Heart failure

Heart Failure http://emedicine.medscape.com/article/163062-overview

Author: Ioana Dumitru, MD; Chief Editor: Henry H Ooi, MBBCh more...

Updated: Aug 30, 2011

Background
Signs and symptoms of heart failure include tachycardia and manifestations of venous congestion (eg, edema) and
low cardiac output (eg, fatigue). Breathlessness, a cardinal symptom of left ventricular (LV) failure, may manifest with
progressively increasing severity. (See Clinical Presentation.)

Heart failure can be classified according to a variety of factors. The New York Heart Association (NYHA) classification
for heart failure is based on the relation between symptoms and the amount of effort required to provoke them, and
The American College of Cardiology/American Heart Association (ACC/AHA) heart failure guidelines complement the
NYHA classification to reflect the progression of disease. (See Clinical Presentation.)

Laboratory studies should include a complete blood count (CBC), electrolytes, and renal and liver function studies, and
2-dimensional echocardiography is recommended in the initial evaluation of patients with known or suspected heart
failure. Two principal features of the chest radiograph are the size and shape of the cardiac silhouette and edema at
the lung bases, and pulse oximetry is highly accurate for assessing the presence of hypoxemia and, therefore, the
severity of heart failure. (See Workup.)

In acute heart failure, patient care consists of stabilizing the patients’ clinical condition; establishing the diagnosis,
etiology, and precipitating factors; and initiating therapies to provide rapid symptom relief. Surgical options for heart
failure include heart transplantation, coronary artery bypass grafting (CABG), valve replacement or repair, ventricular
restoration, cardiac resynchronization therapy (CRT, implantable cardioverter-defibrillators (ICDs), and ventricular
assist devices (VADs). (See Treatment and Management.)

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Along with oxygen, medications
assisting with symptom relief include diuretics, digoxin, inotropes, oxygen, and morphine. Drugs that can exacerbate
heart failure should be avoided (NSAIDs, calcium channel blockers, most antiarrhythmic drugs). (See Medications.)

Pathophysiology
The common pathophysiologic state that perpetuates the progression of heart failure is extremely complex,
regardless of the precipitating event. Compensatory mechanisms exist on every level of organization, from subcellular
all the way through organ-to-organ interactions. Only when this network of adaptations becomes overwhelmed does
heart failure ensue.

Most important among the adaptations are the Frank-Starling mechanism, in which an increased preload helps to
sustain cardiac performance; alterations in myocyte regeneration and death; myocardial hypertrophy with or without
cardiac chamber dilatation, in which the mass of contractile tissue is augmented; and activation of neurohumoral
systems. The release of norepinephrine by adrenergic cardiac nerves augments myocardial contractility and includes
activation of the renin-angiotensin-aldosterone system [RAAS], the sympathetic nervous system [SNS], and other
neurohumoral adjustments that act to maintain arterial pressure and perfusion of vital organs.

In acute heart failure, the finite adaptive mechanisms that may be adequate to maintain the overall contractile
performance of the heart at relatively normal levels become maladaptive when trying to sustain adequate cardiac
performance.

The primary myocardial response to chronic increased wall stress is myocyte hypertrophy, death/apoptosis, and
regeneration.[1] This process eventually leads to remodeling, usually the eccentric type. Eccentric remodeling further
worsens the loading conditions on the remaining myocytes and perpetuates the deleterious cycle. The idea of
lowering wall stress to slow the process of remodeling has long been exploited in treating heart failure patients.[2]

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The reduction of cardiac output following myocardial injury sets into motion a cascade of hemodynamic and
neurohormonal derangements that provoke activation of neuroendocrine systems, most notably the above-mentioned
adrenergic systems and RAAS.

The release of epinephrine and norepinephrine, along with the vasoactive substances endothelin-1 (ET-1) and
vasopressin, causes vasoconstriction, which increases afterload and, via an increase in cyclic adenosine
monophosphate (cAMP), causes an increase in cytosolic calcium entry. The increased calcium entry into the myocytes
augments myocardial contractility and impairs myocardial relaxation (lusitropy).

The calcium overload may induce arrhythmias and lead to sudden death. The increase in afterload and myocardial
contractility (known as inotropy) and the impairment in myocardial lusitropy lead to an increase in myocardial energy
expenditure and a further decrease in cardiac output. The increase in myocardial energy expenditure leads to
myocardial cell death/apoptosis, which results in heart failure and further reduction in cardiac output, perpetuating a
cycle of further increased neurohumoral stimulation and further adverse hemodynamic and myocardial responses.

In addition, the activation of the RAAS leads to salt and water retention, resulting in increased preload and further
increases in myocardial energy expenditure. Increases in renin, mediated by decreased stretch of the glomerular
afferent arteriole, reduce delivery of chloride to the macula densa and increase beta1-adrenergic activity as a
response to decreased cardiac output. This results in an increase in angiotensin II (Ang II) levels and, in turn,
aldosterone levels, causing stimulation of the release of aldosterone. Ang II, along with ET-1, is crucial in maintaining
effective intravascular homeostasis mediated by vasoconstriction and aldosterone-induced salt and water retention.

The concept of the heart as a self-renewing organ is a relatively recent development.[3] This new paradigm for myocyte
biology has created an entire field of research aimed directly at augmenting myocardial regeneration.

The rate of myocyte turnover has been shown to increase during times of pathologic stress.[1] In heart failure, this
mechanism for replacement becomes overwhelmed by an even faster increase in the rate of myocyte loss. This
imbalance of hypertrophy and death over regeneration is the final common pathway at the cellular level for the
progression of remodeling and heart failure.

Ang II

Research indicates that local cardiac Ang II production (which decreases lusitropy, increases inotropy, and increases
afterload) leads to increased myocardial energy expenditure. Ang II has also been shown in vitro and in vivo to
increase the rate of myocyte apoptosis.[4] In this fashion, Ang II has similar actions to norepinephrine in heart failure.

Ang II also mediates myocardial cellular hypertrophy and may promote progressive loss of myocardial function. The
neurohumoral factors above lead to myocyte hypertrophy and interstitial fibrosis, resulting in increased myocardial
volume and increased myocardial mass, as well as myocyte loss. As a result, the cardiac architecture changes, which,
in turn, leads to further increase in myocardial volume and mass.

Myocytes and myocardial remodeling

In the failing heart, increased myocardial volume is characterized by larger myocytes approaching the end of their life
cycle. As more myocytes drop out, an increased load is placed on the remaining myocardium, and this unfavorable
environment is transmitted to the progenitor cells responsible for replacing lost myocytes. Progenitor cells become
progressively less effective as the underlying pathologic process worsens and myocardial failure accelerates. These
features, namely the increased myocardial volume and mass, along with a net loss of myocytes, are the hallmark of
myocardial remodeling. This remodeling process leads to early adaptive mechanisms, such as augmentation of stroke
volume (Starling mechanism) and decreased wall stress (Laplace mechanism), and later, to maladaptive mechanisms,
such as increased myocardial oxygen demand, myocardial ischemia, impaired contractility, and arrhythmogenesis.

As heart failure advances, there is a relative decline in the counterregulatory effects of endogenous vasodilators,
including nitric oxide (NO), prostaglandins (PGs), bradykinin (BK), atrial natriuretic peptide (ANP), and B-type natriuretic
peptide (BNP). This occurs simultaneously with the increase in vasoconstrictor substances from the RAAS and the
adrenergic system. This fosters further increases in vasoconstriction and thus preload and afterload, leading to cellular
proliferation, adverse myocardial remodeling, and antinatriuresis, with total body fluid excess and worsening heart
failure (HF) symptoms.

Systolic and diastolic failure

Systolic and diastolic heart failure each result in a decrease in stroke volume. This leads to activation of peripheral and
central baroreflexes and chemoreflexes that are capable of eliciting marked increases in sympathetic nerve traffic.

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While there are commonalities in the neurohormonal responses to decreased stroke volume, the neurohormone-
mediated events that follow have been most clearly elucidated for individuals with systolic heart failure. The ensuing
elevation in plasma norepinephrine directly correlates with the degree of cardiac dysfunction and has significant
prognostic implications. Norepinephrine, while directly toxic to cardiac myocytes, is also responsible for a variety of
signal-transduction abnormalities, such as down-regulation of beta1-adrenergic receptors, uncoupling of beta2-
adrenergic receptors, and increased activity of inhibitory G-protein. Changes in beta1-adrenergic receptors result in
overexpression and promote myocardial hypertrophy.

ANP and BNP

ANP and BNP are endogenously generated peptides activated in response to atrial and ventricular volume/pressure
expansion. ANP and BNP are released from the atria and ventricles, respectively, and both promote vasodilation and
natriuresis. Their hemodynamic effects are mediated by decreases in ventricular filling pressures, owing to reductions
in cardiac preload and afterload. BNP, in particular, produces selective afferent arteriolar vasodilation and inhibits
sodium reabsorption in the proximal convoluted tubule. BNP inhibits renin and aldosterone release and, therefore,
adrenergic activation as well. ANP and BNP are elevated in chronic heart failure. BNP, in particular, has potentially
important diagnostic, therapeutic, and prognostic implications.

For more information, see Natriuretic Peptides in Congestive Heart Failure.

Other vasoactive systems

Other vasoactive systems that play a role in the pathogenesis of heart failure include the ET receptor system, the
adenosine receptor system, vasopressin, and tumor necrosis factor-alpha (TNF-alpha). ET, a substance produced by
the vascular endothelium, may contribute to the regulation of myocardial function, vascular tone, and peripheral
resistance in heart failure. Elevated levels of ET-1 closely correlate with the severity of heart failure. ET-1 is a potent
vasoconstrictor and has exaggerated vasoconstrictor effects in the renal vasculature, reducing renal plasma blood
flow, glomerular filtration rate (GFR), and sodium excretion.

TNF-alpha has been implicated in response to various infectious and inflammatory conditions. Elevations in TNF-alpha
levels have been consistently observed in heart failure and seem to correlate with the degree of myocardial
dysfunction. Experimental studies suggest that local production of TNF-alpha may have toxic effects on the
myocardium, thus worsening myocardial systolic and diastolic function.

Thus, in individuals with systolic dysfunction, the neurohormonal responses to decreased stroke volume result in
temporary improvement in systolic blood pressure and tissue perfusion. However, in all circumstances, the existing
data support the notion that these neurohormonal responses contribute to the progression of myocardial dysfunction in
the long term.

Heart failure with normal ejection fraction

In diastolic heart failure (heart failure with normal ejection fraction [HFNEF]), the same pathophysiologic processes
leading to decreased cardiac output that occur in systolic heart failure also occur, but they do so in response to a
different set of hemodynamic and circulatory environmental factors that depress cardiac output.

In HFNEF, altered relaxation, and increased stiffness of the ventricle (due to delayed calcium uptake by the myocyte
sarcoplasmic reticulum and delayed calcium efflux from the myocyte) occur in response to an increase in ventricular
afterload (pressure overload). The impaired relaxation of the ventricle leads to impaired diastolic filling of the left
ventricle (LV).

Morris et al found that RV subendocardial systolic dysfunction and diastolic dysfunction, as detected by
echocardiographic strain rate imaging, are common in patients with HFNEF. This dysfunction is potentially associated
with the same fibrotic processes that affect the subendocardial layer of the LV and, to a lesser extent, with RV
pressure overload. This may play a role in the symptomatology of patients with HFNEF.[5]

LV chamber stiffness

An increase in LV chamber stiffness occurs secondary to any one of the following 3 mechanisms or to a combination
thereof:

Rise in filling pressure
Shift to a steeper ventricular pressure-volume curve
Decrease in ventricular distensibility

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A rise in filling pressure is the movement of the ventricle up along its pressure-volume curve to a steeper portion, as
may occur in conditions such as volume overload secondary to acute valvular regurgitation or acute LV failure due to
myocarditis.

A shift to a steeper ventricular pressure-volume curve results most commonly not only from increased ventricular mass
and wall thickness, as observed in aortic stenosis and long-standing hypertension, but also from infiltrative disorders
(eg, amyloidosis), endomyocardial fibrosis, and myocardial ischemia.

Parallel upward displacement of the diastolic pressure-volume curve is generally referred to as a decrease in
ventricular distensibility. This is usually caused by extrinsic compression of the ventricles.

Concentric LV hypertrophy

Whereas volume overload, as observed in chronic aortic and/or mitral valvular regurgitant disease, shifts the entire
diastolic pressure-volume curve to the right, indicating increased chamber stiffness, pressure overload that leads to
concentric LV hypertrophy (LVH, as occurs in aortic stenosis, hypertension, and hypertrophic cardiomyopathy) shifts
the diastolic pressure-volume curve to the left along its volume axis so that at any diastolic volume ventricular diastolic
pressure is abnormally elevated, although chamber stiffness may or may not be altered. Increases in diastolic
pressure lead to increased myocardial energy expenditure, remodeling of the ventricle, increased myocardial oxygen
demand, myocardial ischemia, and eventual progression of the maladaptive mechanisms of the heart that lead to
decompensated heart failure.

Arrhythmias

While life-threatening rhythms are more common in ischemic versus nonischemic cardiomyopathy, arrhythmia imparts
a significant burden in all forms of heart failure. In fact, some arrhythmias even perpetuate heart failure. The most
significant of all rhythms associated with heart failure are the life-threatening ventricular arrhythmias. Structural
substrates for ventricular arrhythmias common in heart failure, regardless of the underlying cause, include the
following:

Ventricular dilatation
Myocardial hypertrophy
Myocardial fibrosis

At the cellular level, myocytes may be exposed to increased stretch, wall tension, catecholamines, ischemia, and
electrolyte imbalance. The combination of these factors contributes to an increased incidence of arrhythmogenic
sudden cardiac death in patients with heart failure.

Etiology
Most patients who present with significant heart failure do so because of an inability to provide adequate cardiac output
in that setting. This is often a combination of the causes listed below in the setting of an abnormal myocardium. The list
of causes responsible for presentation of a patient with heart failure exacerbation is very long, and searching for the
proximate cause to optimize therapeutic interventions is important.

From a clinical standpoint, classifying the causes of heart failure into the following 3 broad categories is useful:

Underlying causes
Fundamental causes
Precipitating causes

Underlying causes

Underlying causes include structural abnormalities (congenital or acquired) that affect the peripheral and coronary
arterial circulation, pericardium, myocardium, or cardiac valves, thus leading to the increased hemodynamic burden or
myocardial or coronary insufficiency responsible for heart failure.

Specific underlying factors in various forms of heart failure include systolic heart failure, diastolic heart failure, acute
heart failure, high-output heart failure, and right heart failure.

Systolic heart failure includes the following:

Coronary artery disease

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Diabetes mellitus
Hypertension
Valvular heart disease (stenosis or regurgitant lesions)
Arrhythmia (supraventricular or ventricular)
Infections and inflammation (myocarditis)
Peripartum cardiomyopathy
Congenital heart disease
Drug induced (either recreational like alcohol and cocaine, or therapeutic drugs with cardiac side effects like
doxorubicin)
Idiopathic cardiomyopathy
Rare conditions (endocrine abnormalities, rheumatologic disease, neuromuscular conditions)

Diastolic heart failure includes the following:

Coronary artery disease
Diabetes mellitus
Hypertension
Valvular disease (aortic stenosis)
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy (amyloidosis)
Constrictive pericarditis

Acute heart failure includes the following:

Acute valvular (mitral or aortic) regurgitation
Myocardial infarction
Myocarditis
Arrhythmia
Drug induced (eg, cocaine, calcium channel-blocker or beta-blocker overdose)
Sepsis

High-output heart failure includes the following:

Anemia
Systemic arteriovenous fistulas
Hyperthyroidism
Beriberi heart disease
Paget disease of bone
Albright syndrome (fibrous dysplasia)
Multiple myeloma
Pregnancy
Glomerulonephritis
Polycythemia vera
Carcinoid syndrome

Right heart failure includes the following:

Left ventricular failure
Coronary artery disease (ischemia)
Pulmonary hypertension
Pulmonary valve stenosis
Pulmonary embolism
Chronic pulmonary disease
Neuromuscular disease

Fundamental causes

Fundamental causes include the biochemical and physiologic mechanisms, through which either an increased
hemodynamic burden or a reduction in oxygen delivery to the myocardium results in impairment of myocardial
contraction.

Precipitating causes of heart failure

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Overt heart failure may be precipitated by progression of the underlying heart disease. A previously stable,
compensated patient may develop heart failure that is clinically apparent for the first time when the intrinsic process
has advanced to a critical point, such as with further narrowing of a stenotic aortic valve or mitral valve. Alternatively,
decompensation may occur as a result of failure or exhaustion of the compensatory mechanisms but without any
change in the load on the heart in patients with persistent, severe pressure or volume overload.

The most common cause of decompensation in a previously compensated patient with heart failure is inappropriate
reduction in the intensity of treatment, whether dietary sodium restriction, physical activity reduction, drug regimen
reduction, or, most commonly, a combination of these measures.

Arrhythmias, particularly ventricular arrhythmias, can be life threatening.

Systemic infection or the development of unrelated illness can also lead to heart failure. Systemic infection
precipitates heart failure by increasing total metabolism as a consequence of fever, discomfort, and cough, increasing
the hemodynamic burden on the heart. Septic shock, in particular, can precipitate heart failure by the release of
endotoxin-induced factors that can depress myocardial contractility.

Cardiac infection and inflammation can also endanger the heart. Myocarditis or infective endocarditis may directly
impair myocardial function and exacerbate existing heart disease. The anemia, fever, and tachycardia that frequently
accompany these processes are also deleterious. In the case of infective endocarditis, the additional valvular damage
that ensues may precipitate cardiac decompensation.

Patients with heart failure, particularly when confined to bed, are at high risk of developing pulmonary emboli, which can
increase the hemodynamic burden on the right ventricle by further elevating right ventricular (RV) systolic pressure,
possibly causing fever, tachypnea, and tachycardia.

Intense, prolonged physical exertion or severe fatigue, such as may result from prolonged travel or emotional crisis, is
a relatively common precipitant of cardiac decompensation. The same is true of exposure to severe climate change
(ie, the individual comes in contact with a hot, humid environment or a bitterly cold one).

Excessive intake of water and/or sodium and the administration of cardiac depressants or drugs that cause salt
retention are other factors that can lead to heart failure.

Because of increased myocardial oxygen consumption and demand beyond a critical level, the following high-output
states can precipitate the clinical presentation of heart failure:

Profound anemia
Thyrotoxicosis
Myxedema
Paget disease of bone
Albright syndrome
Multiple myeloma
Glomerulonephritis
Cor pulmonale
Polycythemia vera
Obesity
Carcinoid syndrome
Pregnancy
Nutritional deficiencies (eg, thiamine deficiency, beriberi)

In particular, consider whether the patient has underlying coronary artery disease or valvular heart disease.

Patients with one form of underlying heart disease that may be well compensated can develop heart failure when a
second form of heart disease ensues. For example, a patient with chronic hypertension and asymptomatic LVH may
be asymptomatic until a myocardial infarction (MI) develops and precipitates heart failure.

Epidemiology
United States statistics

According to the American Heart Association, heart failure affects nearly 5.7 million Americans of all ages and is
responsible for more hospitalizations than all forms of cancer combined. It is the number 1 cause for hospitalization
among Medicare patients. With improvement in survival of acute MIs and a population that continues to age, heart
failure will continue to increase in prominence as a major health problem in the United States.

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Heart failure statistics for the United States are as follows[6] :

Heart failure is the fastest-growing clinical cardiac disease entity in the United States, affecting 2% of the
population.
In 2006, 1.1 million patients were admitted to the hospital for acute decompensated heart failure in the United
States, almost double the number seen 15 years prior. In addition, there were 3.4 million outpatient visits for
heart failure.
550,000 new cases of heart failure are diagnosed and 300,000 deaths are caused by heart failure each year.
Rehospitalization rates[7] during the 6 months following discharge are as much as 50%.
Nearly 2% of all hospital admissions in the United States are for decompensated heart failure; and heart failure
is the most frequent cause of hospitalization in patients older than 65 years, with an annual incidence of 10 per
1,000.
The average duration of hospitalization is about 6 days.
In 2008, the estimated total cost of heart failure in the United States was $37.2 billion. This represented 1-2%
of all healthcare expenditures.

The incidence and prevalence of heart failure are higher in African Americans, Hispanics, Native Americans, and
recent immigrants from developing nations, Russia, and the former Soviet republics. The higher prevalence of heart
failure in African Americans, Hispanics, and Native Americans is directly related to the higher incidence and prevalence
of hypertension and diabetes. This problem is particularly exacerbated by a lack of access to health care and to
substandard preventive health care among the most indigent of individuals in these and other groups; many persons in
these groups are without adequate health insurance coverage.

The higher incidence and prevalence of heart failure among recent immigrants from developing nations is largely due
to a lack of prior preventive health care and to a lack of treatment or to substandard treatment for common conditions,
such as hypertension, diabetes, rheumatic fever, and ischemic heart disease.

Men and women have equivalent incidence and prevalence of heart failure. However, many differences between men
and women are observed, including the following:

Women tend to develop heart failure later in life than men do.
Women are more likely than men to have preserved systolic function.
Women develop depression more commonly than men do.
Women have signs and symptoms of heart failure similar to those of men, but they are more pronounced in
women.
Women survive longer with heart failure than men do.

The prevalence of heart failure increases with age. The prevalence is 1-2% of the population younger than 55 years
and increases dramatically to a rate of 10% for persons older than 75 years. Nonetheless, heart failure can occur at
any age, depending on the cause.

Longitudinal data from the Framingham Heart Study suggests that antecedent subclinical left ventricular systolic or
diastolic dysfunction is associated with an increased incidence of heart failure, supporting the notion that heart failure is
a progressive syndrome.[8] Another analysis of over 36,000 patients undergoing outpatient echocardiography reported
that moderate or severe diastolic dysfunction, but not mild diastolic dysfunction, is an independent predictor of
mortality.[9]

International statistics

Heart failure is a worldwide problem, but little accurate financial data are available. The most common cause of heart
failure in industrialized countries is ischemic cardiomyopathy. Other causes, including Chagas disease and valvular
cardiomyopathy, assume a more important role in developing countries than in the United States. However, as
developing nations urbanize and become more affluent, the rate of heart failure increases in concordance with rates of
diabetes, hypertension, a more processed diet, and a more sedentary lifestyle. This was illustrated in a population
study in Soweto, South Africa. As the community transformed into a more urban and westernized city, an increase in
diabetes and hypertension was met with an increased rate of heart failure.[10]

In terms of treatment, a 2006 study of European nations showed few important international differences in uptake of
key therapies among European countries with widely differing cultures and economic status for patients with heart
failure. In contrast, studies of sub-Saharan Africa, where health care resources are more limited, have shown poor
outcomes in certain populations.[11] For instance, hypertensive heart failure carries a 25% 1-year mortality rate in some
countries, and human immunodeficiency virus (HIV)–associated cardiomyopathy generally progresses to death within

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100 days of diagnosis in patients who are not treated with antiretroviral drugs.

While data in developing countries are not as robust as in Western society, the following trends are apparent:

Causes tend to be largely nonischemic
Patients tend to present at a younger age
Outcomes are largely worse where health care resources are limited
Isolated right heart failure tends to be more prominent, with a variety of causes, from tuberculous pericardial
disease to lung disease and pollution, having been postulated

Prognosis
In general, the inpatient mortality rate for patients with heart failure is 5-20%, while outpatient mortality remains 20% at
the end of the first year postdiagnosis and up to 50% at 5 years postdiagnosis, despite marked improvement in
medical and device therapy (AHA published statistics). Each rehospitalization increases mortality by 20-30%.

Cardiopulmonary stress testing can be useful in assessing the chances of a patient’s survival within the next year as
well as in determining the need for referral for either cardiac transplantation or implantation of mechanical circulatory
support.

Patients with NYHA class IV, ACC/AHA stage D heart failure have more than 50% mortality at 1 year.

A study by van Diepen et al suggests patients with heart failure or atrial fibrillation have a significantly higher risk of
noncardiac postoperative mortality than patients with coronary artery disease; thus, patients and physicians should
consider this risk, even if a minor procedure is planned.[12]

Heart failure associated with acute MI has an inpatient mortality rate of 20-40%; mortality approaches 80% in patients
who are also hypotensive (eg, cardiogenic shock).

Patient Education
Stage A patients have risk factors for developing heart failure (eg, hypertension, diabetes mellitus, obesity, metabolic
syndrome, sleep apnea, patients with a family history of dilated cardiomyopathy or using cardiotoxins). They should be
treated with aggressive risk factor modification, education, and angiotensin-converting enzyme inhibitor
(ACEI)/angiotensin receptor blocker (ARB) if diabetes mellitus or vascular disease is present (HOPE, SOLVD-
prevention).

To help prevent recurrence of heart failure, counsel and educate patients in whom heart failure was caused by dietary
factors or medication noncompliance with regard to the importance of proper diet and the necessity of medication
compliance.

For excellent patient education resources, visit eMedicine's Heart Center, Cholesterol Center, Diabetes Center. In
addition, see eMedicine's patient education articles Congestive Heart Failure, High Cholesterol, Chest Pain, Heart
Rhythm Disorders, Coronary Heart Disease, and Heart Attack.

Contributor Information and Disclosures
Author
Ioana Dumitru, MD Assistant Professor, Internal Medicine, Section of Cardiology, Founder and Medical Director,
Heart Failure and Cardiac Transplant Program, University of Nebraska Medical Center; Assistant Professor, Internal
Medicine, Section of Cardiology, Veterans Affairs Medical Center, Omaha, Nebraska

Ioana Dumitru, MD is a member of the following medical societies: American College of Cardiology, Heart Failure
Society of America, and International Society for Heart and Lung Transplantation

Disclosure: Nothing to disclose.

Coauthor(s)
Mathue Baker, MD Fellow, Department of Internal Medicine, Division of Cardiology, University of Nebraska
Medical Center, Omaha


8 of 30 9/3/2011 8:27 AM


David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice
Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians
and Society for Academic Emergency Medicine


William K Chiang, MD Associate Professor, Department of Emergency Medicine, New York University School of
Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center

William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology,
American College of Medical Toxicology, and Society for Academic Emergency Medicine


Joseph Cornelius Cleveland Jr, MD Associate Professor, Division of Cardiothoracic Surgery, University of
Colorado Health Sciences Center

Joseph Cornelius Cleveland Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American
Association for the Advancement of Science, American College of Cardiology, American College of Chest
Physicians, American College of Surgeons, American Geriatrics Society, American Physiological Society, American
Society of Transplant Surgeons, Association for Academic Surgery, Heart Failure Society of America, International
Society for Heart and Lung Transplantation, Phi Beta Kappa, Society of Critical Care Medicine, Society of Thoracic
Surgeons, and Western Thoracic Surgical Association

Disclosure: Thoratec Heartmate II Pivotal Tria; Grant/research funds Principal Investigator - Colorado; Abbott
Vascular E-Valve E-clip Honoraria Consulting; Baxter Healthcare Corp Consulting fee Board membership;
Heartware Advance BTT Trial Grant/research funds Principal Investigator- Colorado; Heartware Endurance DT trial
Grant/research funds Principal Investigator-Colorado

Kavita Garg, MD Professor, Department of Radiology, University of Colorado School of Medicine

Kavita Garg, MD is a member of the following medical societies: American College of Radiology, American
Roentgen Ray Society, Radiological Society of North America, and Society of Thoracic Radiology


Shamai Grossman, MD, MS Assistant Professor, Department of Emergency Medicine, Harvard Medical School;
Director, The Clinical Decision Unit and Cardiac Emergency Center, Beth Israel Deaconess Medical Center

Shamai Grossman, MD, MS is a member of the following medical societies: American College of Emergency
Physicians


Jeffrey A Miller, MD Associate Adjunct Professor of Clinical Radiology, University of Medicine and Dentistry of
New Jersey-New Jersey Medical School; Faculty, Department of Radiology, Veterans Affairs of New Jersey Health
Care System

Jeffrey A Miller, MD is a member of the following medical societies: American Roentgen Ray Society, Society for
Health Services Research in Radiology, and Society of Thoracic Radiology


John D Newell Jr, MD Professor of Radiology, Head, Division of Radiology, National Jewish Health; Professor,
Department of Radiology, University of Colorado School of Medicine

John D Newell Jr, MD is a member of the following medical societies: American College of Chest Physicians,
American College of Radiology, American Roentgen Ray Society, American Thoracic Society, Association of
University Radiologists, Radiological Society of North America, and Society of Thoracic Radiology

Disclosure: Siemens Medical Grant/research funds Consulting; Vida Corporation Ownership interest Board

9 of 30 9/3/2011 8:27 AM


membership; TeraRecon Grant/research funds Consulting; eMedicine Honoraria Consulting; Humana Press
Honoraria Other

David A Nix, MD, PhD Staff Physician, Department of Emergency Medicine, Kaiser Santa Clara

David A Nix, MD, PhD is a member of the following medical societies: American College of Emergency Physicians,
Emergency Medicine Residents Association, and Society for Academic Emergency Medicine


Donald Schreiber, MD, CM Associate Professor of Surgery (Emergency Medicine), Stanford University School
of Medicine

Donald Schreiber, MD, CM is a member of the following medical societies: American College of Emergency
Physicians

Disclosure: Abbott Point of Care Inc Research Grant and Speakers Bureau Speaking and teaching; Nanosphere
Inc Grant/research funds Research; Singulex Inc Grant/research funds Research; Abbott Diagnostics Inc
Grant/research funds None

Craig H Selzman, MD, FACS Associate Professor of Surgery, Surgical Director, Cardiac Mechanical Support and
Heart Transplant, Division of Cardiothoracic Surgery, University of Utah School of Medicine

Craig H Selzman, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American
Association for Thoracic Surgery, American College of Surgeons, American Physiological Society, Association for
Academic Surgery, International Society for Heart and Lung Transplantation, Society of Thoracic Surgeons,
Southern Thoracic Surgical Association, and Western Thoracic Surgical Association


Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division
of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians,
National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management
position; ProceduresConsult.com Royalty Other

Vibhuti N Singh, MD, MPH, FACC, FSCAI Director, Suncoast Cardiovascular Center; Chair, Cardiology Division
and Cath Labs, Department of Medicine, Bayfront Medical Center; Clinical Assistant Professor, Division of
Cardiology, University of South Florida College of Medicine

Vibhuti N Singh, MD, MPH, FACC, FSCAI is a member of the following medical societies: American College of
Cardiology, American College of Physicians, American Heart Association, American Medical Association, and
Florida Medical Association


Specialty Editor Board
George A Stouffer III, MD Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of
Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology,
University of North Carolina Medical Center

George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College
of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for
Cardiac Angiography and Interventions


Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College
of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

10 of 30 9/3/2011 8:27 AM


Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program
Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University
School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American
Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency
Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas
Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic
Emergency Medicine


Brett C Sheridan, MD, FACS Associate Professor of Surgery, University of North Carolina at Chapel Hill School
of Medicine


Chief Editor
Henry H Ooi, MBBCh Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans
Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Henry H Ooi, MBBCh is a member of the following medical societies: American College of Cardiology, American
Heart Association, Heart Failure Society of America, and International Society for Heart and Lung Transplantation


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