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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 becoming increasingly common. More than 20 million people worldwide are estimated to have heart failure. Prevalence is rising because the population is ageing: in both men and women, the prevalence of heart failure in those aged 80-89 years is roughly 10 times the prevalence in those aged 50-59 years. Coronary artery disease is now the most common cause of heart failure. Better treatment of myocardial infarction means that more people survive with impaired myocardial function, and some of these will develop heart failure in time. Hypertension is also an important contributing factor. Valvular disease, once a major cause of heart failure, has become less prevalent. The median survival after diagnosis of heart failure was only 1.7 years for men and 3.2 years for women, according to Framingham data for the years 1948 to 1988. After five years, only 25% of men and 38% of women were still alive. Preventive and treatment measures have improved this picture somewhat: deaths from heart failure have decreased by about 12% per decade. However, heart failure continues to carry a grave prognosis.
J Renin Angiotensin Aldosterone Syst 2004 Sep
PMID:The epidemiology of heart failure. 1552 38

Aldosterone plays a key role in the pathophysiology of heart failure. Angiotensin converting enzyme inhibitors and angiotensin II receptor blockers may not suppress aldosterone production in the long term. This allows aldosterone to exert its effects on myocardial fibrosis and cardiac remodelling, endothelial function, electrolytes and baroreceptor response. The Randomized Aldactone Evaluation Study (RALES) tested spironolactone against placebo in patients with severe heart failure. The study found a 30% reduction in the risk of death among patients treated with spironolactone and a 31% reduction in the risk of death from cardiac causes. Patients in the spironolactone group had significantly lower risks of death from progression of heart failure and sudden cardiac death. The Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) investigated the effects of eplerenone against placebo in patients with myocardial infarction complicated by left ventricular dysfunction. Compared to placebo, the relative risk of death from any cause was 0.85 in eplerenone-treated patients, and the relative risk of death or hospitalisation for cardiovascular events was 0.87. The reduction in the risk of sudden death from cardiac causes was statistically significant. In conclusion, aldosterone blockade should form part of optimal therapy for patients with heart failure.
J Renin Angiotensin Aldosterone Syst 2004 Sep
PMID:Aldosterone blockade in heart failure. 1552 39

Significant progress has been made in the last few years in the management of heart failure. In particular, several trials have given significant results. It has become apparent that heart failure may be prevented in some patients by treatment of risk factors such as coronary artery disease. Experience with angiotensin-converting enzyme (ACE) inhibitors has shown that the survival and symptomatic benefits do last in the long term, and confirm that they are the first-line treatment in heart failure. The results of a number of trials using the angiotensin receptor blockers (ARBs) candesartan, valsartan and losartan are presented and discussed. There is also some experience now in the use of candesartan for patients with heart failure and preserved left ventricular systolic function. The COMET trial compared the beta-blockers carvedilol and metoprolol tartrate, and suggests that there may be differences in clinical effect between beta-blockers. The selective aldosterone receptor blocker eplerenone was evaluated in the EPHESUS trial in post-MI patients with signs of heart failure. Based on these clinical trials, heart failure guidelines are now being updated.
J Renin Angiotensin Aldosterone Syst 2004 Sep
PMID:Reassessing guidelines for heart failure. 1552 40

Activity of the renin-angiotensin-aldosterone system (RAAS) is increased in heart failure. Agents which act on the RAAS can be expected to benefit these patients. Recent trials which have furthered our understanding of drugs which are of benefit in heart failure--angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, beta-blockers and aldosterone antagonists--are discussed. It is desirable to use multiple agents for best results in patients with heart failure. New European Society of Cardiology guidelines on the management of heart failure are expected later this year.
J Renin Angiotensin Aldosterone Syst 2004 Sep
PMID:Conclusions on the management of heart failure. 1552 41

Activity of the renin-angiotensin-aldosterone system (RAAS) is increased in patients with heart failure, and its maladaptive mechanisms may lead to adverse effects such as cardiac remodelling and sympathetic activation. Elevated renin activity has been demonstrated in patients with dilated cardiomyopathy. (Third- generation synthetic non-peptide renin inhibitors, with more favourable properties than earlier renin inhibitors, lower ambulatory blood pressure and may have a role to play in other cardiovascular disease.) Chymase, a protease inhibitor stored in mast cells that generates angiotensin II (Ang II) (in addition to angiotensin-converting enzyme [ACE]), has been linked to extracellular matrix remodelling in heart failure. Again, chymase inhibitors have been developed to investigate its functions in vitro and in vivo . Bradykinin is thought to contribute to the cardioprotective effect of ACE inhibition through modification of nitric oxide release, calcium handling and collagen accumulation. Ang II is believed to influence a number of molecular and structural changes in the heart, mostly mediated through the AT1-receptor. The importance of the RAAS in heart failure is shown by the survival benefit conferred by treatment with ACE inhibitors.
J Renin Angiotensin Aldosterone Syst 2004 Sep
PMID:The role of the renin-angiotensin-aldosterone system in heart failure. 1552 42

The Valsartan Antihypertensive Long-Term Use Evaluation (VALUE) Trial compared coronary heart disease outcome in two anti-hypertensive treatment strategies based on either an angiotensin receptor blocker, valsartan, or a calcium channel blocker (CCB), amlodipine. In both patient groups a diuretic was added, if necessary, in an attempt to achieve blood pressure (BP) goals. Follow-up of over 15,000 patients was maintained for 4.2 years. There were no differences in the primary composite endpoint of cardiac morbidity and mortality (which included interventional procedures, hospitalised heart failure, non-fatal myocardial infarction and fatal coronary heart disease, however myocardial infarction and stroke events occurred less commonly on amlodipine than on valsartan the former achieving statistical significance [p=0.02 and p=0.08 respectively]). There was a non-significant excess of hospitalised heart failure on amlodipine (p=0.012). However, lower BPs early in the trial probably accounted for most of the observed benefits in favour of the CCB. The angiotensin receptor blocker arm was associated with less new onset diabetes. The results of VALUE add further support to the evidence that blood pressure control is the major determinant in outcome in trials of antihypertensive therapy.
J Renin Angiotensin Aldosterone Syst 2004 Sep
PMID:The VALUE trial: a commentary. 1552 43

Renin angiotensin system inhibitor therapy is seldom offered to individuals who have diabetes and advanced chronic kidney disease because of safety concerns. In this post hoc, secondary analysis of the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial, angiotensin antagonism risk/benefit profile was assessed in 1513 individuals with type 2 diabetes and overt nephropathy. Incidence of ESRD, hospitalizations for heart failure, withdrawals for adverse events, and proteinuria during losartan or conventional treatment were compared within three tertiles of baseline serum creatinine concentration (highest, 2.1 to 3.6 mg/dl; middle, 1.6 to 2.0 mg/dl; lowest, 0.9 to 1.6 mg/dl). Losartan decreased the risk of ESRD by 24.6, 26.3, and 35.3% in highest, middle, and lowest tertiles, respectively. For every 100 patients with serum creatinine >2.0, 1.6 to 2.0, or <1.6 mg/dl, respectively, 4 yr of losartan therapy was estimated to save 18.9, 8.4, and 2.9 ESRD events and US$1,502,855, US$1,021,770, and US$528,591 costs for renal replacement therapy. Losartan also decreased the hospitalizations for heart failure by 50.2 and 45.1, in the highest and middle tertile, respectively. Withdrawals for adverse events other than heart failure were comparable between tertiles and treatment groups. Proteinuria decreased more on losartan than on placebo in all tertiles (highest, 24 versus -8%; middle, 16 versus -8%; lowest, 15 versus -10%). In proteinuric individuals with type 2 diabetes, losartan therapy reduced ESRD and hospitalizations for heart failure and was well tolerated at all levels of renal function. Angiotensin II antagonism is a suitable and well-tolerated treatment for individuals with type 2 diabetes even with GFR levels approaching renal replacement therapy.
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PMID:Continuum of renoprotection with losartan at all stages of type 2 diabetic nephropathy: a post hoc analysis of the RENAAL trial results. 1557 15

Many studies have investigated the process of left ventricular (LV) dilatation and the effects of angiotensin-converting enzyme (ACE) inhibitors after myocardial infarction (MI). It has been generally accepted that progression of LV dilatation is a major predictor of heart failure and death after MI. Also, attenuation of LV dilatation is thought to be one of the main mechanisms by which ACE inhibitors (ACE-Is) produce their beneficial effects. However, evidence for this hypothesis came from studies that were performed before thrombolytic therapy and primary percutaneous coronary intervention (PCI) were routinely used after acute MI. Nowadays, reperfusion is obtained much more frequently and LV dilatation after MI has become less prevalent. Nevertheless, ACE-Is proved effective in reducing cardiac morbidity and mortality. Therefore, mechanisms other than attenuation of LV dilatation, such as anti-atherosclerotic effects or plaque stabilisation, may explain the long-term beneficial effects of ACE-Is after MI. In the present overview, we evaluate the role of LV dilatation and the effects of ACE-Is after MI in the thrombolytic/primary PCI era and provide recommendations on ACE-I use in clinical practice.
J Renin Angiotensin Aldosterone Syst 2004 Dec
PMID:The revised role of ACE-inhibition after myocardial infarction in the thrombolytic/primary PCI era. 1580 34

Chronic elevation of plasma aldosterone contributes to heart failure. Mineralocorticoid receptor (MR) antagonism is cardioprotective in such a setting, but whether such protection occurs in the presence of low-aldosterone concentrations remains unclear. We investigated whether MR blockade attenuates cardiac hypertrophy and failure in rats with salt-sensitive hypertension. Dahl salt-sensitive (DS) rats fed a high-salt diet from 7 weeks develop concentric left ventricular (LV) hypertrophy secondary to hypertension at 12 weeks followed by heart failure at 19 weeks (DS-CHF). DS rats on such a diet were treated with a non-antihypertensive dose of the selective MR antagonist eplerenone from 12 to 19 weeks. Renin activity and aldosterone concentration in plasma were decreased in DS-CHF rats compared with controls. LV hypertrophy and fibrosis, as well as macrophage infiltration around coronary vessels, were apparent in DS-CHF rats. The amounts of mRNAs for 11beta-hydroxysteroid dehydrogenase type 1, MR, monocyte chemoattractant protein 1, and osteopontin were increased in these hearts. Treatment of DS-CHF rats with eplerenone inhibited these changes in gene expression, as well as coronary vascular inflammation and heart failure. Eplerenone attenuated both the decrease in the ratio of reduced to oxidized glutathione and the increase in NADPH oxidase activity apparent in DS-CHF rat hearts. MR blockade with eplerenone thus resulted in attenuation of LV hypertrophy and failure, without an antihypertensive effect, in rats with low-aldosterone hypertension. The beneficial cardiac effects of eplerenone are likely attributable, at least in part, to attenuation of myocardial oxidative stress and coronary vascular inflammation induced by glucocorticoid-activated MRs.
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PMID:Mineralocorticoid receptor antagonism attenuates cardiac hypertrophy and failure in low-aldosterone hypertensive rats. 1650 9

Combined therapy with optimum doses of a beta-blocker and an angiotensin-converting enzyme inhibitor (ACE-I) is the mainstay for the treatment of chronic heart failure (CHF). However, patients cannot be started on full doses of both drugs and treatment has to be initiated one way or the other. The Cardiac Insufficiency Bisoprolol Study (CIBIS) III was the first trial investigating the optimum sequence of initiating treatment of CHF, in terms of mortality and morbidity. CIBIS III compared randomised, open-label initial monotherapy with bisoprolol or enalapril for six months, followed by their combination for six to 24 months, in 1,010 patients at least 65 years of age, with stable, mildly or moderately symptomatic, systolic CHF. The two strategies were similarly efficacious in terms of the combined primary endpoint of mortality or all-cause hospitalisation, and showed similar safety. The bisoprolol-first approach showed a 28% lower mortality at the end of the monotherapy phase (p=0.24) and a 31% lower mortality at the end of the first year (p=0.06), but a 25% increase in worsening of CHF events (p=0.23). The main conclusion is that, CHF therapy may be started with bisoprolol or enalapril in patients like those in CIBIS III. However, it may be argued that the primary therapeutic goal in the early phase of CHF should be improved survival, whereas the long-term aim, achievable during combined therapy with optimum doses of several drugs, should be improved quality of life, physical function, morbidity and survival. In such case, the CIBIS III findings would tend to support starting CHF therapy with bisoprolol rather than enalapril in stable patients with mild or moderate symptoms.
J Renin Angiotensin Aldosterone Syst 2005 Dec
PMID:Implications of CIBIS III: a commentary. 1652 41


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