Annals of Internal Medicine䊛

In the Clinic®

Heart Failure Prevention

H
eart failure affects more than 6 million
people in the United States and incurs a
heavy toll in morbidity, mortality, and Diagnosis
health care costs. It frequently coexists with
other important disorders, including hyperten-
sion, coronary artery disease, diabetes, and Treatment
obesity. Decades of clinical trials have shown
that several medications and interventions are
effective for improving outcomes; however,
mortality and hospitalization rates remain high. Practice Improvement
More recently, additional medications and de-
vices have shown promise in reducing the
health burden of heart failure.

CME/MOC activity available at Annals.org.

Physician Writer doi:10.7326/AITC201806050

Audrey Wu, MD
From the University of CME Objective: To review current evidence for prevention, diagnosis, and treatment of heart
Michigan, Ann Arbor, failure.
Michigan. Funding Source: American College of Physicians.
Disclosures: Dr. Wu, ACP Contributing Author, has nothing to disclose. The form can be
viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M18
-0070.
Acknowledgment: The author thanks Lee R. Goldberg, MD, MPH, author of the previous
version of this In the Clinic.
With the assistance of additional physician writers, the editors of Annals of Internal Medi-
cine develop In the Clinic using MKSAP and other resources of the American College of
Physicians.
In the Clinic does not necessarily represent official ACP clinical policy. For ACP clinical
guidelines, please go to https://www.acponline.org/clinical_information/guidelines/.

© 2018 American College of Physicians

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 Approximately 6.5 million per- and heart failure with preserved
sons in the United States have ejection fraction (HFPEF, or dia-
heart failure, and the number is stolic dysfunction). In reality, the
rising. Heart failure incidence disease process occurs on a con-
1. Benjamin EJ, Blaha MJ, increases with age, with lifetime tinuum between preserved and
Chiuve SE, Cushman M, risk ranging from 20%– 45%. At reduced ejection fraction, and
Das SR, Deo R, et al;
American Heart Associa- age 75 years or younger, inci- elements of both conditions fre-
tion Statistics Committee dence is higher in black persons quently coexist.
and Stroke Statistics Sub-
committee. Heart disease than in white persons. Although
and stroke statistics-2017
survival after diagnosis has im- The distinction between HFREF and
update: a report from the
American Heart Associa- proved over time, mortality is still HRPEF heart failure is important in
tion. Circulation. 2017;
high: Roughly 50% of patients determining treatment. There are far
135:e146-e603. [PMID:
28122885] die within 5 years after diagnosis. more data to guide therapy for the
2. Yancy CW, Jessup M,
Bozkurt B, Butler J, Casey Primary risk factors for incident former condition than for the latter.
DE Jr, Drazner MH, et al.
heart failure include coronary Studies generally use a cutoff of
2013 ACCF/AHA guideline
for the management of artery disease, hypertension, 35%–45% to distinguish between
heart failure: executive
diabetes, obesity, and smoking. the 2 conditions, although that
summary: a report of the
American College of Cardi- Hospitalization rates have re- threshold is artificial and more firmly
ology Foundation/Ameri-
can Heart Association Task mained fairly stable, with 1.023 established in research than in clini-
Force on Practice Guide-
million hospital discharges in cal practice. The American College
lines. Circulation. 2013;
128:1810-52. [PMID: 2010. Heart failure was listed as a of Cardiology Foundation (ACCF)
23741057]
cause of death for more than and American Heart Association
3. Pocock SJ, Ariti CA, Mc-
Murray JJ, Maggioni A, 300 000 persons in 2014. In (AHA) guidelines define HFREF as
Køber L, Squire IB, et al;
Meta-Analysis Global 2012, the estimated total cost of ejection fraction of 40% or less and
Group in Chronic Heart
heart failure was $30.7 billion. It HFPEF as ejection fraction of 50% or
Failure. Predicting survival
in heart failure: a risk is also a major problem in the greater. Borderline HFPEF is de-
score based on 39 372
rest of the world, but information fined as ejection fraction between
patients from 30 studies.
Eur Heart J. 2013;34: is less available and less accurate 41% and 49%. For the remainder of
1404-13. [PMID:
23095984] for many areas. The most com- this article, the term “heart failure”
4. Barlera S, Tavazzi L, Fran-
mon cause of heart failure in in- will refer to HFREF unless otherwise
zosi MG, Marchioli R,
Raimondi E, Masson S, dustrialized countries is ischemic specified.
et al; GISSI-HF Investiga-
tors. Predictors of mortality cardiomyopathy, whereas other The ACCF and AHA have devel-
in 6975 patients with causes, such as infectious and
chronic heart failure in the oped a staging system to help clini-
Gruppo Italiano per lo inflammatory diseases, assume a cians select therapies that improve
Studio della Streptochinasi
nell’Infarto Miocardico- larger role in less developed ar- outcomes for persons at risk for
Heart Failure trial: pro- eas (1). Risk factors vary substan- heart failure or those with estab-
posal for a nomogram.
Circ Heart Fail. 2013;6: tially among regions (1). lished heart failure (see the Box:
31-9. [PMID: 23152490]
5. Levy WC, Mozaffarian D,
Heart failure is a clinical syn- ACCF/AHA Stages of Heart Failure).
Linker DT, Sutradhar SC,
Anker SD, Cropp AB, et al. drome characterized by fluid re- In this staging system, the New
The Seattle Heart Failure
Model: prediction of sur- tention resulting in effort intoler- York Heart Association (NYHA)
vival in heart failure. Circu- ance and congestion in many classification is used to describe
lation. 2006;113:1424-
33. [PMID: 16534009] parts of the body. There is a wide functional status (see the Box:
6. Avery CL, Loehr LR,
Baggett C, Chang PP,
range of causes, including abnor- NYHA Functional Classification).
Kucharska-Newton AM, malities of the pericardium, myo-
Matsushita K, et al. The
population burden of cardium, cardiac valves, and Although this system is based on
heart failure attributable sometimes systemic diseases. subjective assessment, it has
to modifiable risk factors:
the ARIC (Atherosclerosis The terms “cardiomyopathy” and proved to be a robust predictor
Risk in Communities)
Study. J Am Coll Cardiol.
“ventricular dysfunction” indicate of mortality (2). Other more ob-
2012;60:1640-6. [PMID: a specific structural or functional jective predictors have been de-
23021327]
7. Arnold JM, Yusuf S, Young cause of heart failure symptoms. veloped, and most include older
J, Mathew J, Johnstone D, Ventricular dysfunction is broadly age, lower ejection fraction,
Avezum A, et al; HOPE
Investigators. Prevention divided into heart failure with worse renal function, lower sys-
of heart failure in patients
in the Heart Outcomes
reduced ejection fraction tolic blood pressure, and poor
Prevention Evaluation (HFREF, or systolic dysfunction) functional status (3–5).
(HOPE) study. Circulation.
2003;107:1284-90.
[PMID: 12628949]

姝 2018 American College of Physicians ITC82 In the Clinic Annals of Internal Medicine 5 June 2018

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What are the risk factors for
heart failure?
Over the past decade, treat-
ment of heart failure has shifted
from focusing on acute exacer-
bations to treating it as a
chronic and potentially prevent-
able syndrome with more em-
phasis on modifying risk factors.
The major risk factors for heart
failure are hypertension, coro-
nary artery disease, diabetes,
obesity, and smoking. These
factors contribute to more than
half of all cases of incident heart
failure (1). Other factors, such as
dyslipidemia, also influence risk
for incident heart failure be-
cause they are so closely tied to
risk for coronary artery disease.
Nonmodifiable risk factors in-
clude race, sex, and family his-
tory. Even modest decreases in
modifiable risk factors substan-
tially reduce the incidence of
heart failure (6).
Coronary artery disease
Coronary artery disease is the
most common cause of heart
failure. It exerts its effects
through global myocardial isch-
emia from diffuse or microvas-
cular disease or from regional
dysfunction due to disease in
epicardial coronary arteries.
Coronary artery disease confers
a 3-fold increased risk for heart
failure and as much as an 8-fold
increased risk for myocardial
infarction (1, 7). Treatment with
the angiotensin-converting en-
zyme (ACE) inhibitor ramipril
significantly reduces the inci-
dence of heart failure in pa-
tients at high risk for cardiovas-
cular events, including those
who have had myocardial in-
farction.
The CAPRICORN (Carvedilol Post-Infarct Sur-
vival Control in Left Ventricular Dysfunction)
5 June 2018 Annals of Internal Medicine
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trial included patients with a left ventricular
ejection fraction of 40% or less after an acute
myocardial infarction and found that treatment
with the ␤-blocker carvedilol significantly re-
duced rates of all-cause mortality; cardiovascu-
lar mortality; and recurrent, nonfatal myocar-
dial infarction (8).
Hypertension
Long-standing untreated hyper-
tension is associated with both
HFREF and HFPEF and is an inde-
pendent risk factor for coronary
artery disease. Hypertension
leads to maladaptive ventricular
hypertrophy or enlargement and
causes myocardial dysfunction
through hemodynamic overload,
global myocardial ischemia, neu-
rohormonal activation, and other
mechanisms. Intensive hyperten-
sion control reduces develop-
ment of new left ventricular hy-
pertrophy and increases
regression of left ventricular hy-
pertrophy (9, 10). It also reduces
risk for new heart failure and for
death. One meta-analysis
showed that each 10 –mm Hg
reduction in blood pressure is
associated with a 28% reduction
in incident heart failure and a
13% reduction in all-cause
mortality (11).
Diabetes mellitus
Diabetes more than doubles the
risk for heart failure (12, 13) and
frequently exists in conjunction
with other risk factors, such as
hypertension, coronary artery
disease, and obesity. It indepen-
dently increases predisposition
to other risk factors, such as coro-
nary artery disease, and is associ-
ated with adverse changes in
myocardial structure and function
related to microvascular disease
that constitute diabetic cardiomy-
opathy. Poor glycemic control is
associated with greater risk for
incident heart failure (14). In a
large population study, the
In the Clinic ITC83
Prevention
ACCF/AHA Stages of Heart
Failure
A: High risk for heart failure without
structural heart disease or
symptoms of heart failure.
B: Structural heart disease without
signs or symptoms of heart
failure.
C: Structural heart disease with
prior or current symptoms of
heart failure.
D: Refractory heart failure
requiring specialized
interventions.
ACCF = American College of
Cardiology Foundation; AHA =
American Heart Association.
NYHA Functional
Classification
I: No limitation of physical
activity. Ordinary physical
activity does not cause
symptoms of heart failure.
II: Slight limitation of physical
activity. Comfortable at rest,
but ordinary physical activity
results in symptoms of heart
failure.
III: Marked limitation of physical
activity. Comfortable at rest,
but less than ordinary activity
causes symptoms of heart
failure.
IV: Unable to carry out any
physical activity without
symptoms of heart failure, or
symptoms of heart failure at
rest.
NYHA = New York Heart
Association.
8. Dargie HJ. Effect of carve-
dilol on outcome after
myocardial infarction in
patients with left-
ventricular dysfunction:
the CAPRICORN ran-
domised trial. Lancet.
2001;357:1385-90.
[PMID: 11356434]
姝 2018 American College of Physicians

9. Whelton PK, Carey RM,
Aronow WS, Casey DE Jr,
Collins KJ, Dennison Him-
melfarb C, et al. 2017
ACC/AHA/AAPA/ABC/
ACPM/AGS/APhA/ASH/
ASPC/NMA/PCNA guide-
line for the prevention,
detection, evaluation, and
management of high
blood pressure in adults:
A report of the American
College of Cardiology/
American Heart Associa-
tion Task Force on Clinical
Practice Guidelines. J Am
Coll Cardiol. 2017. [PMID:
29146535]
10. Soliman EZ, Ambrosius
WT, Cushman WC,
Zhang ZM, Bates JT,
Neyra JA, et al; SPRINT
Research Study Group.
Effect of intensive blood
pressure lowering on left
ventricular hypertrophy
in patients with hyper-
tension: SPRINT (Systolic
Blood Pressure Interven-
tion Trial). Circulation.
2017;136:440-50.
[PMID: 28512184]
11. Ettehad D, Emdin CA,
Kiran A, Anderson SG,
Callender T, Emberson J,
et al. Blood pressure
lowering for prevention
of cardiovascular disease
and death: a systematic
review and meta-
analysis. Lancet. 2016;
387:957-67. [PMID:
26724178]
12. Thrainsdottir IS, Aspe-
lund T, Thorgeirsson G,
Gudnason V, Hardarson
T, Malmberg K, et al. The
association between
glucose abnormalities
and heart failure in the
population-based Reykja-
vik study. Diabetes Care.
2005;28:612-6. [PMID:
15735197]
13. Dei Cas A, Khan SS,
Butler J, Mentz RJ, Bo-
now RO, Avogaro A, et al.
Impact of diabetes on
epidemiology, treat-
ment, and outcomes of
patients with heart fail-
ure. JACC Heart Fail.
2015;3:136-45. [PMID:
25660838]
14. Lind M, Bounias I, Ol-
sson M, Gudbjörnsdottir
S, Svensson AM, Rosen-
gren A. Glycaemic control
and incidence of heart
failure in 20,985 pa-
tients with type 1 diabe-
tes: an observational
study. Lancet. 2011;378:
140-6. [PMID:
21705065]
15. Rawshani A, Rawshani A,
Franzén S, Eliasson B,
Svensson AM, Miftaraj
M, et al. Range of risk
factor levels: control,
mortality, and cardiovas-
cular outcomes in type 1
diabetes mellitus. Circu-
lation. 2017;135:1522-
1531. [PMID:
28416524]
姝 2018 American College of Physicians
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greater the number of modifiable
risk factors (hemoglobin A1c, hy-
pertension, albuminuria, smok-
ing, and elevated levels of low-
density lipoprotein cholesterol)
that could be reduced to target
levels, the lower the risk for heart
failure hospitalization, acute myo-
cardial infarction, and all-cause
mortality (15). However, even
when all risk factors were ade-
quately controlled, risk for heart
failure hospitalization and acute
myocardial infarction remained
significantly higher than in the
nondiabetic control group.
Moreover, the relationship be-
tween glycemic control and out-
comes seems to be U-shaped,
with greater risk at higher and
lower hemoglobin A1c levels
(16, 17).
The HOPE (Heart Outcomes Prevention Evalua-
tion) trial studied patients aged 55 years or
older who had coronary artery disease, stroke,
peripheral vascular disease, or diabetes and at
least 1 other risk factor for heart failure (hyper-
tension, elevated total cholesterol levels, low
high-density lipoprotein cholesterol levels, ciga-
rette smoking, or microalbuminuria) but no his-
tory of heart failure or systolic dysfunction (left
ventricular ejection fraction <40%). In this study,
the ACE inhibitor ramipril reduced the risk for
stroke, myocardial infarction, and death from car-
diovascular disease by 22% (relative risk, 0.78
[95% CI, 0.70 – 0.86]; P < 0.001) while also re-
ducing the development of heart failure by 23%
(7, 18).
Specific causes
Cardiomyopathy may be caused
by conditions other than coro-
nary artery disease, and knowing
the specific cause may affect
prognosis and management, par-
ticularly if the cause is reversible.
For example, over time, specific
structural abnormalities may lead
to clinical heart failure from pres-
sure or volume overload. These
abnormalities include valvular
disease, such as mitral or aortic
regurgitation; aortic stenosis;
and congenital lesions, such as
hemodynamically significant ven-
ITC84 In the Clinic
tricular septal defects or other
shunts.
Alcohol is a direct myocardial
toxin—it can be the primary cause
of heart failure, and abstinence
can reverse left ventricular dys-
function (19). Cocaine can cause
cardiomyopathy as a result of
induced coronary artery disease,
myocardial infarction, or vasculi-
tis and myocarditis from direct
toxicity. The chemotherapeutic
agents trastuzumab and anthra-
cycline have the potential for car-
diac toxicity.
Hyperthyroidism can cause
atrial fibrillation and tachycar-
dia, which may induce or
worsen heart failure, and resto-
ration of a euthyroid state can
improve ventricular function
(20, 21). Incessant tachycardia
from other causes also can lead
to ventricular dysfunction and
overt heart failure that are po-
tentially reversible with rate
control or elimination of tachy-
cardia (22). Obesity-related car-
diomyopathy probably results
from myocardial and myocyte
adipose accumulation, in-
creased cardiac workload from
elevated systemic blood pres-
sure and circulating blood vol-
ume, and other mechanisms.
Nutritional deficiencies may
also result in cardiomyopathy,
most notably thiamine defi-
ciency, which can occur with
alcoholism or anorexia nervosa.
Inflammation leading to myocardi-
tis can be caused by infections or
toxins, be part of a systemic disor-
der (such as systemic lupus ery-
thematosus or HIV infection), or be
idiopathic (23). Giant cell myo-
carditis is a rare disorder charac-
terized by severe heart failure
and a poor prognosis that gener-
ally requires advanced therapy,
such as implantation of a ventric-
ular assist device and cardiac
transplant. Hypersensitivity myo-
Annals of Internal Medicine 5 June 2018
 carditis is an allergic reaction to
any of a variety of antigens, in-
cluding sulfonamides and
penicillins.
Peripartum cardiomyopathy mani-
fests as left ventricular dysfunc-
tion in the last trimester of preg-
nancy or the early postpartum
period. The underlying mecha-
nisms are not completely under-
stood, and clinical manifestations
may range from asymptomatic
left ventricular dysfunction to se-
vere cardiogenic shock (24).
defined. Hypertrophic cardio-
16. Nichols GA, Joshua-
myopathy is caused by auto- Gotlib S, Parasuraman S.
Glycemic control and risk
somal dominant mutations in of cardiovascular disease
genes that code for compo- hospitalization and all-
cause mortality. J Am
nents of the myocardial sarco- Coll Cardiol. 2013;62:
mere. Its characteristic presen- 121-7. [PMID:
23665365]
tation is marked left ventricular 17. Aguilar D, Bozkurt B,
Ramasubbu K, Deswal A.
hypertrophy with no obvious Relationship of hemoglo-
explanation. Arrhythmogenic bin A1C and mortality in
heart failure patients
right ventricular dysplasia is with diabetes. J Am Coll
Cardiol. 2009;54:422-8.
characterized by fibrofatty re- [PMID: 19628117]
placement of the myocardium, 18. Yusuf S, Sleight P, Pogue
J, Bosch J, Davies R,
usually the right ventricular free Dagenais G; Heart Out-
comes Prevention Evalu-
wall. Ventricular noncompaction ation Study Investigators.
cardiomyopathy results from Effects of an angiotensin-
converting-enzyme in-

Other systemic disorders that arrest in embryogenesis of the hibitor, ramipril, on

cardiovascular events in
cause heart failure include amy- myocardium, which produces a high-risk patients. N Engl
J Med. 2000;342:145-
loidosis, which deposits insoluble spongy, trabeculated myocar- 53. [PMID: 10639539]

fibrillar proteins in various or-
gans, including the heart (25).
Sarcoidosis is frequently a sys-
dial architecture that can be 19. Walsh CR, Larson MG,
Evans JC, Djousse L,
seen on echocardiography and Ellison RC, Vasan RS,
et al. Alcohol consump-
magnetic resonance imaging. tion and risk for conges-

temic or primarily a pulmonary Inherited muscular dystrophies, tive heart failure in the
Framingham Heart
disease characterized by the such as Duchenne muscular Study. Ann Intern Med.
2002;136:181-91.
presence of noncaseating granu- dystrophy or Becker muscular [PMID: 11827493]

lomata. Cardiac involvement is
uncommon and generally mani-
fests as conduction abnormali-
dystrophy, are genetic disor- 20. Klein I, Ojamaa K. Thy-
roid hormone and the
ders characterized by progres- cardiovascular system. N
Engl J Med. 2001;344:
sive weakness in striated mus- 501-9. [PMID:

ties, ventricular arrhythmias, and cles, but they may also involve 11172193]
21. Gerdes AM, Iervasi G.
heart failure (26). Iron overload the cardiac muscle. Thyroid replacement
therapy and heart failure.
can cause HFREF or HFPEF from What drugs or Circulation. 2010;122:
385-93. [PMID:
excess iron deposition in the 20660814]
nonpharmacologic 22. Shinbane JS, Wood MA,
myocardium, resulting from he-
interventions should be used Jensen DN, Ellenbogen
reditary hemochromatosis or KA, Fitzpatrick AP, Schei-
for primary prevention? nman MM. Tachycardia-
other genetic disorders of iron induced cardiomyopa-
metabolism or from the repeated Although there is no definitive thy: a review of animal
models and clinical stud-
transfusions necessary to treat evidence that routine use of nu- ies. J Am Coll Cardiol.

some hereditary anemias. tritional supplements can prevent 1997;29:709-15. [PMID:

9091514]
heart failure, incidence can be 23. Kindermann I, Barth C,
Mahfoud F, Ukena C,
There are many genetic cardio- reduced by modification of hy- Lenski M, Yilmaz A, et al.
myopathies, and they have a pertension, diabetes, obesity, Update on myocarditis. J
Am Coll Cardiol. 2012;
diverse range of clinical mani- coronary artery disease, and 59:779-92. [PMID:
22361396]
festations. Many are not fully smoking (15). 24. Arany Z, Elkayam U.
Peripartum cardiomyopa-
thy. Circulation. 2016;
133:1397-409. [PMID:
27045128]
25. Maurer MS, Elliott P,
Comenzo R, Semigran
M, Rapezzi C. Addressing
common questions en-
Prevention... The most recognized risk factors for heart failure are hy- countered in the diagno-
pertension, coronary artery disease, diabetes, obesity, and smoking. sis and management of
cardiac amyloidosis.
Modification of these factors reduces the risk for heart failure. Preven- Circulation. 2017;135:
tion from specific causes other than coronary disease requires preven- 1357-77. [PMID:
tion and treatment of the specific cause. 28373528]
26. Birnie DH, Nery PB, Ha
AC, Beanlands RS. Car-
diac sarcoidosis. J Am
CLINICAL BOTTOM LINE Coll Cardiol. 2016;68:
411-21. [PMID:
27443438]

5 June 2018 Annals of Internal Medicine In the Clinic ITC85 姝 2018 American College of Physicians

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 Diagnosis
27. Goldberg LR, Jessup M.
Stage B heart failure:
management of asymp-
tomatic left ventricular
systolic dysfunction.
Circulation. 2006;113:
2851-60. [PMID:
16785351]
28. Morrison LK, Harrison A,
Krishnaswamy P, Kazane-
gra R, Clopton P, Maisel
A. Utility of a rapid
B-natriuretic peptide
assay in differentiating
congestive heart failure
from lung disease in
patients presenting with
dyspnea. J Am Coll Car-
diol. 2002;39:202-9.
[PMID: 11788208]
29. Maisel AS, Krishnaswamy
P, Nowak RM, McCord J,
Hollander JE, Duc P,
et al; Breathing Not
Properly Multinational
Study Investigators.
Rapid measurement of
B-type natriuretic peptide
in the emergency diag-
nosis of heart failure. N
Engl J Med. 2002;347:
161-7. [PMID:
12124404]
30. Dao Q, Krishnaswamy P,
Kazanegra R, Harrison A,
Amirnovin R, Lenert L,
et al. Utility of B-type
natriuretic peptide in the
diagnosis of congestive
heart failure in an
urgent-care setting. J Am
Coll Cardiol. 2001;37:
379-85. [PMID:
11216950]
31. Ledwidge M, Gallagher
J, Conlon C, Tallon E,
O’Connell E, Dawkins I,
et al. Natriuretic peptide-
based screening and
collaborative care for
heart failure: the
STOP-HF randomized
trial. JAMA. 2013;310:
66-74. [PMID:
23821090]
32. Daniels LB, Maisel AS.
Natriuretic peptides. J
Am Coll Cardiol. 2007;
50:2357-68. [PMID:
18154959]
33. Wang TJ, Larson MG,
Levy D, Benjamin EJ,
Leip EP, Wilson PW,
et al. Impact of obesity
on plasma natriuretic
peptide levels. Circula-
tion. 2004;109:594-600.
[PMID: 14769680]
34. Masson S, Latini R,
Anand IS, Barlera S,
Angelici L, Vago T, et al;
Val-HeFT Investigators.
Prognostic value of
changes in N-terminal
pro-brain natriuretic
peptide in Val-HeFT
(Valsartan Heart Failure
Trial). J Am Coll Cardiol.
2008;52:997-1003.
[PMID: 18786480]
姝 2018 American College of Physicians
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What symptoms and signs
should prompt clinicians to
consider a diagnosis of heart
failure?
The history and physical exami-
nation are essential during the
initial evaluation for suspected
heart failure. The history may re-
veal the presence of risk factors;
clues to specific causes, such as
prior chemotherapy or a family
history of cardiomyopathy; and
clinical manifestations, such as
weight gain, shortness of breath,
and edema. The physical exami-
nation may identify congestion or
low cardiac output by identifying
tachycardia, elevated jugular ve-
nous pressure, a third heart
sound, ascites, peripheral
edema, or cool extremities. A
heart murmur may signal valvular
heart disease. Identifying early
evidence of heart failure in
asymptomatic patients is impor-
tant because very strong evi-
dence shows that treatment of
asymptomatic left ventricular dys-
function delays onset of symp-
tomatic heart failure and im-
proves survival (27).
What diagnostic tests should
clinicians consider in the
evaluation of patients with
suspected heart failure?
Echocardiography and other
noninvasive imaging
Two-dimensional Doppler echo-
cardiography should be done in
all patients with new-onset heart
failure. It measures important
characteristics of the left ventri-
cle, such as ejection fraction, cav-
ity size and function, wall thick-
ness, and diastolic relaxation as
well as wall-motion abnormali-
ties. It also measures right ven-
tricular function, estimates pul-
monary artery pressure,
documents valvular abnormali-
ties, and differentiates between
ITC86 In the Clinic
HFREF and HFPEF. Repeated or
serial echocardiography is indi-
cated only when there has been
a change in clinical status or for
assessment of the effects of treat-
ment. Radionuclide ventriculog-
raphy and magnetic resonance
imaging are alternative imaging
methods for measuring ejection
fraction if echocardiography can-
not be used.
Laboratory tests
The initial laboratory evaluation
for patients with new-onset heart
failure should include blood
counts; serum levels of electro-
lytes, glucose, and lipids; blood
tests for renal function, liver func-
tion, and thyroid-stimulating hor-
mone levels; and urinalysis. If
hemochromatosis, HIV infection,
rheumatologic diseases, amy-
loidosis, or pheochromocytoma
are suspected, the initial labora-
tory evaluation might also in-
clude tests for those conditions.
B-type natriuretic peptide (BNP)
and N-terminal pro–B-type natri-
uretic peptide (NT-proBNP) are
the cleavage products of a com-
mon precursor molecule whose
serum level rises with increased
ventricular volume and pressure.
This means that levels of these
peptides can be used as markers
for volume and pressure over-
load. For example, they can help
determine whether acute dys-
pnea is caused by acute decom-
pensated heart failure; they can
also be used for screening high-
risk populations for undiagnosed
heart failure (28 –31). Interpreta-
tion of the results must also take
into account that values can be
higher in women; older patients;
and those who have renal dis-
ease, acute coronary syndrome,
or acute pulmonary disease. Lev-
els can be lower in patients with
obesity (32, 33). In addition, BNP
and NT-proBNP levels can help
Annals of Internal Medicine 5 June 2018
 stratify risk and determine prog-
nosis (34). For example, patients
being discharged from the hospi-
tal after treatment for heart fail-
ure with higher BNP levels have
an increased risk for death and
are more likely to be readmitted
(35). However, studies have pro-
vided conflicting evidence that
usually does not support use of
BNP or NT-proBNP for other
treatment decisions (36, 37).
In the multicenter GUIDE-IT (Guiding Evidence
Based Therapy Using Biomarker Intensified
Treatment in Heart Failure) study, high-risk pa-
tients with heart failure (elevated BNP in the
past 30 days and history of hospitalization for
heart failure) were randomly assigned to NT-
proBNP– guided care or usual care. The enroll-
ment goal was 1100 participants, but the
study was stopped early because of futility
when no significant differences were observed
between the groups in the primary outcome (a
composite of time to first hospitalization for
heart failure or cardiovascular death) (36).
Electrocardiography
The ACCF/AHA guidelines rec-
ommend electrocardiography for
all patients with new-onset heart
failure. Results may show ventric-
ular hypertrophy, atrial abnor-
mality, arrhythmia, conduction
abnormalities, previous myocar-
dial infarction, or active ischemia.
Electrocardiographic monitoring
should continue for up to 2
weeks if there are clinical sugges-
tions of episodic arrhythmia.
Stress testing
Noninvasive imaging to diagnose
myocardial ischemia is reason-
able in patients with new-onset
heart failure who have coronary
artery disease but no angina. It
also can identify the extent of
viable myocardium and thus help
with some decisions regarding
revascularization. Cardiopulmo-
nary exercise testing can mea-
sure the extent of disability and
differentiate between cardiac
and pulmonary causes of exer-
cise limitation. Either a cardiopul-
5 June 2018 Annals of Internal Medicine
Downloaded from https://annals.org by Laura Laura Rodriguez on 10/15/2019
monary exercise test or the
6-minute walk test can establish
functional class, which could be
useful in patients who are candi-
dates for cardiac transplant. The
6-minute walk test is easier to
administer and also provides
prognostic information (see the
Box: How to Perform the
6-Minute Walk Test).
Invasive evaluation
Coronary angiography by cathe-
terization or noninvasive com-
puted tomographic angiography
is indicated in suspected cases of
myocardial ischemia. Right heart
catheterization may be indicated
for hemodynamic monitoring in
seriously ill hospitalized patients
whose volume status or cardiac
pump function cannot be deter-
mined by clinical assessment. In
addition, right heart catheteriza-
tion can be useful in patients who
continue to have signs of cardio-
genic shock despite therapy and
patients who are being evaluated
for mechanical circulatory sup-
port or cardiac transplant. Endo-
myocardial biopsy is generally
done only when a specific type of
cardiomyopathy is suspected
and establishing the diagnosis
would affect management. Im-
plantable pulmonary artery pres-
sure monitors that communicate
wirelessly can also be useful. The
CHAMPION (CardioMEMS Heart
Sensor Allows Monitoring of
Pressure to Improve Outcomes in
NYHA Functional Class III Heart
Failure Patients) trial included a
heterogeneous group of outpa-
tients and found significantly
lower rates of hospitalization for
heart failure when daily pulmo-
nary artery pressure readings
were included in decisions about
therapy changes (38). A trend
toward reduced mortality was
also noted in the subset of pa-
tients who had HFREF (39).
In the Clinic ITC87
How to Perform the 6-Minute
Walk Test
Ask the patient to walk for 6
minutes in a straight line
back and forth between 2
points separated by 60 feet.
Allow the patient to stop and
rest or even sit if necessary.
At either end of the course,
place chairs that can quickly
be moved if the patient
needs to sit. Note the total
distance walked in 6 minutes,
which correlates well with
other measures of functional
capacity. Sex-specific
equations have been
developed that use age,
height, and weight to
calculate predicted distances
for healthy adults.
35. Logeart D, Thabut G,
Jourdain P, Chavelas C,
Beyne P, Beauvais F,
et al. Predischarge B-type
natriuretic peptide assay
for identifying patients at
high risk of re-admission
after decompensated
heart failure. J Am Coll
Cardiol. 2004;43:635-
41. [PMID: 14975475]
36. Felker GM, Anstrom KJ,
Adams KF, Ezekowitz JA,
Fiuzat M, Houston-Miller
N, et al. Effect of natri-
uretic peptide-guided
therapy on hospitaliza-
tion or cardiovascular
mortality in high-risk
patients with heart fail-
ure and reduced ejection
fraction: a randomized
clinical trial. JAMA.
2017;318:713-20.
[PMID: 28829876]
37. Jourdain P, Jondeau G,
Funck F, Gueffet P, Le
Helloco A, Donal E, et al.
Plasma brain natriuretic
peptide-guided therapy
to improve outcome in
heart failure: the STARS-
BNP Multicenter Study. J
Am Coll Cardiol. 2007;
49:1733-9. [PMID:
17448376]
38. Abraham WT, Steven-
son LW, Bourge RC,
Lindenfeld JA, Bau-
man JG, Adamson PB;
CHAMPION Trial Study
Group. Sustained effi-
cacy of pulmonary
artery pressure to
guide adjustment of
chronic heart failure
therapy: complete
follow-up results from
the CHAMPION ran-
domised trial. Lancet.
2016;387:453-61.
[PMID: 26560249]
姝 2018 American College of Physicians

39. Givertz MM, Steven-
son LW, Costanzo MR,
Bourge RC, Bauman
JG, Ginn G, et al;
CHAMPION Trial Inves-
tigators. Pulmonary
artery pressure-guided
management of pa-
tients with heart fail-
ure and reduced ejec-
tion fraction. J Am
Coll Cardiol. 2017;70:
1875-86. [PMID:
28982501]
40. The Cardiac Insufficiency
Bisoprolol Study II (CIBIS-
II): a randomised trial.
Lancet. 1999;353:9-13.
[PMID: 10023943]
41. Effect of metoprolol
CR/XL in chronic heart
failure: Metoprolol CR/XL
Randomised Intervention
Trial in Congestive Heart
Failure (MERIT-HF). Lan-
cet. 1999;353:2001-7.
[PMID: 10376614]
42. Packer M, Coats AJ,
Fowler MB, Katus HA,
Krum H, Mohacsi P,
et al; Carvedilol Prospec-
tive Randomized Cumu-
lative Survival Study
Group. Effect of carve-
dilol on survival in severe
chronic heart failure. N
Engl J Med. 2001;344:
1651-8. [PMID:
11386263]
43. CONSENSUS Trial Study
Group. Effects of enal-
april on mortality in
severe congestive heart
failure. Results of the
Cooperative North Scan-
dinavian Enalapril Sur-
vival Study
(CONSENSUS). N Engl J
Med. 1987;316:1429-
35. [PMID: 2883575]
44. Yusuf S, Pitt B, Davis CE,
Hood WB, Cohn JN;
SOLVD Investigators.
Effect of enalapril on
survival in patients with
reduced left ventricular
ejection fractions and
congestive heart failure.
N Engl J Med. 1991;
325:293-302. [PMID:
2057034]
45. Yusuf S, Pitt B, Davis CE,
Hood WB Jr, Cohn JN;
SOLVD Investigators.
Effect of enalapril on
mortality and the devel-
opment of heart failure
in asymptomatic patients
with reduced left ventric-
ular ejection fractions.
N Engl J Med. 1992;
327:685-91. [PMID:
1463530]
46. Pitt B, Segal R, Martinez
FA, Meurers G, Cowley
AJ, Thomas I, et al. Ran-
domised trial of losartan
versus captopril in pa-
tients over 65 with heart
failure (Evaluation of
Losartan in the Elderly
Study, ELITE). Lancet.
1997;349:747-52.
[PMID: 9074572]
姝 2018 American College of Physicians
Downloaded from https://annals.org by Laura Laura Rodriguez on 10/15/2019
Diagnosis... Dyspnea, congestion, and fatigue are the primary symp-
toms of heart failure, and the presence of risk factors should raise clini-
cal suspicion for heart failure. In this setting, the clinician should take a
history, perform a physical examination, and use 2-dimensional Dopp-
ler echocardiography to assess cardiac structure and function. If heart
failure is present, the clinician should use additional diagnostic testing
to determine the cause and to identify any exacerbating factors.
CLINICAL BOTTOM LINE
Treatment
Which drugs should be used for controlled clinical trials have
therapy? What are the shown that ACE inhibitors sig-
alternatives for patients who nificantly reduce mortality and
cannot tolerate these drugs? adverse events, such as hospi-
talization, worsening heart fail-
β-Blockers ure, and myocardial infarction,
␤-Blockers are first-line therapy even in patients without symp-
for heart failure and are indi- toms. Mortality was reduced by
cated for all patients regardless as much as 30% (43– 45). Impor-
of NYHA class. Patients with less tant adverse effects include
severe heart failure have the cough, worsening renal insuffi-
greatest long-term benefit, in- ciency, and hyperkalemia.
cluding those with left ventricu-
Angiotensin-receptor blockers
lar HFREF but no symptoms.
Angiotensin-receptor blockers
Many large randomized con-
(ARBs) can be used in patients
trolled studies that included a
who have intolerable adverse
variety of patients with heart
effects from ACE inhibitors, pri-
failure and the ␤-blockers carve- marily cough. There are no sig-
dilol, bisoprolol, and long- nificant differences in other ad-
acting metoprolol succinate
verse effects. Large randomized
found significant reductions in controlled trials have shown re-
hospitalizations, sudden death, duced mortality (30%– 45% in
and overall mortality. Reduc- some studies) and morbidity
tions in mortality ranged from similar to that associated with
23%– 65% (8, 40 – 42). Significant ACE inhibitor therapy (46 – 49).
data on other ␤-blockers are Although some studies have
lacking, so it is generally prefer- suggested that combining ACE
able to use the agents tested in
inhibitors and ARBs may be
clinical trials. beneficial in reducing left ven-
ACE inhibitors tricular size and decreasing hos-
ACE inhibitors should be used pitalizations, the effect on mor-
for all patients with left ventricu- tality was equivocal and this
lar systolic dysfunction or combination is not routinely
recommended.
HFREF regardless of functional
class (even in the absence of Angiotensin receptor–neprilysin
symptoms) except in patients inhibitors
with an intolerance or a contra- In patients with mild to severe
indication, such as angioedema. symptoms (NYHA class II to IV)
These vasodilators alter the nat- who tolerate adequate doses of
ural history of the disease and ACE inhibitors or ARBs, substitut-
improve survival and quality of ing an angiotensin receptor–
life. Many large randomized neprilysin inhibitor (ARNI) for the
ITC88 In the Clinic Annals of Internal Medicine 5 June 2018
 ACE inhibitor or ARB further re- When should clinicians add
duces risk for cardiovascular other medications?
47. Cohn JN, Tognoni G;
death or heart failure hospitaliza- Valsartan Heart Failure
tion by 20%. Potential adverse Aldosterone antagonists Trial Investigators. A
effects include hypotension and If patients continue to have mild randomized trial of the
angiotensin-receptor
renal insufficiency. These drugs to severe symptoms (NYHA class blocker valsartan in
chronic heart failure.
should not be given to patients II to IV) despite therapy with ACE N Engl J Med. 2001;
with a history of angioedema or inhibitors and ␤-blockers, treat- 345:1667-75. [PMID:
11759645]
administered concurrently or ment with low doses of an aldo- 48. Maggioni AP, Anand I,
Gottlieb SO, Latini R,
within 36 hours of the last dose sterone antagonist is indicated to Tognoni G, Cohn JN;
of an ACE inhibitor because of an reduce morbidity and mortality. Val-HeFT Investigators
(Valsartan Heart Failure
increased risk for angioedema. Spironolactone has been most Trial). Effects of valsartan
on morbidity and mortal-
extensively studied but can occa- ity in patients with heart
In the PARADIGM-HF (Prospective Comparison sionally cause painful gyneco- failure not receiving
of ARNI with ACEI to Determine Impact on angiotensin-converting
mastia in men. enzyme inhibitors. J Am
Global Mortality and Morbidity in Heart Fail- Coll Cardiol. 2002;40:
ure) trial, 8442 patients with NYHA class II RALES (Randomized Aldactone Evaluation 1414-21. [PMID:
12392830]
through IV heart failure and ejection fraction of Study) was a large randomized controlled trial 49. Granger CB, McMurray
40% or less were randomly assigned to enal- involving 1663 patients with NYHA class III or JJ, Yusuf S, Held P, Mi-
chelson EL, Olofsson B,
april (an ACE inhibitor) or the combination of IV heart failure receiving appropriate therapy et al; CHARM Investiga-
sacubitril (an ARNI) with valsartan (an ARB) in tors and Committees.
with or without spironolactone. The trial was Effects of candesartan in
addition to standard therapy. Compared with
stopped early because there were significantly patients with chronic
the enalapril group, risk for death and heart heart failure and reduced
fewer deaths in the spironolactone group than left-ventricular systolic
failure hospitalization was significantly lower
in the placebo group (284 vs. 386 deaths; P < function intolerant to
in the sacubitril–valsartan group (21.8% vs. angiotensin-converting-
0.001) (53). enzyme inhibitors: the
26.5%; hazard ratio [HR], 0.80 [CI, 0.73– CHARM-Alternative trial.
0.87]; P < 0.001) (50). Eplerenone is a more selective Lancet. 2003;362:772-6.
[PMID: 13678870]
Hydralazine and nitrates aldosterone antagonist that is 50. McMurray JJ, Packer M,
Desai AS, Gong J,
A suitable alternative for patients less often associated with gyne- Lefkowitz MP, Rizkala AR,
comastia. It has been shown to et al; PARADIGM-HF
who cannot tolerate ACE inhibi- Investigators and Com-
tors or ARBs is the combination decrease all-cause mortality in mittees. Angiotensin-
neprilysin inhibition
of hydralazine and isosorbide patients with ejection fraction versus enalapril in heart
dinitrate. Although the reduction less than 40% after acute myocar- failure. N Engl J Med.
2014;371:993-1004.
in mortality associated with this dial infarction (54). [PMID: 25176015]
51. Loeb HS, Johnson G,
combination is not as great as Henrick A, Smith R, Wil-
that seen with ACE inhibitors, the The EMPHASIS-HF (Eplerenone in Mild Pa- son J, Cremo R, et al.
tients Hospitalization and Survival Study in Effect of enalapril, hydral-
benefit exceeds that of placebo azine plus isosorbide
Heart Failure) trial was a large double-blind dinitrate, and prazosin
(51). In African American patients
trial of 2737 patients with NYHA class II on hospitalization in
with severe symptomatic heart heart failure receiving standard therapy who
patients with chronic
congestive heart failure.
failure (NYHA class III or IV), hy- were randomly assigned to eplerenone (up The V-HeFT VA Coopera-
dralazine plus isosorbide dini- to 50 mg/d) or placebo. The trial was
tive Studies Group. Circu-
lation. 1993;87:VI78-87.
trate should be added to stan- stopped early because of a significant reduc- [PMID: 8500244]
52. Taylor AL, Ziesche S,
dard therapy, including an ACE tion in death and risk for heart failure hos- Yancy C, Carson P,
inhibitor or ARB and ␤-blocker, pitalization in the eplerenone group (18.3% D’Agostino R Jr, Ferdi-
nand K, et al; African-
because it favorably affects myo- vs. 25.9%; HR, 0.63 [CI, 0.54 – 0.74]; P < American Heart Failure
cardial remodeling and mortality 0.001) (55). Trial Investigators. Com-
bination of isosorbide
in these patients. dinitrate and hydralazine
Higher rates of hyperkalemia in blacks with heart fail-
ure. N Engl J Med.
A-HeFT (African American Heart Failure Trial) have been found in patients re- 2004;351:2049-57.
compared hydralazine plus isosorbide dini- ceiving ACE inhibitors and spi- [PMID: 15533851]
53. Pitt B, Zannad F, Remme
trate with placebo in African Americans with ronolactone, necessitating care- WJ, Cody R, Castaigne A,
NYHA class III or IV heart failure who were re- ful monitoring of serum
Perez A, et al. The effect
of spironolactone on
ceiving standard therapy that included ACE in- morbidity and mortality
potassium levels (56). The combi-
hibitors and ␤-blockers. This trial showed that in patients with severe
adding hydralazine and isosorbide dinitrate nation of ACE inhibitors, ARBs, heart failure. Random-
ized Aldactone Evalua-
significantly reduced mortality by 43% and and spironolactone should be tion Study Investigators.
first hospitalization for heart failure by 33%. It avoided because of significantly N Engl J Med. 1999;
341:709-17. [PMID:
also improved quality of life (52). increased risk for hyperkalemia. 10471456]

5 June 2018 Annals of Internal Medicine In the Clinic ITC89 姝 2018 American College of Physicians

Downloaded from https://annals.org by Laura Laura Rodriguez on 10/15/2019


54. Pitt B, Remme W, Zan-
nad F, Neaton J, Marti-
nez F, Roniker B, et al;
Eplerenone Post-Acute
Myocardial Infarction
Heart Failure Efficacy and
Survival Study Investiga-
tors. Eplerenone, a selec-
tive aldosterone blocker,
in patients with left ven-
tricular dysfunction after
myocardial infarction.
N Engl J Med. 2003;
348:1309-21. [PMID:
12668699]
55. Zannad F, McMurray JJ,
Krum H, van Veldhuisen
DJ, Swedberg K, Shi H,
et al; EMPHASIS-HF
Study Group. Eplerenone
in patients with systolic
heart failure and mild
symptoms. N Engl J
Med. 2011;364:11-21.
[PMID: 21073363]
56. Juurlink DN, Mamdani
MM, Lee DS, Kopp A,
Austin PC, Laupacis A,
et al. Rates of hyperkale-
mia after publication of
the Randomized Aldac-
tone Evaluation Study. N
Engl J Med. 2004;351:
543-51. [PMID:
15295047]
57. Swedberg K, Komajda
M, Böhm M, Borer JS,
Ford I, Dubost-Brama A,
et al; SHIFT Investigators.
Ivabradine and outcomes
in chronic heart failure
(SHIFT): a randomised
placebo-controlled study.
Lancet. 2010;376:875-
85. [PMID: 20801500]
58. Matsue Y, Damman K,
Voors AA, Kagiyama N,
Yamaguchi T, Kuroda S,
et al. Time-to-furosemide
treatment and mortality
in patients hospitalized
with acute heart failure.
J Am Coll Cardiol. 2017;
69:3042-51. [PMID:
28641794]
59. Felker GM, Lee KL, Bull
DA, Redfield MM, Ste-
venson LW, Goldsmith
SR, et al; NHLBI Heart
Failure Clinical Research
Network. Diuretic strate-
gies in patients with
acute decompensated
heart failure. N Engl J
Med. 2011;364:797-
805. [PMID: 21366472]
60. Digitalis Investigation
Group. The effect of
digoxin on mortality and
morbidity in patients
with heart failure. N Engl
J Med. 1997;336:525-
33. [PMID: 9036306]
61. Rathore SS, Curtis JP,
Wang Y, Bristow MR,
Krumholz HM. Associa-
tion of serum digoxin
concentration and out-
comes in patients with
heart failure. JAMA.
2003;289:871-8. [PMID:
12588271]
姝 2018 American College of Physicians
Downloaded from https://annals.org by Laura Laura Rodriguez on 10/15/2019
Ivabradine
Ivabradine is a new agent that
slows heart rate by selectively
inhibiting the depolarizing If cur-
rent in the sinoatrial node. It re-
duces heart failure hospitaliza-
tions in patients who have mild to
moderate symptoms (NYHA class
II or III), are receiving standard
medical therapy that includes a
maximally tolerated dose of
␤-blockers, are in sinus rhythm,
and have a resting heart rate of at
least 70 beats/min. Ivabradine is
not indicated for patients with
chronic atrial fibrillation or a
slower sinus rate. Adverse effects
are rare but include symptomatic
bradycardia and vision distur-
bances.
SHIFT (Systolic Heart failure treatment with the
If inhibitor ivabradine Trial) included 6558 pa-
tients with symptomatic heart failure who had
a left ventricular ejection fraction of 35% or
less, were in sinus rhythm with a resting heart
rate of at least 70 beats/min, and were receiv-
ing standard medical therapy that included a
maximally tolerated dose of a ␤-blocker. Pa-
tients were randomly assigned to ivabradine
(titrated to a maximum dose of 7.5 mg twice
daily) or placebo. Patients in the ivabradine
group had better outcomes in a composite end
point that included cardiovascular death and
heart failure hospitalization (24% vs. 29%; HR,
0.82 [CI, 0.75– 0.90]; P < 0.0001) (57).
Diuretics
Diuretics are the only therapy
that produces short-term symp-
tomatic benefits. They reduce
pulmonary capillary wedge pres-
sure and edema and increase
exercise capacity. A recent ob-
servational study found that pa-
tients presenting to the emer-
gency department for acute
decompensated heart failure
who received early treatment
(<60 minutes after arrival) with
intravenous loop diuretics had
lower in-hospital mortality (58).
Another randomized trial of pa-
tients hospitalized with acute de-
compensated heart failure found
no significant difference in sub-
jective symptoms or change in
renal function between intrave-
ITC90 In the Clinic
nous bolus dosing every 12
hours or continuous infusion, ei-
ther at low doses (equivalent to
the patient's outpatient oral di-
uretic dose) or high doses (2.5
times the outpatient dose) (59).
However, no prospective clinical
trials have assessed long-term
safety or the effect of diuretics on
mortality in heart failure.
Loop diuretics should be com-
bined with a low-sodium diet to
control volume overload, main-
tain a stable weight, and improve
the functional capacity of patients
with NYHA class II to IV heart fail-
ure. Diuretics should not be used
alone to treat heart failure due to
HFREF because they do not pre-
vent disease progression. The
commonly used loop diuretics
differ primarily in speed of ab-
sorption and bioavailability.
Compared with furosemide,
torsemide and bumetanide are
more rapidly absorbed and have
greater bioavailability. If a patient
does not respond to oral furo-
semide therapy and is stable
enough to continue oral diuretic
therapy, changing to oral
torsemide or bumetanide may
facilitate diuresis. In addition, thi-
azide diuretics, which act more
distally in the nephron, may be
added to augment diuresis. A
thiazide diuretic, such as metola-
zone, combined with a loop di-
uretic can be an effective “slid-
ing” regimen based on the
patient's daily weight and symp-
toms. Patients receiving diuretics
should have renal function and
electrolyte levels, especially po-
tassium, checked frequently.
Digoxin
Digoxin can alleviate symptoms
and decrease hospitalization in
patients with HFREF; however, it
should be reserved for patients
with symptomatic NYHA class II
to IV heart failure because it pro-
vides no survival advantage com-
Annals of Internal Medicine 5 June 2018
 pared with placebo (60). Be- found that treatment with cande- 62. Yusuf S, Pfeffer MA,
Swedberg K, Granger CB,
cause it primarily provides rate sartan reduced hospitalizations Held P, McMurray JJ,
et al; CHARM Investiga-
control at rest, digoxin alone but had no significant effect on tors and Committees.
may be insufficient for rate con- cardiovascular death (62). Effects of candesartan in
patients with chronic
trol in patients with atrial fibrilla- TOPCAT (Treatment of Preserved heart failure and pre-
tion; the ACCF/AHA guidelines Cardiac Function Heart Failure served left-ventricular
ejection fraction: the
recommend use of a ␤-blocker with an Aldosterone Antagonist), CHARM-Preserved Trial.
Lancet. 2003;362:777-
with digoxin for this purpose. a recent large randomized trial of 81. [PMID: 13678871]
Because hypokalemia and hy- patients with preserved ejection 63. Pitt B, Pfeffer MA, Ass-
mann SF, Boineau R,
pomagnesemia increase risk for fraction (≥45%), found no signifi- Anand IS, Claggett B,
digoxin toxicity, regular mea- et al; TOPCAT Investiga-
cant difference between spirono- tors. Spironolactone for
surement of electrolytes is rec- lactone and placebo in the com- heart failure with pre-
served ejection fraction.
ommended. Renal function posite outcome of cardiovascular N Engl J Med. 2014;
should also be followed closely death, aborted cardiac arrest, 370:1383-92. [PMID:
24716680]
because digoxin is excreted by and heart failure hospitalization. 64. Lip GY, Shantsila E. Anti-
coagulation versus pla-
the kidneys. Renal excretion of A subset of patients with increased cebo for heart failure in
digoxin is diminished and BNP did benefit, but the implica- sinus rhythm. Cochrane
Database Syst Rev. 2014:
plasma digoxin levels are in- tions are uncertain (63). CD003336. [PMID:
creased by drugs inhibiting 24683002]
65. Homma S, Thompson JL,
P-glycoprotein, such as amioda- When should clinicians use Pullicino PM, Levin B,
rone, verapamil, erythromycin, inotropic agents? Freudenberger RS, Teer-
link JR, et al; WARCEF
quinidine, or cyclosporine. Continuous intravenous adminis- Investigators. Warfarin
and aspirin in patients
When these drugs are given, tration of inotropic agents, such as with heart failure and
the digoxin dose will likely need dobutamine and milrinone, can sinus rhythm. N Engl J
Med. 2012;366:1859-
to be reduced. Some contro- increase cardiac output and de- 69. [PMID: 22551105]
66. O’Connor CM, Whellan
versy exists over the appropri- crease afterload in patients with DJ, Lee KL, Keteyian SJ,
ate serum level of digoxin. A severe decompensated heart fail- Cooper LS, Ellis SJ, et al;
HF-ACTION Investigators.
post hoc analysis of a large ran- ure who do not respond to stan- Efficacy and safety of
dard oral heart failure medications exercise training in pa-
domized controlled trial tients with chronic heart
showed that higher serum and have evidence of end-organ failure: HF-ACTION ran-
domized controlled trial.
digoxin levels (≥1.2 ng/mL) hypoperfusion or signs of impend- JAMA. 2009;301:1439-
were associated with increased ing or overt cardiogenic shock. In 50. [PMID: 19351941]
67. Moss AJ, Zareba W, Hall
mortality and suggested an op- addition, continuous intravenous WJ, Klein H, Wilber DJ,
Cannom DS, et al; Multi-
timal therapeutic range of 0.5– inotropic agents can be used on a center Automatic Defibril-
0.8 ng/mL (61). short-term basis to treat cardio- lator Implantation Trial II
Investigators. Prophylac-
genic shock and prepare the pa- tic implantation of a
What drug therapy is tient for more definitive therapies, defibrillator in patients
with myocardial infarc-
appropriate for patients with such as coronary revascularization. tion and reduced ejec-
HFPEF? Moreover, intravenous inotropic tion fraction. N Engl J
Med. 2002;346:877-83.
The goal of treatment for patients agents can be used for intermedi- [PMID: 11907286]
68. Bardy GH, Lee KL, Mark
with HFPEF is to control exacer- ate and longer periods as “bridge DB, Poole JE, Packer DL,
bating and causative factors. Hy- therapy” in patients waiting for Boineau R, et al; Sudden
Cardiac Death in Heart
pertension should be controlled mechanical circulatory support or Failure Trial (SCD-HeFT)
with ␤-blockers, ACE inhibitors, cardiac transplant. Finally, in se- Investigators. Amioda-
rone or an implantable
and ARBs. If angina or evidence lected patients with end-stage cardioverter-defibrillator
for congestive heart
of myocardial ischemia is present heart failure who are not eligible failure. N Engl J Med.
in patients with coronary disease, 2005;352:225-37.
for mechanical circulatory support [PMID: 15659722]
coronary revascularization is rea- or cardiac transplant, long-term 69. Kadish A, Dyer A,
Daubert JP, Quigg R,
sonable. Atrial fibrillation should inotropic infusion may help palli- Estes NA, Anderson KP,
be managed according to prac- ate symptoms. Intravenous inotro- et al; Defibrillators in
Non-Ischemic Cardiomy-
tice guidelines to mitigate symp- pic agents have not been shown to opathy Treatment Evalua-
tion (DEFINITE) Investiga-
toms, which probably are related improve survival and may increase tors. Prophylactic
to reduced diastolic filling time. the risk for arrhythmia, so long- defibrillator implantation
in patients with nonisch-
One large randomized con- term use of this regimen without a emic dilated cardiomyop-
trolled trial of patients with pre- specific clinical indication may be athy. N Engl J Med.
2004;350:2151-8.
served ejection fraction (>40%) harmful. [PMID: 15152060]

5 June 2018 Annals of Internal Medicine In the Clinic ITC91 姝 2018 American College of Physicians

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70. Køber L, Thune JJ,
Nielsen JC, Haarbo J,
Videbæk L, Korup E,
et al; DANISH Investiga-
tors. Defibrillator implan-
tation in patients with
nonischemic systolic
heart failure. N Engl J
Med. 2016;375:1221-
30. [PMID: 27571011]
71. Young JB, Abraham WT,
Smith AL, Leon AR,
Lieberman R, Wilkoff B,
et al; Multicenter InSync
ICD Randomized Clinical
Evaluation (MIRACLE
ICD) Trial Investigators.
Combined cardiac resyn-
chronization and im-
plantable cardioversion
defibrillation in ad-
vanced chronic heart
failure: the MIRACLE ICD
Trial. JAMA. 2003;289:
2685-94. [PMID:
12771115]
72. Cleland JG, Daubert JC,
Erdmann E, Freemantle
N, Gras D, Kappenberger
L, et al; Cardiac
Resynchronization-Heart
Failure (CARE-HF) Study
Investigators. The effect
of cardiac resynchroniza-
tion on morbidity and
mortality in heart failure.
N Engl J Med. 2005;
352:1539-49. [PMID:
15753115]
73. Moss AJ, Hall WJ, Can-
nom DS, Klein H, Brown
MW, Daubert JP, et al;
MADIT-CRT Trial Investi-
gators. Cardiac-
resynchronization ther-
apy for the prevention of
heart-failure events. N
Engl J Med. 2009;361:
1329-38. [PMID:
19723701]
74. Goldenberg I, Kutyifa V,
Klein HU, Cannom DS,
Brown MW, Dan A, et al.
Survival with cardiac-
resynchronization ther-
apy in mild heart failure.
N Engl J Med. 2014;
370:1694-701. [PMID:
24678999]
75. Doukky R, Avery E, Man-
gla A, Collado FM, Ibra-
him Z, Poulin MF, et al.
Impact of dietary sodium
restriction on heart fail-
ure outcomes. JACC
Heart Fail. 2016;4:24-
35. [PMID: 26738949]
76. Kavalieratos D, Gelfman
LP, Tycon LE, Riegel B,
Bekelman DB, Ikejiani
DZ, et al. Palliative care
in heart failure: rationale,
evidence, and future
priorities. J Am Coll
Cardiol. 2017;70:1919-
30. [PMID: 28982506]
姝 2018 American College of Physicians
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When should clinicians
consider using anticoagulants?
Routine anticoagulation is not
recommended for patients with
chronic HFREF who do not have
another indication for anticoagu-
lation due to lack of demon-
strated clinical benefit (64). For
example, in patients with re-
duced ejection fraction (≤35%)
who were in sinus rhythm and
did not have another indication
for anticoagulation, no significant
difference between warfarin and
aspirin was found in a composite
outcome of ischemic stroke, in-
tracerebral hemorrhage, and all-
cause mortality because the re-
duced risk for ischemic stroke
was offset by an increased risk for
major hemorrhage (65). The
novel oral anticoagulants have
improved safety profiles and are
an attractive possibility in this
population, but current guide-
lines do not recommend them
because their benefit has not yet
been shown in clinical trials. Cur-
rent guidelines do recommend
anticoagulation for patients with
chronic heart failure and nonval-
vular atrial fibrillation using the
strategies that are recommended
for patients without heart failure.
What should clinicians advise
patients about exercise? Are
formal exercise programs
beneficial?
A structured cardiac rehabilita-
tion program that provides su-
pervised exercise and support in
making lifestyle modifications
can improve functional capacity
and quality of life, although no
effects on mortality have been
found.
In a large multicenter randomized clinical
trial of medically stable outpatients with
heart failure, participation in a structured
aerobic exercise program in addition to
usual care showed that exercise training was
well-tolerated and safe, and improvements
in exercise capacity (6-minute walk test and
peak oxygen consumption) were also noted.
ITC92 In the Clinic
However, exercise did not significantly re-
duce all-cause mortality or hospitalizations
(66).
When should clinicians
consider an intracardiac device
for primary prophylaxis or
treatment?
Candidates for a prophylactic
implantable cardioverter-
defibrillator (ICD) should have a
reasonable expectation of
meaningful survival of more
than 1 year, be at least 40 days
beyond any acute myocardial
infarction, and be receiving
standard medical therapy for
heart failure. Current guidelines
recommend ICD implantation
for primary prevention of sud-
den death in patients with isch-
emic or nonischemic cardiomy-
opathy, ejection fraction of 35%
or less, and mild to moderate
symptoms (NYHA class II or III).
In addition, ICD implantation for
primary prevention is indicated
for asymptomatic (NYHA class I)
patients with ischemic cardio-
myopathy and ejection fraction
of 30% or less (67, 68). The indi-
cation for prophylactic implan-
tation in patients with nonisch-
emic cardiomyopathy is less
certain (69). In the randomized
trial DANISH (Danish Study to
Assess the Efficacy of ICDs in
Patients with Non-ischemic Sys-
tolic Heart Failure on Mortality),
no significant difference in mor-
tality with prophylactic ICD im-
plantation versus usual clinical
care was found in patients with
nonischemic cardiomyopathy
(70). The ability of ICD implan-
tation to meaningfully prolong
survival is uncertain in patients
at high risk for nonsudden
death because of advanced
end-stage heart failure, severe
comorbidities, or overall frailty.
In these situations, the decision
to use an ICD should be tai-
lored to the patient's circum-
stances.
Annals of Internal Medicine 5 June 2018
 Progression of heart failure is of-
ten associated with development
of ventricular dyssynchrony, most
readily diagnosed by QRS pro-
longation on electrocardiogra-
phy and manifesting clinically as
impaired and inefficient ventricu-
lar contractile function, develop-
ing or worsening functional
mitral regurgitation, and mala-
daptive ventricular remodeling.
Cardiac resynchronization ther-
apy (CRT, or biventricular pacing)
can reverse these adverse
changes and improve outcomes.
This therapy is not indicated for
asymptomatic patients (NYHA
class I), patients with non–left
bundle branch block with QRS
duration less than 150 millisec-
onds, or those with expected sur-
vival less than 1 year. It is indi-
cated for patients who have an
ejection fraction of 35% or less,
are in sinus rhythm, have left
bundle branch block and a QRS
duration of at least 150 millisec-
onds, have mild to severe symp-
toms (NYHA class II through IV),
and are receiving standard medi-
cal therapy. CRT is reasonable for
other patients with ejection frac-
tion of 35% or less who are re-
ceiving standard medical therapy
for heart failure. It is also indi-
cated for patients with atrial fibril-
lation who require ventricular
pacing and otherwise meet crite-
ria for CRT or who require near
100% ventricular pacing with
CRT, and those having implanta-
tion of a new or replacement de-
vice anticipated to require signifi-
cant (>40%) ventricular pacing
(71–74).
When should patients be
hospitalized?
Clinicians should consider hospi-
talizing patients with acute de-
compensated heart failure. Clini-
cal characteristics of this
condition include progressive or
severe signs and symptoms of
volume overload or low cardiac
5 June 2018 Annals of Internal Medicine
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output, or laboratory evidence of
end-organ hypoperfusion de-
spite outpatient medical therapy.
Signs and symptoms of decom-
pensated heart failure include
shortness of breath, orthopnea,
paroxysmal nocturnal dyspnea,
lower-extremity edema, abdo-
minal bloating, early satiety, an-
orexia, lightheadedness, syn-
cope, weight gain, and hypoten-
sion. Patients should be
hospitalized if they have hemody-
namically significant ventricular
or atrial arrhythmia or there is
concern for acute coronary
syndrome.
When should clinicians consult
a cardiologist?
Clinicians should consider con-
sulting a cardiologist when the
patient's clinical status worsens
despite optimal medical ther-
apy. Under these circum-
stances, the cardiologist can
help treat such reversible car-
diac conditions as coronary ar-
tery disease, valvular heart dis-
ease, and incessant tachycardia.
Consultation should also be
considered when newly diag-
nosed or chronic heart failure is
associated with markedly re-
duced ejection fraction, there is
suspicion that the cardiomyopa-
thy is caused by a systemic dis-
ease or a heritable disorder, or
77. Yancy CW, Jessup M,
the patient has signs and symp- Bozkurt B, Butler J,
toms of decompensated heart Casey DE Jr, Colvin MM,
et al. 2017 ACC/AHA/
failure. Finally, a cardiologist HFSA focused update of
the 2013 ACCF/AHA
should be consulted when the guideline for the man-
patient does not tolerate agement of heart failure:
a report of the American
afterload-reducing agents or College of Cardiology/
␤-blockers; develops hypona- American Heart Associa-
tion Task Force on Clini-
tremia, worsening renal func- cal Practice Guidelines
and the Heart Failure
tion, or poor functional status; Society of America. Circu-
lation. 2017;136:e137-
or is hospitalized frequently.
e161. [PMID:
28455343]
What is the role of lifestyle 78. Lindenfeld J, Albert NM,
Boehmer JP, Collins SP,
modifications? Ezekowitz JA, Givertz
MM, et al; Heart Failure
Patients who have such cardio- Society of America. HFSA
vascular risk factors as hyperlipid- 2010 comprehensive
heart failure practice
emia, obesity, or diabetes should guideline. J Card Fail.
follow dietary recommendations 2010;16:e1-194. [PMID:
20610207] doi:10.1016/
specific to those conditions. Cig- j.cardfail.2010.04.004
In the Clinic ITC93 姝 2018 American College of Physicians
 arette smoking should be dis-
continued, and alcohol should
be consumed in moderation.
Weight monitoring and sodium
and fluid restriction may help for
long-term management of heart
failure, particularly in symptom-
atic and advanced stages. Daily
weight checks may prevent
heart failure exacerbations by
allowing for prophylactic di-
uretic adjustments. Patients can
weigh themselves daily and con-
tact their clinician for instructions
on adjustments if their weight
exceeds a predetermined
threshold (usually a 2-lb increase
overnight or a 5-lb increase over
3 days). Some patients can use a
sliding dose of diuretic to main-
tain their weight. Support from
nurses, dietitians, home health
staff, and physical therapists can
help prevent exacerbations. In
advanced heart failure, particu-
larly in patients with hyponatre-
mia, fluid restriction (1.5–2 L/d)
and dietary sodium restriction
are reasonable to assist diuretic
effectiveness and reduce con-
gestion. However, these recom-
mendations are based on expert
opinion and data from small,
uncontrolled, and observational
studies with heterogeneous
study populations. The data are
conflicting, and some studies
even suggest a detrimental ef-
fect of sodium restriction on clin-
ical outcomes (75). Current AHA
guidelines recommend restrict-
ing sodium intake to no more
than 1500 mg/d in patients with
hypertension or left ventricular
hypertrophy, and this may also
be reasonable for patients with
less advanced disease (AHA
stage A or B). For patients with
more advanced heart failure
(AHA stage C [Figure] or D),
there are not enough data to
guide decisions about sodium
restriction, except to aim for a
lower level than in the general
population (<2000 –3000 mg/d).
姝 2018 American College of Physicians
Downloaded from https://annals.org by Laura Laura Rodriguez on 10/15/2019
Figure. Evidence-based guideline– directed medical therapy for stage C
heart failure.
NYHA I–IV
ACE inhibitor or ARB or ARNI
AND
β-blocker
NYHA II–IV NYHA II–III
On maximally tolerated β-blocker dose,
ADD aldosterone antagonist (if GFR
>30 mL/min and K <5 mEq/dL)
in sinus rhythm, resting HR >70 bpm
ADD ivabradine
ADD loop diuretic if volume overloaded
NYHA III–IV
African American and persistently symptomatic
ADD hydralazine–isosorbide dinitrate
ACE = angiotensin-converting enzyme; ARB = angiotensin-receptor blocker; ARNI = angioten-
sin receptor–neprilysin inhibitor; bpm = beats per minute; GFR = glomerular filtration rate; HR =
heart rate; K = potassium; NYHA = New York Heart Association.
What is the role of palliative depression, the level of social
care? support, unrealistic expectations
The natural progression of heart about the prognosis of the dis-
failure includes recurrent fre- ease or the effectiveness of the
quent and unpredictable exacer- interventions, discordance be-
bations followed by recovery. tween objective measures of dis-
Palliative care provides different ease status and the patient's sub-
types of care for different stages jective experience, anxiety
of heart failure. Basic palliative
related to advanced therapies,
care primarily involves symptom
and adjustment to new social or
management, but advanced pal-
liative care addresses more re- professional roles. Several con-
fractory symptoms, complex psy- sensus guidelines now recom-
chosocial issues, and end-of-life mend including palliative care as
management. Areas that may part of routine care for patients
need to be addressed include with heart failure (76).
Treatment... The patient's NYHA functional class guides treatment. Re-
gardless of the presence or severity of symptoms, first-line drug therapy
should be initiated with ␤-blockers and either ACE inhibitors or ARBs (or, if
these are not tolerated, hydralazine and nitrates). In symptomatic patients,
ARNI treatment leads to a better prognosis and should be substituted for
the ACE inhibitor or ARB. For patients with mild to severe symptoms
(NYHA class II through IV), an aldosterone antagonist should be added.
Loop diuretics and digoxin are available for symptomatic management in
patients with NYHA class II to IV heart failure. Symptomatic patients with an
ejection fraction irreversibly reduced below 35% should be considered for
a prophylactic ICD even in the absence of arrhythmia. Consultation with a
cardiologist should be considered in patients with left bundle branch block
or severe heart failure, especially those with recurrent hospitalizations;
need for an ICD, a pacemaker, or CRT; or need for evaluation regarding
mechanical circulatory support or cardiac transplant.
CLINICAL BOTTOM LINE
ITC94 In the Clinic Annals of Internal Medicine 5 June 2018

What do professional
organizations recommend with
regard to the care of patients
with heart failure?
In 2013, the ACCF/AHA pub-
lished the Guideline for the Man-
agement of Heart Failure, which
was updated in conjunction with
the Heart Failure Society of
America in 2016 (2, 77). Other
important guidelines include the
Heart Failure Society of America
2010 Comprehensive Heart Fail-
ure Practice Guideline (78).
What measures do
stakeholders use to evaluate
the quality of care for patients
with heart failure?
The Centers for Medicare & Medic-
aid Services (CMS) started a Physi-
cian Quality Reporting System
(PQRS)—previously known as the
Physician Quality Reporting
Initiative—that clinicians can use to
earn bonus payments by reporting
quality measures on claims for ser-
In the Clinic
Tool Kit
Heart Failure
5 June 2018 Annals of Internal Medicine
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Practice Improvement
vices. Of the current measures in
the PQRS, 2 relate specifically to
heart failure. The first calls for ACE
inhibitors or ARBs in patients older
than 18 years with a diagnosis of
heart failure and left ventricular
dysfunction, and the second calls
for ␤-blocker therapy in the same
population. Other relevant PQRS
quality measures include influenza
immunization, documentation of
current medications, and tobacco
use screening and counseling. The
Agency for Healthcare Research
and Quality is using quality indica-
tors to measure the hospital ad-
mission rate for heart failure, and
CMS publicly reports hospital-level
30-day mortality for patients with
myocardial infarction and heart
failure. Other performance mea-
sures that are evaluated by several
regulatory agencies include hospi-
tal readmission rates within 30
days of discharge and documenta-
tion of discharge teaching and
instructions.
Clinical Guidelines
www.acc.org/latest-in-cardiology/ten-points-to
-remember/2017/04/27/15/50/2017-acc-aha-hfsa
-focused-update-of-hf-guideline
Update of the 2013 guideline on heart failure from the
American Heart Association, the American College of
Cardiology, and the Heart Failure Society of America.
www.escardio.org/Guidelines/Clinical-Practice
-Guidelines/Acute-and-Chronic-Heart-Failure
Guidelines on heart failure from the European Society of
Cardiology.
IntheClinic
Information for Patients and Clinicians
www.heart.org/HEARTORG/Conditions/HeartFailure
/Heart-Failure-Guidelines-Toolkit_UCM_491412
_SubHomePage.jsp
Information on heart failure, including a downloadable
guideline algorithm, provided by the American Heart
Association for clinicians and patients.
Patient Information
http://circ.ahajournals.org/content/129/3/e293
Self-care guide for patients, provided by the journal
Circulation.
www.mayoclinic.org/diseases-conditions/heart-failure
/symptoms-causes/syc-20373142
Heart failure information provided by the Mayo Clinic.
www.cdc.gov/heartdisease/materials_for_patients.htm
Educational material provided by the Centers for Disease
Control and Prevention.
In the Clinic ITC95 姝 2018 American College of Physicians
 WHAT YOU SHOULD KNOW In the Clinic
Annals of Internal Medicine
ABOUT HEART FAILURE
What Is Heart Failure?
Your heart is a strong muscle about the size of your fist.
It pumps oxygen-rich blood throughout the body.
Heart failure doesn't mean your heart has stopped
working; it means that it doesn't pump as well as it
should, and your body doesn't get enough of the
blood it needs to work well.
What Are the Risk Factors?
You are at higher risk for heart failure if you:
• Have high blood pressure, diabetes, or heart
disease
• Are overweight
• Smoke cigarettes
• Have a family history of heart failure
• Drink alcohol heavily
What Are the Symptoms?
• Feeling weak or tired
• Feeling short of breath when lying flat
• Swollen feet and ankles
• Unexplained weight gain
How Is It Diagnosed?
• Angiotensin-converting enzyme (ACE) inhibitors.
• Your doctor will perform a physical exam and ask
These medicines help lower your blood pressure
you questions about your medical history and
symptoms. and help improve your shortness of breath. This
• You will have an echocardiogram, a safe, painless helps your heart work better.
procedure that uses sound waves to see what your • Angiotensin-receptor blockers (ARBs). These
heart looks like and how it functions. medicines provide many of the same benefits as
• Your doctor will perform or refer you for other ACE inhibitors.

tests.
How Is It Treated?
• Heart failure is a serious health condition, but treat-
ment can make you feel better and live longer.
Modification of risk factors
• Don't smoke cigarettes.
• If you're overweight, lose weight.
• If you drink alcohol heavily, reduce the
amount you drink.
• If you have high blood pressure, diabetes, or
coronary artery disease, make sure those
conditions are treated.
Other lifestyle changes
• It's important to check your weight often. A lot
of weight gain in a few days or weight gain
every day for more than a few days can mean
that heart failure is getting worse.
• People with heart failure may need a low-salt
diet. Ask your doctor.
Medications
• ␤-blockers. These medicines help slow your
heart rate and reduce your blood pressure.
This can help your heart work better.
Patient Information
• Hydralazine and nitrates. These medicines can
be used for people who can't use ACE
inhibitors or ARBs. Sometimes they are added
to ACE inhibitors or ARBs.
• Angiotensin receptor–neprilysin inhibitors.
These medicines help blood flow and fluid
retention and help your heart work better.
Devices or implants
• These might include a pacemaker to make
your heart beat regularly or an implantable
cardioverter-defibrillator to restart your heart
automatically if it stops beating.
Questions for Your Doctor
• What type of heart failure do I have?
• Do I need to lose weight?
• What physical activities are good for me?
• Which medicines will I be taking for my heart
failure, and what do they do?
• What changes in my condition should make
me call the office?
• If I'm doing well, when should I come back to
see you?

For More Information

American College of Physicians
www.acponline.org/patient_ed/cardiovascular
MedlinePlus
https://medlineplus.gov/heartfailure.html
American Heart Association
www.heart.org

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