Best of heart failure

4 in particular, classifies patients into rogressive worsening of symptoms t daily activities, and multiple hospi- ptimal HF therapy. Recurrent hospi- uropean EPICAL registry of more d that patients were admitted to the spent nearly 28 days per year in the ms at rest despite being on medical venous (IV) inotropic therapy, ven- lantation. Similarly, New York Heart nto class I–IV based on the severity noted by marked limitation of phys- hysical activity without discomfort, all into NYHA Class III–IV catego- ms of HF, it is imperative to find the F is extensive, some of the common ons, thyroid dysfunction, ischemia, and hypertension. Of note, however, ailure but no structural disease or nt but patient is asymptomatic nt along with symptoms apy and requiring advanced interventions f daily living without experiencing any ctivities of daily living ity triggers symptoms of HF g fatigue, inability to ambulate G. Murtaza and W. G. Cotts patients with HF to avoid nephrotoxicity and volume overload. Dihydropyridine calcium channel blockers, in particular amlodipine, should be avoided in HF as they have been shown to cause peripheral edema by causing arteriolar dilatation and fluid extravasation [19]. PRAISE II Trial concluded that amlodipine does not exert favorable effects on the clinical course of patients with HF, regardless of the presence or absence of coronary artery disease. Verapamil has a negative inotropic effect and should ideally be avoided in HF with reduced ejection fraction. Diltiazem has a lesser inotropic effect and can be used with caution with patients with HF, particularly when control of supraventricular tachyarrhythmias is required [20, 21]. Weight reduction should be emphasized. Smoking cessation and vaccinations including influenza and pneumococcal should be encouraged. Alcohol should be limited and completely avoided in cases of alcoholic cardiomyopathy [22]. Medical Management Over the last 30 years, great advances have been taken in the research of appropriate medicines that improve survival and outcomes in HF. In the 1980s and early 1990s several large randomized clinical trials demonstrated a survival benefit with ACE inhibitors in both asymptomatic patients with LV dysfunction and patients with severe HF. The SOLVD prevention and treatment trials demonstrated survival benefits in symptomatic and asymptomatic patients with left ventricular dysfunction treated with enalapril [23]. In 1987, the CONSENSUS trial showed a significant survival benefit of adding enalapril, to conventional medical therapy in patients with severe congestive HF [24]. Careful attention to side effects of ACE inhibitors such as cough and angioedema should be considered. ARBs may considered as substitutes with such side effects. With regards to ARBs, the CHARM Trial in 2004 showed improved outcomes when candesartan, an ARB, was added to standard medical therapy including a beta blocker, ACE inhibitor, and aldosterone antagonist [25]. However, the benefit was not enough to recommend the use of both ACE inhibitors and ARBs. Combined use can lead to hyperkalemia, worsen renal function and lead to hypotension [26]. Sacubitril/valsartan, an angiotensin receptor-neprilysin inhibitor, was recently approved for HF patients with NYHA Class II–IV with an EF of 35%. The Paradigm trial showed a significant reduction in risk of death and hospitalization for HF with sacubitril/valsartan when compared with enalapril. Patients with GFR less than 30 mL/h. were excluded from the study, limiting its use in patients with poor kidney function [27]. A number of randomized multicenter clinical trials evaluating the efficacy of beta-blockers in patients with HF showed significant survival benefits. Trials such as MERIT-HF, CIBIS II, the US Carvedilol Trials and COPERNICUS showed that metoprolol succinate, carvedilol, and bisoprolol improve survival, improve EF and symptoms in HF [28–31]. Carvedilol may have an added advantage of alfa blocking activity which causes peripheral dilation and carvedilol also has an effect on improving insulin sensitivity [32, 33]. Beta blockers should be gradually uptitrated at 2-week intervals with attention paid to hypotension and bradycardia. Beta-blockers should not be initiated or uptitrated with patients with evidence of acute HF. Abrupt discontinuation of beta blocker therapy in HF should be avoided as rebound effects can occur. In such a situation, a decrease in dosage is warranted. However, in cardiogenic shock, beta blockers should be held. The A-HeFT trial in 2004, which looked at combined hydralazine and isosorbide dinitrate therapy in advanced HF African American patients with low ejection fraction, NYHA class III to IV symptoms, was terminated early when it demonstrated improved survival and reduced hospitalization in the treatment group [34, 35]. Several studies have demonstrated a survival benefit with aldosterone inhibitors. The first was the RALES trial which showed survival benefit with spironolactone in patients with class III and IV HF [36]. The Ephesus trial demonstrated a survival benefit in post myocardial infarction patient receiving eplerenone [37]. In general, all HF patients should be on a beta blocker, ACE inhibitors (ARBs if ACE inhibitors cannot be tolerated). Loop diuretics should be added for symptomatic improvement of dyspnea and relief of congestion. Aldosterone receptor antagonists are recommended in addition to ACE inhibitors, beta blockers and diuretics unless contraindications are present. Nitrates may be added to help improve dyspnea and angina [4] (Table 3). Diuresis is an important part of therapy as it reduces filling pressures and central and pulmonary vascular congestion. Inmost patients, diuresis is achieved through the use of a loop diuretics. Loop diuretics are considered first line diuretic therapy because they are effective and retain their effectiveness with worsening of renal function. Usually, patients are on diuretic therapy at home. In hospitalized patients with ADHF, IV furosemide is generally used to target a net negative fluid balance. IV furosemide is preferred because compared to oral, IV has greater bioavailability. The IV dose should be at least equivalent to the home dose when initiating therapy in the hospital, and uptitration can be done depending on the volume status of the patient. Loop diuretics are the recommended diuretics for patients with advanced CKD as other diuretics are less effective with GFR less than 30 mL/h. However, even loop diuretics may lose their efficacy in the setting of hypotension, significant intrinsic renal disease, and as GFR decreases, as only 15–20% of furosemide is delivered to the kidney tubules in CKD stage 5. In the setting of a severe edematous state, increased gut edema impairs absorption of furosemide. In this setting, either switching to IV furosemide or oral bumetanide or torsemide, loop diuretics with predictable bioavailability, can be considered [38]. Generally speaking, of the three loop diuretics, furosemide, bumetanide, and torsemide, torsemide has the