heart failure in fact

8/14/2019 Heart Failure in Fact

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in the clinic

Heart Failure

Diagnosis page ITC12-2

Treatment page ITC12-6

Practice Improvement page ITC12-14

Patient Information page ITC12-15

CME Questions page ITC12-16

Section EditorsChristine Laine, MD, MPHDavid Goldmann, MD

Science WriterJennifer F. Wilson

The content ofIn the Clinic is drawn from the clinical information and

education resources of the American College of Physicians (ACP), including

PIER (Physicians Information and Education Resource) and MKSAP (Medical

Knowledge and Self-Assessment Program). Annals of Internal Medicine

editors develop In the Clinic from these primary sources in collaboration with

the ACPs Medical Education and Publishing Division and with the assistance

of science writers and physician writers. Editorial consultants from PIER and

MKSAP provide expert review of the content. Readers who are interested in these

primary resources for more detail can consult http://pier.acponline.org and other

resources referenced in each issue ofIn the Clinic.

The information contained herein should never be used as a substitute for clinical

judgment.

2007 American College of Physicians


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What patients should cliniciansconsider to be at risk for heartfailure?Elderly persons are at highest risk.The overall prevalence of heart fail-ure in persons over 80 years of ageis approximately 10% compared

with just 1% among persons underage 50 (2). African Americans alsoface an increased risk for heart fail-ure. African Americansbetween 45 and 64years of age are 2.5times more likely to diefrom heart failure thanCaucasians in the sameage range (3). Menhave a higher rate ofheart failure than

women, although thisdifference narrows aswomen get older.

Certain conditions and behaviorsalso increase the risk for heart fail-ure, and these conditions shouldbe treated to reduce the risk (seeBox). In addition to these, epi-demiologic study has linked in-creased risk for heart failure tophysical inactivity, obesity, and

lower levels of education (4).Hypertension

Longstanding untreated hyperten-sion is associated with the develop-ment of both systolic and diastolicheart failure as well as an inde-pendent risk for coronary arterydisease (CAD). Clinical trials haveshown that a reduction in systolic

or diastolic blood pressure can re-duce the subsequent risk for devel-oping heart failure (5). Even mod-est decreases in systolic bloodpressure reduce mortality and therisk for heart failure (6).

DiabetesDiabetes markedly increases therisk for heart failure and is an inde-

pendent risk factor forCAD.

The HOPE (Heart Out-comes Prevention Evalu-taion) trial found thatamong patients at least 55

years of age with eitheratherosclerosis or diabetesand at least 1 other riskfactor but without a historyof heart failure, theangiotensin-convertingenzyme (ACE) inhibitor

ramipril reduced the risk for stroke, my-ocardial infarction (MI), and death fromcardiovascular disease by 22% while alsosignificantly reducing heart failure (6).

Cardiotoxic Substance Use

Alcohol is a direct myocardial toxinand can be the primary cause ofheart failure. Abstinence from alco-hol may reverse left ventricular dys-function. Tobacco and cocaine usesignificantly increase the risk forCAD, which in turn can lead toheart failure. Cocaine also hasdirect effects on the myocardium.Chemotherapeutic agents, such asanthracycline and trastuzumab,can also exert toxic effects on themyocardium.

2007 American College of Physicians ITC12-2 In the Clinic Annals of Internal Medicine 4 December 2007

Approximately 5 million people in the United States have heart failure,and the number is on the rise, according to the National Heart Lungand Blood Institute. Heart failure is the most frequent cause of hos-

pitalization in U.S. patients older than 65 years, and the disease leads toabout 300 000 deaths per year (1). Heart failure is a significant problemthroughout the rest of the world as well, but few accurate data are available.The most common cause of heart failure in industrialized countries is is-chemic cardiomyopathy, whereas other causes, such as infectious diseases,assume a larger role in underdeveloped countries. Despite recent advances in

the management of patients with heart failure, morbidity and mortality ratesremain high. The estimated 5-year mortality rate is 50%.

Diagnosis

1. Finn P. AmericanHeart Associationscientific sessions2005. 13-16 Novem-ber 2005, Dallas, TX,USA. IDrugs.2006;9:13-5.[PMID: 16374724]

2. Kannel WB. Currentstatus of the epi-demiology of heartfailure. Curr CardiolRep. 1999;1:11-9.[PMID: 10980814]

3. Centers for DiseaseControl and Preven-tion (CDC). Mortality

from congestiveheart failureUnitedStates, 1980-1990.MMWR Morb MortalWkly Rep. 1994;43:77-81. [PMID: 8295629]

4. He J, Ogden LG, Baz-zano LA, et al. Riskfactors for congestiveheart failure in USmen and women:NHANES I epidemio-logic follow-up study.Arch Intern Med.2001;161:996-1002.[PMID: 11295963]

5. The sixth report ofthe Joint NationalCommittee on pre-vention, detection,

evaluation, and treat-ment of high bloodpressure. Arch InternMed. 1997;157:2413-46. [PMID: 9385294]

6. HOPE Investigators.Effects of ramipril oncoronary events inhigh-risk persons: re-sults of the HeartOutcomes PreventionEvaluation Study. Cir-culation.2001;104:522-6.[PMID: 11479247]

Common Conditions andBehaviors that Increasethe Risk for Heart Failure

Hypertension

Diabetes

Cardiotoxic substance use

Hyperlipidemia

Thyroid disorders

Tachycardia

Coronary artery disease


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7. Sacks FM, Pfeffer MA,Moye LA, et al. Theeffect of pravastatinon coronary eventsafter myocardial in-farction in patientswith average choles-terol levels. Choles-terol and RecurrentEvents Trial investiga-tors. N Engl J Med.1996;335:1001-9.

[PMID: 8801446]8. Klein I, Ojamaa K. Thy-

roid hormone andthe cardiovascularsystem. N Engl J Med.2001;344:501-9.[PMID: 11172193]

9. Fadel BM, Ellahham S,Ringel MD, et al. Hy-perthyroid heart dis-ease. Clin Cardiol.2000;23:402-8.[PMID: 10875028]

10. Coleman HN III, Tay-lor RR, Pool PE, et al.Congestive heartfailure followingchronic tachycardia.Am Heart J.1971;81:790-8.[PMID: 5088355]

11. Peters KG, KienzleMG. Severe car-diomyopathy due tochronic rapidly con-ducted atrial fibrilla-tion: complete re-covery afterrestoration of sinusrhythm. Am J Med.1988;85:242-4.[PMID: 3400701]

12. Grogan M, SmithHC, Gersh BJ, WoodDL. Left ventriculardysfunction due toatrial fibrillation inpatients initially be-lieved to have idio-pathic dilated car-diomyopathy. Am JCardiol.1992;69:1570-3.[PMID: 1598871]

13. Dargie HJ. Effect ofcarvedilol on out-come after myocar-dial infarction in pa-tients withleft-ventricular dys-function: the CAPRI-CORN randomisedtrial. Lancet.2001;357:1385-90.[PMID: 11356434]

2007 American College of PhysiciansITC12-3In the ClinicAnnals of Internal Medicine4 December 2007

Hyperlipidemia

Hyperlipidemia is strongly associ-ated with CAD, which may ulti-mately lead to heart failure. Large-scale clinical trials have shown thebenefit of lipid lowering for pri-mary and secondary prevention ofcardiovascular events.

The CARE (Cholesterol and Recurrent

Events) trial found that pravastatin treat-

ment significantly reduced mortality as well

as subsequent cardiovascular events and

reduced the incidence of heart failure (7).

Thyroid Disorders

Both hyperthyroidism and hypo-thyroidism are associated withheart failure, and correction to aeuthyroid state can potentiallyreturn ventricular function to nor-mal (8, 9). Hyperthyroidism is

associated with atrial fibrillationand tachycardia, which may com-plicate or worsen heart failure.

Tachycardia

Studies have shown that rapid pro-longed ventricular rates can lead tocardiomyopathy. Restoration ofnormal rhythm or rate control inpatients with poorly controlledatrial fibrillation and othersupraventricular tachycardias can

improve function and potentiallyprevent left ventricular dysfunction(1012).

Coronary Artery Disease

Aggressive risk-factor modificationwith cholesterol-lowering drugsand aspirin, ACE inhibitors, and -blockers can significantly reducemortality and the risk for futurecardiovascular complications, in-cluding heart failure.

The CAPRICORN (Carvedilol Post-Infarct

Survival Control in Left Ventricular Dys-

function) trial demonstrated that the -

blocker carvedilol significantly benefited

mortality in patients with left ventricular

dysfunction with or without heart failure

after MI in the setting of background ther-

apy with ACE inhibitors, revascularization,

and aspirin (13).

What symptoms and signs shouldprompt clinicians to consider thediagnosis of heart failure?Patients with underlying risk fac-tors, including CAD, valvular heartdisease, and longstanding hyperten-sion, may be asymptomatic, andclinicians should not wait forsymptoms to develop before evalu-ating and treating them for earlyleft ventricular dysfunction. Oncestructural or functional heart dis-ease affects the ability of the my-ocardium to fill and pump bloodnormally, patients may developdyspnea, fatigue, exercise intoler-ance, and fluid retention manifest-ed by pulmonary congestion andedema. Sometimes the breathingdifficulties and cough of heart fail-ure are initially misdiagnosed asbronchitis, pneumonia, or asthma,especially in young patients. Physi-cal signs of heart failure may reflectthe underlying cause, as shown byelevated blood pressure or an abnor-mal cardiac murmur, or the result-ing fluid retention, as shown byelevated jugular venous pressure,pulmonary crackles, a third heartsound, and lower extremity edema.

What tests should cliniciansconsider in the evaluation of

patients with suspected heartfailure?Electrocardiography

The American College of Cardiol-ogy (ACC)/American Heart Asso-ciation (AHA) recommends elec-trocardiography (ECG) in anypatient at risk for or with a historyof cardiac disease, including new-onset or exacerbated heart failure.If possible, the tracing should becompared with a previous baseline

tracing. Results can help documentthe presence of ventricular hyper-trophy, atrial abnormality, arrhyth-mias, conduction abnormalities,prior MI, and evidence of active is-chemia.

Echocardiography

Two-dimensional echocardiographywith Doppler should be performed


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in all patients with suspected heartfailure. It is a key study for deter-mining left ventricular cavity sizeand function, identifying wall mo-tion abnormalities, measuring leftand right ventricular ejection frac-tions, documenting the presence ofvalvular abnormalities, and differ-entiating between systolic and dias-tolic heart failure. In diastolic heartfailure, the ejection fraction is nor-mal (>50%), and there is evidenceof ventricular hypertrophy. In sys-tolic dysfunction, the ejection frac-tion is


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heart failure, the heart is dilatedwith an ejection fraction below50%, whereas in diastolic heart fail-ure, which occurs more often inelderly patients with hypertension,there is less dilatation and a normal

ejection fraction. Among patientswith heart failure, those withpreserved ejection fraction repre-sent a significant proportion andhave a similar survival rate to thosewith systolic heart failure (16, 17)

17. Bhatia RS, Tu JV, LeeDS, et al. Outcomeof heart failure withpreserved ejectionfraction in a popula-tion-based study. NEngl J Med.2006;355(3):260-9.[PMID: 16855266]


Table 1. Underlying Causes of Heart Failure*

Causes Characteristics

Dilated cardiomyopathies

Ischemic heart disease Occurs in people with a history of MI, presence of infarction pattern on ECG, or risk factors forcoronary disease.

Hypertension Presents in people with a history of poorly controlled blood pressure, presence of an S4 on physicalexamination, or left ventricular hypertrophy on echocardiogram or ECG. Hypertension can also causehypertrophic as well as dilated caridomyopathy.

Valvular heart disease Mitral regurgitation: ejection murmur at apex, dyspnea on exertion, atrial fibrillation. Aortic stenosis:dyspnea with exertion, ejection murmur at base that radiates to carotid arteries, decreased carotidupstroke, syncope, angina.

Bacterial myocarditis Fever, exposure to known agent, or positive blood cultures. Includes Borrelia burgdorferi(Lymedisease), diphtheria, rickettsia, streptococci, and staphylococci.

Parasitic myocarditis Travel history to endemic areas, fever, or peripheral stigmata of infection. Rare in United States.Includes Trypanosoma cruzi(Chagas disease), leishmaniasis, and toxoplasmosis.

Giant cell myocarditis Intractable ventricular or supraventricular arrhythmias with rapidly progressive left ventriculardysfunction: Endomyocardial biopsy specimen may be used to confirm the diagnosis. Effectiveimmunotherapy may be available, but prognosis is poor without ventricular assist device ortransplantation.

Familial dilated cardiomyopathies Family history of heart failure or sudden cardiac death in blood relatives.

Toxic cardiomyopathies History of exposure to toxic agents, such as alcohol, anthracycline, radiation, cocaine, orcatecholamines.

Collagen vascular disease History, positive serology results, or other stigmata of a collagen vascular disease, including systemiclupus erythematosus, polyarteritis nodosa, scleroderma, or dermatomyositis.

Granulomatous disease, such Atrial and ventricular arrhythmias that are difficult to control, rapidly progressive leftas sarcoidosis ventricular dysfunction, heart block.

Endocrinologic or metabolic disorders Clinical history of hyperthyroidism, acromegaly, hypothyroidism, uremia, pheochromocytoma, diabetesmellitus, thiamine deficiency, selenium deficiency, carnitine deficiency, kwashiorkor, carcinoid tumor,

or obesity; serum test for endocrine abnormality; long-term resident of a developing country or anarea with endemic nutritional deficiency. Nutritional deficiencies are rare in the United States.

Peripartum cardiomyopathy Heart failure symptoms with left ventricular dysfunction within 6 months of a pregnancy.

Neuromuscular disorders Clinical history of Becker muscular dystrophy, myotonic dystrophy, Friedreich ataxia, limb-girdlemuscular dystrophy, or Duchenne muscular dystrophy. Physical examination findings depend on theunderlying disease.

Cardiac transplant rejection History of cardiac transplant, medication noncompliance, shortness of breath, atrial or ventriculararrhythmias, or tachycardia, summation gallop on examination.

Hypertrophic cardiomyopathies

Hypertrophic obstructive History or family history of hypertrophic cardiomyopathy, echocardiographic and ECG findings ofcardiomyopathy hypertrophy. Screen for outflow tract gradient by physical examination, echocardiography, or cardiac

catheterization. Significant hypertrophy can also be seen in hypertension.

Restrictive cardiomyopathies

Infiltrative diseases affecting History of amyloidosis, sarcoidosis, hemochromatosis, Fabry disease, glycogen storage diseases,the myocardium Gaucher disease, mucopolysaccharidosis, endomyocardial fibrosis, or hypereosinophilic syndrome;

thickening of the myocardium on echocardiogram, suggesting an infiltrative process; cardiac MRIshowing infiltration; family history of an inborn error of metabolism or amyloidosis; presence ofS

4on examination; right-sided heart failure more severe than left-sided failure; other organs

involved in underlying disease process.

* ECG = electrocardiography; MI = myocardial infarction; MRI = magnetic resonance imaging.


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18. Sullivan MJ, CobbFR. The anaerobicthreshold in chronicheart failure. Rela-tion to blood lactate,ventilatory basis, re-producibility, and re-sponse to exercisetraining. Circulation.1990;81:II47-58.[PMID: 2295152]

19. Myers J, Gianrossi R,Schwitter J, et al. Ef-fect of exercise train-ing on postexercise

oxygen uptake ki-netics in patientswith reduced ven-tricular function.Chest.2001;120:1206-11.[PMID: 11591562]

20. Sullivan MJ, CobbFR. Central hemody-namic response toexercise in patientswith chronic heartfailure. Chest.1992;101:340S-346S.[PMID: 1576862]

How should clinicians evaluatefunctional capacity in patientswith suspected heart failure todetermine treatment?Clinicians should determine func-tional capacity by using the NewYork Heart Association (NYHA)classification system (see Box).

Tracking changesin clinicalNYHA class atevery visit mayidentify patientswith progressiveheart failure whomay eventuallybenefit from spe-cialized care orcardiac trans-plantation.

Additional func-tional capacitytests that can befollowed overtime include the6-minute walk test (see Box) andformal exercise or pharmacologicstress testing. Measuring peak oxy-gen consumption (VO

2) at the time

of exercise testing can be useful indetermining prognosis.

What is the role of diet in themanagement heart failure?Despite a paucity of definitiveevidence, ACC/AHA and otherguidelines recommend sodium re-striction in patients with sympto-matic heart failure as well as avoid-ance of salt-retaining medications,

such as nonsteroidal anti-inflam-matory drugs. Some clinicians rec-ommend that patients with moreadvanced heart failure limit intaketo 2 grams of sodium and 2 quartsof fluid per day to increase the ef-fectiveness of diuretic therapy.Limitation of salt and fluid intake

results in fewer hos-pitalizations fordecompensated heartfailure. Patients whohave cardiovascularrisk factors, such ashyperlipidemia, obe-sity, or diabetes,should also beencouraged to followdietary recommenda-tions specific to

these underlyingconditions.

What shouldclinicians advisepatients about

exercise? Do formal exerciseprograms provide benefit?Exercise improves physical and psy-chological well-being. In patientswith heart failure, it improves peakVO

2(18, 19) as well as metabolic

and hemodynamic indices and de-lays the onset of anaerobic thresh-old (18, 20). Clinicians should en-roll patients with medically stableNYHA class II, III, and perhapsclass IV heart failure in a long-termaerobic exercise program tailored tothe patients functional capacity. Astructured cardiac rehabilitationprogram may be particularly

Diagnosis... Be alert for the development of heart failure in older persons; AfricanAmericans; men; and in patients with hypertension, hyperlipidemia and diabetes,and those who smoke, drink alcohol, or use illicit drugs. Dyspnea and fatigue arethe primary symptoms of heart failure. In addition to history and physical exami-nation, use 2-dimensional Doppler echocardiography to assess left ventricularfunction along with ECG and additional studies to determine the cause of theheart failure and to identify exacerbating factors.

CLINICAL BOTTOM LINE

How to Perform the 6-minuteWalk Test

Ask the patient to walk for 6minutes in a straight line back andforth between 2 points separated by60 feet. Allow the patient to stopand rest or even sit, if necessary. Ateither end of the course, placechairs that can quickly be moved ifthe patient needs to sit. Note thetotal distance walked in 6 minutes,which correlates well with other

measures of functional capacity.Gender-specific equations havebeen developed using age, height,and weight to calculate predicteddistance for healthy adults.

New York Heart Association(NYHA) Classification System:

NYHA class I (mild): Patient hasasymptomatic left ventricular dys-function. Normal physical activitydoes not cause undue fatigue, pal-pitation, or shortness of breath.

NYHA class II (mild): Patient has fa-tigue, palpitation, or shortness ofbreath with normal physical activity.

NYHA class III (moderate): Patienthas shortness of breath with mini-mal activity, including usual activi-ties of daily living.

NYHA class IV (severe): Patient hasshortness of breath at rest and isunable to carry out any physicalactivity without discomfort. Physicalactivity of any kind increasesdiscomfort.

Treatment


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21. The CONSENSUS Tri-al Study Group. Ef-fects of enalapril onmortality in severecongestive heart fail-ure. Results of theCooperative NorthScandinavianEnalapril Survival

Study (CONSENSUS).N Engl J Med.1987;316:1429-35.[PMID: 2883575]

22. The SOLVD Investi-gators. Effect ofenalapril on survivalin patients with re-duced left ventricu-lar ejection fractionsand congestiveheart failure. N EnglJ Med. 1991;325:293-302. [PMID: 2057034]

23. The SOLVD Investi-gators. Effect ofenalapril on mortali-ty and the develop-ment of heart failurein asymptomatic pa-

tients with reducedleft ventricular ejec-tion fractions. N EnglJ Med. 1992;327:685-91. [PMID: 1463530]

24. Pitt B, Segal R, Mar-tinez FA, et al. Ran-domised trial oflosartan versus cap-topril in patientsover 65 with heartfailure (Evaluation ofLosartan in the El-derly Study, ELITE).Lancet.1997;349:747-52.[PMID: 9074572]

25. Pitt B, Poole-WilsonPA, Segal R, et al. Ef-fect of losartan com-

pared with captoprilon mortality in pa-tients with sympto-matic heart failure:randomised trialthe Losartan HeartFailure SurvivalStudy ELITE II.Lancet.2000;355:1582-7.[PMID: 10821361]

26. Cohn JN, Tognoni G.A randomized trialof the angiotensin-receptor blocker val-sartan in chronicheart failure. N EnglJ Med.2001;345:1667-75.[PMID: 11759645]

27. Maggioni AP, AnandI, Gottlieb SO, et al.;Val-HeFT Investiga-tors (Valsartan HeartFailure Trial). Effectsof valsartan on mor-bidity and mortalityin patients withheart failure not re-ceiving angiotensin-converting enzymeinhibitors. J Am CollCardiol.2002;40:1414-21.[PMID: 12392830]

effective because it can providesupervised exercise as well as sup-port in making lifestyle modifica-tions. Exercise should be stoppedtemporarily in patients with wors-ening heart failure until symptomsare stabilized. In addition, if pa-tients show evidence of exercise-induced ischemia, exercise shouldbe stopped until further evaluationand therapy are initiated.

When should clinicians beginfirst-line drug therapy with ACEinhibitors or angiotensin-receptorblockers? What are thealternatives for patients whocannot tolerate these drugs?ACE Inhibitors

ACE inhibitors should be used byall patients with heart failure re-gardless of functional class except

those with intolerance or a contra-indication, such as angioedema.These vasodilators alter the naturalhistory of the disease and improvesurvival and quality of life. Numer-ous randomized, placebo-controlledclinical trials have demonstratedthat ACE inhibitors reduce mortal-ity in patients with left ventriculardysfunction, even in those withoutsymptoms.

The CONSENSUS (Cooperative North Scan-

dinavian Enalapril Survival Study) trial

evaluated 253 patients with NYHA class I

to IV heart failure who were randomly as-

signed to enalapril or placebo in a blinded

study. All patients were also receiving di-

uretics, and 93% received digitalis glyco-sides. The mortality rate was reduced by

27% (P < 0.001) in the patients receiving

enalapril compared with placebo (21).

The SOLVD (Studies of Left Ventricular Dys-function) treatment trial randomly as-

signed 2569 patients with NYHA class I to

IV heart failure to enalapril vs. placebo. In patients with heart failure receiving

enalapril compared with placebo, there

was a 16% (P < 0.005) reduction in mor-

tality rate, a 30% (P < 0.0001) reduction in

heart failure hospitalizations, a 7% (P 130 msec on ECG, and symptomsdespite maximal medical therapy.

In the MIRACLE-ICD (Multicenter InSync

ICD Randomized Clinical Evaluation) trial,

369 patients with class III or IV heart failure,

ejection fraction, and QRS interval < 130

msec received an ICD with resynchroniza-

tion device. Those in whom the latter de-

vice was turned on demonstrated im-

proved quality of life, functional status,

and exercise capacity but no change in

heart failure status, rates of hospitaliza-

tion, or survival (50).

In the CARE-HF (Cardiac Resynchroniza-

tion in Heart Failure) study, 813 patients

with NYHA class III or IV heart failure due to

left ventricular systolic dysfunction andcardiac dyssynchrony who were receiving

standardized drug therapy were randomly

assigned to receive medical therapy alone

or with cardiac resynchronization. The

study concluded that, in these patients,

cardiac resynchronization improved

symptoms and quality of life and reduced

the risk for death (51).

When should clinicians useinotropic agents in patients withheart failure?Inotropic agents, such as dobuta-mine and milrinone, can improvecardiac output in patients with lowcardiac output and decrease after-load in patients with severe heartfailure unresponsive to the tradi-tional heart failure medications.However, all inotropic agents withthe exception of digoxin have beenassociated with excess mortalityand should be reserved for patientsunresponsive to traditional oralheart failure medications. Becauseof the increased risk for suddencardiac death, they should only beused in a monitored setting or forpalliation of end-stage disease.

When should clinicians consider

using anticoagulants in patientswith heart failure?Dilated cardiomyopathy with de-pressed ejection fraction below35%, valvular lesions (especially mi-tral stenosis), and atrial fibrillationare all associated with embolicstroke. The incidence of throm-boembolic events was about 2.7 per100 patient-years in the 1 large tri-al database of patients with heartfailure (52). Although many experts

advocate anticoagulation to reducethe risk for stroke for patients withheart failure and significantly de-pressed ejection fraction who haveno contraindications, anticoagula-tion remains controversial for pa-tients with an ejection fraction be-low 35% without atrial fibrillation,documented clot, or valvular heartdisease; and in another trial data-base, the use of warfarin in suchpatients was not associated with a

reduction in all-cause mortality(53). Therefore, it seems most ap-propriate to initiate anticoagulationwith warfarin in patients with doc-umented left ventricular clot onechocardiogram or ventriculogram,atrial fibrillation, or prior embolicevent and to use aspirin or clopi-dogrel in patients with coronary


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Table 2. Drug Treatment for Heart Failure*

Agent, Dosage Mechanism of Action Benefits Side Effects Notes

ACE inhibitors

Enalapril, 520 mg PO bid Inhibits angiotensin-converting Improves patient Cough, angioedema, Follow BUN, creatinine, and potassiumenzyme; results in decreased exercise tolerance, renal insufficiency, levels; withdraw or decrease dose if renal

Captopril, 12.550.0 mg PO tid conversion of angiotensin I to hemodynamic status, hyperkalemia insufficiency exacerbated. For all classesangiotensin II and decreased survival; may halt of heart failure.

Lisinopril, 540 mg PO qd metabolism of bradykinin. The progression and causeor 520 mg PO bid latter produces prostaglandins regression of HF

and nitric oxide

Angiotensin-receptor antagonists

Losartan, 25100 mg PO qd Inhibits reninangiotensin system Improvement in hemo- Hyperkalemia, exacer- Follow BUN, creatinine, and potassiumat angiotensin receptor level dynamics and symptoms. bation of renal in- levels. May use these agents in additionValsartan, 80320 mg PO qd Should be used in patients sufficiency, hypotension to ACE inhibitors in patients with severe

who cannot take ACE in- HF.Candesartan, 1632 mg PO qd hibitors. May be detrimental

in patients already on ACEinhibitors and -blockers

-blockers

Carvedilol, 3.12525.0 mg Inhibits adrenergic nervous Improves hemodynamic Bradycardia, depression, Avoid in patients with significant asthma,PO bid (50 mg PO bid system; improves survival and status, LVEF, survival; hypotension, diabetes, or high-grade conduction system diseasefor patients weighing LVEF in patients with HF; may halt progression exacerbation of asthma without pacemaker. For all classes of>85 kg) reduces sudden death risk and cause regression or COPD heart failure. Use with caution in patients

of HF with class IV heart failure.Carvedilol CR, 1080 mg qd

Metoprolol XL/CR (succinate),50200 mg PO qd XL

Bisoprolol, 5 mg PO bid

Afterload reducersHydralazine, 25100 mg PO Reduces afterload and preload Combination with nitrates Hypotension, lupus-like Combination with nitrates reserved forqid improves survival in patients syndrome (high doses patients intolerant to ACE inhibitors and ARBs

with HF; survival benefit of hydralazine)not as great as ACE inhibitors

Isosorbide dinitrate, 1040 Reduces afterload and preload Combination with hydralazine Headache Combination with hydralazine reserved formg PO tid improves survival in patients patients intolerant to ACE inhibitors and ARBs

with HF; survival benefit notas great as ACE inhibitors

Aldosterone antagonists

Spironolactone, 12.550.0 Inhibits aldosterone, which can Improves survival in Hyperkalemia, Follow potassium level, especially inmg PO qd escape ACE inhibition and has patients with NYHA gynecomastia patients taking ACE inhibitors. Aldosterone

Eplerenone, 2550 mg numerous deleterious effects on stages III to IV HF. antagonists alone are not an adequatePO qd cardiovascular system in patients Improves survival after subst itute for a loop diuret ic in patients

with HF MI with LV dysfunction. who require diuretics. Eplerenone has fewer

sex-hormonerelated side effects. Avoid withcombination of ACE inhibitors and ARBs.

Loop diuretics

Furosemide, 10160 mg PO Inhibits chloride uptake in the Palliative in patients Hypokalemia, hypo- Follow BUN, creatinine, potassium,qd bid loop of Henle; result is diuresis with congestive magnesemia, volume and magnesium levels and volume status.

Torsemide, 1040 mg PO qd symptoms. No survival depletion, renalbid benefit. insufficiency

Bumetanide, 14 mg POqd bid

Ethacrynic acid, 25100 mgPO qd bid

Digitalis glycoside

Digoxin, 0.1250.25 mg PO Positive inotropic agents. Improves exercise Arrhythmias, bradycardia Follow levels (aim for level


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54. American College ofCardiology/AmericanHeart Association Task

Force on PracticeGuidelines (Commit-tee to Revise the 1995Guidelines for theEvaluation and Man-agement of Heart Fail-ure). ACC/AHA Guide-lines for theEvaluation and Man-agement of ChronicHeart Failure in theAdult: Executive Sum-mary. Circulation.2001;104:2996-3007.[PMID: 11739319]


Treatment... Determine NYHA functional class to guide treatment in patients withheart failure. Limit salt and fluid intake in patients with symptomatic heart fail-ure, and recommend regular exercise as tolerated. Begin first-line drug therapywith ACE inhibitors or ARBs (or hydralazine and nitrates if these are not tolerated)as well as -blockers in patients who are not volume overloaded. Add loop diureticsand digoxin in patients with NYHA classes II, III, and IV heart failure and aldos-

terone antagonists in those with class III and IV and monitor potassium and renalfunction. Consult a cardiologist in patients with severe heart failure who mayrequire hospitalization for inotropic agents; placement of ICD devices, pacemakers,or left ventricular assist devices; or cardiac transplantation. Recognize that anti-coagulation for patients with depressed ejection fractions remains controversial.Teach patients to participate in their own care by encouraging them to monitortheir diet, medical regimen, and weight.

CLINICAL BOTTOM LINE

disease, regardless of ejectionfraction.

What should clinicians advisepatients to do to preventexacerbations of heart failure?Clinicians should advise patients toadhere to their fluid and salt re-striction and medical regimen,

weigh themselves daily, and to re-port deviations from their dryweight before they become symp-tomatic. Some patients can learn touse a sliding dose of diuretic tomaintain their weight. Help fromnurses, dietitians, home health staff,and physical therapists can be in-valuable in helping patients preventexacerbations. Patients should re-ceive pneumococcal vaccine andannual influenza immunization.

Patients with established CADshould begin aggressive risk-factormodification, including attention todiet, exercise, weight control, andsmoking cessation. Behavior modi-fications should be prescribed aswell as pharmacologic therapy un-less contraindicated. Multiple stud-ies have shown that risk-factormodification with cholesterol-low-ering drugs and the use of aspirin

or other antiplatelet drugs, ACEinhibitors, and -blockers can sig-nificantly reduce the risk for futurecardiovascular events and reducemortality.

When should clinicians considerconsulting a cardiologist aboutmanagement of patients withheart failure?If symptoms worsen despite opti-mal medical therapy, consult a car-diologist for help in reviewing theneed for hospitalization for par-enteral inotropic drug treatment;catheterization; placement of anICD, biventricular pacemaker, orleft ventricular assist device; or car-diac transplantation. Consider ob-taining pulmonary consultationwhen primary lung disease, such aschronic obstructive pulmonary dis-ease or sleep apnea, is thought tobe contributing to the patientssymptoms.

When should clinicians hospitalizepatients with heart failure?

Patients with severe NYHA classIV heart failure, characterized bydyspnea at rest, severe fatigue, orvolume overload unresponsive tooral diuretics or that requires inpa-tient evaluation and managementshould be hospitalized. This in-cludes patients with life-threaten-ing ventricular arrhythmias or atrialarrhythmias that worsen heart fail-ure symptoms or cause hypoten-sion. It also includes patients withsyncope, sudden cardiac death,and atrial arrhythmias withworsening clinical signs and symp-toms of heart failure who requireparenteral drug treatment or deviceplacement.


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What do professionalorganizations recommend withregard to the care of patientswith heart failure?The ACC/AHA published guide-lines for the Evaluation and Man-agement of Chronic Heart Failure inthe Adult in 2001 (54), and these

were updated in 2005 (55).Theguidelines contain extensive infor-mation on the characterization ofheart failure as a clinical syndrome,initial and serial clinical assessmentof patients, drug and device therapyfor patients with heart failure at vari-ous stages of the disease, treatmentof special populations, managingpatients with heart failure and con-comitant disorders, end-of-life con-siderations, and issues involved in

implementation of the guidelines.The updated guidelines stress theimportance of early diagnosis to stopor slow disease progression andchanges in drug therapy based onseveral pivotal clinical trials.

In addition to the ACC/AHAguidelines, other significant guide-lines include the Heart Failure Soci-ety of America 2006 ComprehensiveHeart Failure Practice Guideline

(56) and the Department of VeteransAffairs/Veterans Health Administra-tion 2003 guidelines relating to the

pharmacologic management ofchronic heart failure (57).

What measures do stakeholdersuse to evaluate the quality of carefor patients with heart failure?The Centers for Medicare andMedicaid (CMS) has started aPhysician Quality Reporting Initia-tive (PQRI) program, throughwhich clinicians can report a desig-nated set of quality measures onclaims for services provided duringthe period from 1 July through 31December 2007 and earn bonuspayments. Among the currentmeasures in the PQRI program, 2relate to heart failure.The first issimilar to the Ambulatory CareQuality Alliance measure relating touse of ACE inhibitors or ARBs,

calling for use of these agents inpatients over 18 years of age with adiagnosis of heart failure and leftventricular dysfunction. The secondmeasures use of-blocker therapy inthe same population.

In addition, the Agency forHealthcare Research and Quality isusing quality indicators to measurethe hospital admission rate for heartfailure, and CMS has proposed the

public reporting of hospital-level30-day mortality for patients withheart attack and heart failure.

Practice

Improvement

55. American College ofCardiology.ACC/AHA 2005Guideline Update forthe Diagnosis andManagement ofChronic Heart Failurein the Adult: a report

of the American Col-lege of Cardiology/American Heart As-sociation Task Forceon Practice Guide-lines (Writing Com-mittee to Updatethe 2001 Guidelinesfor the Evaluationand Management ofHeart Failure): devel-oped in collabora-tion with the Ameri-can College of ChestPhysicians and theInternational Societyfor Heart and Lung

Transplantation: en-dorsed by the HeartRhythm Society.Circulation.

2005;112:e154-235.[PMID: 16160202]

56. Heart Failure Societyof America. HFSA2006 Comprehen-sive Heart FailurePractice Guideline. JCard Fail. 2006;12:e1-2. [PMID: 16500560]

57. Pharmacy BenefitsManagement Strate-gic Healthcare Groupand the Medical Ad-visory Panel; Depart-ment of Veterans Af-fairs, Veterans HealthAdministration. ThePharmacologic Man-agement of ChronicHeart Failure. Ac-cessed at http://www.oqp.med.va.gov/cpg/CHF/CHF_Base.htm on 11 October2007.

in

the

clinic

Tool Kitin the clinic

Heart Failure

PIER Moduleswww.pier.acponline.org

Heart failure and percutaneous coronary intervention modules with updated informationon current diagnosis and treatment of heart failure, designed for rapid access at the pointof care.

Patient Informationwww.annals.org/intheclinic

Download copies of the Patient Information sheet that appears on the following page forduplication and distribution to your patients.

Quality Improvement Toolswww.ihi.org/ihi/search/searchresults.aspx?searchterm=heart+failure+tools&searchtype=basic

Links to a variety of helpful tools for managing various aspects of heart failure, compiledby the Institute for Healthcare Improvement.

www.gericareonline.net/tools/eng/heartfailure/index.html

Download a complete heart failure toolkit covering various topics in assessment,management, and follow-up with accompanying flowsheets from the Practicing Physicianin Education project, supported by the John A. Hartford Foundation.

www.cardiologyinoregon.org/information/information.html#toolkit

Resources from the Oregon Heart Failure GAP Toolkit, part of an American College ofCardiology project in 3 states to improve heart failure care.


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THINGS PEOPLE SHOULD KNOWABOUT HEART FAILURE

In the Clinic

Annals of Internal Medicine

Web Sites with Good Information on Heart Failure

American College of Physicianswww.doctorsforadults.com/images/healthpdfs/heartfail.pdf

American Heart Associationwww.americanheart.org/presenter.jhtml?identifier=1486

National Heart, Lung, and Blood Institutewww.nhlbi.nih.gov/health/dci/Diseases/Hf/HF_WhatIs.html

Heart failure, sometimes called congestive heart failure, is a condition in which theheart cant pump as well as it should. Because the heart has a hard time getting bloodto the rest of the body, patients with heart failure can feel weak and tired.

In some patients with heart failure, fluid (edema) builds up in the lungs and parts ofthe body, making it hard to breathe and causing swelling in the legs.

Heart failure can result from many different conditions that directly or indirectly af-fect the heart. People with high blood pressure, diabetes, high cholesterol, and coro-nary artery disease can develop heart failure. Treating these conditions may preventheart failure.

Treating heart failure means working together with your doctor to control salt in your

diet, watching your weight, and taking all your medications every day. Its importantto keep your regular doctor appointments.

Heart failure affects nearly 5 million adults, and 550 000 new cases are diagnosedeach year. It is more common in older people but can occur at any age. Althoughthere is no cure yet, heart failure is very treatable and millions of Americans lead afull life by managing their condition through medications and by making healthychanges in their lifestyles.

Heart Failure Symptoms:

Breathlessness during activity, at rest, or while sleeping

Wheezing or coughing that may be dry or may produce white or pink blood-tinged phlegm

Swelling in the feet, ankles, legs or abdomen, or unexplained weight gain

A constant lack of energy and difficulty performing everyday activities

A sense of having a full or sick stomach

A feeling like the heart is racing or pounding

A feeling the heart is skipping beats or occasionally pounding very hard

PatientIn

formation


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CME Questions

A 48-year-old woman with a history ofan ischemic cardiomyopathy and New

York Heart Association class II heart fail-ure symptoms is seeking advice about hermedical therapy. She has no inducibleischemia on stress testing and her last

ejection fraction by echocardiographywas estimated to be 35%. She was lasthospitalized for an exacerbation of heartfailure 1 year ago. She takes extended-release metoprolol, aspirin, lisinopril,digoxin, and furosemide. On physicalexamination, her heart rate is 62/min andblood pressure is 104/78 mm Hg. There isno jugular venous distention, and herchest is clear on auscultation. She has aregular rhythm without gallop or murmur.Her complete blood count and serumelectrolytes are normal.

Which one of the following changes inher medications should be made at thistime?

A. Add an angiotensin-receptorblocker.

B. Add nitroglycerin and hydralazine.

C. Add spironolactone.D. Discontinue metoprolol.E. No changes at this time.

A 56-year-old woman who is new to yourpractice is evaluated for recent exacerba-tion of dyspnea and fatigue. She has

idiopathic dilated cardiomyopathy andreceives a stable heart failure regimen,including lisinopril, 20 mg/d; digoxin, 125mg/d; furosemide, 40 mg/d; and meto-prolol XL, 50 mg/d. She also takes alen-dronate, hormone replacement therapy,glipizide, folic acid, and ibuprofen be-cause of rheumatoid arthritis. Thyroidhormone therapy with thyroxin was initi-ated because of the finding of an elevat-ed serum thyroid-stimulating hormonelevel 4 months earlier. The thyroid-stimulating hormone level returned tonormal after therapy.

On physical examination, blood pressureis 110/72 mm Hg, and heart rate is82/min. Jugular venous pressure is esti-mated at 10 cm H

2O. The lungs are clear.

Cardiac examination shows an S3

gallopand 2+ pitting edema.

Which of the following is most likely tobe exacerbating the heart failure in thispatient?

A. AlendronateB. GlipizideC. IbuprofenD. Thyroxin

E. Estrogen

A 35-year-old man with a 2-year historyof dilated, nonischemic cardiomyopathyand New York Heart Association func-tional class III symptoms is admitted tothe hospital with worsening shortness ofbreath for the third time in 6 months. Hehas normal coronary arteries and an ejec-tion fraction of 25%. His current medica-tions include extended-release metopro-lol, lisinopril, furosemide, digoxin, and

spironolactone. On physical examination,his blood pressure is 96/70 mm Hg, hispulse rate is 84/min, and his respirationrate is 22/min. He has crackles halfwayup his lung fields bilaterally, a displacedcardiac apex, and an S

3gallop. His electro

cardiogram shows sinus rhythm with aleft bundle branch block and a QRSduration of 170 msec.

Which of the following outcomes canthis patient expect from a cardiacresynchronization procedure?

A. Decreased risk for all-cause

mortalityB. Decreased risk for cardiac deathC. Decreased risk for sudden cardiac

deathD. Improved heart failure symptoms

and exercise tolerance

E. No benefit

A 65-year-old man who had an acutemyocardial infarction 10 years ago isreevaluated. Despite diet and exercisetherapy, he has had recurrent ischemicevents, and over the past 2 years, he has

been hospitalized several times for exacer-bations of heart failure. Six months ago,a dipyridamole thallium scan showed noischemia and echocardiogram showedanterior akinesia, global hypokinesia,and moderate to severe mitral regurgita-tion, with an ejection fraction of 28%.

Medications include ramipril, carvedilol,furosemide, aspirin, digoxin, and spirono-lactone. His condition is classified asNew York Heart Association functionalclass III.

On physical examination, heart rate is

62/min and blood pressure is 96/60 mm Hg.He has bibasilar crackles and jugularvenous distention. A summation gallopand a 3/6 holosystolic murmur at theapex and radiating to the axilla are pres-ent. Electrocardiogram shows left bundlebranch block and first-degree atrial ven-tricular block.

Which of the following is the mostappropriate next step in the managementof this patient?

A. Coronary artery bypass graft

surgery.B. Left ventricular aneurysmectomy.C. Implantation of a cardiodefibrillator/

atrioventricular sequentialbiventricular pacemaker.

D. Mitral valve repair.

E. Transmyocardial laserrevascularization.

A 72-year-old woman with a 2-year his-tory of ischemic heart disease and NYHAstage I heart failure seeks advice aboutimplantable defibrillators. One year ago, acardiac catheterization demonstrated

nonobstructive coronary artery diseaseand an ejection fraction of 55%. Herelectrocardiogram shows sinus rhythm at76/min with normal perfusion rate, quan-titative radioscintigraphy, and cardiacoutput intervals.

Which of the following outcomes canreasonably be expected with the use ofan implantable cardiac defibrillator inthis patient?

A. Fewer hospital admissions for heartfailure.

B. Decreased risk for acute coronarysyndrome.

C. Decreased risk for sudden cardiac

death.D. Decreased risk for cardiac death.E. No benefit.

Questions are largely from the ACPs Medical Knowledge Self-Assessment Program (MKSAP). Go to www.annals.org/intheclinic/

to obtain up to 1.5 CME credits, to view explanations for correct answers, or to purchase the complete MKSAP program.

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heart failure in fact

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