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• W2000487813 abstract "Class I: 1In patients with severe heart failure and fluid retention, loop diuretics should be used and adjusted to achieve symptom control and/or euvolemia (Level of Evidence: C).2In cases of diuretic resistance, precipitating factors or alternative causes of fluid retention should be investigated and excluded (Table 1) (Level of Evidence: C).Table 1Precipitating Factors or Alternative Causes of Edema in Heart Failure• Non-compliance with diuretic (and other) medication• Non-compliance with salt and fluid restriction• Non-steroidal anti-inflammatory drug usage• Glitazones• Intrinsic renal disease• Hypoproteinemia• Calcium channel antagonists• Acute impairment of left ventricular function (new-onset ischemia, arrhythmias such as atrial fibrillation)Adapted with permission from Nieminen et al.1Nieminen M.S. Bohm M. Cowie M.R. et al.Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Acute Heart Failure of the European Society of Cardiology.Eur Heart J. 2005; 26: 384-416Crossref PubMed Scopus (799) Google Scholar Open table in a new tab 3Diuretic resistance should be treated with an increase in dose or frequency of loop diuretics, change to a loop diuretic with better bioavailability, addition of a thiazide diuretic, or intravenous administration (bolus or continuous infusion) of a loop diuretic (Level of Evidence: C).4All neurohormonal antagonists used in the management of patients with heart failure with low left ventricular ejection fraction (LVEF) should be those shown to be effective in clinical trials and they should be used at maximally tolerated or target dosages (Table 2) (Level of Evidence: A).Table 2Standard Drugs That Antagonize the Neurohormonal SystemsDrugClassStarting doseTarget dose from clinical trialCaptoprilACE inhibitor6.25–12.5 mg tid50 mg tidEnalaprilACE inhibitor2.5–5 mg bid10–20 mg bidRamiprilACE inhibitor2.5 mg bid5 mg bidTrandolaprilACE inhibitor1 mg qd4 mg qdCarvedilolα1 non-selective β-blocker, anti-oxidant properties3.125 mg bid25 mg bid (50 mg bid, if weight >85 kg [187 lb])Metoprolol succinateβ1-selective β-blocker12.5–25 mg qd200 mg qdBisoprololβ1-selective β-blocker1.25 mg qd10 mg qdCandesartanARB4–8 mg qd32 mg qdLosartanARB12.5 mg qd50 mg qdValsartanARB20 mg bid160 mg bidEplerenoneSelective aldosterone receptor blocker25 mg qd50 mg qdSpironolactoneAldosterone receptor blocker12.5–25 mg qd25–50 mg qdACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; bid, twice daily; d, day; qd, once daily; tid, three times daily. Open table in a new tab 5All patients with heart failure and low LVEF should have a trial of angiotensin-converting enzyme (ACE) inhibitors unless there are unequivocal contraindications (Level of Evidence: A).6Angiotensin receptor blockers (ARBs) should be used as an alternative to ACE inhibitors in patients who cannot tolerate ACE inhibitors due to cough or angioedema (Level of Evidence: A).7All patients with heart failure and low LVEF should have a trial of β-blockers unless there are unequivocal contraindications (Level of Evidence: A).8In patients with atrial fibrillation, control of the heart rate should be done and conversion may be performed (Level of Evidence: C).9Patients with heart failure and low LVEF should be anti-coagulated with warfarin if they have a history of an embolic event, atrial fibrillation or evidence of a new left ventricular (LV) thrombus (Level of Evidence: A).10In carefully selected advanced heart failure patients with low LVEF, aldosterone antagonists should be added to maximally tolerated ACE inhibitors and β-blockers. However, this approach requires frequent monitoring of serum potassium and renal function (Level of Evidence: B). Adapted with permission from Nieminen et al.1Nieminen M.S. Bohm M. Cowie M.R. et al.Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Acute Heart Failure of the European Society of Cardiology.Eur Heart J. 2005; 26: 384-416Crossref PubMed Scopus (799) Google Scholar ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; bid, twice daily; d, day; qd, once daily; tid, three times daily. Class IIa: 1In patients with pre–renal azotemia or fluid retention resistant to diuretic therapy, it is reasonable to use hemofiltration or dialysis (Level of Evidence: C).2In heart failure patients with low LVEF, it is reasonable to add ARBs to the combination of maximally tolerated ACE inhibitors and β-blockers (Level of Evidence: B).3In heart failure patients with low LVEF, it is reasonable to continue maximal ARB therapy rather than changing to an ACE inhibitor (Level of Evidence: C).4In patients with heart failure and low LVEF, it is reasonable to consider a combination of hydralazine and nitrates when progressive renal dysfunction or hyperkalemia limits therapy with an ACE inhibitor (ACEI) or ARB (Level of Evidence: C).5In patients with heart failure and low LVEF, it is reasonable to consider the addition of a hydralazine and nitrate combination or nitrates alone for patients with persistent symptoms despite recommended therapy with neurohormonal antagonists and diuretics for fluid retention (Level of Evidence: B).6In patients with persistent, severe heart failure and low LVEF, who are on maximal therapy with ACEIs, β-blockers and diuretics, it is reasonable to use digoxin therapy to reduce symptoms, decrease hospitalizations, or control heart rate in atrial fibrillation. Drug-level monitoring is strongly recommended. Target trough levels should be <1.0 ng/ml (Level of Evidence: C). Class I: 1In heart failure patients with fluid retention, salt and fluid intake should be restricted (Level of Evidence: C).2In addition to optimal medical therapy, regular exercise should be advised in patients with chronic stable heart failure to improve functional capacity (Level of Evidence: A).3Patients with advanced heart failure should be cared for by a multidisciplinary team, and seen at regular intervals (Level of Evidence: A).4Right heart catheterization should be performed to assess pulmonary vascular resistance (PVR) in heart transplant candidates (Level of Evidence: B).5Hemodynamic assessment using an indwelling pulmonary catheter should be used for assessment and management in patients with cardiogenic shock (Level of Evidence: C).6Patients with heart failure should be approached regarding their wishes for resuscitative care and their wishes should be documented in a living will or other advanced medical directive (Level of Evidence: C). Class IIa: 1It is reasonable to consider a formal sleep evaluation for all patients with a history suggestive of sleep apnea prior to consideration of cardiac transplantation (Level of Evidence: C).2In patients with ischemic heart failure and low LVEF, it is reasonable to consider coronary artery bypass grafting (CABG) (Level of Evidence: C).3It is reasonable to use brain natriuretic peptide (BNP) or N-terminal pro–B-type (NT-pro-BNP) levels and trends over time in the management of patients with heart failure (Level of Evidence: B).4Short-term hemodynamic monitoring with a pulmonary artery catheter may be used to assess and manage patients with advanced heart failure (Level of Evidence: B). Class IIb: 1In patients with heart failure and low LVEF, ventricular restoration surgery or mitral valve repair may be considered (Level of Evidence: C). Class III: 1Candidacy for transplantation must not be contingent upon clinical trial participation (Level of Evidence: C). Class I: 1In patients with decompensated heart failure and adequate blood pressure, intravenous vasodilators should be considered before inotropic therapy (Level of Evidence: C).2In patients with decompensated heart failure and hypoperfusion in spite of adequate filling pressures, inotropic or pressor therapy should be used (Level of Evidence: C).3The need for continued inotropic therapy should be frequently re-assessed (Level of Evidence: C).4Long-term use of inotropic therapy should only be used as a pharmacologic bridge to transplantation or for palliation (Level of Evidence: C).5The use of vasoconstrictive agents should be reserved for those patients who are in refractory cardiogenic shock (Level of Evidence: C). In chronic heart failure, neuroendocrine systems are activated to compensate for reduced perfusion of vital organs (e.g., activation of the sympathetic nervous system and renin–angiotensin–aldosterone system [RAAS] and secretion of vasopressin, cytokines and endothelin). Activation of these systems leads to fluid retention. Clinical correlates to fluid retention in heart failure are dyspnea and pulmonary edema (LV failure) as well as peripheral edema and ascites (right ventricular [RV] failure). Repeated decompensation or failure to control fluid retention are important symptomatic criteria for the decision to list a patient for heart transplantation.1Nieminen M.S. Bohm M. Cowie M.R. et al.Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Acute Heart Failure of the European Society of Cardiology.Eur Heart J. 2005; 26: 384-416Crossref PubMed Scopus (799) Google Scholar Measures to control or avoid fluid retention in patients with heart failure include fluid and salt intake restriction and the use of diuretic drugs. Fluid status should be monitored roughly by daily weights. Limited fluid intake (1.5 to 2 liters/day for severe heart failure) limits edema formation and avoids hyponatremia. Diuretic drugs improve dyspnea, exercise tolerance and cardiac performance by reducing LV filling pressures and decreasing dynamic mitral regurgitation. Insufficient diuresis may impair the efficacy of ACEIs. Excessive dehydration should be avoided because it may lead to hypotension, further activation of RAAS, and renal insufficiency. Thiazide diuretics, which block sodium and water re-absorption in the distal convoluted tubule, cause only mild water diuresis; their primary effect in heart failure is sodium excretion with a subsequent effect on hypertension.1Nieminen M.S. Bohm M. Cowie M.R. et al.Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Acute Heart Failure of the European Society of Cardiology.Eur Heart J. 2005; 26: 384-416Crossref PubMed Scopus (799) Google Scholar Loop diuretics (furosemide, bumetanide or torsemide) inhibit sodium uptake in the ascending loop of Henle by blocking the sodium–potassium–chloride transporter. Loop diuretics are the most potent diuretics, have a short duration of action, and are used in the treatment of patients with chronic heart failure or an acute exacerbation of heart failure, as well as in the setting of renal failure in patients with heart failure. As diuretics may induce further activation of the RAAS, diuretics should always be combined with an ACEI or ARB. In advanced stages of heart failure (New York Heart Association [NYHA] Class III or IV) diuretics form the mainstay of symptomatic therapy, affording unquestionable relief from dyspnea, peripheral edema and ascites. Although the effects of diuretics on symptom control are well established, the impact of diuretic therapy on prognosis (mortality) in heart failure is far less clear as large, placebo-controlled mortality trials have not been performed with diuretics. In the Torsemide in Congestive Heart Failure (TORIC) trial, a significant survival advantage was demonstrated for patients treated with torsemide vs furosemide, possibly due to additional anti-aldosterone action and better absorption of torsemide.2Cosin J. Diez J. Torasemide in chronic heart failure: results of the TORIC study.Eur J Heart Fail. 2002; 4: 507-513Crossref PubMed Scopus (81) Google Scholar In advanced heart failure, diuretic resistance, defined as failure to induce clinically sufficient diuresis even with large doses of loop diuretics, may develop. Diuretic resistance is associated with an adverse prognosis,3Neuberg G.W. Miller A.B. O’Connor C.M. et al.Diuretic resistance predicts mortality in patients with advanced heart failure.Am Heart J. 2002; 144: 31-38Abstract Full Text Full Text PDF PubMed Scopus (160) Google Scholar and it may be caused by delayed absorption of the diuretic, reduced secretion into the renal tubule, post-diuretic (rebound) salt retention, and compensatory hypertrophy of the distal tubule.4De Bruyne L.K. Mechanisms and management of diuretic resistance in congestive heart failure.Postgrad Med J. 2003; 79: 268-271Crossref PubMed Google Scholar Management includes: exclusion of precipitating factors (Table 1); salt and volume restriction; increased dosing of diuretics; intravenous application of diuretic; combination therapy of loop diuretic with thiazide or metolazone5Channer K.S. McLean K.A. Lawson-Matthew P. Richardson M. Combination diuretic treatment in severe heart failure: a randomised controlled trial.Br Heart J. 1994; 71: 146-150Crossref PubMed Google Scholar, 6Dormans T.P. Gerlag P.G. Combination of high-dose furosemide and hydrochlorothiazide in the treatment of refractory congestive heart failure.Eur Heart J. 1996; 17: 1867-1874Crossref PubMed Google Scholar; and institution of inodilatory therapy with dopamine, dobutamine or milrinone. Acute exacerbation of fluid retention represents the most common form of acute decompensation (“wet” decompensation) in patients with heart failure, leading to increased hospitalization, morbidity and cost. Diuretic resistance, further compromise of LV function, or intercurrent illness may represent precipitating factors. Rapid restoration of euvolemia, usually via intensified diuretic therapy, achieves symptomatic relief. In therapy-resistant cases hemofiltration or hemodialysis may be required. Activation of the RAAS and the adrenergic system has a pivotal role in the progression of heart failure.7Eichhorn E.J. Bristow M.R. Medical therapy can improve the biological properties of the chronically failing heart A new era in the treatment of heart failure.Circulation. 1996; 94: 2285-2296Crossref PubMed Google Scholar, 8Swedberg K. Importance of neuroendocrine activation in chronic heart failure Impact on treatment strategies.Eur J Heart Fail. 2000; 2: 229-233Crossref PubMed Scopus (27) Google Scholar, 9Weber K.T. Aldosterone in congestive heart failure.N Engl J Med. 2001; 345: 1689-1697Crossref PubMed Scopus (419) Google Scholar These systems are activated by increased myocardial stretch and peripheral hypoperfusion and cause vasoconstriction, hydrosaline retention, myocardial hypertrophy and fibrosis, fetal gene expression and accelerated cell death. Their importance is shown by their independent prognostic value and, more importantly, by the beneficial effects of their long-term pharmacologic inhibition. Hence, the administration of neurohormonal antagonists is the basis of the current medical treatment of chronic heart failure.10Hunt S.A. Baker D.W. Chin M.H. et al.ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary.J Heart Lung Transplant. 2002; 21: 189-203Abstract Full Text Full Text PDF PubMed Scopus (109) Google Scholar, 11Jessup M. Brozena S. Heart failure.N Engl J Med. 2003; 348: 2007-2018Crossref PubMed Scopus (1026) Google Scholar, 12Remme W.J. Swedberg K. Guidelines for the diagnosis and treatment of chronic heart failure.Eur Heart J. 2001; 22: 1527-1560Crossref PubMed Scopus (1305) Google Scholar The impact of neurohormonal antagonists on prognosis is so important that no patient should undergo heart transplantation if not previously treated with or shown to be intolerant of neurohormonal antagonists. As the beneficial effects of neurohormonal antagonists are progressive and may need at least 4 months to become significant,7Eichhorn E.J. Bristow M.R. Medical therapy can improve the biological properties of the chronically failing heart A new era in the treatment of heart failure.Circulation. 1996; 94: 2285-2296Crossref PubMed Google Scholar it is recommended to wait for such a time interval, if possible, before making a decision regarding heart transplantation candidacy in a patient not previously treated. It is also important to note that neurohormonal antagonists are not short-term life-saving agents. They are administered for their long-term beneficial effects on outcome. In the short term, their administration may be associated with worsening of symptoms and hemodynamic variables, so that their initiation may be poorly tolerated or even contraindicated in patients with unstable clinical conditions.7Eichhorn E.J. Bristow M.R. Medical therapy can improve the biological properties of the chronically failing heart A new era in the treatment of heart failure.Circulation. 1996; 94: 2285-2296Crossref PubMed Google Scholar, 13Bristow M.R. Beta-adrenergic receptor blockade in chronic heart failure.Circulation. 2000; 101: 558-569Crossref PubMed Google Scholar, 14Packer M. Neurohormonal interactions and adaptations in congestive heart failure.Circulation. 1988; 77: 721-730Crossref PubMed Google Scholar, 15Stevenson L.W. Beta-blockers for stable heart failure.N Engl J Med. 2002; 346: 1346-1347Crossref PubMed Scopus (11) Google Scholar 1.2.1. Angiotensin-converting enzyme inhibitors. The main mechanisms of action of the ACEIs include inhibiting LV remodeling and myocardial dysfunction, as well as reducing ischemic events in patients with concomitant coronary artery disease (CAD). The beneficial effects of ACEIs on symptoms, hospitalization rate and mortality have been consistently shown in large, placebo-controlled, randomized trials.16Flather M.D. Yusuf S. Kober L. et al.ACE-Inhibitor Myocardial Infarction Collaborative GroupLong-term ACE-inhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual patients.Lancet. 2000; 355: 1575-1581Abstract Full Text Full Text PDF PubMed Google Scholar, 17The CONSENSUS Trial Study GroupEffects of enalapril on mortality in severe congestive heart failure Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS).N Engl J Med. 1987; 316: 1429-1435Crossref PubMed Google Scholar These effects are independent from the baseline characteristics of the patients, except that they are of greater magnitude in patients with more severe LV dysfunction and symptoms.12Remme W.J. Swedberg K. Guidelines for the diagnosis and treatment of chronic heart failure.Eur Heart J. 2001; 22: 1527-1560Crossref PubMed Scopus (1305) Google Scholar, 16Flather M.D. Yusuf S. Kober L. et al.ACE-Inhibitor Myocardial Infarction Collaborative GroupLong-term ACE-inhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual patients.Lancet. 2000; 355: 1575-1581Abstract Full Text Full Text PDF PubMed Google Scholar, 17The CONSENSUS Trial Study GroupEffects of enalapril on mortality in severe congestive heart failure Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS).N Engl J Med. 1987; 316: 1429-1435Crossref PubMed Google Scholar Patients with severe heart failure have a lower tolerance to ACEI administration. Lower cardiac output and peripheral hypoperfusion are associated with a greater activation of the RAAS, with a corresponding increased likelihood of renal failure and hypotension when this system is blocked.14Packer M. Neurohormonal interactions and adaptations in congestive heart failure.Circulation. 1988; 77: 721-730Crossref PubMed Google Scholar, 18Packer M. Interaction of prostaglandins and angiotensin II in the modulation of renal function in congestive heart failure.Circulation. 1988; 77: I-64-I-73Crossref Google Scholar However, a mild 10% to 20% increase in serum creatinine after the initiation of ACEI therapy should not be considered a contraindication to the continuation of treatment. Similarly, hypotension should be a contraindication to treatment only if symptomatic.10Hunt S.A. Baker D.W. Chin M.H. et al.ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary.J Heart Lung Transplant. 2002; 21: 189-203Abstract Full Text Full Text PDF PubMed Scopus (109) Google Scholar, 12Remme W.J. Swedberg K. Guidelines for the diagnosis and treatment of chronic heart failure.Eur Heart J. 2001; 22: 1527-1560Crossref PubMed Scopus (1305) Google Scholar, 18Packer M. Interaction of prostaglandins and angiotensin II in the modulation of renal function in congestive heart failure.Circulation. 1988; 77: I-64-I-73Crossref Google Scholar, 19Packer M. Lee W.H. Kessler P.D. Medina N. Yushak M. Gottlieb S.S. Identification of hyponatremia as a risk factor for the development of functional renal insufficiency during converting enzyme inhibition in severe chronic heart failure.J Am Coll Cardiol. 1987; 10: 837-844Abstract Full Text PDF PubMed Google Scholar, 20Packer M. Lee W.H. Medina N. Yushak M. Kessler P.D. Functional renal insufficiency during long-term therapy with captopril and enalapril in severe chronic heart failure.Ann Intern Med. 1987; 106: 346-354Crossref PubMed Google Scholar Even if initiation and titration of ACEI therapy may be more difficult in patients with advanced heart failure, it must be pointed out that the beneficial effects of ACEIs on prognosis are similar in patients with renal failure21Mann J.F. Gerstein H.C. Pogue J. Bosch J. Yusuf S. Renal insufficiency as a predictor of cardiovascular outcomes and the impact of ramipril: the HOPE randomized trial.Ann Intern Med. 2001; 134: 629-636Crossref PubMed Google Scholar and greater in those with more severe heart failure.8Swedberg K. Importance of neuroendocrine activation in chronic heart failure Impact on treatment strategies.Eur J Heart Fail. 2000; 2: 229-233Crossref PubMed Scopus (27) Google Scholar, 17The CONSENSUS Trial Study GroupEffects of enalapril on mortality in severe congestive heart failure Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS).N Engl J Med. 1987; 316: 1429-1435Crossref PubMed Google Scholar Conversely, hemodynamic intolerance to ACEIs is associated with a worse prognosis.22Kittleson M. Hurwitz S. Shah M.R. et al.Development of circulatory–renal limitations to angiotensin-converting enzyme inhibitors identifies patients with severe heart failure and early mortality.J Am Coll Cardiol. 2003; 41: 2029-2035Abstract Full Text Full Text PDF PubMed Scopus (77) Google Scholar 1.2.2. ARBs. ARBs block the effects of angiotensin II on Type I angiotensin II receptors. These receptors mediate most, if not all, of the untoward effects of angiotensin II. Thus, as opposed to ACEIs, their efficacy cannot be decreased by the activation of non–ACE-dependent angiotensin II synthetic pathways. Hence, ARBs provide a more effective blockade of the Type I angiotensin receptors. Unlike the ACEIs, ARBs do not increase kinin levels. This property accounts for the increased tolerability of ARBs (lack of kinin-mediated side effects), but it may also lower their efficacy, because kinins have been associated with beneficial effects such as peripheral vasodilation and inhibition of myocardial hypertrophy and fibrosis.23Gring C.N. Francis G.S. A hard look at angiotensin receptor blockers in heart failure.J Am Coll Cardiol. 2004; 44: 1841-1846Abstract Full Text Full Text PDF PubMed Scopus (14) Google Scholar, 24McMurray J.J. Pfeffer M.A. Swedberg K. Dzau V.J. Which inhibitor of the renin–angiotensin system should be used in chronic heart failure and acute myocardial infarction?.Circulation. 2004; 110: 3281-3288Crossref PubMed Scopus (49) Google Scholar The Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity (CHARM) Alternative Trial has shown that the administration of an ARB improves prognosis in those heart failure patients who are intolerant of an ACEI.25Granger C.B. McMurray J.J. Yusuf S. et al.Effects of candesartan in patients with chronic heart failure and reduced left-ventricular systolic function intolerant to angiotensin-converting-enzyme inhibitors: the CHARM-Alternative trial.Lancet. 2003; 362: 772-776Abstract Full Text Full Text PDF PubMed Scopus (900) Google Scholar These data are consistent with previous studies in patients with chronic heart failure26Maggioni A.P. Anand I. Gottlieb S.O. Latini R. Tognoni G. Cohn J.N. Effects of valsartan on morbidity and mortality in patients with heart failure not receiving angiotensin-converting enzyme inhibitors.J Am Coll Cardiol. 2002; 40: 1414-1421Abstract Full Text Full Text PDF PubMed Scopus (188) Google Scholar or with post-infarction LV dysfunction or heart failure.27Pfeffer M.A. McMurray J.J. Velazquez E.J. et al.Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both.N Engl J Med. 2003; 349: 1893-1906Crossref PubMed Scopus (1478) Google Scholar The major trials addressing the issue of combined therapy with ARBs and ACEIs in heart failure have been the Valsartan Heart Failure Trial (Val-HeFT)28Cohn J.N. Tognoni G. A randomized trial of the angiotensin-receptor blocker valsartan in chronic heart failure.N Engl J Med. 2001; 345: 1667-1675Crossref PubMed Scopus (1927) Google Scholar and CHARM.29McMurray J.J. Ostergren J. Swedberg K. et al.Effects of candesartan in patients with chronic heart failure and reduced left-ventricular systolic function taking angiotensin-converting-enzyme inhibitors: the CHARM-Added trial.Lancet. 2003; 362: 767-771Abstract Full Text Full Text PDF PubMed Scopus (1238) Google Scholar In the Val-HeFT trial, the administration of valsartan to patients receiving ACEI therapy was associated with an 18.2% lower incidence of hospitalizations for heart failure; however, there was no effect on mortality. The CHARM-Added trial showed that the administration of candesartan to patients with severe heart failure (NYHA Class III or IV) or moderately symptomatic heart failure (NYHA Class II), but with a recent (<6 months) cardiovascular hospitalization, was associated with a reduction in the primary end-point (cardiovascular death or heart failure hospitalization) and a reduction in both cardiovascular death and heart failure hospitalizations. In contrast to the Val-HeFT trial, the beneficial effects of ARB use in the CHARM-Added trial were also observed in the patients on concomitant ACEI and β-blocker therapy. The differences between the two studies are likely influenced by the inclusion of patients with more advanced heart failure and poorer prognosis in the CHARM trial. ARBs should be administered with the same precautions as ACEIs. They lack the kinin-mediated effects of ACEIs, but may cause renal failure and hypotension by the same mechanism as ACEIs.10Hunt S.A. Baker D.W. Chin M.H. et al.ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary.J Heart Lung Transplant. 2002; 21: 189-203Abstract Full Text Full Text PDF PubMed Scopus (109) Google Scholar, 12Remme W.J. Swedberg K. Guidelines for the diagnosis and treatment of chronic heart failure.Eur Heart J. 2001; 22: 1527-1560Crossref PubMed Scopus (1305) Google Scholar 1.2.3. Aldosterone antagonists. In the Randomized Aldactone Evaluation Study (RALES), administration of spironolactone 25 to 50 mg/day was associated with a 35% reduction in mortality, a concomitant decrease in heart failure hospitalizations, and an improvement in symptoms.30Pitt B. Zannad F. Remme W.J. et al.Randomized Aldactone Evaluation Study InvestigatorsThe effect of spironolactone on morbidity and mortality in patients with severe heart failure.N Engl J Med. 1999; 341: 709-717Crossref PubMed Scopus (4822) Google Scholar The Eplerenone in Patients with Heart Failure Due to Systolic Dysfunction Complicating Acute Myocardial Infarction (EPHESUS) trial showed the beneficial effects of the selective aldosterone antagonist eplerenone in patients with recent myocardial infarction (MI) and LV dysfunction or heart failure.31Pitt B. Remme W. Zannad F. et al.Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction.N Engl J Med. 2003; 348: 1309-1321Crossref PubMed Scopus (2517) Google Scholar Aldosterone antagonists should therefore be considered in all candidates for heart transplantation. To minimize the risks of hyperkalemia and renal failure,32Juurlink D.N. Mamdani M.M. Lee D.S. et al.Rates of hyperkalemia after publication of the Randomized Aldactone Evaluation Study.N Engl J Med. 2004; 351: 543-551Crossref PubMed Scopus (867) Google Scholar aldosterone antagonists are generally contraindicated in patients with renal insufficiency (serum creatinine >2.5 mg/dl) or hyperkalemia (serum potassium >5.5 mEq/liter). Careful and frequent monitoring of these laboratory evaluations is required after the initiation of an aldosterone antagonist, and then periodically, at least every 1 to 3 months.10Hunt S.A. Baker D.W. Chin M.H. et al.ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary.J Heart Lung Transplant. 2002; 21: 189-203Abstract Full Text Full Text PDF PubMed Scopus (109) Google Scholar, 12Remme W.J. Swedberg K. Guidelines for the diagnosis and treatment of chronic heart failure.Eur Heart J. 2001; 22: 1527-1560Crossref PubMed Scopus (1305) Google Scholar, 33Metra M. Nodari S. Dei C.L. Current guidelines in the pharmacological management of chronic heart failure.J Renin Angiotensin Aldosterone Syst. 2004; 5: S11-S16Crossref PubMed Google Scholar 1.2.4. β-blockers. Large, randomized trials have consistently shown that β-blocker therapy is associated with a significant reduction in mortality and hospitaliz" @default.
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• W2000487813 title "Optimal Pharmacologic and Non-pharmacologic Management of Cardiac Transplant Candidates: Approaches to Be Considered Prior to Transplant Evaluation: International Society for Heart and Lung Transplantation Guidelines for the Care of Cardiac Transplant Candidates—2006" @default.
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