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Heart Failure
Author: Ioana Dumitru, MD; Chief Editor: Henry H Ooi, MD, MRCPI more...
Updated: Jul 13, 2015
Practice Essentials
Heart failure develops when the heart, via an abnormality of cardiac function
(detectable or not), fails to pump blood at a rate commensurate with the
requirements of the metabolizing tissues or is able to do so only with an elevated
diastolic filling pressure. See the image below.
This chest radiograph shows an enlarged cardiac silhouette and edema at the lung bases,
signs of acute heart failure.
Diagnosis
The Framingham criteria for the diagnosis of heart failure consists of the concurrent
presence of either 2 major criteria or 1 major and 2 minor criteria.[1]
Major criteria include the following:
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Radiographic cardiomegaly
Pulmonary edema, visceral congestion, or cardiomegaly at autopsy
Nocturnal cough
Dyspnea on ordinary exertion
A decrease in vital capacity by one third the maximal value recorded
Pleural effusion
Tachycardia (rate of 120 bpm)
Bilateral ankle edema
The New York Heart Association (NYHA) classification system categorizes heart
failure on a scale of I to IV,[2] as follows:
Testing
The following tests may be useful in the initial evaluation for suspected heart
failure[3, 5, 6] :
Complete blood count (CBC)
Urinalysis
Electrolyte levels
Renal and liver function studies
Fasting blood glucose levels
Lipid profile
Thyroid stimulating hormone (TSH) levels
B-type natriuretic peptide levels
N-terminal pro-B-type natriuretic peptide
Electrocardiography
Chest radiography
2-dimensional (2-D) echocardiography
Nuclear imaging [7]
Maximal exercise testing
Pulse oximetry or arterial blood gas
Management
Surgical options
Background
Heart failure is the pathophysiologic state in which the heart, via an abnormality of
cardiac function (detectable or not), fails to pump blood at a rate commensurate with
the requirements of the metabolizing tissues or is able to do so only with an elevated
diastolic filling pressure.
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Heart failure (see the images below) may be caused by myocardial failure but may
also occur in the presence of near-normal cardiac function under conditions of high
demand. Heart failure always causes circulatory failure, but the converse is not
necessarily the case, because various noncardiac conditions (eg, hypovolemic
shock, septic shock) can produce circulatory failure in the presence of normal,
modestly impaired, or even supranormal cardiac function. To maintain the pumping
function of the heart, compensatory mechanisms increase blood volume, cardiac
filling pressure, heart rate, and cardiac muscle mass. However, despite these
mechanisms, there is progressive decline in the ability of the heart to contract and
relax, resulting in worsening heart failure.
This chest radiograph shows an enlarged cardiac silhouette and edema at the lung bases,
signs of acute heart failure.
A 28-year-old woman presented with acute heart failure secondary to chronic hypertension.
The enlarged cardiac silhouette on this anteroposterior (AP) radiograph is caused by acute
heart failure due to the effects of chronic high blood pressure on the left ventricle. The heart
then becomes enlarged, and fluid accumulates in the lungs (ie, pulmonary congestion).
Stage A patients are at high risk for heart failure but have no structural heart
disease or symptoms of heart failure
Stage B patients have structural heart disease but have no symptoms of
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heart failure
Stage C patients have structural heart disease and have symptoms of heart
failure
Stage D patients have refractory heart failure requiring specialized
interventions
Laboratory studies for heart failure should include a complete blood count (CBC),
electrolytes, and renal function studies. Imaging studies such as chest radiography
and 2-dimensional echocardiography are recommended in the initial evaluation of
patients with known or suspected heart failure. B-type natriuretic peptide (BNP) and
N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels can be useful in
differentiating cardiac and noncardiac causes of dyspnea. (See the Workup Section
for more information.)
In acute heart failure, patient care consists of stabilizing the patient's clinical
condition; establishing the diagnosis, etiology, and precipitating factors; and initiating
therapies to provide rapid symptom relief and survival benefit. Surgical options for
heart failure include revascularization procedures, electrophysiologic intervention,
cardiac resynchronization therapy (CRT), implantable cardioverter-defibrillators
(ICDs), valve replacement or repair, ventricular restoration, heart transplantation,
and ventricular assist devices (VADs). (See the Treatment Section for more
information.)
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.[8, 9, 10, 11, 12]
Adaptations
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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 beta1adrenergic 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.
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.[19] 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.
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.
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 beta1adrenergic receptors result in overexpression and promote myocardial hypertrophy.
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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. It also inhibits renin and aldosterone release and,
therefore, adrenergic activation. ANP and BNP are elevated in chronic heart failure.
BNP, in particular, has potentially important diagnostic, therapeutic, and prognostic
implications.
For more information, see the Medscape Reference article Natriuretic Peptides in
Congestive Heart Failure.
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).[21] 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. Some
studies suggest that local production of TNF-alpha may have toxic effects on the
myocardium, thus worsening myocardial systolic and diastolic function.
In diastolic heart failure (heart failure with normal ejection fraction [HFNEF]), the
same pathophysiologic processes occur that lead to decreased cardiac output in
systolic heart failure, but they do so in response to a different set of hemodynamic
and circulatory environmental factors that depress cardiac output.[22]
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 then 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.[23]
LV chamber stiffness
A rise in filling pressure is the movement of the ventricle up along its pressurevolume 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.
Concentric LV hypertrophy
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pressure-volume curve to the left along its volume axis. As a result, ventricular
diastolic pressure is abnormally elevated, although chamber stiffness may or may
not be altered.
Arrhythmias
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 4
broad categories is useful:
Underlying causes
Specific underlying factors cause various forms of heart failure, such as systolic
heart failure (most commonly, left ventricular systolic dysfunction), heart failure with
preserved LVEF, acute heart failure, high-output heart failure, and right heart failure.
Underlying causes of systolic heart failure include the following:
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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.
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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)
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.[24, 25] 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.[26]
Genetics of cardiomyopathy
Epidemiology
Heart failure is the fastest-growing clinical cardiac disease entity in the United
States, affecting 2% of the population
Heart failure accounts for 34% of cardiovascular-related deaths [28]
Approximately 670,000 new cases of heart failure are diagnosed each year
[28]
About 277,000 deaths are caused by heart failure each year [28]
Heart failure is the most frequent cause of hospitalization in patients older
than 65 years, with an annual incidence of 10 per 1,000 [28]
Rehospitalization rates during the 6 months following discharge are as much
as 50% [34]
Nearly 2% of all hospital admissions in the United States are for
decompensated heart failure, and the average duration of hospitalization is
about 6 days
In 2010, the estimated total cost of heart failure in the United States was
$39.2 billion, [35] representing 1-2% of all health care expenditures
The incidence and prevalence of heart failure are higher in blacks, Hispanics, Native
Americans, and recent immigrants from developing nations, Russia, and the former
Soviet republics. The higher prevalence of heart failure in blacks, 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 by substandard preventive health care available to the
most indigent of individuals in these and other groups; in addition, many persons in
these groups do not have adequate health insurance.
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The higher incidence and prevalence of heart failure in recent immigrants from
developing nations are largely due to a lack of prior preventive health care, a lack of
treatment, or substandard treatment for common conditions, such as hypertension,
diabetes, rheumatic fever, and ischemic heart disease.
Men and women have the same incidence and the same prevalence of heart failure.
However, there are still many differences between men and women with heart
failure, such as the following:
The prevalence of heart failure increases with age. The prevalence is 1-2% of the
population younger than 55 years and increases to a rate of 10% for persons older
than 75 years. Nonetheless, heart failure can occur at any age, depending on the
cause.
International statistics
Heart failure is a worldwide problem. The most common cause of heart failure in
industrialized countries is ischemic cardiomyopathy, with other causes, including
Chagas disease and valvular cardiomyopathy, assuming a more important role in
developing countries. However, in developing nations that have become more
urbanized and more affluent, eating a more processed diet and leading a more
sedentary lifestyle have resulted in an increased rate of heart failure, along with
increased rates of diabetes and hypertension. This change was illustrated in a
population study in Soweto, South Africa, where the community transformed into a
more urban and westernized city, followed by an increase in diabetes, hypertension,
and heart failure.[36]
In terms of treatment, one study showed few important differences in uptake of key
therapies in European countries with widely differing cultures and varying 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
specific populations.[37, 38] For example, in some countries, hypertensive heart
failure carries a 25% 1-year mortality rate, and human immunodeficiency virus
(HIV)associated cardiomyopathy generally progresses to death within 100 days of
diagnosis in patients who are not treated with antiretroviral drugs.
While data regarding developing nations are not as robust as studies of Western
society, the following trends in developing nations are apparent:
Prognosis
In general, the mortality following hospitalization for patients with heart failure is
10.4% at 30 days, 22% at 1 year, and 42.3% at 5 years, despite marked
improvement in medical and device therapy.[28, 39, 40, 41, 42, 43] Each
rehospitalization increases mortality by about 20-22%.[28]
Mortality is greater than 50% for patients with NYHA class IV, ACC/AHA stage D
heart failure. Heart failure associated with acute MI has an inpatient mortality of
20-40%; mortality approaches 80% in patients who are also hypotensive (eg,
cardiogenic shock). (See Heart Failure Criteria and Classification).
A study by van Diepen et al suggests that patients with heart failure or atrial
fibrillation have a significantly higher risk of noncardiac postoperative mortality than
patients with coronary artery disease; this risk should be considered even if a minor
procedure is planned.[45]
A study by Bursi et al found that among community patients with heart failure,
pulmonary artery systolic pressure (PASP), assessed by Doppler echocardiography,
can strongly predict death and can provide incremental and clinically significant
prognostic information independent of known outcome predictors.[46]
Higher concentrations of galectin-3, a marker of cardiac fibrosis, were associated
with an increased risk for incident heart failure (hazard ratio: 1.28 per 1 SD increase
in log galectin-3) in the Framingham Offspring Cohort. Galectin-3 was also
associated with an increased risk for all-cause mortality (multivariable-adjusted
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Patient Education
To help prevent recurrence of heart failure in patients in whom heart failure was
caused by dietary factors or medication noncompliance, counsel and educate such
patients about the importance of proper diet and the necessity of medication
compliance. Dunlay et al examined medication use and adherence among
community-dwelling patients with heart failure and found that medication adherence
was suboptimal in many patients, often because of cost.[48] A randomized controlled
trial of 605 patients with heart failure reported that the incidence of all-cause
hospitalization or death was not reduced in patients receiving multi-session self-care
training compared to those receiving a single session intervention. The optimum
method for patient education remains to be established. It appears that more
intensive interventions are not necessarily better.[49]
For patient education information, see the Heart Health Center, Cholesterol Center,
and Diabetes Center, as well as Congestive Heart Failure, High Cholesterol, Chest
Pain, Heart Rhythm Disorders, Coronary Heart Disease, and Heart Attack.
Clinical Presentation
Author
Ioana Dumitru, MD Associate Professor of Medicine, Division of Cardiology, Founder and Medical Director, Heart
Failure and Cardiac Transplant Program, University of Nebraska Medical Center; Associate Professor of
Medicine, Division of Cardiology, Veterans Affairs Medical Center
Ioana Dumitru, MD is a member of the following medical societies: American College of Cardiology, International
Society for Heart and Lung Transplantation, Heart Failure Society of America
Disclosure: Nothing to disclose.
Coauthor(s)
Mathue M Baker, MD Cardiologist, BryanLGH Heart Institute and Saint Elizabeth Regional Medical Center
Mathue M Baker, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.
Chief Editor
Henry H Ooi, MD, MRCPI Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans
Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine
Disclosure: Nothing to disclose.
Acknowledgements
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 AcademyofSciences,and Society for
Academic Emergency Medicine
Disclosure: Nothing to disclose.
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
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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
Disclosure: Nothing to disclose.
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
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
Disclosure: Nothing to disclose.
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
membership; TeraRecon Grant/research funds Consulting; Medscape Reference Honoraria Consulting; Humana
Press Honoraria Other
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
Disclosure: Nothing to disclose.
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
Brett C Sheridan, MD, FACS Associate Professor of Surgery, University of North Carolina at Chapel Hill School
of Medicine
Disclosure: Nothing to disclose.
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
Disclosure: Nothing to disclose.
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
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