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Scientific Review and Clinical Applications | Clinician's Corner

β-Blockers in Heart Failure Clinical Applications FREE

Michael H. Farrell, MD; JoAnne Micale Foody, MD; Harlan M. Krumholz, MD
[+] Author Affiliations

Author Affiliations: Department of Internal Medicine, Sections of Cardiovascular Medicine (Drs Foody and Krumholz) and General Medicine (Dr Farrell), and the Section of Health Policy and Administration, Department of Epidemiology and Public Health (Dr Krumholz), Yale University School of Medicine, New Haven, Conn; and the Center for Outcomes Research and Evaluation, Yale–New Haven Hospital, New Haven, Conn (Dr Krumholz).


Scientific Review and Clinical Applications Section Editor: Wendy Levinson, MD, Contributing Editor.


JAMA. 2002;287(7):890-897. doi:10.1001/jama.287.7.890.
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Published online

β-Blockers reduce morbidity and mortality in heart failure patients with left ventricular systolic dysfunction and stable fluid status. The successful adoption of β-blocker guidelines for these patients requires an understanding of the value of this therapy and effective systems to maintain safety and ensure high quality of care. This article distills scientific evidence and consensus guidelines into a series of cases and practical answers about patient selection, discussions with patients, management and monitoring, and systems improvements to optimize quality of care, safety, and benefit for all patients with heart failure.

Figures in this Article

Once thought harmful for patients with heart failure,1,2 β-blockers have been shown to reduce morbidity and mortality in heart failure patients with left ventricular (LV) systolic dysfunction and stable fluid status.310 The appropriate use of β-blockers in heart failure is now a key aspect of high-quality cardiovascular care, requiring appropriate prescribing behavior and effective monitoring systems to maintain patient safety. The goal of this article is to distill the current scientific evidence610 and consensus guidelines1113 into practical, immediately useful information about patient selection, discussions with patients, management and monitoring, and systems improvements to optimize quality of care and safety for all heart failure patients.

All heart failure patients with LV systolic dysfunction should be considered for β-blockers to reduce morbidity and prevent mortality.13 Previous guidelines from the American College of Cardiology (ACC) and American Heart Association (AHA)14 and current guidelines from the Heart Failure Society of America11 have recommended β-blockers for certain patients with mild to moderate heart failure according to New York Heart Association functional classification.4,6,7 Prompted by new evidence,5,10 the most recent ACC–AHA guidelines13 have introduced a broader disease-progression staging system (Figure 1) that ranges from patients without structural heart disease but at risk for heart failure (ACC–AHA stage A) to severely ill patients with a need for specialized interventions (ACC–AHA stage D). The ACC–AHA guidelines endorse the use of β-blockers for all patients with heart failure or those at risk for heart failure, except those with a history of intolerance to β-blockers and those with a contraindication. In addition, β-blockers are not recommended without a heart failure specialist first being consulted for patients with refractory heart failure, multiple hospitalizations, or a need for specialized treatments (ACC–AHA stage D) such as a mechanical circulatory-assist device or intravenous inotropic support.

Figure 1. American College of Cardiology–American Heart Association (ACC–AHA) Stage and New York Heart Association (NYHA) Classification of Heart Failure
Graphic Jump Location

The following cases are examples of the typical outpatients who have heart failure and are most appropriate for receiving β-blockers.

Patient 1 is a 60-year-old man who has chronic heart failure and complains of dyspnea upon mild to moderate exertion. A recent LV ejection fraction measurement was 25%. His weight is stable; he has trace pedal edema but no rales. His medications include an angiotensin-converting enzyme (ACE) inhibitor, digoxin, furosemide, and spironolactone.

This patient is ideal for a trial of β-blocker therapy. He has dyspnea with mild to moderate exertion (New York Heart Association functional class II or III; ACC–AHA stage C) and LV systolic dysfunction (LV ejection fraction <35% to 40%) and is similar to many patients enrolled in the first major clinical trials of β-blockers.4,6,7

Like most patients in clinical trials, this patient is receiving stable doses of a diuretic.47 To maximize patient safety, guidelines1113 recommend that β-blockers be initiated only in heart failure patients who are clinically euvolemic or receiving stable doses of diuretics without signs of fluid overload such as pulmonary rales, jugular venous distension, or more than minimal peripheral edema (BOX 1). If fluid status worsens after a β-blocker is started, guidelines13 recommend increasing the diuretic dosage (or initiating a diuretic if one is not already started), provided the patient does well, eg, has no hypotension, evidence of hypoperfusion, or requirement for intravenous positive inotropic support.

Box 1. Selection of Patients With Heart Failure for β-Blocker Therapy*

INDICATIONS
Asymptomatic Left Ventricular Dysfunction (American College of Cardiology– American Heart Association [ACC–AHA] Stage B)
No dyspnea on exertion (New York Heart Association [NYHA] class I)
Left ventricular ejection fraction <35% to 40%
No signs of fluid overload (given diuretic if necessary to maintain fluid balance)
Medications should include an angiotensin-converting enzyme (ACE) inhibitor
Evidence is best for patients with a risk for worsened heart failure caused by concurrent hypertension, coronary artery disease, or another cause

Structural Heart Disease With Prior or Current Symptoms of Heart Failure (ACC–AHA Stage C)
Dyspnea on mild to moderate exertion or dyspnea at rest if otherwise stable (NYHA class II and III and some patients with NYHA class IV)
Left ventricular ejection fraction <35% to 40%
No signs of fluid overload (given diuretic if necessary to maintain fluid balance)
Medications should include an ACE inhibitor and digoxin if indicated

CONTRAINDICATIONS
Hospitalized in an intensive care unit
Evidence of fluid overload or severe volume depletion
Recent requirement for intravenous treatment with positive inotropic agent
Reactive airways disease requiring inhaled β-adrenergic agonist therapy

Symptomatic bradycardia or advanced heart block without a pacemaker

*Abstracted from ACC–AHA guidelines.13 Guidelines also recommend β-blockers for certain patients at risk for developing heart failure (ACC–AHA stage A) caused by hypertension or coronary artery disease. Patients with severe symptoms and recurrent hospitalizations (refractory heart failure or ACC–AHA stage D) should be evaluated by a physician experienced in treating heart failure.

(Return to text.)

Patient 1 is also similar to many patients in clinical trials in that he is receiving stable doses of an ACE inhibitor and digoxin.47 Evidence for β-blocker use is most applicable for patients receiving these medications, since most patients in trials of mild to moderate heart failure were receiving at least a low dose of an ACE inhibitor (90%-97% of patients) and digoxin (50%-68%). The simultaneous initiation of β-blockers and ACE inhibitors, discussed below, is feasible but was not evaluated in the clinical trials.

If patient 1 instead had dyspnea at rest (New York Heart Association class III or IV, ACC–AHA stage C) and stable fluid status, evidence for β-blocker use would be provided by the Carvedilol Prospective Randomized Cumulative Survival (COPERNICUS) Trial,5 a study of patients with severe heart failure (symptoms at minimal exertion or at rest).

Patient 2 is an asymptomatic 62-year-old male jogger presenting for a regular checkup. His only medication is a daily aspirin. His LV ejection fraction was 30% last year following an acute myocardial infarction (AMI) 2 years ago.

This patient has asymptomatic LV dysfunction (New York Heart Association class I, or ACC–AHA stage B) and is a good candidate for β-blockers on the basis of his history of AMI.15 β-Blockers would also be recommended if he had LV systolic dysfunction from some other cause, such as idiopathic dilated cardiomyopathy.13 Although there is currently insufficient clinical trial evidence to recommend β-blocker use in patients with asymptomatic LV dysfunction, studies10,1618 and recent guidelines11,13 suggest that β-blockers should be initiated because they reduce progression to heart failure, as in trials of coronary artery disease or hypertension.17,19

The 2 previous patients are prototypical "ideal" examples of heart failure patients for whom β-blockers are recommended. Clinicians, however, must often decide about the use of β-blockers for a population of patients that is more diverse than the patients included in clinical trials. The following case illustrates an example of the many patients in clinical practice with chronic comorbidities and other factors that have not been well represented in clinical trials.

Patient 3 is an 81-year-old black woman who has dyspnea on minimal exertion and was hospitalized recently for intravenous diuresis. Her LV ejection fraction was measured in the hospital at 28%. She has no signs or symptoms of fluid overload when receiving appropriate doses of diuretic and ACE inhibitor. She has well-controlled diabetes mellitus, chronic obstructive pulmonary disease, and a pacemaker that was placed for sick sinus syndrome.

This patient was only recently discharged from the hospital with fluid overload, but she appears to have good fluid balance after receiving oral diuretics and is still a good candidate for a trial of β-blockers. The results from COPERNICUS5 suggest that heart failure patients who were hospitalized or given intravenous diuretics within 14 days will do well when receiving β-blockers, provided that they have stable fluid status. On the other hand, β-blockers should not be used in patients who require the intensive care unit, intravenous vasodilators, or intravenous positive inotropic agents.13

Patients with symptomatic bradycardia should not receive a β-blocker until the cause of bradycardia is ascertained and treated. The recent ACC–AHA13 and Heart Failure Society of America guidelines11 do not recommend a specific heart-rate threshold in asymptomatic patients, but most major trials4,5,7 excluded even asymptomatic patients with an untreated heart rate of 65/min or less, and the previous ACC–AHA guideline14 recommended avoiding β-blockers in patients with untreated heart rates of less than 60/min. Patient 3 had been found to have sick sinus syndrome, but β-blockers should be safe because she has a pacemaker.

Diabetes mellitus was once thought to be a contraindication to β-blocker use, but β-blockers have since been shown to be well tolerated in trials, with little concern of masking hypoglycemia.14,2022 Patients with bronchospasm requiring inhaled β-agonists should not receive β-blockers, but patients with nonreversible chronic obstructive pulmonary disease have been included in several studies4,7 and can be expected to do well if observed for worsening respiratory status. Additionally, heart failure patients with chronic obstructive pulmonary disease20,23 and diabetes21,22 may have a greater absolute benefit from β-blockers than those without these comorbidities. Thus, the careful use of β-blockers in patients with diabetes or mild chronic obstructive pulmonary disease (not requiring bronchodilators) is prudent.

Some clinicians may be reluctant to initiate a β-blocker on the basis of this patient's age, since patients older than 80 years have been excluded from many trials and may be considered to have a higher risk from the medication. Nevertheless, β-blockers have been found to be safe and effective in smaller studies24,25 and in a large retrospective study of patients after AMI that included more than 10 000 patients older than 75 years and receiving a β-blocker.26 Thus, the potential benefits from β-blockers seem to outweigh the risks in this population.

Some experts have questioned the application of clinical trial results to subgroups such as women4,6,7 and black patients,20,27 but recent data2830 and the expert opinion of consensus groups13 strongly endorse the extension of trial results to such groups not well represented in the trials. Thus, patient 3 has no absolute contraindications to β-blocker use despite several differences between her case and that of subjects in clinical trials. She is likely to benefit from cautious initiation of a β-blocker and close follow-up by a physician experienced in the care of heart failure patients.

You receive a call from the emergency department physician about a 34-year-old man who has heart failure caused by progressive cardiomyopathy and returns to the hospital only 3 days after his most recent hospitalization, at which his LV ejection fraction measurement was 14%. Medications at discharge included a starting dose of a β-blocker, furosemide twice daily, an ACE inhibitor, and digoxin. He has severe dyspnea at rest, orthopnea, and pitting edema to the knees, even with high-dose diuretics and home dobutamine. The emergency physician wishes to admit patient 4 to the intensive care unit for aggressive therapy and suggests consultation with a heart failure specialist.

This patient is an example of a patient with ACC–AHA stage D heart failure. Evidence is limited regarding the general use of β-blockers in such patients, so patients must be individually evaluated to determine the balance of risk and benefit. Given this patient's complexity, β-blockers perhaps should not have been initiated until his condition was somewhat better controlled. At this point, the recent ACC–AHA guidelines13 would recommend that β-blockers be discontinued when the patient enters the intensive care unit or when positive intravenous inotropic support is required, or if the patient develops signs of fluid overload.

Regarding this patient's hospitalization, it would be advisable to consult a heart failure specialist who can help with future management of this patient's β-blocker and other medications. The recent ACC–AHA guidelines13 advocate a model in which primary care physicians and heart failure specialists collaborate. Heart failure specialists have more experience with severe heart failure and often have better access to systems resources such as disease-management programs. Many heart failure patients can be treated by primary care providers, but patients who remain symptomatic or have frequent hospitalizations should be evaluated by a heart failure specialist. Referral is especially recommended for patients with complicated or stage D heart failure, a category reserved for patients with refractory symptoms, recurrent hospitalization, or the need for specialized care.13 Many stage D patients may have difficulty tolerating β-blockers and may develop hypotension, bradycardia, or worsened fluid retention.

When β-blockers are indicated, how should the decision be discussed with the patient? Discussions with heart failure patients about the benefits and risks of β-blockers are important for reasons of professionalism and shared decision making. Also, patient education may help reduce nonadherence with treatment plans and prevent a delay in seeking preventive care, which may avoid readmissions and premature mortality.31,32 In addition, patients should have realistic expectations of benefits and potential adverse effects.

Several key concepts should be conveyed in a standardized fashion to heart failure patients when β-blockers are initiated (BOX 2). First, patients should understand that β-blockers will immediately reduce the chances of death from heart failure or other causes.14 Next, patients should know that 2 to 3 months may elapse before they notice a reduction in symptoms or need for hospitalization and that they may experience a brief worsening of symptoms in the beginning.14,33 Patients should be aware of the potential for adverse effects with β-blockers, as discussed below. They should be trained to weigh themselves daily and contact their physician if their weight increases or if they develop early warning symptoms for hypotension, bradycardia, or fluid retention. Patients should also be aware of the importance of their cooperation with the plan for gradual increases in β-blocker dosage and contacting the clinician if symptoms arise. Finally, they should be counseled to not stop taking a β-blocker abruptly without discussing the change with their clinician. These key concepts can be found in a patient information page here (in PDF format)  Image not available.. Other resources are available for patients to learn more about β-blockers and heart failure, including the guidelines themselves and Web sites sponsored by the AHA (http://www.americanheart.org/chf) and the Heart Failure Society of America (http://www.abouthf.org).

Box 2. Procedures for Using β-Blockers in Chronic Heart Failure

Measures to Aid Implementation in Clinical Settings
Maintain an adequate knowledge base about β-blocker therapy for heart failure
Implement systems changes (such as reminder stickers on charts or an audit and feedback program) to ensure the appropriate use of β-blockers
Periodically review the charts of patients with heart failure to ensure that they are receiving β-blockers and other appropriate medications such as angiotensin- converting enzyme inhibitors or have a documented contraindication
Maintain a relationship with a disease-management program consultant and an experienced heart failure consultant to help heart failure patients at greater risk for developing adverse effects or complications

Assessment Visit on Beginning β-Blockers
Thorough history taking, physical examination, and assessment of left ventricular ejection fraction to verify the cause and extent of heart failure
Record baseline weight, blood pressure, pulse, respiratory rate, and document cardiopulmonary examination, including presence or absence of peripheral edema
Determine stability of fluid status and the need for diuretics
Educate the patient about the appropriate diet and fluid intake
Supply the patient with written instructions for β-blocker dosage. Educate the patient about signs of hypotension, bradycardia, or worsening heart failure. Supply the patient with reliable contact information and instructions in case symptoms develop
Teach patients to weigh themselves daily and, if possible, to monitor their blood pressure at home
Maintain a specialized flow sheet to ensure that dosages are easily appraised in the chart
Determine the date for follow-up or dosage increase according to recent stability of blood pressure, pulse rate, and fluid status (typical range, 2-4 weeks)
After initiation and early dosage increases, schedule interim follow-up by telephone

Follow-up Visit
Repeat measurements of weight, blood pressure, pulse rate, and respiratory rate, and document cardiopulmonary examination, including presence or absence of peripheral edema
Evaluate patient to determine whether signs or symptoms of any of the following have developed: dizziness, fatigue, dyspnea, peripheral edema, hypotension, bradycardia, palpitations, atrioventricular block, bronchospasm, impotence (men), confusion, and memory loss
Reinforce education and practice of weighing at home, blood pressure monitoring, and monitoring for adverse effects

(Return to text.)

A variety of adverse effects have been reported for β-blockers.3437 Patients should be instructed about the most common adverse effects (hypotension, bradycardia, or worsened heart failure) (BOX 2), which can arise in virtually any patient if the dosage of β-blocker is too high or escalated too rapidly. Patients should be provided with an educational handout that they can review at home and advised to contact the clinician immediately if symptoms develop.

At the follow-up visit, patients should be asked whether they have developed adverse effects other than those listed in BOX 2, although the clinician should remain aware that many of these adverse effects have been reported nearly as frequently in clinical trial patients receiving a placebo. Package inserts3537 and the Physicians' Desk Reference34 report many other rare adverse effects ranging from nausea to thrombocytopenic purpura, but these have not been commonly observed in clinical trials.

When patients develop adverse effects that do not resolve, the clinician and patient should discuss the relative risks and benefits of continuing the β-blocker. The patient should be aware that some hypotension and bradycardia is to be expected after β-blockers are initiated and that the appearance of these adverse effects does not preclude continued use of a β-blocker. Some adverse effects such as fatigue, depression, or impotence may resolve over time or may be treatable; some symptoms may be entirely unrelated to the β-blocker. Other adverse effects may be more desirable than the adverse effect of stopping the β-blocker use, eg, worsened heart failure and a shorter life expectancy.

Which β-blocker is the best choice? Opinions diverge about which β-blocker is best, since little published work has compared patient outcomes among the different β-blockers.38,39 Currently, only carvedilol and long-acting metoprolol are approved by the US Food and Drug Administration for use in heart failure; bisoprolol is not yet approved for heart failure, but it has demonstrated efficacy in clinical trials.4 Pharmacologically, metoprolol and bisoprolol are highly selective for cardiac β1 receptors; carvedilol is less cardioselective but also has ancillary vasodilating and antioxidant40 properties. Although some have touted the advantages of one β-blocker over another, there is no evidence that differences between β-blockers are associated with differences in patient outcomes. The ongoing Carvedilol or Metoprolol European Trial (COMET)41 will compare outcomes among more than 3000 heart failure patients randomized to receive either carvedilol or metoprolol. Recruitment for this trial is complete and the 2-year follow-up results are expected to be available later this year.

How should the dose be initiated and titrated to maximize benefit and lessen adverse effects? Once a patient is determined to be appropriate for receiving β-blockers, a key goal should be to initiate the medication safely and titrate the dosage to the maximum tolerable. Suggested initiation and target dosages, based on clinical trials4,6,7 and guidelines,12 are shown in Table 1 for bisoprolol, carvedilol, and extended-release metoprolol.7,11,14 To avoid β-blockers' causing hypotension, they should be titrated upward with the "start low, go slow" approach used in most clinical trials, with a doubling of the dose every 2 to 4 weeks until the target is reached.13 This approach is similar to the 2-week open-label run-in period used before randomization in 2 major trials to determine whether patients could tolerate β-blockers.6,7 Clinicians may wish to increase the titration interval or decrease the increment in patients with a history of systolic blood pressure less than 90 mm Hg or a pulse rate less than 60/min or in patients with a recent change in fluid status. After the 2-week run-in period, up to 90% of the ideal patients in the US Carvedilol Program were able to tolerate the study protocol of doubled dose every 2 to 4 weeks,6 and nearly two thirds of those included in the Metoprolol CR/XL Randomized Intervention Trial in Congestive Heart Failure (MERIT-HF) were receiving the target dose of 200 mg at the conclusion of the study.7

Table Graphic Jump LocationTable. Starting and Target Dosages of β-Blockers in Heart Failure*

After a β-blocker dose is titrated up, the risk for symptomatic hypotension can be expected to be greatest within 24 to 48 hours14 and then improve within the next few doses. Combination effects from diuretics and ACE inhibitors should be considered or drug interactions with agents such as amiodarone, nitrates, or other antihypertensives. If hypotension develops, patients should try to take the β-blocker, ACE inhibitor, and diuretic at different times of the day.14 Patients should not reduce their diuretic dosages but may try temporary reductions in the dosage of an ACE inhibitor. Little evidence is available to guide these decisions, but the trials do suggest that the combination of medications is useful. Finally, other causes of hypotension should be considered, such as worsening fluid status caused by increased intake of salt or medication nonadherence.

A key remaining question is whether or how to initiate β-blockers and ACE inhibitors simultaneously, especially in patients receiving these agents for the first time. There is no evidence to help prioritize the titration of ACE inhibitors and β-blockers together, but recent guidelines observe that patients need not be receiving high doses of an ACE inhibitor to be considered for β-blockers, since most patients in clinical trials were not receiving high doses of an ACE inhibitor. In addition, there is some evidence for benefit with low doses of ACE inhibitors either by themselves or in combination with β-blockers43 as well as for very low doses of β-blockers.13,44 Finally, an early benefit for both agents together is plausible based on their separate mechanisms of action and the antiarrhythmic effects of β-blockers.43 In some cases, heart failure patients with systolic blood pressure below 95 to 100 mm Hg or a pulse rate below 60/min can be treated safely with β-blockers by experienced heart failure clinicians with access to disease-management programs or other ways to arrange for close monitoring at home.

What strategies can help the busy clinician ensure that effective doses of β-blockers are initiated and safely titrated? Changing clinical practice can be challenging, and a busy practice can benefit from a systematic approach to titrating β-blocker dosage and monitoring for adverse effects. A list of specific tasks for baseline and follow-up office visits is shown in BOX 2.13,45,46 The flow sheet in Figure 2 is an example of a simple charting tool that can be replicated on any word processor and placed in the records of all heart failure patients to follow titration of both β-blocker and ACE inhibitor. When hypotension or other adverse effects arise, the clinician can use the flow sheet to determine whether dose titration may have been too rapid or remind the clinician when several previous dose reductions had been necessary. In either case, a complete record of dose titration on 1 page may help the clinician decide whether it will be advisable to refer the patient to a heart failure consultant or a specialized heart failure management clinic13,46,47 while the β-blocker dose is escalated.

Figure 2. Sample Flow Sheet for Heart-Failure Medication
Graphic Jump Location
ACE indicates angiotensin-converting enzyme.

Many strategies can be used to help ensure that all appropriate heart failure patients receive β-blockers, even in a busy clinical practice with many patients in various stages of heart failure. Published evidence has shown that simple provider education and guideline dissemination alone are unlikely to effectively improve processes of care such as β-blocker use in heart failure.48 Rather, systemic change must be accomplished through the multifaceted use of several types of interventions, each of which would probably be ineffective if used alone.4749 In addition to education49,50 and guideline dissemination,51 effective systemic approaches include academic detailing or outreach visits,52 opinion leaders/local champions,53 computer and chart reminders,54,55 disease management programs,46,47 and chart audit and feedback to clinicians.56 Since clinical change is difficult to accomplish all at once, small manageable changes should be made according to feasibility. Care can then be monitored sequentially for effectiveness of the change.57

Although some clinics may not have the resources to provide specific heart failure case management or elaborate quality improvement projects, clinicians can still adopt this approach of small, feasible changes. An initial first step might be to place a prominent heart failure sticker and the flow sheet in Figure 2 in the charts of all heart failure patients, regardless of whether they have recently been treated in the office. A nurse or office manager can go through the list of heart failure patients, calling in each one for an assessment visit throughout a 2- or 3-month period. Heart failure patients not receiving β-blockers can be evaluated at baseline as shown in BOX 1 and treated as indicated in BOX 2. Follow-up can be systematized with the flow sheet in Figure 2. After a 6-month period, the clinician can ask that a sample of heart-failure–labeled charts be pulled for a simple self-directed audit. The point is that adherence to the new guideline will require a system that ensures that eligible patients are identified and appropriately treated.

Heart failure is a progressive and often fatal condition, and many heart failure patients receiving β-blockers will require admission to the hospital. Some patients may develop heart failure exacerbation or fluid overload after being given β-blockers. Other patients' heart failure may progress because of worsened hypertension or myocardial ischemia. Clinicians should be aware of how to manage β-blockers during these exacerbations as well as when they should consult a physician who specializes in the care of patients with severe heart failure.

You receive a call from the inpatient residents about a 62-year-old man with heart failure admitted to the hospital. He has been compliant with medications, and his LV ejection fraction 6 months ago was 30%. He now presents with dyspnea at rest, orthopnea, and peripheral pitting edema after dietary indiscretion while on vacation. He has no chest pain, and 2 sets of laboratory and electrocardiogram test results show no evidence of ischemia. The residents wonder whether his exacerbation could be related to his long-standing use of a β-blocker. Your outpatient chart reminds you that the β-blocker had been successfully titrated to a maximal dosage 4 months ago and was well tolerated at follow-up a month ago.

This patient has experienced an exacerbation of heart failure with evidence of fluid overload. Heart failure patients being admitted to the hospital should be evaluated individually by experienced clinicians to determine whether the β-blocker should be discontinued, on the grounds that the patients may be more likely to undergo adverse consequences of bradycardia, hypotension, and worsened failure if the β-blocker use is continued.13 In general, β-blockers should not be initiated in patients with unstable signs or symptoms of fluid overload,11,12 but they can often be continued during treatment of heart failure exacerbation if diuretic and other therapies are intensified.13 In addition, the COPERNICUS trial5 established the safety and benefit of β-blockers in heart failure patients recently discharged from the hospital. Since it does not appear that this patient will require admission to the intensive care unit or intravenous inotropic support, some experienced clinicians may elect to attempt an aggressive diuresis and restart his β-blocker use as soon as fluid status begins to respond.

The ACC–AHA guidelines13 suggest that primary care physicians with knowledge or experience in heart failure care will be able to direct this patient's inpatient therapy and temporary discontinuation of a β-blocker. A cardiologist will become involved at some level in the care of patients who require echocardiography or catheterization. A heart failure specialist should evaluate patients who fail to respond to diuretics or have multiple exacerbations. In addition, many heart failure patients with exacerbation, such as this patient, will benefit from renewed education or participation in a disease-management program, services that may be provided more efficiently in a heart failure specialist clinic.

The residents' question about a possible association between this patient's β-blocker use and exacerbation reflects the persistence of the long-standing myth that β-blockers are contraindicated in heart failure,3 although it is possible that the patient could be experiencing an adverse effect. The fact that this patient has tolerated a stable dosage of β-blocker for several months suggests that some other cause is likely, providing that no other event has occurred, such as an AMI.

Now that evidence and guidelines are available to recommend β-blockers in patients with and at risk for developing heart failure, clinicians should develop a system to be able to care properly for patients with this common disorder. A key goal of these systems should be to extend in a short time the benefits of β-blockers to all patients who are likely to benefit from them. The components of the system should include (1) appropriate knowledge of β-blockers and their indications, (2) awareness of how some heart failure patients differ from the ideal prototypes for therapy, (3) strategies to assist the clinician in initiating and monitoring patients to ensure that they are treated effectively and safely, (4) effective methods for communicating to patients the risks, benefits, and effective participation in care, (5) the enlistment of support staff where possible, (6) an effective safety net for hospitalization or home therapy, with temporary discontinuation of β-blockers as indicated, and (7) appropriate safeguards for consultation with or referral to a heart failure specialist for patients with complicated heart failure or for those who have difficulty tolerating β-blockers. With better understanding and appropriate involvement of heart failure specialists and disease-management programs, more heart failure patients will be prescribed β-blockers and experience the expected improvements in morbidity and mortality.

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Packer M, Cohn JN. Consensus recommendations for the management of chronic heart failure.  Am J Cardiol.1999;83:1A-38A.
Hennekens CH, Albert CM, Godfried SL, Gaziano JM, Buring JE. Adjunctive drug therapy of acute myocardial infarction: evidence from clinical trials.  N Engl J Med.1996;335:1660-1667.
Vantrimpont P, Rouleau JL, Wun CC.  et al. for the SAVE Investigators.  Additive beneficial effects of beta-blockers to angiotensin-converting enzyme inhibitors in the Survival and Ventricular Enlargement (SAVE) Study.  J Am Coll Cardiol.1997;29:229-236.
Chadda K, Goldstein S, Byington R, Curb JD. Effect of propranolol after acute myocardial infarction in patients with congestive heart failure.  Circulation.1986;73:503-510.
Dargie HJ. Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial.  Lancet.2001;357:1385-1390.
β-Blocker Heart Attack Trial Research Group.  A randomized trial of propranolol in patients with acute myocardial infarction, II: morbidity results.  JAMA.1983;250:2814-2819.
Gottlieb SS, McCarter RJ, Vogel RA. Effect of beta-blockade on mortality among high-risk and low-risk patients after myocardial infarction.  N Engl J Med.1998;339:489-497.
Bristow MR, Gilbert EM, Abraham WT.  et al.  Effect of carvedilol on LV function and mortality in diabetic versus non-diabetic patients with ischemic or non-ischemic dilated cardiomyopathy.  Circulation.1996;94:I-644.
Chen J, Marciniak TA, Radford MJ, Wang Y, Krumholz HM. Beta-blocker therapy for secondary prevention of myocardial infarction in elderly diabetic patients: results from the National Cooperative Cardiovascular Project.  J Am Coll Cardiol.1999;34:1388-1394.
Chen J, Radford MJ, Wang Y, Marciniak TA, Krumholz HM. Effectiveness of beta-blocker therapy after acute myocardial infarction in elderly patients with chronic obstructive pulmonary disease or asthma.  J Am Coll Cardiol.2001;37:1950-1956.
Krum H, Ninio D, MacDonald P. Baseline predictors of tolerability to carvedilol in patients with chronic heart failure.  Heart.2000;84:615-619.
Owen A. Experience of commencing carvedilol in elderly patients with heart failure in a routine outpatient clinic.  Eur J Heart Fail.2000;2:287-289.
Krumholz HM, Radford MJ, Wang Y, Chen J, Heiat A, Marciniak TA. National use and effectiveness of beta-blockers for the treatment of edlerly patients after acute myocardial infarction: National Cooperative Cardiovascular Project.  JAMA.1998;280:623-629.
The Beta-Blocker Evaluation of Survival Trial Investigators.  A trial of the beta-blocker bucindolol in patients with advanced chronic heart failure.  N Engl J Med.2001;344:1659-1667.
Yancy CW, Fowler MB, Colucci WS.  et al.  Race and the response to adrenergic blockade with carvedilol in patients with chronic heart failure.  N Engl J Med.2001;344:1358-1365.
Simon T, Mary-Krause M, Funck-Brentano C, Jaillon P. Sex differences in the prognosis of congestive heart failure: results from the Cardiac Insufficiency Bisoprolol Study (CIBIS II).  Circulation.2001;103:375-380.
Wedel H, Demets D, Deedwania P.  et al.  Challenges of subgroup analyses in multinational clinical trials: experiences from the MERIT-HF trial.  Am Heart J.2001;142:502-511.
Michalsen A, Konig G, Thimme W. Preventable causative factors leading to hospital admission with decompensated heart failure.  Heart.1998;80:437-441.
Vinson JM, Rich MW, Sperry JC, Shah AS, McNamara T. Early readmission of elderly patients with congestive heart failure.  J Am Geriatr Soc.1990;38:1290-1295.
Hall SA, Cigarroa CG, Marcoux L, Risser RC, Grayburn PA, Eichhorn EJ. Time course of improvement in left ventricular function, mass and geometry in patients with congestive heart failure treated with beta-adrenergic blockade.  J Am Coll Cardiol.1995;25:1154-1161.
Medical Economics Co.  Physicians' Desk Reference 200155th ed. Montvale, NJ: Medical Economics; 2001.
 Bisoprolol [package insert]. Research Triangle Park, NC: GlaxoSmithKline; 2002.
 Sustained-release metoprolol [package insert]. Wilmington, Del: AstraZeneca; 2002.
 Carvedilol [package insert]. Pearl River, NY: Lederle; 2002.
Metra M, Giubbini R, Nodari S, Boldi E, Modena M, Dei CL. Differential effects of beta-blockers in patients with heart failure: a prospective, randomized, double-blind comparison of the long-term effects of metoprolol versus carvedilol.  Circulation.2000;102:546-551.
Sanderson J, Chan S, Yip G.  et al.  Beta-blockade in heart failure: a comparison of carvedilol with metoprolol.  J Am Coll Cardiol.1999;34:1522-1528.
Yue TL, Cheng HY, Lysko PG.  et al.  Carvedilol, a new vasodilator and beta adrenoceptor antagonist, is an antioxidant and free radical scavenger.  J Pharmacol Exp Ther.1992;263:92-98.
Poole-Wilson PA, Remme WJ. COMET: a multicenter randomized double-blind study to compare the effect of carvedilol and metoprolol on mortality and morbidity in patients with moderate or severe congestive heart failure (NYHA II-IV).  Cardiovasc Drugs Ther.1999;13:24.
Medical Economics Co.  2001 Drug Topics Red BookMontvale, NJ: Medical Economics Data; 2001.
Packer M, Poole-Wilson PA, Armstrong PW.  et al. for the ATLAS Study Group.  Comparative effects of low and high doses of the angiotensin-converting enzyme inhibitor, lisinopril, on morbidity and mortality in chronic heart failure.  Circulation.1999;100:2312-2318.
Bristow MR, Gilbert EM, Abraham WT.  et al.  Carvedilol produces dose-related improvements in left ventricular function and survival in patients with chronic heart failure.  Circulation.1996;94:2807-2816.
Philbin EF. Comprehensive multidisciplinary programs for the management of patients with congestive heart failure.  J Gen Intern Med.1999;14:130-135.
Albert NM, Young JB. Heart failure disease management: a team approach.  Cleve Clin J Med.2001;68:53-64.
Rich MW. Heart failure disease management: a critical review.  J Card Fail.1999;5:64-75.
Oxman AD, Thomson MA, Davis DA, Haynes RB. No magic bullets: a systematic review of 102 trials of interventions to improve professional practice.  CMAJ.1995;153:1423-1431.
Davis DA, Thomson MA, Oxman AD, Haynes RB. Changing physician performance: a systematic review of the effect of continuing medical education strategies.  JAMA.1995;274:700-705.
O'Brien T, Freemantle N, Oxman AD, Wolf F, Davis DA, Herrin J. Continuing education meetings and workshops: effects on professional practice and health care outcomes (Cochrane Review).  Cochrane Database Syst Rev.2001;(2):CD003030.
Grimshaw JM, Russell IT. Effect of clinical guidelines on medical practice: a systematic review of rigorous evaluations.  Lancet.1993;342:1317-1322.
Thomson O'Brien MA, Oxman AD, Davis DA, Haynes RB, Freemantle N, Harvey EL. Educational outreach visits: effects on professional practice and health care outcomes.  Cochrane Database Syst Rev.2000;(2):CD000409.
Thomson O'Brien MA, Oxman AD, Haynes RB, Davis DA, Freemantle N, Harvey EL. Local opinion leaders: effects on professional practice and health care outcomes.  Cochrane Database Syst Rev.2000;(2):CD000125.
Johnston ME, Langton KB, Haynes RB, Mathieu A. Effects of computer-based clinical decision support systems on clinician performance and patient outcome: a critical appraisal of research.  Ann Intern Med.1994;120:135-142.
Balas EA, Weingarten S, Garb CT, Blumenthal D, Boren SA, Brown GD. Improving preventive care by prompting physicians.  Arch Intern Med.2000;160:301-308.
Thomson O'Brien MA, Oxman AD, Davis DA, Haynes RB, Freemantle N, Harvey EL. Audit and feedback: effects on professional practice and health care outcomes.  Cochrane Database Syst Rev.2000;(2):CD000259.
Berwick DM. Developing and testing changes in delivery of care.  Ann Intern Med.1998;128:651-656.

Figures

Figure 1. American College of Cardiology–American Heart Association (ACC–AHA) Stage and New York Heart Association (NYHA) Classification of Heart Failure
Graphic Jump Location
Figure 2. Sample Flow Sheet for Heart-Failure Medication
Graphic Jump Location
ACE indicates angiotensin-converting enzyme.

Tables

Table Graphic Jump LocationTable. Starting and Target Dosages of β-Blockers in Heart Failure*

References

Epstein S, Robinson BF, Kahler RL, Braunwald E. Effects of beta-adrenergic blockade on the cardiac response to maximal and submaximal exercise in man.  J Clin Invest.1965;44:1745-1753.
Nayler WD, Chipperfield D, Lowe TE. The negative inotropic effect of adrenergic betareceptor blocking drugs on human heart muscle.  Cardiovasc Res.1969;3:30-36.
Foody JM, Farrell MH, Krumholz HM. β-Blocker therapy in heart failure: scientific review.  JAMA.2002;287:883-889.
CIBIS-II Investigators and Committees.  The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial.  Lancet.1999;353:9-13.
Packer M, Coats AJS, Fowler MB.  et al.  Effect of carvedilol on survival in severe chronic heart failure.  N Engl J Med.2001;344:1651-1658.
Packer M, Bristow MR, Cohn JN.  et al.  The effect of carvedilol on morbidity and mortality in patients with chronic heart failure: US Carvedilol Heart Failure Study Group.  N Engl J Med.1996;334:1349-1355.
International Steering Committee, Merit-HF.  Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF).  Lancet.1999;353:2001-2007.
Hjalmarson A, Goldstein S, Fagerberg B.  et al. for the MERIT-HF Study Group.  Effects of controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart failure: the Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF).  JAMA.2000;283:1295-1302.
Brophy JM, Joseph L, Rouleau JL. Beta-blockers in congestive heart failure: a Bayesian meta-analysis.  Ann Intern Med.2001;134:550-560.
Colucci WS, Packer M, Bristow MR.  et al.  Carvedilol inhibits clinical progression in patients with mild symptoms of heart failure: US Carvedilol Heart Failure Study Group.  Circulation.1996;94:2800-2806.
Heart Failure Society of America (HFSA).  HFSA guidelines for management of patients with heart failure caused by left ventricular systolic dysfunction: pharmacological approaches.  J Card Fail.1999;5:357-382.
Remme WJ, Swedberg K. Guidelines for the diagnosis and treatment of chronic heart failure.  Eur Heart J.2001;22:1527-1560.
Hunt SA, Baker DW, Chin MH.  et al.  ACC/AHA guidelines for the evaluation 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 (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). American College of Cardiology Web site. Available at: http://www.acc.org/clinical/guidelines/failure/pdfs/hf_fulltext.pdf. Accessed January 10, 2002.
Packer M, Cohn JN. Consensus recommendations for the management of chronic heart failure.  Am J Cardiol.1999;83:1A-38A.
Hennekens CH, Albert CM, Godfried SL, Gaziano JM, Buring JE. Adjunctive drug therapy of acute myocardial infarction: evidence from clinical trials.  N Engl J Med.1996;335:1660-1667.
Vantrimpont P, Rouleau JL, Wun CC.  et al. for the SAVE Investigators.  Additive beneficial effects of beta-blockers to angiotensin-converting enzyme inhibitors in the Survival and Ventricular Enlargement (SAVE) Study.  J Am Coll Cardiol.1997;29:229-236.
Chadda K, Goldstein S, Byington R, Curb JD. Effect of propranolol after acute myocardial infarction in patients with congestive heart failure.  Circulation.1986;73:503-510.
Dargie HJ. Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial.  Lancet.2001;357:1385-1390.
β-Blocker Heart Attack Trial Research Group.  A randomized trial of propranolol in patients with acute myocardial infarction, II: morbidity results.  JAMA.1983;250:2814-2819.
Gottlieb SS, McCarter RJ, Vogel RA. Effect of beta-blockade on mortality among high-risk and low-risk patients after myocardial infarction.  N Engl J Med.1998;339:489-497.
Bristow MR, Gilbert EM, Abraham WT.  et al.  Effect of carvedilol on LV function and mortality in diabetic versus non-diabetic patients with ischemic or non-ischemic dilated cardiomyopathy.  Circulation.1996;94:I-644.
Chen J, Marciniak TA, Radford MJ, Wang Y, Krumholz HM. Beta-blocker therapy for secondary prevention of myocardial infarction in elderly diabetic patients: results from the National Cooperative Cardiovascular Project.  J Am Coll Cardiol.1999;34:1388-1394.
Chen J, Radford MJ, Wang Y, Marciniak TA, Krumholz HM. Effectiveness of beta-blocker therapy after acute myocardial infarction in elderly patients with chronic obstructive pulmonary disease or asthma.  J Am Coll Cardiol.2001;37:1950-1956.
Krum H, Ninio D, MacDonald P. Baseline predictors of tolerability to carvedilol in patients with chronic heart failure.  Heart.2000;84:615-619.
Owen A. Experience of commencing carvedilol in elderly patients with heart failure in a routine outpatient clinic.  Eur J Heart Fail.2000;2:287-289.
Krumholz HM, Radford MJ, Wang Y, Chen J, Heiat A, Marciniak TA. National use and effectiveness of beta-blockers for the treatment of edlerly patients after acute myocardial infarction: National Cooperative Cardiovascular Project.  JAMA.1998;280:623-629.
The Beta-Blocker Evaluation of Survival Trial Investigators.  A trial of the beta-blocker bucindolol in patients with advanced chronic heart failure.  N Engl J Med.2001;344:1659-1667.
Yancy CW, Fowler MB, Colucci WS.  et al.  Race and the response to adrenergic blockade with carvedilol in patients with chronic heart failure.  N Engl J Med.2001;344:1358-1365.
Simon T, Mary-Krause M, Funck-Brentano C, Jaillon P. Sex differences in the prognosis of congestive heart failure: results from the Cardiac Insufficiency Bisoprolol Study (CIBIS II).  Circulation.2001;103:375-380.
Wedel H, Demets D, Deedwania P.  et al.  Challenges of subgroup analyses in multinational clinical trials: experiences from the MERIT-HF trial.  Am Heart J.2001;142:502-511.
Michalsen A, Konig G, Thimme W. Preventable causative factors leading to hospital admission with decompensated heart failure.  Heart.1998;80:437-441.
Vinson JM, Rich MW, Sperry JC, Shah AS, McNamara T. Early readmission of elderly patients with congestive heart failure.  J Am Geriatr Soc.1990;38:1290-1295.
Hall SA, Cigarroa CG, Marcoux L, Risser RC, Grayburn PA, Eichhorn EJ. Time course of improvement in left ventricular function, mass and geometry in patients with congestive heart failure treated with beta-adrenergic blockade.  J Am Coll Cardiol.1995;25:1154-1161.
Medical Economics Co.  Physicians' Desk Reference 200155th ed. Montvale, NJ: Medical Economics; 2001.
 Bisoprolol [package insert]. Research Triangle Park, NC: GlaxoSmithKline; 2002.
 Sustained-release metoprolol [package insert]. Wilmington, Del: AstraZeneca; 2002.
 Carvedilol [package insert]. Pearl River, NY: Lederle; 2002.
Metra M, Giubbini R, Nodari S, Boldi E, Modena M, Dei CL. Differential effects of beta-blockers in patients with heart failure: a prospective, randomized, double-blind comparison of the long-term effects of metoprolol versus carvedilol.  Circulation.2000;102:546-551.
Sanderson J, Chan S, Yip G.  et al.  Beta-blockade in heart failure: a comparison of carvedilol with metoprolol.  J Am Coll Cardiol.1999;34:1522-1528.
Yue TL, Cheng HY, Lysko PG.  et al.  Carvedilol, a new vasodilator and beta adrenoceptor antagonist, is an antioxidant and free radical scavenger.  J Pharmacol Exp Ther.1992;263:92-98.
Poole-Wilson PA, Remme WJ. COMET: a multicenter randomized double-blind study to compare the effect of carvedilol and metoprolol on mortality and morbidity in patients with moderate or severe congestive heart failure (NYHA II-IV).  Cardiovasc Drugs Ther.1999;13:24.
Medical Economics Co.  2001 Drug Topics Red BookMontvale, NJ: Medical Economics Data; 2001.
Packer M, Poole-Wilson PA, Armstrong PW.  et al. for the ATLAS Study Group.  Comparative effects of low and high doses of the angiotensin-converting enzyme inhibitor, lisinopril, on morbidity and mortality in chronic heart failure.  Circulation.1999;100:2312-2318.
Bristow MR, Gilbert EM, Abraham WT.  et al.  Carvedilol produces dose-related improvements in left ventricular function and survival in patients with chronic heart failure.  Circulation.1996;94:2807-2816.
Philbin EF. Comprehensive multidisciplinary programs for the management of patients with congestive heart failure.  J Gen Intern Med.1999;14:130-135.
Albert NM, Young JB. Heart failure disease management: a team approach.  Cleve Clin J Med.2001;68:53-64.
Rich MW. Heart failure disease management: a critical review.  J Card Fail.1999;5:64-75.
Oxman AD, Thomson MA, Davis DA, Haynes RB. No magic bullets: a systematic review of 102 trials of interventions to improve professional practice.  CMAJ.1995;153:1423-1431.
Davis DA, Thomson MA, Oxman AD, Haynes RB. Changing physician performance: a systematic review of the effect of continuing medical education strategies.  JAMA.1995;274:700-705.
O'Brien T, Freemantle N, Oxman AD, Wolf F, Davis DA, Herrin J. Continuing education meetings and workshops: effects on professional practice and health care outcomes (Cochrane Review).  Cochrane Database Syst Rev.2001;(2):CD003030.
Grimshaw JM, Russell IT. Effect of clinical guidelines on medical practice: a systematic review of rigorous evaluations.  Lancet.1993;342:1317-1322.
Thomson O'Brien MA, Oxman AD, Davis DA, Haynes RB, Freemantle N, Harvey EL. Educational outreach visits: effects on professional practice and health care outcomes.  Cochrane Database Syst Rev.2000;(2):CD000409.
Thomson O'Brien MA, Oxman AD, Haynes RB, Davis DA, Freemantle N, Harvey EL. Local opinion leaders: effects on professional practice and health care outcomes.  Cochrane Database Syst Rev.2000;(2):CD000125.
Johnston ME, Langton KB, Haynes RB, Mathieu A. Effects of computer-based clinical decision support systems on clinician performance and patient outcome: a critical appraisal of research.  Ann Intern Med.1994;120:135-142.
Balas EA, Weingarten S, Garb CT, Blumenthal D, Boren SA, Brown GD. Improving preventive care by prompting physicians.  Arch Intern Med.2000;160:301-308.
Thomson O'Brien MA, Oxman AD, Davis DA, Haynes RB, Freemantle N, Harvey EL. Audit and feedback: effects on professional practice and health care outcomes.  Cochrane Database Syst Rev.2000;(2):CD000259.
Berwick DM. Developing and testing changes in delivery of care.  Ann Intern Med.1998;128:651-656.
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