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Dilated Cardiomyopathy

  • Author: Vivek J Goswami, MD; Chief Editor: Henry H Ooi, MD, MRCPI  more...
 
Updated: Oct 06, 2014
 

Practice Essentials

Dilated cardiomyopathy is a progressive disease of heart muscle that is characterized by ventricular chamber enlargement and contractile dysfunction with normal left ventricular (LV) wall thickness. The right ventricle may also be dilated and dysfunctional. Dilated cardiomyopathy is the third most common cause of heart failure and the most frequent reason for heart transplantation.

Signs and Symptoms

Symptoms are a good indicator of the severity of dilated cardiomyopathy and may include the following:

  • Fatigue
  • Dyspnea on exertion, shortness of breath
  • Orthopnea, paroxysmal nocturnal dyspnea
  • Increasing edema, weight, or abdominal girth

On physical examination, look for signs of heart failure and volume overload. Assess vital signs with specific attention to the following:

  • Tachypnea
  • Tachycardia
  • Hypertension

Other pertinent findings include the following (the level of cardiac compensation or decompensation determines which signs are present):

  • Signs of hypoxia (eg, cyanosis, clubbing)
  • Jugular venous distension (JVD)
  • Pulmonary edema (crackles and/or wheezes)
  • S 3 gallop
  • Enlarged liver
  • Peripheral edema

Look for the following on examination of the neck:

  • Jugular venous distention (as an estimate of central venous pressure)
  • Hepatojugular reflux
  • a wave
  • Large cv wave (observed with tricuspid regurgitation)
  • Goiter

Findings on examination of the heart may include the following:

  • Cardiomegaly (broad and displaced point of maximal impulse, right ventricular heave)
  • Murmurs (with appropriate maneuvers)
  • S 2 at the base (paradoxical splitting, prominent P 2), S 3, and S 4
  • Tachycardia
  • Irregularly irregular rhythm
  • Gallops

See Clinical Presentation for more detail.

Diagnosis

The workup in a patient with suspected cardiomyopathy may include the following:

  • Complete blood count
  • Metabolic panel
  • Thyroid function tests
  • Cardiac biomarkers
  • B-type natriuretic peptide assay
  • Chest radiography
  • Echocardiography
  • Cardiac magnetic resonance imaging (MRI)
  • Electrocardiography (ECG)

In many cases of cardiomyopathy, endomyocardial biopsy is class II (uncertain efficacy and may be controversial) or class III (generally not indicated). Class II indications for endomyocardial biopsy include the following:

  • Recent onset of rapidly deteriorating cardiac function
  • Patients receiving chemotherapy with doxorubicin
  • Patients with systemic diseases with possible cardiac involvement (eg, hemochromatosis, sarcoidosis, amyloidosis, Löffler endocarditis, endomyocardial fibroelastosis)

See Workup for more detail.

Management

Treatment of dilated cardiomyopathy is essentially the same as treatment of chronic heart failure (CHF). Some therapeutic interventions treat symptoms, whereas others treat factors that affect survival.

Drug classes used include the following:

  • Angiotensin-converting enzyme (ACE) inhibitors
  • Angiotensin II receptor blockers (ARBs)
  • Beta-blockers
  • Aldosterone antagonists
  • Cardiac glycosides
  • Diuretics
  • Vasodilators
  • Antiarrhythmics
  • Human B-type natriuretic peptide
  • Inotropic agents

Anticoagulants may be used in selected patients.

Surgical options for patients with disease refractory to medical therapy include the following:

  • Left ventricular assist devices
  • Cardiac resynchronization therapy (biventricular pacing)
  • Automatic implantable cardioverter-defibrillators
  • Ventricular restoration surgery
  • Heart transplantation

See Treatment and Medication for more detail.

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Background

Dilated cardiomyopathy is a progressive disease of heart muscle that is characterized by ventricular chamber enlargement and contractile dysfunction with normal left ventricular (LV) wall thickness. The right ventricle may also be dilated and dysfunctional. Dilated cardiomyopathy is the third most common cause of heart failure and the most frequent reason for heart transplantation.

Dilated cardiomyopathy is 1 of the 3 traditional classes of cardiomyopathy, along with hypertrophic and restrictive cardiomyopathy. However, the classification of cardiomyopathies continues to evolve, based on the rapid evolution of molecular genetics as well as the introduction of recently described diseases.

Multiple causes of dilated cardiomyopathy exist, one or more of which may be responsible for an individual case of the disease (see Etiology). All alter the normal muscular function of the myocardium, which prompts varying degrees of physiologic compensation for that malfunction.

The degree and time course of malfunction are variable and do not always coincide with a linear expression of symptoms. Persons with cardiomyopathy may have asymptomatic LV systolic dysfunction, LV diastolic dysfunction, or both. When compensatory mechanisms can no longer maintain cardiac output at normal LV filling pressures, the disease process is expressed with symptoms that collectively compose the disease state known as chronic heart failure (CHF).

Continuing ventricular enlargement and dysfunction generally leads to progressive heart failure with further decline in LV contractile function. Sequelae include ventricular and supraventricular arrhythmias, conduction system abnormalities, thromboembolism, and sudden death or heart failure–related death.

Cardiomyopathy is a complex disease process that can affect the heart of a person of any age, but it is especially important as a cause of morbidity and mortality among the world's aging population. It is the most common diagnosis in persons receiving supplemental medical financial assistance via the US Medicare program.

Nonpharmacologic interventions are the basis of heart failure therapy. Instruction on a sodium diet restricted to 2 g/day is very important and can often eliminate the need for diuretics or permit the use of reduced dosages. Fluid restriction is complementary to a low-sodium diet. Patients should be enrolled in cardiac rehabilitation involving aerobic exercise.

For patient education information, see the Heart Center, as well as Congestive Heart Failure.

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Pathophysiology

Dilated cardiomyopathy is characterized by ventricular chamber enlargement and systolic dysfunction with greater LV cavity size with little or no wall hypertrophy. Hypertrophy is judged as the ratio of LV mass to cavity size; this ratio is decreased in persons with dilated cardiomyopathies.

The enlargement of the remaining heart chambers is primarily due to LV failure, but it may be secondary to the primary cardiomyopathic process. Dilated cardiomyopathies are associated with both systolic and diastolic dysfunction. The decrease in systolic function is by far the primary abnormality. This leads to an increase in the end-diastolic and end-systolic volumes.

Progressive dilation can lead to significant mitral and tricuspid regurgitation, which may further diminish the cardiac output and increase end-systolic volumes and ventricular wall stress. In turn, this leads to further dilation and myocardial dysfunction.

Early compensation for systolic dysfunction and decreased cardiac output is accomplished by increasing the stroke volume, the heart rate, or both (cardiac output = stroke volume ´ heart rate), which is also accompanied by an increase in peripheral vascular tone. The increase in peripheral tone helps maintain appropriate blood pressure. Also observed is an increased tissue oxygen extraction rate with a shift in the hemoglobin dissociation curve.

The basis for compensation of low cardiac output is explained by the Frank-Starling Law, which states that myocardial force at end-diastole compared with end-systole increases as muscle length increases, thereby generating a greater amount of force as the muscle is stretched. Overstretching, however, leads to failure of the myocardial contractile unit.

These compensatory mechanisms are blunted in persons with dilated cardiomyopathies, as compared with persons with normal LV systolic function. Additionally, these compensatory mechanisms lead to further myocardial injury, dysfunction, and geometric remodeling (concentric or eccentric).

Neurohormonal activation

Decreased cardiac output with resultant reductions in organ perfusion results in neurohormonal activation, including stimulation of the adrenergic nervous system and the renin-angiotensin-aldosterone system (RAAS). Additional factors important to compensatory neurohormonal activation include the release of arginine vasopressin and the secretion of natriuretic peptides. Although these responses are initially compensatory, they ultimately lead to further disease progression.

Alterations in the adrenergic nervous system induce significant increases in circulating levels of dopamine and, especially, norepinephrine. By increasing sympathetic tone and decreasing parasympathetic activity, an increase in cardiac performance (beta-adrenergic receptors) and peripheral tone (alpha-adrenergic receptors) is attempted.

Unfortunately, long-term exposure to high levels of catecholamines leads to down-regulation of receptors in the myocardium and blunting of this response. The response to exercise in reference to circulating catecholamines is also blunted. Theoretically, the increased catecholamine levels observed in cardiomyopathies due to compensation may in themselves be cardiotoxic and lead to further dysfunction. In addition, stimulation of the alpha-adrenergic receptors, which leads to increased peripheral vascular tone, increases the myocardial workload, which can further decrease cardiac output. Circulating norepinephrine levels have been inversely correlated with survival.

Activation of the RAAS is a critical aspect of neurohormonal alterations in persons with CHF. Angiotensin II potentiates the effects of norepinephrine by increasing systemic vascular resistance. It also increases the secretion of aldosterone, which facilitates sodium and water retention and may contribute to myocardial fibrosis.

The release of arginine vasopressin from the hypothalamus is controlled by both osmotic (hyponatremia) and nonosmotic stimuli (eg, diuresis, hypotension, angiotensin II). Arginine vasopressin may potentiate the peripheral vascular constriction because of the aforementioned mechanisms. Its actions in the kidneys reduce free-water clearance.

Natriuretic peptide levels are elevated in individuals with dilated cardiomyopathy. Natriuretic peptides in the human body include atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide. ANP is primarily released by the atria (mostly the right atrium). Right atrial stretch is an important stimulus for its release. The effects of ANP include vasodilation, possible attenuation of cell growth, diuresis, and inhibition of aldosterone. Although BNP was initially identified in brain tissue (hence its name), it is secreted from cardiac ventricles in response to volume or pressure overload. As a result, BNP levels are elevated in patients with CHF. BNP causes vasodilation and natriuresis.

Counterregulatory responses to neurohormonal activation involve increased release of prostaglandins and bradykinins. These do not significantly counteract the previously described compensatory mechanisms.

The body's compensatory mechanisms for a failing heart are evidently shortsighted. Compensation for decreased cardiac output cannot be sustained without inducing further decompensation. The rationale for the most successful medical treatment modalities for cardiomyopathies is therefore based on altering these neurohormonal responses.

Circulating cytokines as mediators of myocardial injury

Tissue necrosis factor-alpha (TNF-alpha) is involved in all forms of cardiac injury. In cardiomyopathies, TNF-alpha has been implicated in the progressive worsening of ventricular function, but the complete mechanism of its actions is poorly understood. Progressive deterioration of LV function and cell death (TNF plays a role in apoptosis) are implicated as some of the mechanisms of TNF-alpha. It also directly depresses myocardial function in a synergistic manner with other interleukins.

Elevated levels of several interleukins have been found in patients with left ventricular dysfunction. Interleukin (IL)–1b has been shown to depress myocardial function. One theory is that elevated levels of IL-2R in patients with class IV CHF suggest that T-lymphocytes play a role in advanced stages of heart failure.

IL-6 stimulates hepatic production of C-reactive protein, which serves as a marker of inflammation. IL-6 has also been implicated in the development of myocyte hypertrophy, and elevated levels have been found in patients with CHF. IL-6 has been found to correlate with hemodynamic measures in persons with left ventricular dysfunction.

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Etiology

Dilated cardiomyopathy has many causes, including inherited disease, infections, and toxins. Finding a specific cause for an individual case may be difficult, especially in patients with multiple risk factors.

Causes of dilated cardiomyopathy include the following:

  • Genetics
  • Secondary to other cardiovascular disease: ischemia, hypertension, valvular disease, tachycardia induced
  • Infectious: viral, rickettsial, bacterial, fungal, metazoal, protozoal
  • Probable infectious: Whipple disease, Lyme disease
  • Metabolic: endocrine diseases (eg, hyperthyroidism, hypothyroidism, acromegaly, myxedema, hypoparathyroidism, hyperparathyroidism), diabetes mellitus, electrolyte imbalance (eg, potassium, phosphate, magnesium)
  • Nutritional: thiamine deficiency (beriberi), protein deficiency, starvation, carnitine deficiency
  • Toxic: drugs, poisons, foods, anesthetic gases, heavy metals, ethanol
  • Collagen vascular disease
  • Infiltrative: hemochromatosis, amyloidosis, glycogen storage disease
  • Granulomatous (sarcoidosis)
  • Physical agents: extreme temperatures, ionizing radiation, electric shock, nonpenetrating thoracic injury
  • Neuromuscular disorders: muscular dystrophy (limb-girdle [Erb dystrophy], Duchenne dystrophy, fascioscapulohumeral [Landouzy-Dejerine dystrophy]), Friedreich disease, myotonic dystrophy
  • Primary cardiac tumor (myxoma)
  • Senile
  • Peripartum
  • Immunologic: postvaccination, serum sickness, transplant rejection

In many cases of dilated cardiomyopathy, the cause remains unexplained. However, some idiopathic cases may result from failure to identify known causes such as infections or toxins. The idiopathic category should continue to diminish as more information explaining pathophysiologic mechanisms, specifically genetic-environmental interactions, becomes available.

Toxins are a significant cause. Almost a third of cases may result from severe ethanol abuse.

Viral myocarditis

Viral myocarditis is an important entity within the category of infectious cardiomyopathy. Viruses have been implicated in cardiomyopathies as early as the 1950s, when coxsackievirus B was isolated from the myocardium of a newborn baby with a fatal infection. Advances in genetic analysis, such as polymerase chain reaction testing, have aided in the discovery of several viruses that are believed to have roles in viral cardiomyopathies.

Viral infections and viruses associated with myocardial disease may be caused by the following:

  • Coxsackievirus (A and B) [1]
  • Influenza virus (A and B)
  • Adenovirus
  • Echovirus
  • Rabies
  • Hepatitis
  • Yellow fever
  • Lymphocytic choriomeningitis
  • Epidemic hemorrhagic fever
  • Chikungunya fever
  • Dengue fever
  • Cytomegalovirus
  • Epstein-Barr virus
  • Rubeola
  • Rubella
  • Mumps
  • Respiratory syncytial virus
  • Varicella-zoster virus
  • Human immunodeficiency virus

Viral myocarditis can produce variable degrees of illness, ranging from focal disease to diffuse pancarditis involving myocardium, pericardium, and valve structures. Viral myocarditis is usually a self-limited, acute-to-subacute disease of the heart muscle. Symptoms are similar to those of CHF and often are subclinical. Many patients experience a flulike prodrome.

Confirming the diagnosis can be difficult because symptoms of heart failure can occur several months after the initial infection. Patients with viral myocarditis (median age, 42 years) are generally healthy and have no systemic disease.

Acute viral myocarditis can mimic acute myocardial infarction, with patients sometimes presenting in the emergency department with chest pain; nonspecific electrocardiographic (ECG) changes; and abnormal, often highly elevated serum markers such as troponin, creatine kinase, and creatine kinase-MB.

The diagnosis of viral myocarditis is mainly indicated by a compatible history and the absence of other potential etiologies, particularly if it can be confirmed with acute or convalescent sera. An ECG demonstrates varying degrees of ST-T wave changes reflecting myocarditis and, sometimes, varying degrees of conduction disturbances. Echocardiography is a crucial aid in classifying this disease process, which manifests mostly as a dilated type of cardiomyopathy.

Myocarditis is almost always a clinically presumed diagnosis because it is not associated with any pathognomonic sign or specific, acute diagnostic laboratory test result. In the past, percutaneous transvenous right ventricular endomyocardial biopsy has been used, but the Myocarditis Treatment Trial revealed no advantage for immunosuppressive therapy in biopsy-proven myocarditis, so biopsy is not routinely performed in most cases.

If a patient is thought to have viral myocarditis, the initial diagnostic strategies should be to evaluate cardiac troponin I or T levels and to perform antimyosin scintigraphy. Positive troponin I or T findings in the absence of myocardial infarction and the proper clinical setting confirm acute myocarditis. Negative antimyosin scintigraphy findings exclude active myocarditis.

The exact mechanism for myocardial injury in viral cardiomyopathy is controversial. Several mechanisms have been proposed based on animal models. Viruses affect myocardiocytes by direct cytotoxic effects and by cell-mediated (T-helper cells) destruction of myofibers. Other mechanisms include disturbances in cellular metabolism, vascular supply of myocytes, and other immunologic mechanisms.

Viral myocarditis may resolve over several months during the treatment of left ventricular systolic dysfunction. However, it can progress to a chronic cardiomyopathy. The main issue in recovery is ventricular size. Reduction of ventricular size is associated with long-term improvement; otherwise, the course of the disease is characterized by progressive dilation.

Because of an immunologic mechanism of myocyte destruction, several trials have investigated the use of immunomodulatory medications. (Other trials are currently being conducted.) According to Mason et al in 1995, the Myocarditis Treatment Trial demonstrated no survival benefit with prednisone plus cyclosporine or azathioprine in patients with viral (lymphocytic) myocarditis.[2] Randomized trials are under way to evaluate intravenous immunoglobulin as treatment for viral myocarditis.

Familial cardiomyopathy

Familial cardiomyopathy is a term that collectively describes several different inherited forms of heart failure. Familial dilated cardiomyopathy is diagnosed in patients with idiopathic cardiomyopathy who have 2 or more first- or second-degree relatives with the same disease (without defined etiology). Establishing a diagnosis with more-distant affected relatives (third degree and greater) simply requires identifying more family members with the same disease. Genetic screening has been recommended for patients fulfilling the above criteria.

A study by van Spaendonck-Zwarts et al suggested that a subset of peripartum cardiomyopathy is an initial manifestation of familial dilated cardiomyopathy. This may have important implications for cardiologic screening in such families.[3]

Several forms of familial cardiomyopathy have been described, and theories postulate its association with other causes of cardiomyopathy. Inheritance is autosomal dominant; however, autosomal recessive and sex-linked inheritance have been reported.

Several different genes and chromosomal aberrations have been described in studied families. One example is the gene that codes for actin, a cardiac muscle fiber component. Other forms of familial cardiomyopathy involve a strong association with conduction system disease. As research continues, the knowledge database regarding familial cardiomyopathies is likely to expand.[4, 5]

Doxorubicin-induced cardiomyopathy

Anthracyclines, which are widely used as antineoplastic agents, have a high degree of cardiotoxicity and cause a characteristic form of dose-dependent toxic cardiomyopathy. Both early acute cardiotoxicity and chronic cardiomyopathy have been described with these agents. Anthracyclines can also be associated with acute coronary spasm. The acute toxicity can occur at any point from the onset of exposure to several weeks after drug infusion. Radiation and other agents may potentiate the cardiotoxic effects of anthracyclines.

Cardiac injury occurs even at doses below the empiric limitation of 550 mg/m2. However, whether injury results in clinical CHF varies. The development of heart failure is very rare at total doses less than 450 mg/m2 but is dose dependent.

The history of these patients, in addition to having classic heart failure symptoms or symptoms of acute myocarditis, involves a previous history of malignancy and treatment with doxorubicin.

Anatomically, these patients' hearts vary from having bilaterally dilated ventricles to being of normal size. The mechanism of myocardial injury is related to degeneration and atrophy of myocardial cells, with loss of myofibrils and cytoplasmic vacuolization. The generation of free radicals by doxorubicin has also been implicated. Progressive deterioration is the norm for this toxic cardiomyopathy.

Prevention is based on limiting dosing after 450 mg/m2 and on serial functional assessments (ie, resting and exercise evaluation of ejection fraction). The drug should be discontinued if the ejection fraction is less than 0.45, if it falls by more than 0.05 from baseline, or if it fails to increase by more than 0.05 with exercise. Dexrazoxane is an iron-chelating agent approved by the FDA to reduce toxicity; however, it increases the risk of severe myelosuppression.

Cardiomyopathy associated with collagen-vascular disease

Several collagen-vascular diseases have been implicated in the development of cardiomyopathies. These include the following:

  • Rheumatoid arthritis
  • Systemic lupus erythematosus
  • Progressive systemic sclerosis
  • Polymyositis
  • HLA-B12–associated cardiac disease

Diagnosis is based on identification of the underlying disease in conjunction with appropriate clinical findings of heart failure.

Granulomatous cardiomyopathy (sarcoidosis)

Endomyocardial biopsy may be helpful in establishing the diagnosis, especially in sarcoidosis in which the myocardium may be involved. Involvement may be patchy, resulting in a negative biopsy finding. The diagnosis can also be made if some other tissue diagnosis is possible or available in conjunction with the appropriate clinical picture for heart failure. Cardiac involvement in sarcoidosis reportedly occurs in approximately 20% of cases.

Patients have signs and symptoms of sarcoidosis and CHF. Patients rarely present with CHF without evidence of systemic sarcoid. Bilateral mediastinal, paratracheal, and/or hilar lymphadenopathy may be evident.

Noncaseating granulomatous infiltration of the myocardium occurs as with other organs affected by this disease. Sarcoid granulomas can show a localized distribution within the myocardium. The granulomas particularly affect the conduction system of the heart, left ventricular free wall, septum, papillary muscles, and, infrequently, heart valves. Fibrosis and thinning of the myocardium occurs as a result of the infiltrative process affecting the normal function of the myocardium.

Diagnosis involves finding noncaseating granulomas from cardiac biopsy or other tissues. Often, patients present with conduction disturbances or ventricular arrhythmias. In fact, in patients with normal left ventricular function, these conduction disturbances may be the primary clinical feature.

Treatment of cardiac sarcoidosis with low-dose steroids may be beneficial, especially in patients with progressive disease, conduction defects, or ventricular arrhythmias. The true benefit is unknown because of the lack of placebo-controlled studies. This also holds true for the use of other immunosuppressive agents (eg, chloroquine, hydroxychloroquine, methotrexate) in the treatment of cardiac sarcoidosis.

Carnitine deficiency

A carnitine transporter defect is characterized by severely reduced transport of carnitine into skeletal muscle, fibroblasts, and renal tubules. All children with dilated cardiomyopathy or hypoglycemia and coma should be evaluated for this transporter defect because it is readily amenable to therapy, which results in prolonged prevention of cardiac failure. The prognosis for long-term survival in pediatric dilated cardiomyopathy is poor.

Tachycardia-induced cardiomyopathy

Generally, when detected early, this type of cardiomyopathy is reversible once treatment of the tachycardia is successful. Common etiologies include chronic untreated atrial fibrillation with rapid ventricular response and frequent (several thousand daily) premature ventricular contractions. Persistent tachycardia is known to lead to myocyte dysfunction and cardiomyopathy. If the tachycardia-induced cardiomyopathy is left untreated, the left ventricular dysfunction can become irreversible. The exact mechanisms by which tachycardia affects cell function are poorly understood. The following are possible mechanisms by which myocyte dysfunction arises from tachycardia:

  • Depletion of energy stores
  • Abnormal calcium channel activity
  • Abnormal subendocardial oxygen delivery secondary to abnormalities in blood flow
  • Reduced responsiveness to beta-adrenergic stimulation
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Epidemiology

The true incidence of cardiomyopathies is unknown. As with other diseases, authorities depend on reported cases (at necropsy or as a part of clinical disease coding) to define the prevalence and incidence rates. The inconsistency in nomenclature and disease coding classifications for cardiomyopathies has led to collected data that only partially reflect the true incidence of these diseases.

Whether secondary to improved recognition or other factors, the incidence and prevalence of cardiomyopathy appear to be increasing. The reported incidence is 400,000-550,000 cases per year, with a prevalence of 4-5 million people.

Cardiomyopathy is a complex disease process that can affect the heart of a person of any age, and clinical manifestations appear most commonly in the third or fourth decade.

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Prognosis

Although some cases of dilated cardiomyopathy reverse with treatment of the underlying disease, many progress inexorably to heart failure. With continued decompensation, heart transplantation may be necessary.

The prognosis for patients with heart failure depends on several factors, with the etiology of disease being the primary factor. Other factors play important roles in determining prognosis; for example, higher mortality rates are associated with increased age, male sex, and severe CHF. Prognostic indices include the New York Heart Association functional classification.

The Framingham Heart Study found that approximately 50% of patients diagnosed with CHF died within 5 years.[6] Patients with severe heart failure have more than a 50% yearly mortality rate. Patients with mild heart failure have significantly better prognoses, especially with optimal medical therapy.

A study by Yamada et al indicated that in patients with nonischemic dilated cardiomyopathy, low peak oxygen consumption (VO2) and the presence of late gadolinium enhancement (LGE) on cardiovascular MRI increase the likelihood of cardiac events (ie, cardiac death, lethal arrhythmia, hospitalization for decompensated heart failure). In the study, of 57 patients with dilated cardiomyopathy, Yamada and colleagues determined over a 71-month follow-up period (± 32 months) that in patients with both LGE and a peak VO2 of less than 18.5 mL/kg/min, the incidence of cardiac events was higher than in patients with no LGE and a peak VO2 of 18.5 mL/kg/min or greater or in those with either LGE or a peak VO2 of less than 18.5 mL/kg/min. Multivariate analysis indicated that LGE and peak VO2 are independent prognostic factors.[7]

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Contributor Information and Disclosures
Author

Vivek J Goswami, MD Director of Nuclear Cardiology, Austin Heart; Clinical Assistant Professor, Texas A&M Health Science Center College of Medicine

Vivek J Goswami, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Medical Association, Illinois State Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Amer Suleman, MD Private Practice

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, Society for Cardiovascular Angiography and Interventions, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine

Disclosure: Nothing to disclose.

Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH Professor of Medicine, Director of CME Programs, Team Leader, Root Cause Analysis, Tulane University Heart and Vascular Institute; Director of In-Patient Cardiology, Tulane Service, University Hospital; Visiting Physician, Medical Center of Louisiana at New Orleans; Faculty, Pennington Biomedical Research Institute, Louisiana State University; Professor, Tulane University School of Medicine

Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH is a member of the following medical societies: Alpha Omega Alpha, American Chemical Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Society for Pharmacology and Experimental Therapeutics, American Society of Hypertension, American Thoracic Society, Heart Failure Society of America, National Lipid Association, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Murat M Celebi, MD Clinical Assistant Professor of Medicine, Louisiana State University School of Medicine in New Orleans; Consulting Staff, Crescent City Cardiovascular Associates

Murat M Celebi, MD is a member of the following medical societies: American College of Cardiology, Louisiana State Medical Society, Heart Rhythm Society, Orleans Parish Medical Society

Disclosure: Nothing to disclose.

Frank E Wilklow, MD Principal Investigator, Sub-Investigator, Cardiovascular Research Lab, Louisiana State University Health Sciences Center; Principal Investigator, Sub-Investigator, Gulf Regional Research and Education

Frank E Wilklow, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians

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

Uche A Blackstock, MD Staff Physician, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate

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

Disclosure: Nothing to disclose.

Robert E Fowles, MD Clinical Professor of Medicine, University of Utah College of Medicine; Consulting Staff, Intermountain Medical Center and LDS Hospital; Director and Consulting Staff, Department of Cardiology, Salt Lake Clinic

Robert E Fowles, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Heart Association

Disclosure: Nothing to disclose.

A Antoine Kazzi, MD Chair and Medical Director, Department of Emergency Medicine, American University of Beirut, Lebanon

A Antoine Kazzi, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Heather Murphy-Lavoie, MD, FAAEM Assistant Professor, Section of Emergency Medicine and Hyperbaric Medicine, Louisiana State University School of Medicine in New Orleans; Clinical Instructor, Department of Surgery, Tulane University School of Medicine

Heather Murphy-Lavoie, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society

Disclosure: Nothing to disclose.

Ronald J Oudiz, MD, FACP, FACC, FCCP Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Director, Liu Center for Pulmonary Hypertension, Division of Cardiology, LA Biomedical Research Institute at Harbor-UCLA Medical Center

Ronald J Oudiz, MD, FACP, FACC, FCCP is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Heart Association, and American Thoracic Society

Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research funds Clinical Trials + honoraria; LungRx Clinical Trials + honoraria; Bayer Grant/research funds Consulting

Charles Preston, MD Clinical Associate Professor, Department of Medicine, Section of Emergency Medicine, Charity Hospital, Louisiana State University

Charles Preston, MD is a member of the following medical socities: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Richard H Sinert, DO Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine

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 Reference Salary Employment

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