease. The prognosis of diastolic heart failure is variable; it is related to age, severity of heart failure, and associated comorbid diseases such as coronary artery disease. The prognosis of severe diastolic heart failure is similar to that of systolic heart failure. However, cautious use of diuretics and/or nitrates may cause hypotension and low output state. Heart rate control is essential to improving ventricular filling. Pharmacologic agents such as angiotensin receptor blockers, angiotensin-converting enzyme inhibitors, and calcium channel blockers are used in selected patients to decrease left ventricular hypertrophy. To decrease myocardial fibrosis, aldosterone antagonists have a potential therapeutic role. However, prospective controlled studies will be required to establish their efficacy in primary diastolic heart failure.
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PMID:Primary diastolic heart failure. 1198 32

Recent trials have helped to clarify indications for the initial pharmacological therapy of hypertension. Both the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI) and World Health Organization-international Society of Hypertension (WHO-ISH) recommendations should be revised. The more recent trials indicate that: (1) diuretics and beta-blockers appear to be as effective in reducing overall morbidity/ mortality as other agents (Swedish Trial in Old Patients with Hypertension [STOP-2], United Kingdom Prospective Diabetes Study [UKPDS], Intervention as a Goal in Hypertension Treatment [INSIGHT], Nordic diltiazem [NORDIL]); (2) the use of an a-blocker results in more cardiovascular events, especially congestive heart failure, when compared with a diuretic (Antihypertensive Therapy and Lipid Lowering Heart Attack Trial [ALLHAT]); (3)the use of an angiotensin-converting enzyme (ACE) inhibitor results in fewer myocardial infarctions and episodes of heart failure than calcium channel blockers in the elderly and in diabetic patients (Fosinopril vs. Amlodipine Cardiovascular Events Randomized Trial [FACET], Appropriate Blood Pressure Control in Diabetes [ABCD], STOP-2) - other data (Captopril Prevention Project [CAPPP]) suggest that the use of an ACE inhibitor is preferred in diabetic patients; (4) overall cardiovascular events are similar with calcium channel blockers compared with a diuretic - however, there are fewer strokes with non-dihydropyridine calcium channel blockers (NORDIL) and a trend towards an increase in heart failure and myocardial infarctions with either a dihydropyridine or non-dihydropyridine calcium channel blockers compared with a diuretic (INSIGHT, NORDIL); (5) angiotensin receptor blockers (ARBs) will decrease proteinuria and slow progression of renal disease in type 2 diabetic patients when compared with regimens that do not include an ARB or an ACE inhibitor (Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan [RENAAL], Irbesartan Type II Diabetic Nephropathy Trial [IDNT], Irbesartan Type II Diabetes with Microalbuminuria [IRMA Il]). The debate over initial therapy may be moot. High-risk hypertensive patients should probably be treated initially with combination therapy, one of which should be a diuretic. The use of diuretics and beta-blockers as well as ACE-inhibitors alone or with a diuretic should be considered as initial therapy (a change from JNCVI). Alpha-blockers should be reserved for special situations, i.e. prostatic hypertrophy (in contrast to WHO-ISH recommendations). An ACE-inhibitor or ARB, usually along with a diuretic, can be considered as preferred therapy in hypertensive diabetic patients. Some data suggest equal or greater reduction in strokes with a calcium channel blocker than other medications.
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PMID:Current recommendations for the treatment of hypertension: are they still valid? 1199 97

Treatment strategies for patients with heart failure and left ventricular systolic dysfunction continue to evolve as the complex pathophysiology of this disease is better understood. A number of advances have been made in recent years, most notably the addition of beta-receptor antagonists. In addition, recent studies have provided important information regarding the utility of angiotensin receptor antagonists, aldosterone receptor antagonists, and natriuretic peptides in the management of heart failure. Nonpharmacologic advances include resynchronization therapy, which appears to confer symptomatic improvement in some patients, and improvements in ventricular assist device technology. As the importance of neurohormonal activation in the progression of heart failure becomes increasingly apparent, new therapeutic strategies targeting these neurohormonal systems are being investigated.
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PMID:Recent advances in the treatment of heart failure. 1199 34

The most common etiologies for mitral regurgitation (MR) include mitral valve prolapse syndrome, coronary artery disease, infective endocarditis, rheumatic heart disease, collagen vascular disease, and, recently, anoretic drugs have also been reported to cause MR. In chronic severe MR, forward cardiac output is maintained for the development of afterload reduction with increase in compensatory left ventricular (LV) end-diastolic volume and LV ejection fraction. It is well established that some patients with asymptomatic mitral regurgitation develop irreversible contractile dysfunction of the LV, which is often masked by the afterload-reducing effect of the regurgitant flow; cardiologist have to use some variables, like LV chamber elastance, LV End-Systolic dimensions and volumes, left atrial area combined with ejection fraction, in their clinical evaluations tube able to predict surgery mortality. Careful and periodic evaluation of left ventricular function and size is essential to optimize the timing of surgical intervention in these patients. After symptoms occur, outcome is improved with surgical interventions compared to medical therapy, with a reported survival of only 45% at 5 years without surgical intervention. Vasodilators, diuretics, and recently, angiotensin receptor antagonists have been used in MR medical therapy. Long-term carvedilol therapy in patients with chronic heart failure may prevent or partially reverse progressive left ventricular dilatation. Concomitant by, it has been associated with recovery of diastolic reserve and a decrease in mitral regurgitation.
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PMID:[Heart failure and pure mitral failure. Prognostic impact and its best treatment]. 1200 70

Type 2 diabetes is the most common cause of end-stage renal disease in the United States, and type 2 diabetes has been shown to be a myocardial infarction equivalent in regard to risk of death from a cardiovascular event. Proteinuria is a surrogate marker for renal disease progression, and although data favor both the angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) in reducing proteinuria, data for renal outcomes, such as time to dialysis, only exist for the ARBs, which clearly increase the duration to dialysis. Conversely, ACE inhibitors have overwhelming data that show substantial risk reduction from cardiovascular events and death in people with type 2 diabetes. Similar data on cardiovascular risk reduction are not yet available with ARBs, although two trials of renal disease progression did have cardiovascular endpoints as secondary outcomes. There were no significant differences between the ARB and control group except for first hospitalization with heart failure, where losartan reduced the risk by 32%, but there was a trend, albeit not significant, toward reduction of myocardial infarction. The first information regarding ARB effects on cardiovascular events as primary outcomes will come from the Losartan Intervention for Endpoint (LIFE) Reduction in Hypertension study. Therefore, as of this writing, all patients with type 2 diabetes and no evidence of nephropathy, ie, proteinuria and an elevated creatinine > 1.5 mg/dL, should be placed on an ACE inhibitor for cardiovascular risk reduction. If nephropathy is present, the evidence would support an ARB for therapy in concert with a b-blocker for cardiovascular risk reduction and renoprotection.
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PMID:Angiotensin converting enzyme inhibitors or angiotensin receptor blockers in nephropathy from type 2 diabetes. 1200 99

Chronic heart failure is a common condition with a poor prognosis, usually associated with poor exercise tolerance and debilitating symptoms despite optimal modern therapy. Standard therapy includes diuretics, digoxin, angiotensin-converting enzyme inhibitors (ACEIs) and beta-blockers. Despite this, many patients remain symptomatic, and interest is high as to whether the angiotensin receptor blockers (ARBs) would offer further advantage to a patient already receiving quadruple therapy. In addition, some patients are intolerant of ACEIs, and for this group the ARBs seem a logical choice. This article reviews the evidence for the use of ARBs as a class in heart failure concentrating on clinical recommendations and clinical needs and evidence rather than purely on statistical issues of significance in trials. The trials to date have demonstrated clearly similar hemodynamic effects to those seen with ACEIs and variety of ancillary benefits such as improvements in endothelial function, anti-thrombotic effects, and effects on neurohormonal inhibition. There is consistent evidence of a preservation of exercise tolerance when patients with heart failure are crossed over from stable ACEI therapy, and when added to ACEIs exercise tolerance appears to increase with ARBs. In terms of major outcomes, the two largest trials, Elite-II and Val-Heft, demonstrate that angiotensin receptor blockers probably have a clinical role in improving mortality and morbidity as an alternative to ACEIs in those patients unable to tolerate these agents, which remain, however, the first choice in unselected patients with heart failure. There is a worrying suggestion of a negative interaction when ARBs are added to beta-blockers, which is a reason for caution in using the ARBs, not a reason not to use beta-blockers.
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PMID:Angiotensin type-1 receptor blockers in heart failure. 1200 79

Although angiotensin-converting enzyme (ACE) inhibitors decrease mortality in heart failure, they incompletely suppress angiotensin II with long-term therapy. Since angiotensin receptor blockers (ARBs) block the biologic effects of angiotensin II more completely than ACE inhibitors, they could be beneficial in the treatment of heart failure.
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PMID:ACE inhibitors vs ARBs: is one class better for heart failure. 1202 88


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