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Heart Failure

Amanda Ryan, D.O.

Cardiology Fellow
February 14th, 2008

Learning Objectives

this presentation, the

participant should be able to:

1. Recognize the magnitude of heart failure epidemic and its public

health implications

2. Distinguish the different classifications and stages of heart failure

3. Review underlying pathophysiology of heart failure

4. Discuss signs and symptoms of heart failure exacerbation

5. Identify current practice guidelines for treatment of acute

decompensated heart failure

What is Heart Failure


failure occurs when the heart cannot

pump enough blood fast enough to meet the
metabolic needs of the body.
No longer use the term congestive because
all heart failure does not result in clinically
apparent volume overload

It is an Epidemic

Estimated that over 5 million Americans have heart

Estimated 500,000 new cases per year
Within 5 years, half of those diagnosed will be dead
Over 1 million hospitalizations per year with HF as
primary diagnosis
Most common reason for hospitalization in those >65
years old
85% of HF cases are in adults 65 and older
Heart failure is 4th in a list of quality of care initiatives in
vulnerable older adults

Costs of Heart Failure

It is the leading cause of hospitalization in patients older than 65 years

of age and is a primary hospital discharge diagnosis in 1.1 million
people of all ages each year.

It is one medical condition for which mortality continues to increase.

From 1994 to 2004, the overall death rate declined 2.0% in the United
States, but deaths from HF increased 28% in the same time period.

According to the National Heart, Lung, and Blood Institute, the

estimated direct and indirect costs associated with HF care in the US is
$33.2 billion yearly.

The majority of the costs approximately two-thirds are attributable to

the management of episodes of acute HF decompensation (i.e.,


at Henry Ford Heart and

Vascular Institute found that the annual
number of heart failure cases more than
doubled for Henry Ford Health System in
Detroit from 1989-1997. Over that nine-year
period, 26,442 cases were identified.
Strikingly, the annual prevalence rose from 9
to 20 cases per 1000 health system patients .

Our Aging Population

Different Ways to Define HF

Dilated (congestive) cardiomyopathy is a group of heart muscle

disorders in which the ventricles enlarge but are not able to
pump enough blood for the body's needs, resulting in heart
failure. (Example - CAD, myocarditis, EtOH, HIV)
Hypertrophic cardiomyopathy includes a group of heart disorders
in which the walls of the ventricles thicken (hypertrophy) and
become stiff, even though the workload of the heart is not
increased. (Example congenital HOCM, or acquired)
Restrictive (infiltrative) cardiomyopathy includes a group of heart
disorders in which the walls of the ventricles become stiff, but not
necessarily thickened, and resist normal filling with blood
between heartbeats. (Example radiation, amyloidosis)

Different Ways to Define HF

Diastolic Versus Systolic Heart Failure

A. Systolic cardiac (heart) dysfunction (or systolic

heart failure) occurs when the heart muscle doesn't
contract with enough force, so there is not enough
oxygen-rich blood to be pumped throughout the
B. Diastolic cardiac dysfunction (or diastolic heart
failure) occurs when the heart contracts normally,
but the ventricle doesn't relax properly so less
blood can enter the heart.

Different Ways to Define HF


patients are classified as having HF

of ischemic or nonischemic etiology based on
a history of myocardial infarction (MI) or
based on objective evidence of coronary
artery disease (CAD) such as angiography or
functional testing.

Controversial Definitions

Staging of Heart Failure

New York Heart Association

Class I: No obvious symptoms, no limitations on patient

physical activity (35 percent).

Class II: Some symptoms during or after normal activity,

mild physical activity limitations (35 percent).

Class III: Symptoms with mild exertion, moderate to

significant physical activity limitations (25 percent).

Class IV: Significant symptoms at rest, severe to total

physical activity limitations (5 percent).

Causes of Heart Failure

Coronary artery disease

Problems with the heart muscle itself [known as
cardiomyopathy (myocarditis, etc)]
Problems with any of the heart valves
Abnormal heart rhythms (also called arrhythmias)
Toxic substances (EtOH, cocaine)
Congenital heart disease
Thyroid problems

Diastolic HF

Diastolic heart failure is defined as a condition caused by increased resistance

to the filling of one or both ventricles; this leads to symptoms of congestion from
the inappropriate upward shift of the diastolic pressure-volume relation.
40% of patients

Increasing incidence with age

More common in women

HTN and cardiac ischemia are most common causes

Common precipitating factors include volume overload; tachycardia; exercise;

hypertension; ischemia; systemic stressors (e.g., anemia, fever, infection,
thyrotoxicosis); arrhythmia (e.g., atrial fibrillation, atrioventricular nodal block);
increased salt intake; and use of nonsteroidal anti-inflammatory drugs.

More About Diastolic


involve relaxation and/or

filling and/or distensibility.
Arterial hypertension associated to LV
concentric remodelling is the main
determinant of DD but several other
cardiac diseases, including myocardial
ischemia, and extra-cardiac pathologies
also possible.

Stages of Diastole

1. Isovolumetric relaxation, period occurring between the end of LV

systolic ejection (= aortic valve closure) and the opening of the mitral
valve, when LV pressure keeps going its rapid fall while LV volume
remains constant.
2. LV rapid filling, which begins when LV pressure falls below left
atrial pressure and the mitral valve opens. During this period the blood
has an acceleration which achieves a maximal velocity, direct related to
the magnitude of atrio-ventricular pressure, and stops when this
gradient ends.
3. diastasis, when left atrial and LV pressures are almost equal and LV
filling is essentially maintained by the flow coming from pulmonary
veins with left atrium representing a passive conduit with an
amount depending of LV pressure, function of LV "compliance".
4. atrial systole, which corresponds to left atrial contraction and ends
at the mitral valve closure. This period is mainly influenced by LV
compliance, but depends also by the pericardial resistance, by the atrial
force and by the atrio-ventricular synchronicity (= ECG PR interval).

Patient Differences

is a hemodynamic disorder but there is a

poor relationship between measures of
cardiac performance and patient symptoms
For example, pts with very low EF may be
asymptomatic while someone with preserved
EF may be severely disabled with symptoms

Body Compensatory

Epinephrine and norepinephrine release which increases heart rate and

contractility which increased myocardial work load
Decrease salt and water excretion from kidneys which helps maintain
BP by increasing blood volume, this leads to stretching of hearts
chambers which can impair ability to contract
Hypertrophy and thickening of heart muscle which initially increases
contractility but over time leads to stiff chambers and can impair
HF patients have higher levels of epinephrine, norepinephrine,
aldosterone, angiotensin II, endothelin, inflammatory cytokines, and
vasopressin which contribute to heart remodeling, progression of HF,
and higher levels are associated with increased mortality

Potential Reasons

Alternation in ventricular distensibility

Valvular regurgitation
Pericardial restraint
Cardiac rhythm
Conduction abnormalities
RV function
Also several non-cardiac factors including peripheral
vascular fxn, reflex autonomic activity, renal sodium
handling, etc.

HF Risk Factors - History

EtOH use
Thyroid disorder

Cardiotoxic drugs
Fam Hx of sudden
death, CAD, conduction
problems, HCM
HIV status

Cardiovascular Medical Hx

Hx of heart failure

Embolic events
Rheumatic Dx
Other valvular hx

Signs and Symptoms of HF

Exercise intolerance
Abdominal Fullness

Pulmonary edema
Hepatojugular reflex
Peripheral Edema

HF Diagnosis and Assessment


primarily a clinical diagnosis but

additional information via other diagnostics
can be beneficial
Evaluation depends on if this is first
presentation, change in clinical symptoms,
certainty of diagnosis, etc


BNP levels have been associated

with reduced LVEF, LVH, elevated LV filling
pressures, and acute MI
Evidence supports baseline levels for acute
exacerbations at this time
Evaluation with coronary angiography on
initial dx or presentation is recommended

TTE Recommendations in Heart



The Acute Decompensated Heart Failure National Registry

(ADHERE) is the largest clinical database of patients with acute
decompensated heart failure (ADHF). It provides a crosssectional evaluation of the HF population in the United States
and provides insights into how patients with ADHF are managed
during hospitalization.


The data gathered for this registry include demographic

information, medical history, baseline clinical characteristics,
initial evaluation, treatment received, procedures performed,
hospital course, and patient disposition.

Importantly, registry participation does not require any alteration

of treatment or hospital care, and entry of data into the registry is
not contingent on the use of any particular therapeutic agent or
treatment regimen

Lessons From ADHERE

Prior studies on chronic systolic HF have demonstrated that body mass index
(BMI) is inversely associated with mortality, the so-called obesity paradox.
ADHERE investigators sought to determine whether BMI influences the mortality
risk in ADHF, a subject not previously studied. In the large ADHERE cohort of
hospitalized patients with HF, higher BMI was associated with significantly lower inhospital mortality risk. The authors noted that the relationship between BMI and
adverse outcomes in HF appears to be complex and deserving of further study.

Since most ADHF patients present for hospital care via the emergency department
(ED), the ADHERE investigators studied the impact of early ED initiation of ADHFspecific therapy, as indicated by nesiritide use, on subsequent outcomes.
Nesiritide was started in the ED in 1,613 patients (EDN group) and after admission
to an in-patient unit in 2,687 patients (INN group). Nesiritide was initiated a median
of 2.8 and 15.5 hours after presentation in EDN and INN patients, respectively (p <

Clinical Use of BNP


BNP levels within 24 hours of presentation were obtained in 48,629 (63%)

out of 77,467 hospitalization episodes entered into the ADHERE registry.

BNP levels were <100 pg/ml in only 3.3% of hospitalization episodes in

ADHERE. (The normal plasma level of BNP is currently accepted as <100

In-hospital mortality risk for the overall patient population was 3.6%. When
stratified by BNP level, there was a near linear relationship between BNP
quartiles and in-hospital mortality.

Overall, mortality risk varied more than three- to four-fold on the basis of
the patients initial BNP.

More Implications

BNP quartile remained highly predictive of mortality even after

adjusting for age, gender, systolic blood pressure, blood urea
nitrogen, creatinine, sodium, pulse, and dyspnea at rest

BNP quartiles independently predicted mortality in patients with

reduced and preserved systolic function. BNP quartile groups
also predicted other clinical outcomes including need for
mechanical ventilation, length of stay, time in the intensive care
unit, and percent hospitalization in the intensive care unit


Signs and Symptoms

Sign or Symptom + Why It Happens + People with Heart Failure May Experience...

Shortness of breath or dyspnea

A. Blood "backs up" in the pulmonary veins because

the heart can't keep up with the supply. This
causes fluid to leak into the lungs
a. Breathlessness during activity (most commonly),
at rest, or while sleeping, which may come on
suddenly and wake them up. They often have
difficulty breathing while lying flat and may need
to prop up the upper body and head on two
pillows. They often complain of waking up tired or
feeling anxious and restless.

More Signs and Symptoms

2. Persistent coughing or wheezing
A. Fluid builds up in the lungs
a. coughing that produces white or pink
blood-tinged mucus.
3. Lack of appetite of nausea
A. Digestive system receives less blood
causing problems with digestion
a. Full feeling, early satiety, nausea

Additional Signs
4. Confusion, impaired thinking
A. Changing levels of certain substances in
the blood, such as sodium, can
cause confusion..
a. memory loss and feelings of
disorientation. A caregiver or relative
may notice this first.

More Signs & Symptoms

5. Increased heart rate
A. To "make up for" the loss in pumping
capacity, the heart beats faster.. . .
a. heart palpitations, which feel like the
heart is racing or throbbing.
6. More symptoms weight gain, frequent
urination, cough, decreased physical activity

Physical Examination


Signs that suggest heart failure include:

Third heart sound (S3) (LISTEN LL RECUMBANT)
Increased jugular venous pressure
Positive hepatojugular reflux
Bilateral rales (not always present)
Peripheral edema not due to venous insufficiency
Laterally displaced apical impulse
Weight gain

Limitation of ADLs

particularly geriatric aged persons,

are much more likely to have difficulties with
55% of pts with heart disease over the age of
70 are limited in their ADLs versus 26% of
those who do not have heart disease

What We Should Know about

the Individual Patients HF


Identify the patients with HF

Assess for S/S and risk factors for HF
Initial work up should have been included
work up for reversible causes if appropriate
(TSH, HIV, etc.)
Echocardiogram to determine systolic and
diastolic LV performance, cardiac output
(ejection fraction), and pulmonary artery and
ventricular filling pressures

Individual Patients HF



Chest X-ray to help identify vascular

congestion, infiltrates, effusions
Evaluation and classification of severity of
heart failure
Nuclear imaging for assessment of ejection
fraction or areas of ischemia (as

Non-Pharmacologic Tx

A. Loop diuretics [furosemide (THRESHOLD
DRUG), bumentanide, torsemide] to treat
volume overload may add metolazone to any
B. Management of systolic dysfunction with an
ACE inhibitor like captopril, lisinopril
1. Main side effects cough,
hyperkalemia, angioedema, orthostasis





B-blocker such as carvedilol (coreg),

metoprolol XL (toprol),
Addition of ARB may be substituted for ACE-I
Spironolactone for patients with Stage III or IV heart failure,
the RALES trial
** Watch for hyperkalemia
Digoxin helps with morbidity not mortality
**10-18% of nursing home pts develop toxicity
Side effects include arrhythmias, visual changes, GI
complaints, altered mental status
Nitrates and Hydralazine particularly in African Americans

Basic Pharmacotherapy for HF


All patients with systolic heart failure should be on ACE-I and blockers unless contraindications are present (ARBs can substitute if
there is intolerance to these drug classes, i.e.: ARBs can be used in
combination with ACE-I or with blockers).

Concerns about blood pressure may occur as these drugs are titrated
upwards limitations should relate to symptoms of low BP rather than
actual BP values (for systolic BP above 80 mm Hg) so persistence with
the titration should occur unless such symptoms occur. Concerns about
renal function may occur as these drugs are titrated upwards.


remember that many of these

medications have severe impacts on patients
electrolyte panels.
Check electrolytes on a regular basis in
patients with heart failure
Have open communication with your
physicians regarding medications/plans of
care for your HF patients.

Role of RAS in HF

Role of ACE-I


receptor blockers act as

antagonist at the AT1 receptor


ARBs have been proven beneficial as

alternative to ACE-I in HF treatment and
Some studies suggest concurrent use has
additional benefit

ARB Data

trial: added valsartan to standard

therapy (including ACE)

Findings included decreased morbidity but not mortality in

valsartan group
Slight increase in side effects


trial: added candesartan

Clinically significant reduction in mortality and morbidity

Higher rates of renal dysfunction


The Carvedilol Or Metoprolol European Trial (COMET) study randomized more than 3,000
subjects with mild to severe heart failure (ejection fraction <35%) to either carvedilol 3.125
mg twice a day or metoprolol tartrate 5 mg twice a day. Study treatment doses were
doubled every 2 weeks until the target dose of carvedilol, 25 mg twice a day, or
metoprolol, 50 mg twice a day, was reached.
Patients were followed for 58 months for vascular endpoints including cardiovascular
death, stroke, stroke death, myocardial infarction (MI), and unstable angina. Carvedilol
reduced the likelihood of death by 20%.
Remme and colleagues also found that carvedilol resulted in improved hazard ratios
(HRs) for MI (0.71), stroke (0.79), and fatal stroke or fatal MI (0.46). This study suggests
that the full adrenergic blockade of carvedilol and its antioxidative effects may lead to
improved vascular protection relative to beta-1 blockade alone.



found that five years of

treatment for heart failure without betablockers cost a total of $52,999. With betablockers added to treatment, total treatment
costs fell by $3,959, patient survival
increased by an average of about three-anda-half months, and patients needed fewer
overnight hospital stays.



of Vasopressin antagonism in Heart

Failure Outcome Study with Tolvaptan
(included 4,133 ADHF patients)

EVEREST is a landmark, prospective, international, multicenter, randomized,

double-blind, placebo-controlled study conducted at 432 sites in North America,
South America and Europe conducted between 2003 and 2006. EVEREST
investigators randomized patients with worsening congestive heart failure and
who had a left ventricular ejection fraction (LVEF) of 40 per cent or less within 48
hours of their hospitalization to receive either 30 milligrams (mg) tolvaptan oncedaily or a placebo until the end of the long-term outcome study.

Tolvaptan continued

Short-term studies, tolvaptan, the first oral vasopressin

antagonist, resulted in a statistically significant improvement
relative to placebo on the primary endpoint, the composite of
patient-assessed global clinical status and body weight change
at day 7 or discharge

Long-term study, tolvaptan use was NOT different from placebo

on either of the long-term study's two primary endpoints: deaths
from all causes (P=0.68) or the combined endpoint of
cardiovascular (CV) deaths or hospitalization for worsening heart

Initial Data on Tolvaptan

Tolvaptan added to standard meds rapidly lowered body weight,

and the weight was kept off during therapy.

Low doses were as effective as higher doses.

Tolvaptan did not lower blood pressure or change blood levels of

potassium, BUN or creatinine (it did not reduce kidney function).

Tolvaptan brought low blood sodium levels back up to normal.

Tolvaptan did not worsen heart failure (risk of death,

rehospitalization, and unscheduled visits for CHF).

There was a trend toward lower mortality in tolvaptan patients with

serious congestion, low blood sodium, or weak kidney function.

The greatest benefit with tolvaptan is seen in the sickest patients.


Device Therapy

What is an ICD

The abbreviation for automatic internal cardiac
defibrillator, an amazing device that is often
implanted in individuals suffering from Iifethreatening disordered heart beating. The
AICD device is able to deliver a jolt of
electricity to an abnormally beating heart; the
shock restores normal orderly heart beating.
Thus, on its own, this device is able to ward
off sudden death.

High Tech Devices


devices are designed to pick up lethal

heart rhythms such as ventricular fibrillation
and ventricular tachycardia and deliver an
appropriate shock
However, if atrial fibrillation or other
supraventicular tachycardias go fast enough
and look a certain way to the computer it
WILL shock fast afib
Pt often describes a mule kicking them in
the chest feeling


An estimated one-third of patients with low EF and class III to IV symptoms of

HF manifest a QRS duration >120 ms. This electrocardiographic representation
of abnormal cardiac conduction has been used to identify patients with
dyssynchronous ventricular contraction. While imperfect, the ACC/AHA
guidelines acknowledge that no other consensus definition of cardiac
dyssynchrony exists as yet, although several echocardiographic measures
appear promising.
The mechanical consequences of dyssynchrony include suboptimal ventricular
filling, a reduction in LV dP/dt (rate of rise of ventricular contractile force or
pressure), prolonged duration (and therefore greater severity) of mitral
regurgitation, and paradoxical septal wall motion. Ventricular dyssynchrony is
associated with increased mortality in HF patients.

Evidence for CRT


a meta-analysis of several CRT trials, HF

hospitalizations were reduced by 32% and
all-cause mortality by 25%. The effect on
mortality in this meta-analysis became
apparent after approximately 3 months of

Guidelines for CRT

ICD Support

that ICDs save lives comes from

trials such as MADIT II, DEFINITE, and SCDHeFT

Ventricular Assist Devices

A VAD is a temporary life-sustaining device. VADs

can replace the left ventricle (LVAD), the right
ventricle (RVAD), or both ventricles (BIVAD). They
are used when the heart muscle is damaged and
needs to rest in order to heal or when blood flow
from the heart is inadequate. VADs can also be
used as a bridge in patients awaiting heart
transplantation or in patients who have rejected a
transplanted heart.

Inpatient Vs Outpatient

is a new drug that is a synthetic

BNP that vasodilates vessels and serves as a
potent diuretic agent
Inotropic agents (dobutamine, milrinone)
often used inpt, potent inotropic agents used
to increase cardiac output use is
controversial in outpt settings, may improve
morbidity, definite use in hospice setting,
increase risk of arrhythmias which is
important in those with AICDs

Definition of Stage

Usual Therapies

Those at high risk for developing heart

failure. Includes people with:
Diabetes mellitus
Coronary artery disease (including heart
History of cardiotoxic drug therapy
History of alcohol abuse
History of rheumatic fever
Family history of cardiomyopathy.

Exercise regularly
Quit smoking
Treat hypertension
Treat lipid disorders
Discourage alcohol or illicit drug use
If previous heart attack or current diabetes mellitus or
hypertension angiotensin converting enzyme inhibitor

Stage A

Stage B

Those diagnosed with systolic heart failure

but have never had symptoms of heart
failure (usually by finding an ejection
fraction of less than 40% on

Care measures in Stage A +

All patients should be on ACE-I
Beta-blockers should be added
Surgical consultation for coronary artery revascularization
and valve repair/replacement (as appropriate)

Stage C

Patients with known heart failure with

current or prior symptoms.
Symptoms include:
Shortness of breath
Reduced exercise intolerance.

In this group, care measures from Stage A apply, ACE-I and

beta-blockers should be used +
Diuretics (water pills)
Dietary sodium (salt) restriction
Weight monitoring
Fluid restriction (as appropriate)
Withdrawal of drugs that worsen the condition
Spironolactone when symptoms remain severe with other

Stage D

Presence of advanced symptoms, after

assuring optimized medical care

All therapies under Stages A, B and C + evaluation for:

Cardiac transplantation
Ventricular assist devices
Surgical options
Research therapies
Continuous intravenous inotropic infusions
End-of-life care

Major Outcome Measurements


Accuracy of diagnostic instruments

Quality of life
Symptoms of heart failure
Exercise tolerance and functional capacity
Effects of medications to treat systolic HF on
morbidity and mortality
Adverse effects of drugs
LVEF per echo or radionuclide
Hospitalization rate

Health System HF Intervention


medical management for HF is

consistent with national guidelines
Provide residents with essential information
for self-care
Prevent avoidable hospital readmissions
Reduce financial burden to health care
system through clinically appropriate
utilization of resources and length of stay
Administer preventive vaccinations

Interdisciplinary Interventions

of protocol for heart failure in

the long-term care setting has been proven to
standardize management and strengthen the
continuum of care
Nursing facility in Michigan which consisted
of 150 nursing home beds designed such a


director, director of nursing, key

nursing unit leaders developed
Nursing staff then received education
regarding specifics of protocol
Admission personnel play an important role
by early recognition and requesting certain
documentation from d/c hospitals
Recent weight and immunization hx obtained

Protocol continued
Diagnosis verification by reviewing records,
admission Chest X-ray, echo reports, medication
Pharmacists were utilized when appropriate
Weight monitoring program established (three times
weekly) and if more than 2 lb gain, a standard
nursing assessment
a. Included physical exam and history is possible
focusing on shortness of breath, fatigue, night
cough, LE edema, cough, change in vital signs

More Protocol

vaccination policy
Patient education heart failure booklet,
family counseling when appropriate, input
from dietary and nursing staff

Quality Assurance via CMS HF


echo report
Use of ACE-I where appropriate
Standardized nursing assessments
Effective tx for heart failure symptoms
90% immunization rate
Education for resident and families for HF

Results Echo documented

Ejection Fractions

More Results Symptom


Results ACE-I utilization

Hospital Readmissions

22 noted clinical deteriorations at 5

months, only one resulted in a hospital
readmission in this study.
The other declines or changes in status were
managed in the facility with early, aggressive
Required several training sessions with
nurses, educating attending physicians, and
the involvement of facility administrator

End of Life Care

Realization that heart failure is often a terminal

disease and while we have made great strides in
treatment, there often comes a point where the
focus of care changes to a palliative focus
May include shutting off defibrillator
Symptom relief, psychosocial and spiritual
considerations are of key importance
End-of-life predominating symptoms are often
dyspnea, dry mouth, nausea, fatigue, pain,
restlessness, and apprehension.

Final Reminder Continue to

Break Barriers

staff, mid-level practitioners,

physicians, dietary staff, therapist, patients &
families, and other ancillary staff must realize
that together we can make the greatest
difference in treating heart failure
HF is an epidemic with primary care staff
having the greatest potential impact by early
realization of decline and appropriate
intervention &/or referral


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Poole-Wilson PA, Swedberg K, Cleland JGF, et al. Comparison of carvedilol and metoprolol on clinical
outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial (COMET):
randomized controlled trial. Lancet 2003;362:7-13.

Remme WJ, Torp-Pedersen C, Cleland JGF, et al. Carvedilol protects better against vascular events than
metoprolol in heart failure Results from COMET. J Am Coll Cardiol 2007;49:963-71.

Rosamond W, Flegal K, Friday G, et al. Heart disease and stroke statistics--2007 update: a report from
the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation

Adams Jr. KF, Fonarow GC, Emerman CL, et al. Characteristics and outcomes of patients hospitalized for
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cases in the Acute Decompensated Failure National Registry (ADHERE). Am Heart J 2005;149:209-216.

Higgins SL, Hummel JD, Niazi IK, et al. Cardiac resynchronization therapy for the treatment of heart
failure in patients with intraventricular conduction delay and malignant ventricular tachyarrhythmias. JACC

Citations Continued

Peacock WF 4th, Fonarow GC, Emerman CL, Mills RM, Wynne J; ADHERE Scientific Advisory
Committee and Investigators; Adhere Study Group. Impact of early initiation of intravenous therapy for
acute decompensated heart failure on outcomes in ADHERE. Cardiology 2007;107:44-51.
Galvao M, Kalman J, DeMarco T, et al. Gender differences in in-hospital management and outcomes in
patients with decompensated heart failure: analysis from the Acute Decompensated Heart Failure
National Registry (ADHERE). J Card Fail 2006;12:100-7.
Fonarow GC, Peacock WF, Phillips CO, et al. Admission B-Type Natriuretic Peptide Levels and InHospital Mortality in Acute Decompensated Heart Failure. J Am Coll Cardiol 2007;49:1943-50

Hunt SA American College of Cardiology; American Heart Association Task Force on Practice Guidelines
(Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure).
ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a
report of the American College of Cardiology/American Heart Association Task Force on Practice
Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of
Heart Failure). JACC 2005;46:e1-e82

Abraham WT, Fisher WG, Smith AL, et al. Cardiac resynchronization in chronic heart failure. N Engl J
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