Heart Failure Evaluation and Long-Term Management

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Chapter 23

Heart Failure Evaluation and Long-Term Management

This chapter deals specifically with the evaluation and long-term management of patients with heart failure caused by depressed ejection fraction. The management of patients with heart failure with preserved ejection fraction (diastolic dysfunction) is discussed in Chapter 24. The management of patients with acute decompensated heart failure is discussed in Chapter 22. Specific discussions of the evaluation and management of myocarditis, dilated cardiomyopathy, hypertrophic cardiomyopathy, and restrictive/infiltrative cardiomyopathy, as well as consideration with cardiac transplantation, are discussed in other dedicated chapters in this section of the book. The roles of pacemakers and implantable cardioverter-defibrillators in patients with heart failure are discussed in this chapter, as well as in the chapters on pacemakers (Chapter 37) and implantable cardioverter-defibrillators (Chapter 38).

1. What are the most common causes of heart failure?

    Ischemic heart disease, hypertension, and valvular heart disease are the most common causes of heart failure. Less common causes include diabetes; microvascular disease; genetic cardiomyopathies and muscular dystrophies; autoimmune and collage vascular diseases such as systemic lupus, dermatomyositis, or scleroderma; toxic cardiomyopathies, including alcohol or illicit drugs such as cocaine; chemotherapy induced cardiomyopathies (e.g., Adriamycin); myocarditis and viral cardiomyopathy; postpartum cardiomyopathy; tachycardia-mediated heart failure; hypothyroidism- or hyperthyroidism-related cardiomyopathies; infiltrative disorders such as sarcoidosis, hemochromatosis, and amyloidosis; high-output states (thyrotoxicosis, beriberi, systemic arteriovenous shunting, chronic anemia); and stress-induced (Tako-tsubo) cardiomyopathy.

2. What elements should the initial assessment of the patient with heart failure include?

    Initial assessment of the patient with heart failure should include:

image Evaluation of heart failure symptoms and functional capacity (dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea [PND], fatigue, and lower extremity edema)

image Evaluation for the presence of diabetes; hypertension; smoking; prior cardiac disease; family history of cardiac disease; history of heart murmur, congenital heart disease, or rheumatic fever; sleep disturbances (obstructive sleep apnea [OSA]); thyroid disease history; exposure to infectious agents; exposure to cardiotoxins; mediastinal irradiation; and past or current use of alcohol and illicit drugs

image Physical examination, including heart rate and rhythm; blood pressure and orthostatic blood pressure changes; measurements of weight, height, and body mass index; overall volume status; jugular venous distension; carotid upstroke and presence or absence of bruits; lung examination for rales or effusions; cardiac examination for systolic or diastolic murmurs; displaced point of maximal impulse (PMI); presence of left ventricular heave; intensity of S2; presence of S3 or S4; liver size; presence of ascites; presence of renal bruits; presence of abdominal aortic aneurysm; peripheral edema; peripheral pulses; and checking whether the extremities are cold and clammy

image Laboratory tests, including complete blood cell count (CBC), creatinine and blood urea nitrogen (BUN), serum electrolytes, natriuretic peptide (BNP or NT-proBNP), fasting blood glucose, lipid profile, liver function tests, thyroid-stimulating hormone (TSH), and urine analysis; and screening for hemochromatosis and human immunodeficiency virus (HIV), pheochromocytoma, amyloidosis, or rheumatologic diseases reasonable in selected patients, particularly if there is clinical suspicion for testing

image Twelve-lead electrocardiogram (ECG), assessing for rhythm, conduction abnormalities, QRS voltage and duration, QT duration, chamber enlargement, presence of ST/T changes, and Q waves

image Chest radiograph

image Transthoracic echocardiogram to asses for left ventricular (LV) and right ventricular (RV) function: wall motion; chamber sizes; filling pressures; morphology of the valves; presence of ventricular hypertrophy; and diastolic parameters

image Consideration of ischemia workup; depending on patient’s age, history, symptoms, and ECG, this may be no workup, stress testing, or cardiac catheterization.

image Endomyocardial biopsy is not part of routine workup but can be considered in highly specific circumstances (see later).

image Consider cardiac MRI if infiltrative causes, such as cardiac sarcoidosis or amyloidosis, are suspected.

3. How are heart failure symptoms classified?

    Symptoms are most commonly classified using the New York Heart Association (NYHA) classification system:

4. What is the stage system for classifying heart failure?

    In 2001, the American College of Cardiology/American Heart Association (ACC/AHA) introduced a system to categorize the stages of heart failure. This system is somewhat different in focus than the previous NYHA classification system and was intended, in part, to emphasize the prevention of the development of symptomatic heart failure. In addition, the 2009 update on the 2005 Heart Failure Guidelines suggest appropriate therapy for each stage (Figure 23-1).

image Stage A: Patient is at high risk for developing heart failure but is without structural heart disease or symptoms of heart failure. Includes patients with hypertension, coronary artery disease (CAD), obesity, diabetes, history of drug or alcohol abuse, history of rheumatic fever, family history of cardiomyopathy, or treatment with cardiotoxins

image Stage B: Patient with structural heart disease but is without signs or symptoms of heart failure. Includes patients with previous myocardial infarction (MI), LV remodeling (including left ventricular hypertrophy [LVH] or low ejection fraction), or asymptomatic valvular disease

image Stage C: Patient with structural heart disease and with prior or current symptoms of heart failure

image Stage D: Patient with refractory heart failure requiring specialized interventions

5. Which patients with heart failure should be considered for endomyocardial biopsy (EMB)?

    In 2007, the ACC/AHA/European College of Cardiology (ACC/AHA/ECC) issued a scientific statement on the role of EMB. Most patients who are seen for heart failure should not be referred for EMB. Biopsy results are often nonspecific or unrevealing, and in most cases there is no specific therapy based on biopsy results that have been shown to improve prognosis. However, in certain clinical scenarios, EMB should be performed (class I recommendation) or can be considered and is considered reasonable (class IIa recommendation). As given in that document, these scenarios include the following:

image New-onset heart failure of less than 2 weeks duration associated with a normal-sized or dilated left ventricle and hemodynamic compromise (class I; level of evidence B)

image New-onset heart failure of 2 weeks to 3 months duration associated with a dilated left ventricle and new ventricular arrhythmias, second- or third-degree heart block, or failure to respond to usual care within 1 to 2 weeks (class I; level of evidence B)

image Heart failure of more than 3 months duration associated with a dilated left ventricle and new ventricular arrhythmias, second- or third-degree heart block, or failure to respond to usual care within 1 to 2 weeks (class IIa; level of evidence C)

image Heart failure associated with a dilated cardiomyopathy of any duration associated with suspected allergic reaction or eosinophilia (class IIa; level of evidence C)

image Heart failure associated with suspected anthracycline cardiomyopathy (class Ia; level of evidence C)

image Heart failure with unexplained restrictive cardiomyopathy (class IIa; level of evidence C)

6. What are the general treatments for patients with heart failure?

image Diuretics are indicated for volume overload. Starting doses of furosemide are often 20 to 40 mg once or twice a day, but higher doses will be required in patients with significant renal dysfunction. The dose should be uptitrated to a maximum of up to 600 mg daily in divided doses. Failure of therapy is often the result of inadequate diuretic dosing. Torsemide is more expensive than furosemide but has superior absorption and longer duration of action. Bumetanide is approximately 40 times more potent milligram-for-milligram than furosemide and can also be used in patients who are unresponsive or poorly responsive to furosemide. Synergistic diuretics that act on the distal portion of the tubule (thiazides such as metolazone, or potassium-sparing agents) are often added in those who fail to respond to high-dose loop diuretics alone. In addition, a new recommendation from 2009 Focused Update states that for hospitalized heart failure patients, if diuresis is inadequate to relieve congestion, higher doses of loop diuretics should be used, addition of second diuretic should be made or continuous infusion of a loop diuretic should be considered.

image Inhibition of the renin-angiotensin-aldosterone system should be initiated. Angiotensin-converting enzyme (ACE) inhibitors are first-line agents in those with depressed ejection fraction because they have been convincingly shown to improve symptoms, decrease hospitalizations, and reduce mortality. Angiotensin II receptor blockers (ARBs) are used in those who are ACE-inhibitor intolerant because of persistent cough. ARBs may also be considered in addition to ACE inhibitors in select patients (this latter decision is best left to a heart failure specialist). The aldosterone antagonists spironolactone or eplerenone can be considered as additional therapy in carefully selected patients with preserved renal function already on standard heart failure therapies.

image Hydralazine and isosorbide are used in patients who are unable to tolerate both ACE inhibitors and ARBs because of renal failure. Hydralazine and isosorbide should be considered in addition to an ACE inhibitor or ARB in African Americans, and can be considered as an add-on therapy in others. They may be considered in patients who are ACE inhibitor and ARB intolerant.

image The beta-adrenergic blocking agents (β-blockers) metoprolol succinate (Toprol XL), carvedilol (Coreg), and bisoprolol have been shown to decrease mortality in appropriately selected patients. These agents should be initiated in euvolemic patients on stable background heart failure therapy, including ACE inhibitors or ARBs.

image Implantable cardioverter-defibrillators (ICDs) are considered for primary prevention in patients whose ejection fractions remain less than 30% to 35% despite optimal medical therapy, and who have a good-quality life expectancy of at least 1 year.

image Biventricular pacing for resynchronization therapy should be considered. According to the 2009 American College of Cardiology Foundation/AHA (ACCF/AHA) guidelines, biventricular pacing for cardiac resynchronization therapy (CRT) should be considered for patients in sinus rhythm with NYHA class III-IV symptoms, left ventricular ejection fraction (LVEF) less than 35%, and QRS greater than 120 ms. Consultation with an electrophysiologist is recommended.

The elements of long-term management of patients with CHF resulting from depressed LV systolic function are summarized in Table 23-1.

TABLE 23-1

ELEMENTS OF THE LONG-TERM MANAGEMENT OF PATIENTS WITH CONGESTIVE HEART FAILURE DUE TO LEFT VENTRICULAR SYSTOLIC DYSFUNCTION

Treatment/Intervention Recommendation (Level of Evidence)
Diuretics for fluid retention Class I (LOE: C)
Salt restriction Class I (LOE: C)
ACE inhibitors (ACEIs) Class I (LOE: A)
Angiotensin II receptor blockers (ARB) in ACEI-intolerant patients Class I (LOE: A)
ARB in persistently symptomatic patients with reduced LVEF already being treated with conventional therapy Class IIb (LOE: C)
Hydralazine + Isosorbide in patients ACEI and ARB intolerant Class IIb (LOE: C)
Hydralazine + Isosorbide in patients already on ACEI and β-blocker with persistent symptoms Class IIa (LOE: A)
β-Blockers Class I (LOE: A)
Digoxin in patients with heart failure symptoms. Generally used in those with continued symptoms and/or hospitalizations despite good therapy with diuretics and ACEIs Class IIa (LOE: B)
Aldosterone antagonists in patients with moderate-severe symptoms who can carefully be monitored for renal function and potassium level and with baseline creatinine < 2-2.5 mg/dL and potassium < 5.0 mEq/L Class I (LOE: B)
Exercise training in ambulatory patients Class I (LOE: B)
ICD for “secondary prevention” (history of cardiac arrest, ventricular fibrillation, or hemodynamically destabilizing ventricular tachycardia) Class I (LOE: A)
ICD for “primary prevention” for LVEF < 30%-35% and symptomatic heart failure (see text) Class I-IIa (LOE: A-B)
Cardiac resynchronization therapy for patients in sinus rhythm with class III-IV symptoms despite medical therapy, LVEF < 35%, and QRS > 120 ms (see text) Class I (LOE: A)

ACE, Angiotensin-converting enzyme; ICD, implantable cardioverter-defibrillator; LVEF, left ventricular ejection fraction.

Modified from Hunt SA, Abraham WT, Chin MH, et al: ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol 46:e1-e82, 2005.

7. How do ACE inhibitors and ARBs work?

    ACE inhibitors inhibit ACE, thus blocking the conversion of angiotensin I to angiotensin II. ACE is predominantly found in the pulmonary and to a lesser extent in the renal endothelium. By decreasing the production of angiotensin II, ACE inhibitors attenuate sympathetic tone, decrease arterial vasoconstriction, and attenuate myocardial hypertrophy. Because angiotensin II stimulates aldosterone production, circulating levels of aldosterone are reduced. This results in decreased in sodium chloride absorption, decreased potassium excretion in the distal tubules, and decreased water retention. Through a decrease in antidiuretic hormone (ADH) production, ACE inhibitors also decrease water absorption in the collecting ducts.

    ARBs selectively block the binding of angiotensin II to the AT1 receptor, thereby blocking the effect of angiotensin II on end organs. This results in attenuation of sympathetic tone, decrease in arterial vasoconstriction, and attenuation of myocardial hypertrophy. Because angiotensin II stimulates aldosterone production, circulating levels of aldosterone are reduced. This results in a decrease in sodium chloride absorption, potassium excretion in the distal tubules, and water retention.

8. What approach should be taken if a patient treated with an ACE inhibitor develops a cough?

    Nonproductive cough related to ACE inhibitors occurs in 5% to 10% of white patients of European descent and in up to 50% of Chinese patients. The cough is believed related to kinin potentiation. The cough usually develops within the first months of therapy and disappears within 1 to 2 weeks of discontinuation of therapy. ACC/AHA guidelines suggest one should first make sure the cough is related to treatment and not to another condition. The guidelines state that the demonstration that the cough disappears after drug withdrawal and recurs after rechallenge with another ACE inhibitor strongly suggests that ACE inhibition is the cause of the cough. They emphasize that patients should be rechallenged, because many will not redevelop a cough, suggesting the initial development of cough was coincidental and may have been related to heart failure. Patients who do have ACE inhibitor–related cough and cannot tolerate symptoms should be treated with an ARB.

9. What is the efficacy of ARBs compared with ACE inhibitors in patients with chronic heart failure?

    Trials comparing the efficacy of ARBs with ACE inhibitors in chronic heart failure revealed that treatment with ARB was equivalent to ACE inhibition (trials using valsartan and candesartan); however, a trend toward improved outcomes was noted with ACE inhibitors in a trial using the ARB losartan.

    In view of the vast experience with the ACE inhibitors as compared with ARBs, ACE inhibitors continue to be the recommended agents of choice for patients with heart failure and depressed LV systolic function. That said, ARBs—specifically, candesartan and valsartan—confer significant benefit on mortality and morbidity in patients with heart failure who are intolerant of ACE inhibitors, and therefore offer a good alternative strategy in these patients. Candesartan and valsartan are the recommended ARBs for patients with heart failure who are intolerant of ACE inhibitors.

10. When should ARBs be added to ACE inhibitors in patients with chronic heart failure?

    Theoretically, the more complete angiotensin II inhibition using a combination of ACE inhibitors and ARBs in patients with heart failure may translate into improved clinical outcomes.

    Two large clinical trials in patients with heart failure, the Val-HeFT and the CHARM-Added trial, evaluated the impact on morbidity and mortality of adding ARBs to ACE inhibitors. Both trials suggest that adding an ARB to an ACE inhibitor leads to a reduction in heart failure hospitalizations, although combination therapy had no impact on mortality. Thus, the current Heart Failure Society of America guidelines recommend the addition of ARBs to ACE inhibitors in patients who meet the following conditions:

11. How do aldosterone antagonists work?

    Aldosterone receptor blockers block the mineralocorticoid receptor in the distal renal tubules, thereby decreasing sodium chloride absorption, potassium excretion, and water retention. In addition, they block the direct deleterious effects of aldosterone on the myocardium and may thus decrease myocardial fibrosis and its consequences.

12. List the indications and recommended dosing of aldosterone antagonists in heart failure.

    Current indications include the following:

Dosing is as follows:

The initial and target doses for aldosterone antagonists and other drugs used to treat patients depressed systolic ejection fraction and/or CHF are listed in Table 23-2.

TABLE 23-2

INITIAL AND TARGET DOSES FOR COMMONLY USED DRUGS FOR PATIENTS WITH DEPRESSED SYSTOLIC EJECTION FRACTION AND/OR CONGESTIVE HEART FAILURE

image

image

ACE, Angiotensin-converting enzyme; bid, twice a day; qd, one a day; tid three times a day.

Extended-release carvedilol now available, although this preparation not specifically tested in heart failure.

Modified from Hunt SA, Abraham WT, Chin MH, et al: ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol 46:e1-e82, 2005.

13. Can all patients with heart failure safely be started on an aldosterone antagonist?

    No. Aldosterone antagonists should not be started in men with creatinine more than 2.5 mg/dL or women with creatinine more than 2 mg/dL, patients with potassium more than 5 mEq/L, those in whom monitoring for hyperkalemia and renal function is not anticipated to be feasible, and those not already on other diuretics.

14. Describe common adverse effects of ACE inhibitors, ARBs, and aldosterone antagonists.

    Common adverse effects include the following:

ARBs are as likely as ACE inhibitors to produce hypotension, worsening renal function, and hyperkalemia. Otherwise, ARBs are better tolerated than ACE inhibitors. The incidence of cough is much lower in ARBs (approximately 1%) compared with ACE inhibitors (approximately 10%). The incidence of angioedema with ACE inhibitors is rare (less than 1%; more common in African Americans) and even more rare with ARBs. However, because there have been case reports of patients developing angioedema on ARBs, the guidelines advise that ARBs may be considered in patients who have had angioedema while taking an ACE inhibitor, albeit with extreme caution. Practically, if a patient develops angioedema while taking an ACE inhibitor, an ARB is generally not initiated.

Gynecomastia and other antiandrogenic effects can occur with spironolactone and are not generally seen with eplerenone.

15. What are the indications and dosing of nitrates/hydralazine in patients with chronic heart failure?

    The vasodilator combination of isosorbide dinitrate (Isordil) and hydralazine (I/H) has been shown to produce modest benefit in patients with heart failure, compared with placebo. The combination has, however, been shown to be less effective than ACE inhibitors. The recent A-Heft trial, which was limited to African-American patients with class III-IV heart failure, showed that the addition of I/H to standard therapy with ACE inhibitor or a β-blocker conferred significant morbidity and mortality benefit.

    Taking all the evidence together, the I/H combination is indicated in the following patients:

Dosages are as follows:

16. How should patients be treated with β-blockers?

    Certain β-blockers have been convincingly shown to decrease mortality in patients with depressed ejection fraction and symptoms of heart failure, and thus it is a class I indication to treat such patients with β-blockers, with an attempt to reach target doses. The β-blockers shown to decrease mortality, their starting doses, and their target doses are given in Table 2. Recommendations from the Heart Failure Society of America and other organizations include the following:

image Patients should not be initiated on β-blocker therapy during decompensated or hemodynamically unstable state heart failure.

image β-Blocker therapy should only be initiated when patients are euvolemic and hemodynamically stable, are usually on a good maintenance dose of diuretics (if indicated), and receiving ACE inhibitors or ARBs.

image β-Blockers should be initiated at low doses, uptitrated gradually (in at least 2-week intervals), and titrated to target doses shown to be effective in clinical trials (see Table 23-2). Practitioners should aim to achieve target doses in 8 to 12 weeks from initiation of therapy and to maintain patients at maximal tolerated doses.

image If patient symptoms worsen during initiation or dose titration, the dose of diuretics or other concomitant vasoactive medications should be adjusted, and titration to target dose should be continued after the patient’s symptoms return to baseline.

image If uptitration continues to be difficult, the titration interval can be prolonged, the target dose may have to be reduced, or the patient should be referred to a heart failure specialist.

image If an acute exacerbation of chronic heart failure occurs, therapy should be maintained if possible; the dose can be reduced if necessary, but abrupt discontinuation should be avoided. If the dose is reduced (or discontinued), the β-blocker (and prior dose) should be gradually reinstated before discharge, if possible.

17. What is the mechanism of action of digoxin?

    Digoxin is a cardiac glycoside and is an inhibitor of the Na+,K+-ATPase pump in the sarcolemmal membrane of the myocyte and other cells. This inhibition causes intracellular accumulation of Na+, which makes the Na+-Ca2+ pump extrude less Ca2+, causing Ca2+ to accumulate inside the cell. This effect results in increased force of contraction. Cardiac glycosides also have effects in the central nervous system, enhancing parasympathetic and reducing sympathetic outputs to the heart, through carotid sinus baroreceptor reflex sensitization. This is the mechanism that underlies the reduction in sinus node activity and slowing in atrioventricular (AV) conduction, which makes digoxin the only agent with a positive inotropic-bradycardic effect and is the basis for its use in the control of some supraventricular arrhythmias.

18. Is there scientific evidence for the use of digoxin?

    The Digitalis Investigation Group (DIG) trial was a multicenter, randomized, double-blinded, placebo-controlled study of 6801 symptomatic patients with heart failure and ejection fraction less than 45%, who were in sinus rhythm. Mean follow-up was 37 months. Patients already receiving digoxin were allowed into the trial and randomized to digoxin or placebo without a washout period. About 95% of patients in both groups received ACE inhibitors; β-blockers were not in use for heart failure at the time. The primary outcome was total mortality. Digoxin did not improve total mortality (34.8% versus 35.1% in the placebo group, P = 0.80) or deaths from cardiovascular causes (29.9% versus 29.5%, P = 0.78). Hospitalizations as a result of worsening heart failure (a secondary endpoint) were significantly reduced by digoxin (26.8% versus 34.7% in the placebo group, risk ratio 0.72, P < 0.001). Hospitalizations for suspected digoxin toxicity were higher in the digoxin group (2% versus 0.9%, P < 0.001). In an ancillary, parallel trial in patients with ejection fraction greater than 45% and sinus rhythm, the findings were consistent with the results of the main trial. Whether these results hold with contemporary heart failure treatment that includes β-blockers, aldosterone-receptor blockers, and resynchronization therapy is not known.

19. What are some of the relevant drug interactions of digoxin?

20. What are the clinical manifestations of digoxin toxicity?

    Digoxin has a narrow safety margin (the difference in plasma drug concentrations between therapeutic and toxic levels is small). Patients with digoxin toxicity may manifest nausea, vomiting, anorexia, diarrhea, fatigue, generalized malaise, visual disturbances (green or yellow halos around lights and objects), and arrhythmias. In the presence of hypokalemia, digoxin toxicity may occur within the therapeutic level. Digoxin dose should be reduced in elderly patients, in patients with renal insufficiency (glomerular filtration rate [GFR] less than 60 mL/min), and when combined with certain drugs. To guide dosing during chronic therapy, digoxin levels should be measured 6 to 8 hours after a dose.

21. What are the electrocardiographic findings of digoxin toxicity?

    Digoxin toxicity can result in a variety of ventricular and supraventricular arrhythmias and AV conduction abnormalities, including:

These arrhythmias result from the electrophysiologic effects of digoxin: Increased intracellular Ca2+ levels predispose to Ca2+-induced delayed afterdepolarizations and, hence, increased automaticity (especially in the junction, Purkinje system, and ventricles); excessive vagal effects predispose to sinus bradycardia and/or arrest, and AV block. Bradyarrhythmias and blocks are more common when the patient is also taking amiodarone.

22. How is digoxin toxicity treated?

    It depends on the clinical severity. Digoxin withdrawal is sufficient with only suggestive symptoms. Activated charcoal may enhance the gastrointestinal (GI) clearance of digoxin if given within 6 hours of ingestion. Drugs that increase plasma digoxin levels (see Question 19) should be discontinued (except amiodarone, because of its long half-life). Correction of hypokalemia is vital (intravenous [IV] replacement through a large vein is preferred with life-threatening arrhythmias), but judgment is needed in the presence of high degrees of AV block. Symptomatic AV block may respond to atropine or to phenytoin (100 mg IV every 5 minutes up to 1000 mg until response or side effects); if no response, use digoxin immune Fab (ovine) (Digibind). The use of temporary transvenous pacing should be avoided. Patients with severe bradycardia should be given Digibind, even if they respond to atropine. Lidocaine and phenytoin may be used to treat ventricular arrhythmias, but for potentially life-threatening bradyarrhythmias or tachyarrhythmias, Digibind should be used. IV magnesium may be given 2 grams over 5 minutes and has been shown to help with digoxin toxicity related arrhythmias. Dialysis has no role because of the high tissue-binding of digoxin.

23. What are the indications for Digibind?

    The indications for Digibind include life-threatening bradyarrhythmias and tachyarrhythmias; hemodynamic instability caused by digoxin, potassium level of more than 5 mEq/L in the setting of acute ingestion, regardless of symptoms or ECG findings; and digoxin level of more than 10 ng/mL or the ingestion of more than 10 mg of digoxin, regardless of symptoms or ECG findings. Digibind is an antibody that binds to digoxin in the plasma and interstitial space, creating a concentration gradient for the exit of intracellular digoxin. As poisoning of the Na+,K+-ATPase is relieved, K+ is pumped intracellularly with the potential of causing hypokalemia; potassium levels should be monitored when Digibind is used. The half-life of the digoxin-Digibind complex is 15 to 20 hours if renal function is normal. Serum digoxin concentration rises significantly after Digibind use (as tissue digoxin is released into the bloodstream, bound to the antibody) and should not be measured.

24. What three classes of drugs exacerbate the syndrome of CHF and should be avoided in most CHF patients?

25. Is dietary restriction of sodium recommended in patients with symptomatic heart failure?

    Yes. In general, patients should restrict themselves to 2 to 3 g sodium daily, and less than 2 g daily in moderate to severe cases of heart failure.

26. Is fluid restriction recommended in all patients with heart failure?

    Not necessarily. Expert opinion differs, although some believe fluid restriction generally is not necessary unless the patient (a) is hyponatremic (sodium less than 130 mEq/L) or (b) fluid retention is difficult to control despite high doses of diuretics and sodium restriction. In such cases, patients are generally restricted to less than 2 L/day.

27. Should patients with CHF be told to use salt substitutes instead of salt?

    In some cases, the answer is no. Many salt substitutes contain potassium chloride in place of sodium chloride. This could lead to potential hyperkalemia in patients on potassium-sparing diuretics, ACE inhibitors or ARBs, or aldosterone antagonists, and those with chronic kidney disease (or those with the potential to develop acute renal failure). Patients who are permitted to use salt substitutes need to be cautioned about potassium issues.

28. What are the current criteria for consideration of CRT with biventricular pacing?

    Patients who should be considered for referral of CRT (class I indication) with or without ICD are those who meet the following criteria:

29. Which patients with heart failure should be considered for an ICD?

    In the 2008 ACC/AHA/Heart Rhythm Society (ACC/AHA/HRS) guidelines on device-based therapy, the writing group stated that they believed guidelines for ICD implantation should reflect the ICD trials that were conducted. Thus, there are many very specific indications for ICD placement, based on symptom class, ischemic or nonischemic causes of heart failure, and ejection fraction. Because ejection fraction may improve significantly after MI (as a result of myocardial salvage and myocardial stunning) and with optimal medical therapy (including ACE inhibitors/ARBs and β-blockers), patients being considered for ICD implantation for primary prevention should be optimally treated and have their ejection fraction reassessed on optimal medical therapy. ICD should only be considered in patients with a reasonable expectation of survival with an acceptable functional status for at least 1 year. Class I recommendations for ICD include the following:

The 2005 European Society of Cardiology guidelines for the diagnosis and treatment of CHF distill their recommendations into three concise points:

image ICD therapy is recommended to improve survival in patients who have survived cardiac arrest or who have sustained VT, which is either poorly tolerated or associated with reduced systolic LV function (class I; level of evidence A).

image ICD implantation is reasonable in selected patients with LVEF less than 30% to 35%, not within 40 days of an MI, on optimal background therapy including ACE inhibitor, ARB, β-blocker, and an aldosterone antagonist, where appropriate, to reduce likelihood of sudden death (class I; level of evidence A).

image ICD implantation in combination with biventricular pacing can be considered in patients who remain symptomatic with severe heart failure, NYHA class III-IV, with LVEF 35% or less and QRS 120 ms or more to improve mortality or morbidity (class IIa; level of evidence B).

Bibliography, Suggested Readings, and Websites

1. Arnold, J.M.O., Heart Failure (HF) 2012 Available at http://www.merckmanuals.com/professional/cardiovascular_disorders/heart_failure/heart_failure_hf.html Accessed March 19, 2013

2. Cooper, L.T., Baughman, K.L., Feldman, A.M., et al. The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology. Endorsed by the Heart Failure Society of America and the Heart Failure Association of the European Society of Cardiology. J Am Coll Cardiol. 2007;50:1914–1931.

3. Epstein, A.E., DiMarco, J.P., Ellenbogen, K.A., et al. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008;51:e1–e62.

4. Heart Failure Society of America. The HFSA website. Available at http://www.hfsa.org. Accessed March 19, 2013

5. Heart Failure Society of America. Heart failure in patients with left ventricular systolic dysfunction. J Card Fail. 2006;12:e38–e57.

6. Hunt, S.A., Abraham, W.T., Chin, M.H., et al. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol. 2005;46:e1–e82.

7. Jessup, M., Abraham, W.T., Casey, D.E., et al. Focused Update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults. Circulation. 2009;119:1977–2016.

8. Mann, D.L. Management of heart failure patients with reduced ejection fraction. In Libby P., Bonow R., Mann D., eds.: Braunwald’s heart disease: a textbook of cardiovascular medicine, ed 8, Philadelphia: Saunders, 2008.

9. Swedberg, K., Cleland, J., Dargie, H., et al. Guidelines for the diagnosis and treatment of chronic heart failure: executive summary (update 2005): the Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology. Eur Heart J. 2005;26:1115–1140.

10. Dumitru, I. Heart Failure. Available at http://www.emedicine.com. Accessed March 19, 2013